Neuropsychology Boards Integrated Study Notes 2006
Galit A. Dori, Ph.D.
Page 1
A clinical neuropsychologist is a professional psychologist trained in the science of brainbehavior relationships.
The clinical neuropsychologist specializes in the application of assessment and intervention
principles based on the scientific study of human behavior across the lifespan as it relates
to normal and abnormal functioning of the central nervous system.
(Houston Conference)
STUDY SOURCES
Adams, Victor & Rooper (1996) Principles of Neurology
**Blumenfeld, (2002) Neuroanatomy through Clinical Cases
* Darby & Walsh (2005) Walsh’s Neuropsychology: A Clinical Approach
Feinberg & Farah (1997) Behavioral Neurology and Neuropsychology
Goldberg (2000) Clinical Neuroanatomy Made Ridiculously Simple
*Heilman & Valenstein (2003) Clinical Neuropsychology
*Hendelman (2000) Atlas of Functional Neuroanatomy
**Kaufman (2001) Clinical Neurology for Psychiatrists
Kolb & Whishaw (1990) Fundamentals of Human Neuropsychology
**Lezak (2004) Neuropsychological Assessment
**Loring (1999) INS Dictionary of Neuropsychology
Mesulam (2000) Principles of Behavioral and Cognitive Neurology
Sattler (1992) Assessment of Children
**Sidman & Sidman (1965) Neuroanatomy: A Programmed Text
*Snyder, Nussbaum & Robins (2006) Clinical Neuropsychology: A Pocket Handbook for
Assessment
*Spreen & Strauss (1998) A Compendium of Neuropsychological Tests
** a must
* highly recommended
your choice
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Neuropsychology Boards Integrated Study Notes 2006
Galit A. Dori, Ph.D.
Page 2
A
Abasia – inability to walk
Agensia – loss of taste
Agrammatism – loss of function words and words endings; also known as telegraphic speech
Alexithymia – difficulty recognizing and describing own emotions
Aphagia – decreased eating
Aphrosexia – disturbance of attention and concentration associated with psychomotor insufficiency,
complaints include difficulty remembering and keeping the mind on a task, associated with
insomnia and fatigue
Atrophy – tissue wasting associated with a reduction in the size and number of cells
B
Bradyphrenia – abnormal slowness of mentation
C
Categorical perception – perception of distinct sounds resulting from a continuous change in physical
characteristics of speech
Chronotarxis – inability to identify date, time of day, or season
Classical conditioning – a neutral (conditioned) stimulus becomes capable of eliciting a response by
pairing with an unconditioned stimulus
Cognition – mental processes associated with attention, perception, thinking, learning, and memory
Competency – capacity to make personal decisions and manage one’s financial affairs
Comportment – appetite, grooming, activity, social behavior
Conation – a constant willing or desire, volition, or striving, including instincts, drives, wishes and
cravings
Confusion – disorientation to time and place
Contracture – a permanent tightening of muscle, tendons, ligaments, or skin that prevents normal
movement and often result in deformity, develops from immobilization or inactivity
Craniotomy – a surgical opening of the skull for access to the brain
Critical flicker fusion – temporal frequency at which a rapidly flashing visual stimulus appears to be a
steady light
Crowding –
1. a decline in visuospatial abilities associated with a shift in language dominance to the right
cerebral hemisphere following left hemisphere damage early in life
2. the tendency to copy several stimuli into a space intended for a single item, to copy a shape
on top of the original stimuli, or to incorporate the original stimuli into the copy (closing-in);
associated with unilateral visual neglect
Current Procedural Terminology (CPT) – a list of descriptive terms associated with digit codes that is
used in reporting medical services and procedures
Cutaneous sense – the sense of pressure, pain, cold, warmth, and touch; receptors lie beneath the skin or
in the mucous membranes
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Neuropsychology Boards Integrated Study Notes 2006
Galit A. Dori, Ph.D.
Page 3
D
Decubitus/pressure ulcer – bedsore occurring from constant pressure restricting blood flow or continuous
exposure to chemical or mechanical irritation (e.g., urine, plaster cast)
Deep structure – the underlying meaning of a spoken or written expression
Delayed response tasks – tasks developed to assess memory in primates in which the animal is required
to remember the location of a reward until a response is permitted (match-to-sample or response
alteration)
Demyelination – destruction of the myelin sheath surrounding a nerve fiber that disrupts neural
conduction; most common is MS but also from leukodystophies (metabolically related), viruses,
and toxins; most common peripheral demyelinating disease is Guillain-Barré
Denervate – a block of a nerve from its normal connections
Derivational error – a reading, writing or speaking error at the single word level in which the correct
morphemic root is retained but differs in part of speech (e.g., “confuse” for “confusion”)
Differential reinforcement of appropriate behavior – behavior modification through reinforcing
prosocial behaviors and ignoring inappropriate behaviors
Disorientation – confusion or loss of information about ones location in time, space (place), social
surroundings (persons in immediate surrounding), and recent events leading to all three
(circumstances); impaired orientation to self-identity usually due to psychological disturbance;
nonresponsiveness to name calling seen in psychosis, cerebral disease, and sensory/motor deficits
Displacement – memory process by which information is lost from one’s attention span or STM
because of the arrival of new information (e.g., Trigrams)
Dissociation – loss of mental integration in which mental processes become separated from normal
consciousness (such as on “automatic pilot”); may be used to describe incongruity between
emotional responses and cognitive content or between verbal expression and actions
Double dissociation – technique in which two functions are found to be selectively and independently
affected
Drug potentiation – the synergistic action of two or more drugs that is greater than their additive effects
Dual task performance – experimental technique in which two tasks are simultaneously performed; tasks
sharing common resources will interfere with each other and will be performed less quickly and
with more errors than tasks with non-overlapping demands
Dysfluent speech – disturbed speech rhythm; most commonly associated with stuttering
Dysphoria – unpleasant mood or affect including anger, irritability, sadness, jealousy, anxiety, fear,
restlessness, or malaise
Dysplasia – abnormal tissue development
Dystrophy – degeneration with loss of function
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Neuropsychology Boards Integrated Study Notes 2006
Galit A. Dori, Ph.D.
Page 4
E
Echographia – pathological copying of written material
Ecphory – the process by which retrieval cues interact with stored information during the reconstruction
of information into memory
Electroconvulsive Therapy (ECT) – form of treatment for depression, schizophrenia (e.g., catatonia) and
bipolar disorder in which an electrical current is passed through the brain to produce a
generalized seizure
Electrolyte imbalance – a condition of disturbed electrolytes (e.g., sodium, potassium) commonly
produced by extreme dietary insufficiency or dehydration GI abnormalities (e.g., vomiting,
diarrhea) that may give rise to an acute confusional state
Emotional lability – abnormal variability in emotional expression characterized by repetitive and abrupt
shifts in affect; common in mania, delirium, and orbitofrontal lobe damage
Epicritic – the discrete quality of somatosensory stimulation including light or localized touch, light
pressure, sharp pain, and temperature stimulation
Errorless learning – learning in which errors are prevented during the training process; more efficient than
trial and error learning for neurological impairment, especially severe anterograde amnesia
Errors of action – functional breakdown in the perception-action cycle, particularly misuse of objects and
sequencing deficits; overlaps with behaviors attributed to apraxias, agnosias, and severe
attentional disturbance
Extinction – in learning theory, the discontinuation of a learned response after cessation of reinforcement
Extinction burst – dramatic increase in response frequently following withdrawal of reinforcement,
followed by rate decrease or cessation of behavior
Extubation – removal of an endotracheal or tracheostomy tube
F
Face-Hand Test –
1) technique used to demonstrate psychogenic hemiparesis; paretic arm is raised above the face
and dropped; those with psychogenic hemiparesis typically avoid hitting their face
2) method of double simultaneous stimulation to assess tactile extinction (a hand and face, both
hands, or both cheeks)
Fantastic confabulation – confabulation based on fictitious events that could not possibly have happened
to the individual
Featural analysis – perceptual process whereby a percept is constructed by analysis of the individual
features
Fluent speech – easily articulated verbal output that is normal in quantity (50-200 words/minute), phrase
length (5-8 words/phrase), prosody/melody, articulation, and content
Fundus – the portion of an organ that is farthest away from its opening (e.g., the fundus of the eye
contains the optic disk, optic nerve, and blood vessels)
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Neuropsychology Boards Integrated Study Notes 2006
Galit A. Dori, Ph.D.
Page 5
G
Galvanic Skin Response (GSR) – activity of sweat glands that is accompanied by changes in voltage and
resistance of the skin; often used to record levels of arousal and emotion
Genetic imprinting – when the same autosomal dominant abnormality produces different syndromes
depending on whether it is transmitted maternally or paternally (e.g., Prader-Willi/Angelman)
Give-way weakness – a sign of poor effort during muscle strength testing that may be due to psychogenic
illness, malingering, or pain; when requested to prevent the examiner from moving the affected
limb during strength training, muscle resistance is only briefly present and then returns to no
resistance; in contrast, patients with neurologic injury display fairly consistent resistance,
gradually giving way to force
Grapheme – a letter or letter combination that represents a specific sound or phoneme
H
Hallucination – false perceptual experiences in the absence of sensory stimuli; auditory most common in
psychiatric disorders, olfactory and gustatory most common in epilepsy and migraines, tactile
most common in drug intoxication; visceral most common in schizophrenia
HEENT – head, eyes, ears, nose, and throat
Hemosiderin – protein residual of the breakdown of blood; on the brain this can cause siderosis
(nervous system dysfunction)
Heterophone – a word with two alternative pronunciations (e.g., read)
Heterotopic ossification – abnormal bone growth into joint space of the arms and legs, causing pain and
contracture; frequently occurs after severe TBI
Homeopathic dosage – a medication dosage that is smaller than that required to produce a therapeutic
effect
Homonymous – having the same effect on both sides
Homophone – words having the same pronunciation but different spelling and meaning
Hyperesthesia – increased sensitivity to sensory stimulation such as pain or touch
Hypertelorism – an abnormally large distance between the eyes
Hypertrophy – enlargement in tissue bulk that is not due to tissue formation
Hypesthesia – decreased sensitivity to stimulation
Hypotelorism – abnormal closeness of eyes
I
Iatrogenic effect – unfavorable and unintended response to medical or surgical treatment that results from
the treatment itself
Idioglossia – unintelligible speech
Idiopathic – a disease process of unknown cause
Imperception – impairments in visual perception and spatial thinking
J
Just-noticeable-difference – the smallest change in the value of a stimulus that can be detected as
different from the comparison stimulus
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Neuropsychology Boards Integrated Study Notes 2006
Galit A. Dori, Ph.D.
Page 6
K
Karyotype – the chromosomal characteristics of an individual
Kinesthesia – perception of various parameters of movement (e.g., range, extent, direction, force,
momentum) generated by receptors in the muscles, tendons, and joints
L
La belle indifference – lack of concern for sensory and motor impairment, commonly applied to
psychogenic conditions
Labile – unstable, easily changed
Language – a communication system of symbolic expression that has an organized grammar and syntax
to convey semantic content
Learning – the process of acquiring new information into memory
Leucotomy/leukotomy – surgical separation of thalamo-frontal fibers, used with mood disorders; become
concrete, difficulty maintaining and shifting set, disassociation between verbalizations and
actions
Leukoaraiosis – attenuation of the cerebral white matter
Lexicon – knowledge of the phonological representation and grammatical aspects of words
Lipid – elements that are fat soluble
Lipophilic – solvents that readily permeate the nervous system and damage lipid-rich myelin, causing
neuropathy and encephalopathy (e.g., glu–n-hexane)
Lipoprotein – compound containing lipids and proteins, with the higher the density the lower the lipid
content; Low-density lipoprotein (LDL) associated with increased risk of coronary artery disease
and stroke, HDL may reduce risk
Lobectomy – surgical resection of a lobe or portion of a lobe in the brain; most common is anterior
temporal lobectomy for seizure control
Lobotomy – surgical destruction of tracts and cell bodies to isolate a cerebral lobe
Lymphocyte – type of white blood cells; can become T cells or B cells
M
Malignant – a condition that is progressive or fatal
Mass effect – impaired brain function from increased intracerebral/intracranial volume
Mental agraphia – metaphorical term for the inability to put thoughts into written phrases
Method of Loci – mnemonic technique in which to-be-remembered items are visualized in separate
locations within an imaginary space
Mirror reading – an implicit memory task in which the reflected images of words are read
Mirror tracing/drawing – an implicit memory task in which a shape is traced or copied while viewing the
shape and hand in a mirror
Mnemonics – techniques or devices for improving memory
Mood – prevailing and sustained subjective emotional state or experience (e.g., anger, elation, depression)
Morbidity – any deviation from psychological or physiological well-being
Morpheme – the smallest unit of meaning in a language, including words as well as meaningful prefixes,
suffixes, and affixes
Mortality – a fatal outcome
Multidimensional scaling – multivariate technique used to assess the scaling of a stimulus through
similarities and differences (e.g., is A more similar to B or C)
Myalgia – muscle pain
Myelitis – inflammation of the spinal cord
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Neuropsychology Boards Integrated Study Notes 2006
Galit A. Dori, Ph.D.
Page 7
Myopathy – disorder of the muscle
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certification process, but there is no guarantee that they will work for you. The notes’ authors, web site host, and everyone else involved in the
creation and distribution of these study notes make no promises as to the complete accuracy of the material, and invite you to suggest changes.
Neuropsychology Boards Integrated Study Notes 2006
Galit A. Dori, Ph.D.
Page 8
N
Nasolabial fold – a crease running from the sides of the nose to the corners of the mouth; flattening may
indicate facial weakness
Neuralgia – paroxysmal pain that extends along the course of one or more nerves
Neuritis – nerve inflammation accompanied by pain and tenderness; also may be associated with
anesthesia, paresthesias, paralysis, wasting, and reflex disappearance
Neurofibrillary tangles – thickened, twisted strands of neural elements within neurons present in AD,
dementia pugilistica, and other diseases; also present in small numbers in healthy individuals
Neuromuscular junction – the terminal of a motor neuron innervating a skeletal muscle fiber by
acetylcholine
Neuropathy – broad term for functional disturbances or pathological changes in the peripheral nervous
system, often designating nonspecific lesion
Neurotoxin – drugs that kill brain cells
Nociception – perception of painful sensations
Non compos mentis – “not of sound mind”; used to describe not being able to manage one’s own affairs
O
Orthography – the written form of language
Orthostatic hypotension – sudden decline in blood pressure occurring after rapid change in body position
(e.g., from lying to standing)
O-sign – continuous open mouth seen in advanced dementia or severe head trauma
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Neuropsychology Boards Integrated Study Notes 2006
Galit A. Dori, Ph.D.
Page 9
P
Paragrammatism – inaccurate selection of function words
Parallel distributed processing – neural processing with parallel and serial features, with memory and
knowledge dependent on connectivity
Paresthesia – somatic sensation in the absence of external stimulation, generally unpleasant
(e.g., formication – feeling of insects crawling)
Paroxysmal – a sudden onset of symptoms
Pathognomonic signs – findings that are disease specific
Phonation – the utterance of vocal sounds
Phoneme – the smallest, distinct unit of sound that is the basic unit of spoken language
Phonemics – the study of the sound system of a spoken language
Phonetics – the science of vocal sound production and perception
Phonology – the study of speech sounds of a language and the rules behind their production
Physiatrist – a physician specializing in physical medicine and rehabilitation (PM&R) for disorders
affecting the nervous system (e.g., stroke, TBI, spinal cord injury), sports injury, orthopedic
injury, and amputation
Physical therapy (PT) – therapy designed for the evaluation and rehabilitation of mobility limitations
resulting from physical injury, somatic effects or nervous system injury
Polygot – an individual who is fluent in more than one language; may display different patterns of
language impairment and recovery for each language
Pragmatics – the correct use of language within a given context or environment
Praxis – the ability to perform skilled movements
Pre-conscious processing – stimulus processing that occurs before, or in the absence of, awareness
Prevalence – the total number of cases of a particular phenomenon that develops within a given period
Prion – a protein particle smaller than a virus that may infect cells and reproduce itself (e.g.,
Creutzfeldt-Jakob, kuru)
PRN – as needed (“pro re nata” - as the occasion rises)
Probability – frequency of an occurrence of an event relative to the number of opportunities for the
event to occur
Procedural discourse analysis – a technique commonly used when analyzing a person’s communication
abilities in which they are asked to describe the procedures associated with an act or skill (e.g.,
cohesion)
Prodrome – symptoms that signal the approach of a full-blown clinical disease
Prepositional/symbolic language – means of linguistic exchange that substitutes articulated sounds,
gestures, or marks for objects, persons, and concepts so that novel relationships can be expressed
Prosody – a component of speech that conveys meaning through pitch, loudness, tempo, stress, and
rhythm; conveys emotional content
Prosthesis – a device used to replace a missing body part; the term cognitive prosthesis is used to
describe compensatory devices (e.g., memory books, to-do lists)
Psychogenic – having a psychological or psychiatric etiology
Psychometrics – the measurement of psychological functions and individual behavioral differences
Psychomotor – the motor effect of cognitive or behavioral activity
Psychomotor retardation – slowed mental and motor activity that may be a common feature of both
psychiatric and neurological illness
Pursuit rotor task – manual tracking task used in the assessment of procedural learning skills
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Neuropsychology Boards Integrated Study Notes 2006
Galit A. Dori, Ph.D.
Page 10
Q
Q-sign – colloquial term for an open mouth with a deviated tongue, often seen in severe acute stroke
Quality of life – the characterization of health concern or disease effects on patient lifestyle and daily
functioning from the patient’s perspective
Quantitative data – data represented numerically, either continuous or discrete
R
Radiculopathy – lesion of the nerve root
Reversal/transposition/sequencing error – reading error due to the reversal of letters
Rule-based reading – phonologically based process in which words are sounded out, occurring
from grapheme-to-phoneme/print-to-sound conversion rules
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Neuropsychology Boards Integrated Study Notes 2006
Galit A. Dori, Ph.D.
Page 11
S
Segmentation – a process during reading by which a string of letters is broken down into graphemic
segments that are then assigned phonology
Semantic – word meanings and the rules for their use
Semantic system – cognitive system for the representation of meaning
Semiology – symptomatology
Serial learning – any learning task in which items to be learned are presented over multiple trials
Shadowing – a dichotic listening task in which the message presented to one ear is repeated by the subject
while a competing message presented to the contralateral ear must be ignored
Signal detection theory – ability to detect the presence of a signal from background noise, based on
perceptual sensitivity and certainty that a threshold for detection has been reached (response
bias); incorporates speed-accuracy tradeoff; used to characterize response style for recognition
memory testing
Somatic – pertaining to the body, in contrast to viscera
S/p – status post; the event being described has already occurred
Speech – the process of language (symbol-based representation) vocalization; may be disrupted by brain
lesions (generally perisylvian) and injuries to peripheral muscles and nerves that serve
articulation and vocalization
Speech-language pathology – the study of speech and language disorders and their treatment
Speech pragmatics – nonlinguistic social rules of verbal communication, including initiating and
terminating speech, maintaining eye contact, and staying on topic
Speech rate – the rate of spontaneous, conversational speech; normally at least 100 words per
minute; slow speech is associated with anterior lesions (i.e., expressive or Broca’s aphasia)
Speech therapy – therapy to maximize the recovery of speech and language in individuals with acquired
language impairment or to facilitate speech and language development in children with
developmental disorders, central and noncentral (e.g., stuttering, phonation difficulty)
Speed-accuracy tradeoff – a phenomenon associated with tests requiring response accuracy that must be
performed within a limited time
Splitting the midline – a sign of psychogenic sensory loss in which sensory perception stops abruptly at
the midline of the body, but should not occur because normal sensory fibers spread across the
midline
Spontaneous speech – spoken discourse produced at the discretion of the speaker
Stenosis – narrowing of vessel wall
Stereograms – meaningful visual stimuli that can be identified only with binocular vision
Subacute – between acute and chronic; denotes a disease course of moderate duration
Subclinical – the presence of a disease without associated symptoms
Supine – the position of lying down with face upward
Supported employment – subcompetitive employment model in which disabled persons are supported by
job coaching or by specialized training and supervision in an enclave/crew
Surface structure – the specific linguistic form of an utterance
Sx – shorthand notion for “symptom”
Syndrome – signs and symptoms that often occur together and that suggest a common etiology,
prognosis, and treatment
Synesthesia – multisensory perception from single sensory stimulation, such as “hearing” colors and
“seeing” sounds
Syntax – the rules of language structure governing the assembly of words into coherent and
meaningful sentences
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Neuropsychology Boards Integrated Study Notes 2006
Galit A. Dori, Ph.D.
Page 12
T
Tachistoscope – an apparatus that allows for brief presentation of visual stimuli
Temporal context – contextual knowledge that allows events to be discriminated in time
Transelectrical nerve stimulation (TENS) – an approach to pain treatment in which electrical stimulation
is applied to the nerve to decrease its sensitivity
Tip-of-the-tongue-phenomenon – inability to retrieve word despite knowledge of meaning and phonology
Topectomy – a surgical resection of a small area of cortex
Topographical disorientation – the inability to find one’s way about, as in mental or paper maps
Tracheostomy/tracheotomy – an opening of the neck to allow placement of a tube through the trachea to
establish a direct airway for artificial ventilation
Trisomy – a genetic abnormality in which there are three rather than two chromosomes
Twist-drill hole – a small hole of several millimeters made into the skull to place intracranial electrodes,
obtain a biopsy, or drain a subdural hematoma
Two-route model – a theory of language processing that postulates two separate means for successful
production; in reading, words can be sounded out or sight read for meaning, and, in writing,
words can be spelled phonetically or from a memorized vocabulary
U
V
Vasculitis – inflammation of a vessel
Ventriculomegaly – enlarged ventricles
Verbal code – the linguistic representation of a word
Vertigo – the illusion of motion involving either the environment or self
Viscosity – an interpersonal style characterized by cohesive and “sticky” behavior that produces
prolonged contact, with speech repetitive and circumstantial; seen in some epilepsy patients
W
Word attack – a reading strategy in which a string of letters is segmented before they are read
X
Y
Yerkes-Dodson law – a relationship between anxiety and performance in which performance is facilitated
by mild anxiety, but after a certain point increasing anxiety produces a rapid performance decline
(∩)
Z
Zebra – a colloquial expression for the diagnosis of a rare condition given a constellation of common
clinical signs
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Neuropsychology Boards Integrated Study Notes 2006
Galit A. Dori, Ph.D.
Page 13
ACALCULIA – acquired disturbance of computational ability
Primary – dominant angular gyrus/inferior parietal lobule, dominant or nondominant perisylvian lesion
Spatial – impaired spatial organization affecting computation (misalignment, number reversal);
post-rolandic lesion of right hemisphere
Left parietal – inability to read or write numbers
Left – alexia for arithmetic signs
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Neuropsychology Boards Integrated Study Notes 2006
Galit A. Dori, Ph.D.
Page 14
AGNOSIA
Loss of meaning not due to sensory deficit, attentional disturbance, or naming disorder; only in single
sensory modality (Freud 1891, Lissauer 1890); test visual fields and acuity, color perception,
anomia/confrontation naming, aphasia, apraxia, apperception (matching, drawing, copying), perception
(figure/ground, closure), visual memory (objects, faces), associations (sorting, usage)
-
-
-
-
Ahylognosia – impaired discrimination of distinctive qualities of objects such as density, weight,
texture, heat
Amorphognosia – impaired identification an object by proprioception/recognition by size and
shape
Apperceptive agnosia – impaired perception (e.g., visual shape and object naming)
 Visual – unable to draw misidentified objects or match to sample; often seen with patchy
visual field defects and recovery from cortical blindness
* bilateral damage to lateral occipital lobes (CO poisoning, mercury, cardiac arrest,
stroke, basilar artery occlusion)
Associative agnosia – impaired attribution of meaning
 Visual – can draw objects and match to sample but not identify; associated with right
homonymous hemianopia
*typically from bilateral occiptotemporal lesions (PCA strokes)
Astereognosis/Somatosensory agnosia – loss of higher-order tactual recognition with intact
elementary recognition (e.g., shape, size, weight, texture)
Auditory affective agnosia – impaired comprehension of prosody; associated with neglect
* right temporoparietal lesions
Auditory sound agnosia – inability to recognize meaningful nonspeech auditory stimuli
* nondominant temporal
Autotopagnosia – inability to identify body parts (e.g., finger; also Lt-Rt confusion)
* dominant parietal region
Barognosia – inability to estimate weight when objects are placed in the affected hand
Color agnosia – unable to name colors yet perform normally on tasks of color perception
 Central achromatopsia – loss of color vision due to CNS disease, but can name color of
object described verbally; associated with visual agnosia and prosopagnosia
* visual association cortex
 Color anomia – loss of color naming, often in conjunction with alexia without agraphia,
associated with right homonymous hemianopia
* left occ-temp mesial lesion/lingual gyrus, extending into CC
 Specific color aphasia – can sort colors and name, associated with aphasia
Color amnesia – loss of knowledge about color in the context of normal color vision; involves
forgetting how objects with intrinsic color should be colored
Cortical deafness – lack of awareness of/ability to interpret auditory stimuli
* bilateral auditory radiations or primary auditory cortex (Heschl’s gyrus)
Metamorphopsia – objects can be identifies but look odd (fragmented, compressed, tilted,
macroposia, micropsia)
Nonverbal auditory agnosia – understand speech but cannot identify nonverbal sounds
* nondominant superior temporal gyri
Olfactory agnosia – smell but can’t discriminate/recognize
Optic aphasia – visually presented objects can be recognized but not named; auditory and tactile
naming intact
Phonagnosia – inability to recognize familiar voices
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Prosopagnosia – inability to recognize familiar faces (associative), associated with color agnosia,
left upper quadrantanopsia common
* bilateral infarct of PCA involving inferior Occ-Temp junction or inferior Par-Occ region;
fusiform gyrus (if unilateral, right hemisphere)
Pure word deafness – intact hearing and comprehension of nonverbal sounds with loss of speech
language comprehension due to disconnection of Wernicke’s area from auditory input; cannot
repeat
* bilateral (or dominant) superior temporal gyri (CVA) or lesion to left auditory area also
cutting off input from contralateral hemisphere
Sensory (receptive) amusia – inability to appreciate various characteristics of heard music
* temporal lobe (dominant if also aphasia)
Simultanagnosia – impaired recognition of whole with preserved ability to describe parts
 Dorsal (bilateral occ-par) – cannot see more than one object at a time
 Ventral (left inferior occ) – can see more than one object at a time
Tactile (apperceptive) – inability to discriminate objects based on physical characteristics of size,
weight, shape, density, or textural cues; often seen with agraphesthesia
* contralateral primary sensory/somatosensory, diffuse areas of perception (e.g., posterior
parietal)
Tactile (associative) – cannot recognize object in hand but can draw object
* inferior parietal cortex
Tactile asymboly – impaired tactile recognition of identify of objects with intact perception of
size, shape, density, weight, texture, heat
Visual object agnosia – inability to recognize, name, or demonstrate use of an object; if static
agnosia, reduced by moving object
* unilateral or bilateral occipitotemporal (lingual, fusiform, parahippocampal gyri)
Theories
Lissauer’s two-stage model (stage):
elementary sensationobject perceptionobject recognitionnaming
(apperception)
(association)
Geschwind (disconnection): disconnection between visual and verbal processes
Marr’s model of 3 types of representation (computational):
primal sketch viewer-centered sketch object-centered sketch
(brightness/shape) (spatial locations)
(surface configuration)
sense
where
what
Damasio’s model (computational): proposes no agnosia without perceptual dysfunction
perception local convergence zones memory binding
(primary and assn cortex)
Ellis and Young’s model (cognitive neuropsychology): recognition by comparing viewer-centered and
object-centered representations to stored structural descriptions of objects known as “object recognition
units”
See Snyder et al. Figures 21.1a, 21.1b
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Page 16
AGRAPHIA
Acquired difficulty in writing or spelling; tested through spontaneous writing, writing to dictation, and
copying
*in isolation (without aphasia) due to damage of dominant superior or inferior parietal lobe
(supramarginal gyrus, angular gyrus) or second frontal gyrus
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Spelling
Deep – impairment in nonlexical spelling, sometimes lexical spelling, and semantic errors; more
trouble with function words than nouns
* supramarginal gyrus or insula, far extending
Surface/Lexical – reliance on spelling by sound
* posterior angular gyrus and parieto-occipital lobule (associated with aphasia)
Phonological – impairment in nonlexical spelling and sometimes lexical (sound-to-letter)
spelling, but no semantic errors
* supramarginal gyrus or insula (associated with alexia), perisylvian region (associated with
aphasia)
Semantic – loss of ability to incorporate meaning, although may be spelled correctly or
homophone
Verbal – cannot combine single letters into words
Jargon – senseless combination of letters or words
Writing
Agraphia with alexia – parietal lobe
Allographic – frequent omissions but well formed letters, copying and oral spelling spared
Aphasic
Apraxic – poor letter formation, poor copy because of impaired program of motor movements,
but oral spelling may be spared
Ideational agraphia (apraxic agraphia without apraxia) – poorly formed graphemes but praxis
intact
* parietal lobe
Pure – poor letter formation, inability to write on a line, writing over the model one is copying
Spatial – slanted, uneven spacing, writing over other words
* usually due to nondominant parietal lesions or frontal lesions
Fluent agraphia – writing of normal quantity and length but with paraphasic errors and lack of substantive
words (e.g., Wernicke, conduction aphasia)
Nonfluent agraphia – effortful, sparse writing, large and messy, spelling errors due to letter omission
(Broca, transcortical motor aphasia)
Optic agraphia – inability to copy words while being able to write from dictation
*lesions in the posterior region of the language-dominant hemisphere
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ALEXIA/DYSLEXIA
Impaired reading and spelling (phonological processing) that does not result from MR, aphasia, cultural
deprivation, lack of motivation to learn, or a psychological disorder
Alexia generally reserved for acquired reading impairment
Dyslexia refers to developmental and acquired reading disability
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Alexia
*Alexia with agraphia (Central) – disturbance of reading and writing; can copy in slavish and
non-comprehensible manner; cannot name letters, read aloud, or comprehend reading; often
accompanied by fluent aphasia, Gerstmann Syndrome, hemisensory loss, right homonymous
visual field defect; also called semantic alexia, parieto-temporal alexia, total (literal and verbal)
alexia, letter and word blindness, surface alexia
* associated with dominant parietal lobe (angular gyrus) lesion, from occlusion of
MCA or distal branches
*Alexia without agraphia (Posterior) – can write but unable to read, can name letters, may
comprehend if spell or pronounce aloud, slavish copy; associated with right homonymous
hemianopia, color naming disturbance; disconnection of visual info from language cortex; also
called pure alexia, visual alexia, verbal alexia, occipital alexia, letter-by-letter reading, word
blindness
* associated with PCA region affecting dominant occipital cortex and posterior corpus
collosum, disconnecting dominant temporo-parietal cortex from visual association cortex
*Literal alexia (Anterior/Frontal) – can read whole words but not recognize individual letters,
severe agraphia, poor copy with omissions, agrammatism, poor spelling; associated with right
hemiplegia, nonfluent aphasia, unilateral sensory/visual field neglect; also called pure letter
blindness
* left frontal lobe, ACA
Alexia with aphasia – reading comprehension and oral reading both impaired
Deep – severe impairment in reading of abstract vs. concrete nouns, modifiers, verbs and functors
vs. nouns, nonwords vs. real words; semantic errors, visual errors, and morphological errors in
prefix or suffix; intact perceptual skills but language dysfunction
Global alexia – total loss of ability to understand written language
Hemi-alexia – inability to read in the left visual field
* posterior CC severed but visual sensory areas intact; right posterior parietal (neglect)
Hemi-spatial alexia – only half the word in read, associated with homonymous visual field or
unilateral attention deficit
Paralexia – substitutions made when reading aloud (literal, semantic, phonemic)
 semantic paralexia (miscomprehension) – substitution of semantically related word;
characteristic of deep dyslexia
 visual paralexia (paraphasic oral reading) – target word is misread with substituted word
sharing many letters with target word
Phonological alexia – impaired sounding out of printed words; substitute real words for
nonwords, poor spelling
* may be related to damage in dominant superior temporal cortex and angular gyrus
Spatial alexia – difficulty keeping location of letters or words or maintaining correct sequence of
lines of print
* right hemisphere dysfunction
Surface – only words that can be sounded out are read and understood, not able to read unusual
pronunciations [includes regularization error, when a word with irregular pronunciation is
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substituted by a word with regular phonemic pronunciation patterns (e.g., “buzzy” for “busy”,
“sue” for “sew”)]; normal language skills but poor visuoperception
* dominant Temp-Par cortex; may have features of Gerstmann
Verbal alexia – can read individul letters but not full words
Dyslexia
Central – a reading disorder affecting lexical and nonlexical reading (deep, phonological,
surface, alexia with agraphia), activating meaning or speech production
Peripheral – visual inputs cannot be associated with stored representation of written
words (attentional, neglect, alexia without agraphia)
Attentional dyslexia – disturbance in reading multiple words, secondary to disturbance in visual
attention, with single word reading preserved
Dyseidetic dyslexia – inability to read words as a whole or as gestalts, words are read and spelled
phonetically, familiar words are sounded out as if not previously encountered
Dysphonetic dyslexia – reading is heavily dependent on sight vocabulary, word attack and
phonetic coding skills are weak, spelling errors are semantic not phonetic
L-type dyslexia – premature reliance on the left hemisphere linguistic strategy through which
semantic and syntactic strategies are generated; results in fast and inaccurate reading and
substantive errors
Mixed dysphonetic-dyseidetic dyslexia – the inability to both develop phonetic-word synthesis
skills and perceive letters and words as visual gestalts
Neglect dyslexia – failure to identify portion of letters or words (mostly on left side)
P-type dyslexia – too much reliance on the right hemisphere that emphasizes perceptual
strategies; reading is accurate but slow and fragmented
Alexia with hemianopsia and achromatopsia suggests dominant Occ-Temp lesion (alexia without
agraphia)
Origin of concept of alexia from case reports by Dejerine (1890s); updated by Geschwind (1962)
Central aphagia – spelling disorder in both written and oral spelling related to linguistic disturbance
Hyperlexia – above-average reading ability in the presence of MR; often with lack of understanding word
meaning
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Page 19
ANOSOGNOSIA
Unawareness of cognitive, linguistic, sensory, and motor deficits, perhaps related to impaired frontal lobe
or parietal lobe functioning; found in hemiparesis, cortical blindness (Anton’s syndrome), Korsakoff’s
amnesia, AD; associated with confabulation
Frontal association – from right or bilateral damage; Geschwind proposes worse on right because of
disconnection from language areas, confabulation to explain what can’t comprehend (not supported);
Bisiach suggests domain specificity
Premorbid personality – associated with insecurity, drive for perfection and superiority
Conscious Awareness System (CAS; Schacter & McGlynn) – conscious awareness received from systems
concerned with specific functions, if low input, lack of awareness (e.g., poor information from parietal
lobe leads to deficient output to frontal lobe)
I. Sensory-Visual denial
1) Hemiplegia – more common on left side (right brain injury), co-occurs with confabulation
a. Anosodiaphoria – lack of concern for serious neurological impairments without denying
their existence, minimize extent of damage in a jocular fashion
b. Somatoparaphrenia – think limb does not belong to them
c. Anosognosic overestimation – overestimate strength of unaffected limb
d. Kinesthetic hallucination – false belief that the limb is moving
e. Phantom supernumerary limb – believe separate limb has appeared on another part of the
body
2) Hemianopia – unaware of visual field cut; associated with larger lesions, more severe
hemiparesis, damage to parietal lobes
a. Anton’s syndrome – unaware of cortical blindness and confabulate; bilateral occipital
lesions
b. Blindsight – perform tasks without conscious visual perception; damage to primary visual
cortex in which residual vision exists in the visual field associated with damage of
cortical areas; occipitotemporal (ventral) pathway
3) Neglect – greater and longer lasting for right hemispheric damage; dissociated from neglect of
somatosensory, motor and visual field cuts
II. Amnesic Syndromes – associated with damage to frontal lobe and diencephalon, not damage to medial
temporal lobe (e.g., AD, Korsakoff)
III. Aphasia – dissociation of awareness of aphasic errors
1) Broca’s – painfully aware of deficits
2) Wernicke’s – often unaware of deficits
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APHASIA/DYSPHASIA
Disorder of symbolic language processing, including naming, fluency, comprehension, and repetition
deficits accompanied by reading and writing impairments; does not include dysarthria (left, frontal lobe)
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Paraphasia – incorrect word selection
*Neologism – invented word
*Phonemic/literal – word distorted by substituting, omitting, or adding phonemic element
*Semantic/verbal – real word substituted for intended word (can be semantically
related or semantically different but still verbal)
 Circumlocution – talking around words or subjects
 Anomia/Dysnomia – impaired ability to name objects or retrieve words
* Temp-Par junction and more general conditions
 Conduite d’approche – successive phonemic approximations toward a target word
Nonfluent (arm more paretic than leg because arm MCA, leg ACA supplied)
Global – nearly complete loss of fluency, comprehension, repetition, naming, reading, and
writing; associated with hemiparesis, hemisensory loss, hemianopsia
* very large lesions affecting dominant frontal-parietal-temporal areas; from MCA
Mixed Transcortical (“isolation”) – isolation of speech area; repetition intact but fluency and
comprehension impaired, unable to name, read, and write
* anterior/posterior border zones affected with perisylvian language areas spared; often from
watershed infarct of MCA-ACA and MCA-PCA, or subcortical lesions, hypoxia, head trauma
Broca’s/Verbal/Expressive/Nonfluent/Anterior/Motor – agrammatic speech limited to function
words, slow speech, dysmelodic, poor repetition, preserved comprehension of single words and
short phrases (although syntax may be impaired); impaired naming with cuing facilitating
performance; poorly formed writing; right hemiplegia common; aware of deficits so frustrated
and depressed
* upper and lower frontal operculum (opercular and triangular inferior frontal gyrus), insula,
adjacent Sylvian fissure, often subcortical involvement; Brodmann’s areas 44 and 45 (near 47, 6,
8, 9, 10); often from CVA of dominant, superior MCA (adjacent to primary motor cortex)
Transcortical Motor/Dynamic – nonfluent and naming difficulties with preserved repetition and
relatively preserved language comprehension
* area superior or anterior to Broca’s or SMA; often from watershed infarct of MCA-ACA
affecting connections to Broca’s area
Fluent
Wernicke’s/Receptive/Fluent/Posterior/Sensory – fluent with semantic paraphasias and severely
impaired comprehension and repetition, naming impaired and cues do not benefit;
jargon aphasia (“word salad”) is an acute expression of Wernicke’s, with fluent speech but may
be incomprehensible and filled with neologisms, paraphasias, and significant perseveration;
logorrhea (excessive and incessant agitated speech characterized by difficulty with grammar, lack
of meaning, and illogical sequences of clauses), may also have anosognosia and/or contralateral,
superior quadrantanopsia; see anger and paranoia
* dominant posterior one-third of the superior temporal gyrus (Heschel’s gyrus and auditory
association cortex); Brodmann’s area 22 (near 37, 39, 40, 41, 42); often from infarct of dominant,
inferior MCA (adjacent to primary auditory cortex)
Transcortical Sensory – speech is fluent and circumlocutory, often with semantic jargon, with
preserved repetition but severely impaired comprehension, naming difficulties; signs include
hemianopsia, visual agnosia, and sensory loss; associated with echolalia; found in late stage AD
* posterior areas along PCA; often from watershed infarct of MCA-PCA affecting
parietal/temporal connections to Wernicke’s area
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Conduction – fluent with severely impaired repetition but relatively preserved language
comprehension and naming, phonemic paraphrases and word finding difficulties; conduite
d’approche/approach behavior; unable to carry out commands or imitate, sometimes hemiparesis
or sensory loss
* posterior perisylvian language areas/supramarginal gyrus in parietal, arcuate fasciculus
Anomic/Amnesic/Nominal/Semantic – word finding and naming difficulties, poverty of
substantive words, circumlocution, few paraphasias, good comprehension, fluent but empty
speech, normal repetition
* left hemisphere, usually temporal lobe/angular gyrus
Other
Perisylvian – impaired repetition
Pure Motor Aphasia/Apraxic Speech/Verbal Apraxia/Aphemia – nonfluent speech marked by
effortful, poorly articulated speech, dysmelodia, dysprosodia, in severe cases mute, with largely
preserved language function demonstrated by the ability to write; often accompanied by akinesia
or paresis of contralateral lower extremity and proximal upper extremity; associated with “foreign
accent”
* small lesions to dominant frontal medial operculum (Broca’s area), SMA, or cingulate gyrus
Subcortical – starts with mutism, or hypophonic voicing (whispering) and hemiparesis and/or
hemisensory loss, improves to paraphasic output, nonaphasic state or residual aphasia; variable
comprehension, repetition, and naming; associated with spastic dysarthria (high pitched, slow and
effortful speech) and hyper/hypokinetic speech (rapid or slow speech with slurred articulation);
usually transient; transcortical aphasia common
* damage to basal ganglia (caudate and putamen), thalamus (often resolves to mild anomia), and
SMA
I. Anterior superior extension – semantic comprehension intact but poor syntactic
comprehension, impaired articulation, short phrases, poor repetition, poor writing,
associated with right hemiplegia
II. Posterior extension – comprehension poor, paraphasias, poor repetition, poor reading
and writing, associated with right hemiplegia
III. Posterior and anterior extension – global aphasia
Crossed aphasia – the occurrence of aphasia in a right-handed patient following right hemisphere
damage; usually based on tumor or trauma and may represent bilateral damage; rare
Developmental dysphasia/aphasia – a language disorder of communication involving failure to develop
language skills normally in the absence of an identifiable neurologic or medical etiology;
primarily expressive, receptive or mixed
Right hemisphere damage – affects prosody, gesturing, emotional aspects, may change vocabulary
selection, responses to complex statements, understanding of metaphors, decreased fluency
Thalamus stimulation (pulvinar and lateral posterior, lateral central complex) – can lead to speech arrest,
naming problems, perseveration, and protracted speech
Pathway between input and output of phonological (speech) and orthographic (print) lexicon and
semantics
Arcuate fasciculus – major association bundle connecting the temporal lobe to the prefrontal cortex,
forming part of the superior longitudinal fasciculus or dorsal pathway; connects Wernicke’s to
Broca’s areas, creating Perisylvian Circuit
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Content/contentive words (open class words) – words with semantic and referential meaning,
consisting primarily of nouns, verbs, adjectives, and adverbs
Function/functor words (closed class) – words primarily conveying grammatical information, such as
articles, auxiliary words, conjunctions, inflections, and pronouns
Word class effects – differential performance of aphasic patients that is related to word type or class; for
example, in Broca’s aphasia omit more function/connecting words than content words (nouns and
verbs) and patients with reading disorders may make more errors reading abstract than concrete
nouns
Word frequency effects – differential performance of aphasic patients that is related to word frequency of
occurrence; in general, high frequency words are less vulnerable to errors in comprehension,
expression, reading, and writing
Phonetic disintegration – a pattern of articulation breakdown associated with aphasia
See Blumenfeld Figure 19.4, Snyder et al. Figure 18.2
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APRAXIA (Steinthal, Liepmann)
Inability to perform learned purposeful movements for reasons other than impaired motor strength,
sensation, coordination, or comprehension (primary motor skills and comprehension intact);
frequently coexists with aphasia (usually cortical or thalamic damage)
Test with gesturing to command, imitation, in response to seeing a tool, and in response to seeing an
object upon which a tool works; discriminate between correct and incorrect movements
pantomimed by the examiner; pantomime and gesture comprehension; serial acts; action-tool and
tool-object association; conceptual knowledge
Programmed mainly by dominant hemisphere
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Ideomotor apraxia – inability to perform transitive (using tool) or intransitive (movement)
gestures on command, performance may or may not be improved with imitation or with the actual
object; common error is using a body part as the object (e.g., hammer, comb); can perform
spontaneously; includes perseverative, sequencing, spatial, postural, verbalization instead of
action, and timing errors; frequently coexists with ideational apraxia; often see bilateral deficits
* lesion of (1) dominant inferior parietal lobe/supramarginal gyrus (seen with conduction aphasia)
or (2) SMA (seen with nonfluent aphasia and hemiparesis) or (3) lesion of CC (no aphasia)
 Colossal/Unilateral – difficulty executing motor sequence of left hand following lesions
of the anterior CC because of disconnect of visuokinetic motor engrams of the left
hemisphere from the motor area of the right hemisphere
Ideational apraxia – inability to perform a series of gestures due to loss or action (ideation) for
movement but can perform individual components; bilateral deficits (e.g., steps to sending letter);
seen in moderately severe dementia with diffuse damage
* large lesion to left parietal lobe
Limb-kinetic/Melokinetic/Innervation – lack of ability to make precise movements with
contralateral limb, clumsiness exceeding weakness or tone impairment, no difficulty in the
selection or sequencing of motor programs is present; typically asymmetric, greater distally, more
in transitive movements (transitioning between movements); and seen with pantomime, imitation,
or the use of real objects
* thought related to contralateral pyramidal motor/premotor area
~~~~~~~~~~~~~~
Apraxia of Speech – difficulty articulating words, practice does not improve
Buccofacial/Oral apraxia – inability to perform movements of face, lips, and tongue on
command; frequently coexists with Broca’s aphasia, dysarthria
* common lesion in dominant central operculum and anterior insula
Conceptual apraxia – inability to perform limb movements on command resulting from
impairment in linking meaning or intent of action to movement plan; movements are well
performed but inaccurate in content
Conduction apraxia – imitation worse than pantomime, with no difficulty comprehending
gestures
Constructional apraxia – inability to copy or assemble items reflecting visual-constructional, not
motor, impairment; associated with dementia and diffuse cerebral impairment
* commonly due to parietal lobe lesions (right – neglect, fragmented, configurational errors; left –
poor planning, omissions)
Dressing apraxia– inability to dress oneself; usually associated with neglect or Balint’s syndrome;
frequent in dementia and confusional states
* right parietal lesions
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Frontal apraxia– inability to perform routine actions because of temporal or sequential
disorganization, action sequence becomes a series of isolated movements; verbal mediation does
not improve performance
Gait apraxia/frontal gait – inability to walk despite the capacity to execute normal walking
movements while lying in bed; may not alternate stepping, foot may seem “magnetized” to floor,
worst when starting to walk, may spontaneously step over obstacle; with dementia, incontinence
* caused by frontal lobe lesions, normal pressure hydrocephalus, and Parkinson Plus syndromes
Graphomotor apraxia/Apraxic agraphia – inability to draw or write despite normal capacity to
hold and manipulate pen or pencil
Ocular apraxia/Oculomotor apraxia/Psychic paralysis of gaze – impaired visual scanning and
volitional eye movement (part of Balint’s syndrome); trouble shifting gaze and maintaining
fixation; vestibular-induced saccades and optico-kinetic nystagmus less severely impaired;
associated with optic ataxia and visual disorientation
* bilateral frontal-parietal lesions
Optic apraxia/Visuomotor apraxia/Optic ataxia – impaired ocular searching movements affecting
visually guided hand movements (part of Balint’s syndrome)
* bilateral posterior parietal lesions
Pantomime agnosia – cannot comprehend or discriminate visual gestures but can perform
gestures normally and imitate
* lesion in dominant temporo-occiptal area
Verbal-Motor dissociation apraxia – imitation and use of objects intact, but difficulty eliciting
correct motor sequences in response to verbal commands
Visuomotor and tactile-motor dissociation apraxia – perform well to verbal commands but
difficulties with visual and tactile stimuli
Disconnection Hypothesis (Liepmann, Geschwind) – disconnection between language areas and
visuokinesthetic engrams, either Wernicke’s to contralateral association area or left to right premotor
areas, or arcuate fasciculus making unable to perform directions understood
Representation/Praxicon Hypothesis (Heilman) – disconnection between visuokinesthetic
engrams/praxicons (cortical movement representations/memories) in inferior parietal lobe to
premotor/motor areas results in poor implementation of skilled movements; would explain apraxia and
inability to recognize correct movement in other
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Page 25
ASSESSMENT
Achievement – maximum performance; recently acquired specific learning
Aptitude – typical performance; innate capacities and older learning
Actuarial/statistical predictions – based on empirically validated relationships between test results and
target criteria (e.g., regression)
Clinical predictions – based on intuition, experience, knowledge (e.g., classification, diagnosis)
Computer Adaptive Testing (CAT) – tailors tests based on previous answers
Computer-Based Tests Interpretation (CBTI)
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Page 26
ATAXIA
Abnormal movements including errors with coordination (rate, range, direction, timing, force) of motor
activity; includes decomposition of movements into component parts, dysmetria (i.e., measuring of
distance; hypermetria when voluntary movements overreach the intended target), dysdiadochokinesia
(i.e., alternating movements), and tremor
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Limb ataxia – lose coordination of limb muscles
* lesion of cerebellar hemispheres
Optic ataxia/apraxia – impaired ocular searching movements affecting visually guided hand
movements (part of Balint’s)
* bilateral posterior parietal lesions
Truncal ataxia – incoordination of the truncal musculature characterized by lurching, unsteady,
and wide-based gait; test tandem walking (heel-toe) and Romberg test (eyes closed); can have
titubation tremor
* tumors of the midline cerebellum (vermis) or chronic alcoholism
Friedrich’s/hereditary spinal ataxia – hereditary (excessive trinucleotide repeats), progressive gait
ataxia; emotional lability may be present, speech may be affected, but cognition unaffected
Appendicular ataxia – movement of extremities affected; dysmetria (past pointing/over- or
undershooting) and dysrhythmia (abnormal rhythm and timing of movements),
dysdiadochokinesia, tremor, myoclonus
* lesions of cerebellar hemispheres and pathways
Sensory ataxia– loss of joint position sense; may improve with visual feedback
*posterior column-medial lemniscus
Spastic ataxia – the combination of spasticity and unsteadiness
Ataxia-hemiparesis caused by lacunar infarcts (contralateral) of corona radiata, internal capsule, or pons
Lesion of pons or prefrontal cortex, hydrocephalus, and disorders of spinal cord also can produce ataxia
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ATTENTION/AROUSAL
Attention – selective awareness or responsiveness, the ability to focus and maintain interest for a
given task or activity
Arousal – state of general alertness
 Tonic – general arousal state, including sleep-wake cycle
 Phasic – sudden increase in attentiveness necessary for rapid response
I. Upper brainstem
1. Ach (pedunculopontine and laterodorsal tegmental nuclei)
2. glutamate (pontomesencephalic) 
II. Thalamus – intralaminar, midline, ventral medial (also receives inhibitory GABA input from thalamic
reticular nucleus)
III. Hypothalamus –
1. histamine (tuberomamillary nucleus in posterior lateral)
IV. Basal forebrain
1. Ach and GABA (nucleus basalis, diagonal band, medial septal) 
V. Cortex
Selective attention, focused attention, sustained attention, response selection and control
Parietal association/inferior parietal cortex – encoding the location of attended objects in space/spatial
selective attention; hemineglect
Frontal heteromodal association – directed and sustained attention, response selection, switching,
searching, eye fields, motor-intention (Dopamine)
Anterior cingulated cortex/limbic pathways – motivating directed and sustained attention, salience
(amygdala, septal nuclei)
Tectum/superior colliculi, pretectal area, and pulvinar – directing visual attention for saccadic
eye movement
Binding = the integration of sensory, motor, emotional, amd mnemonic information from disparate brain
regions into what is perceived as a single unified experience
Mesulum (2000) – Attentional matrix
1. Domain specific – attention processed determined by stimuli (e.g., visual)
2. Domain independent
a. Bottom-up – ascending reticular activating system (ARAS) (not sensory specific)
i. Reticulothalamocortical pathway – cortical arousal after information passed
through thalamus
ii. Extrathalamic pathway – transmitter specific, from brainstem and basal forebrain
to cortex
b. Top-down – cerebral cortex (prefrontal, posterior parietal, limbic lobes)
Posner & Peterson (1990)
1. Functions
a. orienting to sensory events (involuntary)
b. detecting signals for focal processing (voluntary)
c. maintaining vigilant of alert state
2. Systems
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a. posterior for orienting and awareness; dorsal visual pathway, primary cortical
connections to parietal lobe
b. anterior for signal detection; anterior cingulated gyrus, supplemental motor cortex
3. Engagement
a. Engage – pulvinar of thalamus
b. Shift – superior colliculus
c. Disengage – posterior parietal
Mirsky (1996) – factor analysis based; overlaps attention and EF
1. Focus (superior temporal and inferior parietal, corpus striatum) and execute (inferior parietal,
corpus striatum)
2. Sustain (rostral midbrain)
3. Shift (prefrontal, frontal association)
4. Encode (hippocampus, amygdala)
5. Stability (midline thalamus, brainstem)
Cohen, Malloy & Jenkins (1998)
1. Sensory selective attention – filtering, focusing, selecting, disengagement
2. Attentional capacity and focus – influenced by energetic factors (arousal, motivation, effort) and
structural factors (memory, processing speed, cognitive ability)
3. Sustained attention – highly dependent on task duration, vigilance requirement (e.g., high demand
for readiness of low probability target), reinforcement, target-distractor ratio
4. Response selection and control – associated with executive functions (intention, initiation,
generative capacity, persistence, inhibition, switching)
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AUDITION
From vestibulocochlear nerve to cochlea nuclei in medulla (dorsal – information and quality of sounds,
ventral – intensity, then superior olivary nucleus and trapezoid body – localization) to lateral lemniscus to
inferior colliculus in midbrain to MGN of thalamus to Heschel’s gyrus in temporal auditory association
cortex (bilateral representation of auditory impulses on each sidde); accessory nuclei modulate input
Efficient transfer of sound into inner ear related to size of tympanic membranes and oval window
Lesions:
Left sided – poor semantic association; Right sided – poor perceptual discrimination
Lesion in superior temporal gyrus disorders phonemic hearing
Lesion in medial temporal gyrus creates auditory amnesic aphasia (inability to repeat
series of words, mutual inhibition of auditory traces)
Pitch Theory (Sound)
Frequency – low frequencies
Place – high frequencies, location
Volley – mid frequencies, successive firing
Tinnitus – persistent ringing tone or buzzing, usually caused by peripheral auditory disorders affecting the
tympanic membrane, middle ear ossicles, cochlea, or CN VIII
Self-audible bruits – pulsating “whooshing” sounds associated with turbulent flow in AVM, carotid
dissection, elevated ICP
Release phenomenon – elaborate auditory hallucination associated with senosorineural deafness or lesion
of pontine tegmentum
Paracusis – a sound heard previously is heard repeatedly, very rare (analogous to palinopsia)
Presbycusis – hearing loss associated with age, beginning with loss of higher frequencies, associated with
degeneration of CN VIII or cochlear and other middle ear structures
Musical hallucinations – often caused by seizures in right hemisphere
Ear drum 
Middle ear bones (ossicles) including malleus (“hammer”), incus (“anvil”) and stapes (“stirrup”) 
Oval window (sitting in scala vestibuli) and round window (sitting in scala tympani),
separated by promontory; connects to throat via Eustachian tube
From oval window to vestibular system that controls balance (semicircular canals, utricle, saccule) 
Inner ear, including cochlea (two canals for transmission of pressure) and organ of Corti (detects pressure
impulses and turns them into electrical impulses from stimulated hair cells stimulating auditory nerve)
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BASAL GANGLIA
Dyskinesia
Components of extrapyramidal motor system involved in modulation of motor tone and involuntary
motor activity through projections via thalamus, including striatum/neostriatum (caudate nucleus and
putamen joined by cellular bridges), globus pallidus (with putamen called lentiform nucleus; all three
called corpus striatum), substantia nigra (pars reticulata and pars compacta; contains dopamine and
melanin; usually black, hypopigmented in PD), and subthalamic nuclei, plus nucleus accumbens and
ventral pallidum, to pyramidal/corticospinal tract
May be related to procedural learning/habits and limbic functioning through nucleus accumbens;
Ach, DA, GABA, 5HT; damage leads to hypokinetic movement disorders (parkinsonism) and
hyperkinectic (inhibitory) movement disorders (HD – athetosis, chorea, hemiballismus); related to OCD,
Tourette’s; can cause aphasia, apraxia, neglect
CN and P lesions – release signs, rigidity, disconnect
GP lesions – akinesia, mutism
Blood supply:
C, P and GP from lenticulostriate branches of MCA, also ACA Heubner
Also medial GP from ICA Anterior Choroidal
Input through striatum (glutamate, dopamine), output through internal globus pallidus and substantia
nigra pars reticulata through ventral lateral and ventral anterior thalamus via thalamic fasciculus (GABA)
Interneurons in striatum also contain Ach
Direct (disinhibit) to internal GP
Indirect (inhibit) through external GP, subthalamic nucleus, then internal GP
Nigrostriatal – projecting from the substantia nigra to corpus striatum; decreased nigrostriatal
dopamine associated with rigidity, tremor, and akinesia (PD)
Parkinson’s – degeneration of dopamine-containing neurons in substantia nigra (hypokinetic)
Huntington’s – degeneration of striatal neurons (hyperkinetic)
Hemiballismus – damage to subthalamic nucleus
Reduced DA in striatum leads to increase GPi activity
Four Parallel Channels
I. Dorsal striatal
1) Motor – somatosensory cortex, primary motor cortex, premotor cortex
a) BG input – Putamen
b) BG output – GPi, SNr
c) Thalamic Relay – VL, VA
d) Cortical targets – supplementary motor cortex, primary motor cortex, premotor cortex
2) Oculomotor – posterior parietal cortex, prefrontal cortex
a) BG input – Caudate (body)
b) BG output – GPi, SNr
c) Thalamic Relay – VA, MD
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d) Cortical targets – frontal eye fields, supplemental eye fields
3) Prefrontal – posterior parietal cortex, premotor cortex
a) BG input – Caudate (head)
b) BG output – GPi, SNr
c) Thalamic Relay – VA, MD
d) Cortical targets – prefrontal
II. Ventral striatal
4) Limbic – temporal cortex, hippocampus, amygdala (may be involved in schizophrenia)
a) BG input – nucleus accumbens, ventral caudate, ventral putamen
b) BG output – ventral pallidum, GPi, SNr
c) Thalamic Relay – VA, MD
d) Cortical targets – anterior cingulate, orbital frontal
*Pathways
I. Paths from GPi
1) Ansa lenticularis – from GPi looping under internal capsule to reach thalamus
2) Lenticular Fasciculus (H2 field of Forel) – from GPi through internal capsule, between
subthalamic nucleus and zona incerta (part of thalamic reticular nucleus) to reach thalamus
1) and 2) join (at H field of Forel) to form thalamic fasciculus (H1 field of Forel) to enter
thalamus
II. Subthalamic fasciculus – indirect paths from GPe to subthalamic nucleus and from subthalamic
nucleus to GPi
See Hendelman Figure 24, Blumenfeld Figure 16.1, 16.4 (A-D), 16.5, 16.6, 16.9
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BRAIN ASYMMETRY/LATERALIZATION
Asymmetry
1. Right hemisphere larger and heavier and more white matter, more associative cortex and
interconnections
2. Planum temporale, area posterior to the auditory cortex (Heschl’s gyrus), longer and larger on the
left, more gyri and deeper sulci, although Heschl’s gyri larger on right (usually 2)
3. Lateral posterior nucleus (LPN) of thalamus (projecting to parietal cortex) larger on left, medial
geniculate nucleus (MGN) of thalamus (projecting to primary auditory cortex) larger on right
4. Slope of the Sylvian fissure is gentler on the left
5. Frontal operculum (Broca’s area) larger on the right (tone of voice) on the visible surface and
larger on the left (producing language) under the surface
6. Right hemisphere extends farther anteriorly, left hemisphere extended farther posteriorly, and
occiptal horns of lateral ventricles longer on the right
7. Distribution of neurotransmitters (e.g., Ach, GABA, NE, DA) asymmetrical
8. Affected by sex and handedness (asymmetry greatest in right-handed men, associated with
testosterone affecting development of left hemisphere; men smaller posterior body and isthmus of
CC; men larger left planum temporale; men larger brain overall but lower blood flow)
Lateralization/Material-specific learning
Visual system
Auditory system
Left
letters, words
language-related sounds
Somatosensory system
Movement
Memory
Language
complex voluntary movement
verbal memory
speech, reading, writing,
grammar, syntax, arithmetic,
syllable stress
Spatial processes
Music
(sequential, analytic)
note recognition, quality
Right
complex geometric patterns, faces
nonlanguage environmental sounds,
music
tactile recognition of complex patterns,
Braille
movements in spatial patterns
nonverbal memory
prosody, gesturing (frontal operculum)
vocabulary selection, metaphors,
emotional content of speech,
nonverbal sound discrimination
geometry, sense of direction,
mental rotation of shapes, orientation
(creative)
melody recognition, rhythm
Of right-handed, 95+% left-hemisphere language dominant
Of left-handed, 60% left-hemisphere language dominant, right side for 20%, mixed for 20%
Situs inversus – a complete reversal of cerebral laterality and specialization in which the left
hemisphere is dominant for visuospatial processing and the right hemisphere is dominant
for language
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BRAIN CANCER
Adults: 70% supratentorial, 30% infratentorial
Glioblastoma and brain metastases
Children: 30% supratentorial, 70% infratentorial (cerebellum), frequently with hydrocephalus
Astrocytoma, medullablastoma and ependymoma (last two bad outcomes)
General symptoms: change in mental functions, headache, vomiting, seizures
1) primary brain tumors (1%)
a) gliomas – most common, malignant, from glia (glioblastoma - older) or astrocytes
(astrocytoma - younger) or oligodendrocytes (oligodendrogliomas - younger), graded 1-4
(most lethal); more often in men; typically spreads from one hemisphere to the other
through the corpus callosum (60% childhood cerebral neoplasm, 75% all intracranial
tumors); treated with resection
i. Grade I (low) – high differentiation
ii. Grade II and III – astroblastoma
iii. Grade IV (high) – glioblastoma (fatal within year)
b) meningiomas – second most common; a slow-growing benign tumor arising from the
dura/arachnoid; more common along the superior sagittal sinus, sphenoid ridge, and near
the optic chiasm on account of corresponding increases in cerebral vascularization,
creates pressure; more often in women (associated with breast cancer)
c) CNS lymphoma – cluster around ventricles; associated with HIV and immune
compromise; treated with corticosteroids and radiation
d) pituitary adenomas – endocrine disturbance; bitemporal hemianopia by pressure on optic
nerve, elevated prolactic indicator; dopaminergic agonist will shrink
e) pineal – pressure on aqueduct causes Parinaud syndrome (paralysis of upgaze,
convergence or nystagmus, light-near papillary dissociation)
f) schwannoma – most common in CN VIII
g) medullablastoma
h) acoustic neuroma – on covering of CN VIII, may compress CN V and CN VII; associated
with neurofibromatosis type II
2) metastic brain tumors (more common than any other combined) – often multiple because spread
by hematogenous metastasis; lymphomas may be multicentric; most frequent from lung, breast,
melanoma, lymphoma, kidney, ovaries
a) meningeal metastases – breast, lung, leukemia, lymphoma; associated with blunting of
personality, confusion, loss of initiative
b) vertebular and spinal metastases – from breast, lung, prostate, colon
c) nerve and plexis metastases
d) nonmetastastic complications [paraneoplastic syndromes (see below), metabolic
disorders, side effects of chemotherapy and cancer, vascular events, infarctions],
progressive multifocal leukoencephalopathy (demyelinative lesions associated with
hemiparesis, mental status change, language disturbance, and visual disturbance caused
by opportunistic infection in immunologically compromised individuals)
Paraneoplastic syndromes – disorders associated from carcinoma that do not result directly from
tumor effects but antibody formation, resistant to treatment; most common is limbic
encephalitis (personality changes, memory loss, non-systemic cancer, lung/oat cell
carcinoma, ovarian), also dermatomyositis, Lambert-Eaton syndrome (impaired
presynaptic Ach release), pancerebellar degeneration, neuropathy, myoclonus; associated
with small cell lung, breast, testicular, and ovarian cancer
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Treat by surgical resection, radiation (can cause necrosis), chemotherapy, steroids (to reduce edema and
swelling), shunt/stent
Carcinoma – malignant neoplasm
Colloid cyst – benign neoplasm of epithelial cells surrounded by a gelatinous capsule, commonly at the
roof of the third ventricle, which can block the cerebral aqueduct and produce obstructive
hydrocephalus
Craniopharyngioma/suprasella cyst – a calcified/cystic congenital tumor arising from cells derived from
the pituitary stalk (Rathke’s pouch) that often increases intracranial pressure
Ependymoma – a glioma derived from relatively undifferentiated ependymal cells
Neuroma – a tumor consisting primarily of nerve cells and nerve fibers or a tumor growing from a nerve
Neuroblastoma – a tumor composed chiefly of neuroblasts that occurs mainly before age 10, usually
arising in autonomic nervous system or adrenal medulla
Olfactory groove meningioma – tumor originating in arachnoidal cells along the cribiform plate;
may involve anosmia, abulia, confusion, forgetfulness, and inappropriate jocularity
Primitive Neuroectodermal tumors (PNETs) – more malignant
Brain functioning affected by:
1) increased intracranial pressure
2) seizures
3) focal symptoms
4) secreting hormones or altering endocrine patterns
Complications:
1) Radiation associated encephalopathy – from radiation treatment of tumors, associated with
demyelination and necrosis; appears as subcortical dementia; in children 5-7 IQ points
drop a year
2) Chemotherapy – cytokines (interferon-α, interleukin-2, tumor necrosis factor-α) produce cognitive
(fine motor speed, coordination) and mood disturbance; good response to psychostimulants
3) Radiation necrosis – cerebral infarction from occlusion of small cerebral vessels that are damaged
during high-dose radiation therapy for brain tumors, typically appearing 6-18 months after
radiation; in severe cases, vascular dementia may develop
Mass lesions can produce herniation either through mass effect (distorting normal geometry) or
effacement (flattening sulci)
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BRAIN CELLS
Average weight 1400 grams/3 pounds
12-20 billion cells in cerebral cortex, 180 billion in human brain, 1 billion in spine
10-50x more glial cells than neurons
each cell connects to 1,000-100,000 other cell
nerve impulses travel 100m/sec, with speed determined by axonal diameter and myelination
2% of total body weight but consumes 20-25% of total oxygen
10,000 die per day
brain volume peaks in early 20s then progressively declines, with no real change until 40s or 50s;
hippocampus and anterior dorsal frontal lobe most susceptible to neuronal loss, occiptal lobe least
susceptible (blood flow decline greatest in prefrontal and inferior temporal, least in occipital); also
dendretic arborization and decreased synapses
brain changes associated with aging include apoptosis, cumulative biological errors in DNA replication,
protein synthesis, or protein structures; free radical production (oxidative stress)
with age, visual memory declines more than verbal, slowed processing speed, divided attention down,
verbal retrieval down, executive function more concrete and rigid
Neurons
1. Morphological classification (based on number of axons)
a. Multipolar – several dendrites and axons
b. Bipolar – single dendrite and axon (e.g., vision, olfaction, audition)
c. Unipolar – axon and dendrites arise form single process (somatosensory; mainly invertebrates)
d. Interneurons (short or no axon)
2. Functional classification – motor, sensory, interneurons
Stroma – supportive tissue; in the CNS, consists primarily of glia
Stellate cells – neurons with a star-shaped soma (cell body) that typically have an associative function
within a particular brain region rather than an output function to other areas (e.g., pyramidal cells)
Glial Cells – non-neural, supportive cells
1. Oligodendrocytes – form myelin (lipid) in CNS (parallels Schwann cells in PNS), insulate and
speed transmission, offers physical support
2. Astrocytes – large glial cell; structural support, repair, metabolism of synaptic transmission,
regulate ion balance, help form blood-brain barrier; phagocytosis
3. Ependymal cells – epithelial cells that line the brain ventricles and central canal of spinal cord,
assisting in production/secretion and circulation of CSF
4. Microglia – metabolize and remove dead neurons (phagocytosis)
Also supply nutrients and oxygen to neurons, guide migrating neurons
1. Primordial fields myelinate before birth – somesthetic cortex, primary visual cortex, primary
auditory cortex
2. Intermediate fields myelinate birth to 3 months – secondary association areas
3. Terminal fields myelinate 4 months to 14 years – classical association areas
1. Cell body (soma) – brains “gray matter”
a. Cell membrane – semipermeable
b. Nucleus – stores chromosomes (DNA) and nucleolus (rRNA to form proteins)
c. Endoplasmic reticulum – tubes for transporting material within cytoplasm
d. Golgi apparatus – packages peptides and proteins into vesicles
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e. Lysomes – contains enzymes for degrading material, leaving residual lipofuscin granules
f. Mitochondria/Mitochondrial DNA (mtDNA) – ring-shaped, inherited from mother;
produces 90% of energy by taking up glucose and breaking down into ATP; detoxifies
oxidants/free radicals that accelerate aging and death of neurons (has been associated
with PD and familial ALS)
g. Microfilaments/microtubules – structural support and transport
2. Dendrites – most characteristic morphologic feature (e.g., purkinje, pyramidal); dendrictic spines
receive information
3. Axon – transitions at axon hillock, branches called collaterals, terminate in teleodendria, surrounded
by myelin (“white matter”), saltatory conduction with action potential jumping from Nodes of
Ranvier
4. Terminal synaptic buttons – axon ends in terminal buttons, causing release of neurotransmitters into
synapse
Apoptosis – gene-directed cell death, programmed, sequential, energy requiring cell death (e.g., HD)
Necrosis – cell death through inflammatory response
Phagocytosis – removal of dead cells by mitochondria, microglia, and astrocytes
Wallerian/anterograde/orthograde degeneration – atrophy of the distal part of neurons after being severed
from the proximal part (degeneration of severed axon and myelin sheath), associated with trauma,
infarction, or tumor infiltration
Gliosis/sclerosis – scarring associated with hyperplasia glial overgrowth/replacement of cell bodies by
glial cells
Chromatolyses – color dissolution (cell Nissel substance breaks down), so no stain uptake in cell body
(Weigert staining for myelin)
Electrical Communication
Intracellular
I. Resting Potential – negative inside of cell, positive outside of cell
4 ions pass through gates either due to diffusion (equalize) or electrostatic pressure (attraction/repulsion):
1. organic ions (A-) – inside cell, don’t move
2. sodium (Na+) – predominantly outside of cell; diffusion pushes in, attraction pulls in (unbalanced
– pushed out through sodium-potassium pump exchanging 3 Na for 2 K, using up to 40% of
metabolic resources)
3. potassium (K+) – predominantly inside cell; diffusion pushes out, attraction pulls in (balanced)
4. chloride (Cl-) – predominantly outside of cell; diffusion pushes in, repulsion pushes out
(balanced)
II. Action Potential – through depolarization of NA+ rushing into cell, then K+ rushing out of cell, then
gates opening and more NA+ rushing in; intensity of stimulus reflected by frequency of firings and time
interval between; both absolute and relative (requiring greater stimulation to fire) refractory periods (from
–70 to +40), K+ influx restabilizes
Extracellular
1. Neurotransmitters – chemical agent released be a neuron that crosses the synapse and alters the
postsynaptic cell, having either a facilitatory or inhibitory effect; released by terminal buttons and
detected by dendritic receptors; can be gas, peptide, or small molecule
2. Neuromodulators – released by terminal buttons
3. Hormones – most produced by endocrine glands, only detected by target cells
a. peptides – chains of amino acids linked by peptide bonds (insulin, pituitary gland
hormones)
b. steroids – very small, fat-soluble molecules (sex hormones, adrenal cortex hormones)
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Postsynaptic potentials either depolarization or hyperpolarization
Limited transmission by reuptake and enzymatic deactivation (destruction)
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Excitatory (EPSP) when Na+ enters cell (depolarized)
Inhibitory (IPSP) by opening K+ or Cl- channels (hyperpolarized) (both affect through neural integration)
Summative strength temporal or spatial to cause activation of next cell, or can initiate change within the
cell
Neurotrophic factors – naturally occurring peptides that facilitate neuronal growth, promote survival, and
enhance neuronal function [e.g., nerve growth factor (NGF)]
Neurotransmitters – more than 50, in CNS main excitatory is glutamate, main inhibitory is GABA;
acetylcholine in PNS at neuromuscular junctions
1. Acetylcholine (Ach) – stimulates involuntary parasympathetic nervous system, in PNS (spinal
cord horn  skeletal muscles) influencing motor control (at neuromuscular juncture –
preganglionic autonomic and postganglionic parasympathetic), in CNS (basal forebrain nuclei 
nucleus basalis of Meynert (extending from the subthalamic nucleus to the floor of the third
ventricle), medial septal nuclei, nucleus of diagonal band and pontomesencephalic brainstem 
laterodorsal and pedunculopontine tegmental nuclei) influencing memory capacity and
formation, vigilance, processing speed (orbital frontal and temporal lobe functioning); action
terminated by cholinesterase; nicotinic (neuromuscular junction, excitatory) and muscarinic
(cerebral, excitatory or inhibitory) receptors
Synthesis/metabolism: acetyle CoA + CholineAch
a. Tacrine (Cognex) anticholinesterase (↑) – AD
b. Botulinum toxin (Botox) prevents release of Ach (↓) – muscles relax, reduces wrinkles
c. Black widow spider venom stimulates release (↑)
d. Curare blocks nicotinic receptors (↓)
e. Atropine blocks muscarinic receptors (↓), treated with physostigmine (↑)
f. Scopolamine antagonizes muscarinic receptor; memory impairments (↓)
2. Monoamines – neuromodulators
Catecholamines (adrenergic) – personality, mood, drive, movement
a. Dopamine (DA) – generally associated with involuntary motor disorders (PD),
neuropsychiatric problems (schizophrenia, tics, ADHD), modulation of rewards,
initiation and maintanence, working memory, attention switching, processing speed;
produced in midbrain (substantia nigra pars compacta (nigrostriatal), ventral tegmental
(mesolimbic, mesocortical)) and projected to striatum, prefrontal cortex, limbic system,
amygdala; excessive DA (cocaine, amphetamines, L-dopa) can lead to hyperkinetic
movements, visual hallucinations (MAO terminates); potency of antipsychotic drugs
correlated with ability to block D2 receptors in the striatum; precursor of norepinephrine
and epinephrine; produces homovanillic acid (HVA) in CSF
Synthesis/metabolism: phenylalaninetyrosineDOPADA
i.
Nigrostriatal pathway – substantia nigra to extrapyramidal motor system (caudate and
putamen); too little causes rigidity, tremor, akinesia, too much causes dyskinesia
(e.g., PD)
ii.
Mesolimbic pathway – ventral tegmental to amygdala/limbic; positive symptoms of
psychosis, reward
iii.
Mesocortical pathway – ventral tegmental to frontal cortex; negative symptoms of
psychosis, working memory, executive functions
iv.
Tubero-infundibular – connects hypothalamus and pituitary gland; antipsychotics
lead to elevated prolactic level
b. Norepinephrine (NE) (noradrenaline) – regulates mood, memory, hormones, blood flow,
motor behavior, new learning, attention switching, vigilance/arousal, sexual behavior,
appetite, sleep regulation, in locus ceruleus in pons (“blue spot”) and lateral tegmental,
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projecting to forebrain through thalamus; released by the adrenal gland present in
autonomic ganglia; excitatory effect in thalamus; tricyclic increases; depletion reduces
sympathetic activity (e.g., orthostatic hypotension), excess increases sympathetic activity
(e.g., tremor, bronchodilation)
c. Epinephrine (adrenalin) – stimulates sympathetic division of autonomic nervous system
to produce ‘flight or fight’ response, in adrenal medulla
Synthesis/metabolism: DANEepinephrine
Monoamine oxidase (MAO) – a widely distributed enzyme in the body involved in the
breakdown of dopamine, serotonin, and norepinephrine
Indolamines
a. Serotonin (5-HT) – inhibitory; regulates mood, eating, sleeping, temperature, sex,
aggression, arousal, pain (analgesic), in raphe nuclei (raustral and caudal) in pons (and
midbrain and medulla), with projections concentrated in sensory (inhibitory), motor
(excitatory), association, and limbic regions; projecting to cortex, thalamus, and basal
ganglia; low in depression, anxiety, OCD, PD, AD; abnormalities associated with
schizophrenia and hyperaggressive states; SSRI and tricyclic increases; LSD and Ecstacy
(MDMA) increase (psychosis); produces melatonin
Synthesis/metabolism: tryptophan5-hydrotryptophan5-hydrotryptamine/5-HT
Histamine
a. Found in tuberomammillary nucleus of posterior hypothalamus, associated with
maintaining alertness, excitatory effect on thalamus, excitatory and inhibitory affect on
cortical neurons
3. Amino Acids (4)
a. Gamma-aminobutyric acid (GABA) – inhibitory (brain and cord); presynaptic, opens Clchannels and closes CA++ channels, hyperpolarizing cells; increase produces sedative,
anxiolytic, anticonvulsant effects; most in striatum, hypothalamus, spinal cord, temporal
lobes; benzodiazepines and barbiturates bind to the post-synaptic GABA receptor
Synthesized from glutamate
b. Glutamate – excitatory (brain and cord); implicated in neural plasticity, learning,
memory; affected by neurotoxins; synthesized from glutamine; one of four receptors:
A. NMDA (N-methyl-D-aspartate), modulated by inhibitory glycine, that
depolarizes neurons by opening ion channels that chiefly allow an influx of
calcium; involved in memory, embryonic neuron migration; overstimulation
leads to excitotoxicity/cell death by calcium flooding (e.g., HD, epilepsy,
stroke, hypoxia, TBI), binds to ketamine and PCP
c. Glycine – inhibitory (lower brain and cord); modulatory role at interneurons in cord;
blocked by strychnine
d. Aspartate – excitatory
4. Peptides – deactivated by enzymes only
a. Enkephalin, endorphin – endogenous opiates found primarily in the pituitary but also in
the hypothalamus and other brain regions (frontal); physiological roles include pain
perception (to periaqueductal gray matter), stress, respiratory regulation, temperature
control, tolerance development (opiods)
b. Substance P – mediator of inflammation, carry pain signals
c. Vasopressin (antidiuretic) – facilitates water reabsorption by kidneys, may play a role in
memory consolidation
d. Somatostatin – inhibitory neurons; modulation of heat, pain, sleep
e. Angiotensin II – peripherally acts as vasoconstrictor, centrally stimulates pressor
responses and drinking
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Long-term potentiation (LTP) in hippocampus – postsynaptic excitability following stimulation, high
frequency activity causes long-lasting increase in synaptic strength between involved neurons; Ca++
enters postsynsaptic cell through NMDA channels; Hebb’s rule: “neurons that fire together wire
together”, important process in learning and memory
*5HT suppresses LTP, DA and NE facilitate LTP
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BRAIN DEVELOPMENT
Prenatal
1. Proliferation – (2 weeks-6 months) cell generation by mitosis inside neural tube; neurogenesis
describes nerve cell production
2. Mitotic cycle – production of neuroblasts or glioblasts (nerve cell and glial cell precursors)
3. Migration – (6 weeks-6 months) neuroblasts move to permanent location between 6-18 weeks gestation
a. cerebral hemispheres follow inside-out pattern and move in laminae sheets guided by radial
fibers/glia; cerebellum follows outside-in pattern migration and guided by Bergmann glia
b. brain develops neck up, spinal cord develops neck down
4. Aggregation – cellular masses or layers formed by lamination, with neurons adhesing together or
aligning with neighbors
5. Cytodifferentiation
a. development of cell body
b. selective cell death – 40-75% die
c. axonal and dendritic development – (6 weeks-6 months) dendrites sprout through arborization and
grow spines (from birth to 18 months); cells are chemospecific and form connections through
microfilaments
d. synaptogenesis – termination of axonal growth, selection of synaptic sites, formation of synapses
Five stages: in preplate, in cortical plate, in global perinatal “burst”, stabilization from infancy to
adolescence, decline in density throughout adulthood
- visual cortex – dendritic and synaptic growth stops at 8 months, synapse elimination until age 3
- frontal cortex – dendritic and synaptic density peaks in infancy and early childhood and declines
until age 16
6. Pruning – elimination of neuronal overproduction; begins at dendritic spines, eliminates weakly
enforced or redundant connections, promotes neural efficiency
Develop:
head  tail (cephalic  caudal), near  far (proximal  distal), inferior to dorsal (subcortical  cortical)
Development of neural tube
18 days – CNS and PNS develop from midline ectoderm layer of fertilized egg
Neural plate appears from invaginated dorsal ectoderm and forms neural grooves and folds over and
closes in center then out towards ends, neuropores at ends close at 25 days via neurulation to form neural
tube; ectoderm  CNS and skin, mesoderm  meninges, vertebrae, skull
Anterior end gives rise to brain, posterior end forms spinal cord
Neural crest cells adjacent to neural tube pinched off to form bundles to become ganglia
Neural tube defects occur at 3-4 weeks gestation (anterior – anencephaly, caudal – spina bifida)
5-7 weeks brain divisions appear
In vestigial form, the neural tube becomes the cerebral ventricles and cerebral aqueduct
Development of cortex gestationally
6 weeks – basal ganglia
8-10 weeks – early cortical plate, four layers of cortex (ventricular, subventricular, intermediate,
marginal)
lobes formed in order of frontal, parietal, temporal, and occipital
5 months – convolutions and sulci develop
6 months – cortical plate thickens to six-layer composition
Isocortex and external granular layer of cerebellum develop last (hippocampal dentate gyrus and olfactory
bulb neurons generated throughout life)
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In second trimester connection of thalamus to regions of isocortex, appearance of CC (90 days), apoptotic
neuronal death, activity-dependent self-organization of nervous system and first motor activity
In third trimester begin myelination, synaptic connections between isocortex and related structures,
sensory and motor systems near complete
No new neurons develop postnatally
Postnatal development
Brain weighs at birth 25% of adult (300-350 grams), reaches 80% of adult weight at age 4 years
Cortical surface doubles by age 2 years
EEG – at birth irregular and low amplitude, slow rhythm (3-4Hz) primarily over occipital lobes by 4
months, increases until alpha rhythms attained
Primary sensory nuclei in thalamus connects early
Primary zones – modality specific, develop by 1 year
Secondary zones – integrate modality specific information into perceptive information, develops by 5
years
Tertiary zones – associative, supramodal areas integrating information across modalities, develops by age
8 years, and controls executive, purposive, and conative aspects of functioning (prefrontal), develops by
about age 12
Myelination occurs in sensory areas before motor areas
*Myelination of callosal and associational cortical regions continue into 4th decade of life
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BRAIN FREQUENCIES
Beta – >13 Hz, alert awake, mostly in frontal regions; prominent with concentration and anxiety, under
effects of minor tranquilizers
Alpha – 8-13 Hz, quiet awake, occipital and parietal; lost with eye opening, falling asleep, medication that
affects mental functioning; slows in elderly and neurological diseases
Theta – 4-7 Hz and Delta – <4 Hz, in children and upon entering sleep; presence otherwise may indicate a
degenerative illness or metabolic disorder; if focal, may indicate lesion
Triphasic waves: metabolic/toxic encephalopathy, hepatic/renal failure
Periodic complexes (seen as myoclonic jerks): subacute sclerosing panencephalitis (SSPE), CreutzfeldJakob
EEG can differentiate between locked-in syndrome and persistent vegetative state (slow and
disorganized)
Post ECT looks like post-ictal seizure for up to 3 months
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BRAIN LOBES
Parietal lobes – (“where”) somatic/tactile sensation; involved in sense of position and passive movement
(reaching), localize bodily stimuli, distinguish size, shape, and texture (asterognosis), recognize
writing on skin, distinguish simultaneous contacts (two-point discrimination), body image, eye
movements (follow moving target, accommodation and convergence, optic ataxia, fixation, gaze
apraxia, visual search)
Left – disorders of language (alexia, aphasia), acalculia, right-left confusion, agnosia, apraxia
(e.g., Gerstmann syndrome)
Right – constructional apraxia, contralateral neglect (visual attention), disorders of spatial ability,
dressing disability, topographical loss, bilateral ptosis
Posterior: integrating discrete elements into whole; spatial, constructional and topographical skills
inferior – higher order somatosensory and visual cortical fields
superior – somatosensory association cortex
Temporal Lobes – (“what”) auditory sensation and perception (music, speech), selective attention of
auditory and visual input, visual perception, organization and categorization of verbal material,
language comprehension, semantics/meaning, longterm memory (medial), personality and
affective behavior, sexual behavior, paranoia, preoccupation, irritability, aggression
anterior – storage
posterior – retrieval
left temporal lesion – language impairments
right temporal lesion – difficulty recognizing objects from incomplete picture
hippocampus – encodes material-specific
amygdala – emotional memory
Heschle’s gyrus – primary auditory cortex
insula – primary taste cortex
Occipital lobe – posterior brain region involved with vision, separated from the parietal lobe only
medially; larger medially than laterally; damage can result in visual object agnosia, color agnosia,
word blindness (alexia without agraphia), scotomas (blind spots); bilateral damage impairing near
or accommodation reflex
Syndromes of inferior occipitemporal cortex (“what”):
1) prosopagnosia (faces) – fusiform, lingual
2) achromatopsia – color perception (but still can name appropriate color for object verbally
described)
3) micropsia and macropsia
4) metamorphopsia – distorted shape and size (“Alice in Wonderland”)
5) visual reorientation – environment appears inverted or tilted
6) paliopsia – previously seen object reappers (visual association cortex)
7) cerebral diploplia/polyopia
8) erythropsia – unnatural coloring of visual field
9) astereopsis – inability to perceive depth of objects
Syndromes of dorsolateral parieto-occipital cortex (“where”):
1) Balint’s syndrome – simultanagnosia (impaired seeing of whole), optic ataxia (impaired
ability to reach under visual guidance), ocular apraxia (difficulty directing gaze in
periphery)
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Frontal lobe – brain area anterior to the central sulcus and superior to the Sylvian fissure; divided
anatomically into motor, premotor, and prefrontal areas (1/3 of cerebrum in man);
agranular cortex in layers II and IV, III and V well developed (motor cortex);
connection to prefrontal cortex primarily through mediodorsal nucleus of thalamus
Frontal cortex  Striatum Globus pallidus/substantia nigra  thalamus
Glutamate
GABA
1) primary motor – fine motor movement  primary somatosensory area of parietal lobe,
VL thalamic nucleus
2) premotor – praxis, sensorimotor integration  secondary somatosensory area of parietal
lobe, extrapyramidal motor system, primary motor area, VA thalamic nucleus
3) frontal eye fields – voluntary gaze, visual search, directing complex attention  DM
thalamic nucleus
4) dorsolateral prefrontal – executive functions (sequencing, persistence, switching, shifting,
focus), working memory  posterior association cortex, angular and supramarginal gyri,
DM thalamic nucleus
5) orbital prefrontal – smell discrimination, behavioral inhibition and initiation  cingulate,
anterior temporal lobes, limbic system, DM and intralaminar thalamic nuclei
6) supplementary motor and anterior cingulate – initiation and inhibition
7) prefrontal – higher-order heteromodal association cortex
Frontal lobe functions –
 regulation of arousal and behavior
 initiation (generate lists/word fluency)
 adaptive, goal-directed behaviors
 conditional associative learning
 source/contextual memory
 response to changing environmental conditions/contingencies
 planning and sequencing
 shifting attention (Trails B, WCST)
 modulating/stopping ongoing behavior
 meta-awareness/self-monitoring/insight
 searching systematically
 abstract thinking (similarities, proverbs, logic)
 problem solving, decision making, strategy formation
 response inhibition (go-no go, Stroop)
 persistence
Left: elaborative encoding, logical encoding, positive emotions
Right: retrieval, spatial relationships, negative emotions
left frontal lesion – depression; excessive aggression, agitation, anxiety (catastrophic reactions)
right frontal lesion – restricted affect and emotional dyscontrol, euphoria/indifference, mania; false
positive errors
Frontal Lobe symptoms – source amnesia, false recognition, confabulation, poor retrieval, poor selfmonitoring; magnetic gait, urinary incontinence, frontal release signs (grasp, suck, snout, root),
gegenhalten/paratonia (fluctuating resistance to passive stretching of the muscle, increased tone, unable to
relax on command), witzelsucht (facetious, disinhibited, inappropriately euphoric affect); echolalia,
echopraxia (pathological copying of another person’s gestures or movements), pathological inertia (a lack
of drive, initiative, or motivation)
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


dorsolateral frontal/executive dysfunction syndrome – syndrome consisting of difficulty
generating hypotheses, mental inflexibility/rigidity, poor set shifting, reduced fluency,
perseveration (persistence of the same response even when it is shown to be
inappropriate), stereotypy (persistent repetition of purposeless movements, acts, or
words), poor organizational strategies for learning, utilization behavior/environmental
dependency, inability to self-correct, and motor programming deficits (alternating,
reciprocal, or sequential) (WCST, Stroop)
mesial frontal/anterior cingulate syndrome – syndrome characterized by akinetic mutism
from deficit of voluntary regulation of arousal, associated with akinesia and bradykinesia
(abulic hypokinesia); symptoms include apathy, loss of spontaneous speech, thoughts and
actions, monosyllabic speech, reduced movement initiation deficit (inability to initiate
acts despite being able to describe intended action and ability to perform desired
behavior); eating and drinking only if fed, and may be incontinent; indifference to pain;
most severe forms caused by bilateral lesions of the cingulated gyrus whereas unilateral
lesions of the SMA are more likely to result in transient symptoms; neuropsychologically
perform normally on most tasks but show response disinhibition on go/no-go tasks;
Supervisory Attentional System (SAS: Luria’s theoretical system of nonroutine
attentional control)
* often from rupture of ACA/ACoA (damage to cingulate gyrus, supplementary
motor area; partial with left thalamic lesion)
orbital frontal syndrome – syndrome characterized by prominent personality changes,
including emotional lability, impulsivity, disinhibition, poor judgment, irritability, and
occasional imitation and utilization behaviors/environmental dependency/stimulusboundedness (also OCD), undue familiarity, lack of empathy; area extensively connected
to limbic area
Frontal lobe subcortical connections via amygdala (by uncinate fasciculus), hippocampal formation (by
cingulate gyrus and parahippocampal gyrus), thalamus (including mediodorsal nucleus, medial pulvinar,
and intralaminar nuclei), and basal ganglia (by head of caudate)
Direct connection Disinhibits thalamus (inhibitory GABA from striatum to GPi to thalamus)
Indirect connection Inhibits thalamus (inhibitory GABA from striatum to GPe to subthalamic
nucleus to GPi to thalamus)
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BRAIN PLASTICITY
Plasticity includes:
1) maturation/developmental change
2) changing with experience (learning, remembering)
3) recovery after brain injury (reorganization in part)
4) maintaining function despite aging (response to natural cell death – fewer cells but increased
connections)
greater recovery of language functions
increased processing capacity associated with increase in neuronal synapses (axon terminals, dendritic
arborization); dendrictic spine density may be reduced/better pruned; altering of existing synapses
neuronal migration – cells develop along the walls of the ventricle, migrating along radial glial fibers that
then disappear, making repair or regrowth difficult
Stages of cell development: cell proliferation (completed by 5th gestational month), cell differentiation,
cell migration (3rd trimester), dendritic and axonal growth (up to age 2), synaptogenesis, cell and synaptic
death, gliagenesis
Lesions, particularly frontal lobe, occurring <1 year produce more severe IQ deficit than in later life
(usually one standard deviation drop)
Lesions between 1-5 allows relative reorganization and sparing of language functions
Lesions >5 shows little sparing
Removal of either hemisphere leads to compromise of visuospatial and constructional abilities, with
language relatively spared (crowding); hemispheric separation less impairment than for cortical
damage
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BRAINSTEM
Midbrain, pons, and medulla oblongata – where control crosses over
transition between medulla and spinal cord by pyramidal decussation
Midbrain – between the thalamus and pons
Superior colliculi – oculomotor nuclei (CN III) and red nuclei
Inferior colliculi – trochlear nuclei (CN IV) and brachium conjunctivum
Cerebral aqueduct, periaqueductal gray matter (pain modulation – stimulation produces analgesia,
thiamine deprivation causes hemorrhage), midbrain reticular formation (coordinated movements),
medial lemniscus, anterolateral system, cerebral peduncles (substantia nigra and basis
pedunculi), red nucleus [receives input from motor areas of cortex and cerebellum and projects to
spinal cord (rubro-spinal tract), involved in independent head movements], tectum and
tegmentum
Pons – between the medulla and midbrain that bridges the right and left halves of the cerebellum;
includes large ventral portion (descending fiber tracts, cranial nerve nuclei, and middle cerebellar
peduncles to cerebellum) and tegmentum (pontine reticular formation); involved in breathing,
feeding, sleeping, dreaming, integrates bilateral movements, transfers information to cerebellum
Medulla – between the spinal cord and pons, defined at the foramen magnum; autonomic nervous system,
circulation, respiration, audition (pyramids with alternating decussation, inferior olive, nucleus
gigantocellularis); chemotactic trigger zone (area postrema) associated with nausea, modulated by
serotonin
Reticular activating system (RAS)/formation – pontomedullary area regulating level of consciousness
(arousal, sleep) mostly through modulation of thalamus
rostral (upper) – alertness, caudal (lower) – motor, reflex, autonomic functions
associated with respiration, coughing, hiccupping, sneezing, yawning, shivering, gagging,
vomiting, swallowing, laughing, crying, REM
Midbrain dysfunction – third-nerve palsy, pupil dilation, flexor posturing, impaired consciousness
Pontine dysfunction – Babinski’s, generalized weakness, perioral numbness, pins and needles facial
tingling, vision loss/blurring, irregular respiration, shivering, extensor posturing, abducen or
horizontal gaze palsy, ocular bobbing, impaired consciousness, coma
Medullary dysfunction – vertigo, ataxia, nystagmus, nausea, vomiting (area postrema), respiratory arrest,
autonomic instability, hiccups
Doll’s eye reflex/maneuver – reflexive eye movement in the direction opposite to that in which the head
is moving
*absence of this response indicates a brainstem lesion
See Blumenfeld Figures 2.22, 12.2, 14.3, 14.4, 14.5 Hendelman Figure 3
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BRAIN STRUCTURES
Axial/transverse – involving midline structures of the body; horizontal cut
Sagittal – dividing the body into left and right portions
Coronal – as if a crown
Homonculus (Wilder Penfield) – representation of localized functioning of sensory and motor strips by
drawing associated body parts next to the coronal representation
Cytoarchitectonics – study of the architecture (disposition, type, cell density, thickness, cellular
arrangement) of cells and layers (Brodmann – 52 total)
Myeloarchitectonics – study of the fiber structure of the brain
1) Neocortex/isocortex/homogenetic cortex/neopallidum – six layers (counted from surface inward), more
recently developed; 80% of brain; prefrontal, post parietal, lateral temporal, portion of hippocampal
I. Molecular layer – dendrites and axons from other layers
II. Small pyramidal/external granular layer – cortical-cortical connections
III. Medium pyramidal/external pyramidal layer – cortical-cortical connections
IV. Granular/internal granular layer – receives input from thalamus *
V. Large pyramidal/internal pyramidal layer – sends outputs to subcortical structures other than
the thalamus, such as brainstem, spinal cord, and basal ganglia (motor neurons) *
VI. Polymorphic/multiform layer – sends outputs to thalamus *
1 – 0, a, b, c – Tangential layer
2 – Dysfibrous layer
3 – a, b – Suprastriate layer
4 – External band of Baillarger
5 – a, b – Inner striate layer, Internal band of Baillarger
6 – a1, a2, bi, b2 – Infrastriate layer
2) Mesocortex/Limbic cortex – transitions between six and three layers; includes parahippocampal
gyrus, cingulated gyrus, anterior insula, orbitofrontal cortex, temporal pole
3) Allocortex – connected to hypothalamus
I. Archicortex – three-layered hippocampal cortex and dentate gyrus; oldest region of the cortex
II. Paleocortex – three to five-layered olfactory cortex (subiculum, piriform cortex, and
cingulated gyrus)
4) Corticoid areas – simple cortex that merges with subcortical nuclei; includes amygdala, substantia
innominata, septal region
1.
2.
3.
4.
5.
Agranular
Frontal
Parietal
Polar
Granulous
Betz cells – largest cell bodies of all cortical neurons, in precentral gyrus
Luris’ zones –
1) primary zones – high modal specificity, afferent layer IV (sensation)
2) secondary zones – adjacent to primary zones, where information integrated (perception/gnosis),
layers II and III
3) tertiary zones – integrate information across sense modalities
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Somatosensory/somesthetic area – the cortical projection area in the postcentral gyrus (parietal lobe)
involved in the processing of sensory information/conscious perception of somatic sensation from
receptors in skin, joints, muscles, and viscera
Primary receptor areas – the areas of the cerebral cortex that receive the thalamic projections of the
primary sensory modalities (e.g., vision, audition, somesthesis)
Unimodal association cortex – primary, modality specific, adjacent to primary area (somatosensory,
auditory, visual)
Heteromodal association cortex – higher-order integration of information, bi-directional with limbic
cortex (frontal lobes, parieto-occipito-temporal junctions)
Eloquent cortex – cortical regions that, if surgically resected, will produce significant functional
impairments, including language areas and primary motor and sensory regions
Calvaria/calvarium – upper dome-like portion of skull
Centrum semiovale – densely packed white matter tracts from cortex to internal capsule, includes corona
radiata
Decussation – crossing of paired fiber tracts across midline
Nidus – the central portion; used to describe the point of abnormal development in arteriovenous
malformations, nerve origin or nucleus, or infection focus or target
Operculum – the area of the frontal, parietal and temporal lobes covering the insula that borders
on the Sylvian fissure
Parenchyma – essential neural tissue that is supported by the connective tissue framework/stroma
Peduncles – stalk-like connecting structures in the brain (e.g., cerebellar – white matter,
cerebral – white and gray matter)
Periventricular white matter – white matter adjacent to the lateral ventricles; common site of
small vessel disease associated with hypertension
Retrobulbar – located behind the eyeball; located behind the medulla
Rhinencephalon – olfactory and limbic components
Septal area – cortex and unlined septal nuclei, the latter extending to septum pellucidum beneath
the genu and rostrum of the corpus callosum, on the medial side of the frontal lobe
Septum – a thin wall or membrane that divides two chambers
Septum pellucidum – a membrane that separates the frontal horns of the lateral ventricles from
corpus callosum to fornix
Subcortical – brain regions that lie below the cortex (e.g., thalamus, basal ganglia)
Supratentorial – above the tentorium, which is the dural covering of the cerebellum, i.e., the
cerebral hemispheres; used colloquially to describe a functional deficit
Pterion – region over the temple where the frontal, parietal, temporal, and sphenoid bones meet
U fibers – short cortical fibers that connect adjacent cortical gyri
White matter – axonal sheath of myelin on cell fibers that gives the brain tissue a white appearance
1) association – intracerebral connections
2) commissural – intercerebral, connecting equivalent areas of two hemispheres (corpus
callosum, anterior commissure, hippocampal/fornic commissure)
3) projection – between deeper structures (thalamus, hypothalamus, brain stem, cerebellum,
spinal cord) and cortex
Corticofugal – proceeding, conducting, or moving away from the cortex
Corticopetal – proceeding, conducting, or moving toward the cortex
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Gyrus – convolution of the brain surface that is caused by infolding of the cortex
Heschl’s gyrus – transverse temporal gyri on the inferior bank of the Sylvian fissure that serve as
primary auditory cortex
Sulcus – a groove or fissure of the brain that defines a gyrus; major fissures demarcate lobes of the brain
Central sulcus/Rolandic fissure – the major sulcus that runs obliquely across the superior lateral surface of
the cerebral hemisphere, separating the frontal lobes from the parietal lobes, the primary motor
and primary sensory gyri
Longitudinal/interhemispheric fissure – cleft that separates the left and right cerebral hemispheres
Sylvian fissure/lateral fissure – the major sulcus beginning at the base of the brain on the lateral aspect of
the anterior substance, extending laterally between the frontal and temporal lobes, and turning
posteriorly between the temporal and parietal lobes; divides into posterior, ascending, and
anterior branches
Prosencephalon
(forebrain)
Telencephalon
(endbrain)
Diencephalon
(between-brain)
Neocortex (80% of brain)
Basal Ganglia
Limbic System
Olfactory bulb
Lateral Ventricles
(FOREBRAIN)
Thalamus
Epithalamus
Pineal Body
Hypothalamus
Pituitary gland
Third Ventricle
Mesencephalon
(midbrain)
Mesencephalon
(midbrain)
Tectum (“roof”)
Superior/Inferior colliculi
Tegmentum (“covering”)
Cerebral peduncles
Aqueduct
Rhombencephalon
(hindbrain)
Metencephalon
(across-brain)
Cerebellum
Pons
Reticular formation
Fourth ventricle
Myelencephalon
(spinal brain)
Medulla Oblongata
(BRAINSTEM = midbrain, pons, medulla)
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Corpus callosum – genu (anterior portion) tapers into the rostrum (anterior and ventral) and isthmus that
ends enlarged at the splenium, lying over the pineal body and midbrain
1. anterior third (rostrum, genu, and anterior body) – to prefrontal, premotor, and
supplementary motor, possibly anterior inferior parietal
2. anterior midbody – precentral, possibly midtemporal
3. posterior midbody – postcentral, posterior parietal, possibly midtemporal
4. isthmus – posterior parietal, superior temporal
5. splenium – occipital, inferior temporal, ventral temporal, possibly superior parietal
Insula (Island of Reil) – cerebral cortex concealed from the surface and lying at the bottom of the Sylvian
fissure, covered by the frontal operculum, frontoparietal operculum, and temporal operculum;
associated wuth previously acquired memories, non-automatic word processing, taste
Internal capsule – V-shaped fibers going to and from cortex; thalamus (bottom) and caudate (top)
medial, lentiform nucleus (globus pallidus and putamen) lateral
Planum temporale – cortical area of the posterior surface of the superior temporal gyrus between Heschl’s
gyrus and the posterior margin of the Sylvian fissure
Supplementary motor area (SMA) – the area anterior to the primary motor cortex that is important in
temporal organization of movements; involves in sequential performance of multiple movements
and initiation of voluntary movements; at the anterior portion of Brodmann area 6
Uncus – the medially curved, anterior end of the parahippocampal gyrus located near the temporal pole; is
a landmark for the lateral olfactory area
4 c-shaped structures – follow the curve of the lateral ventricles, including caudate nucleus, corpus
callosum, fornix, and stria terminalis
See Darby & Walsh Figures 2.1, 2.2, Blumenfeld Figures 2.10, 2.11 (A-D), 2.25, 6.1, 6.2, 6.9, 19.1 and
Table 2.4
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CEREBELLUM – balance, posture, coordination, timing
Ataxia
Portion of the metencephalon that occupies the posterior fossa behind the brainstem, consisting of median
lobe (vermis) and two lateral hemispheres, connected to the brainstem by three pairs of peduncles
(superior (ouput) and middle (pons input – where info crosses) and inferior (spine input) white matter
tracts), important in the coordination of movements, especially skilled and smooth voluntary movement
(ataxia), control of muscle tone, control of posture and gait, and control of muscle movement and
equilibrium; no direct connection to lower motor neurons, with all output carried by axons of Purkinje
cells into cerebral white matter [through cortex [ventral lateral (VL) nucleus of thalamus] and brainstem];
may modulate procedural/motor learning and classical conditioning; symptoms include deficit of rapidly
alternating movements/dysdochokinisia (smooth movements), decomposition of movements into parts,
muscle fatigue, disorders of speech (slowing/slurring or scanning dysarthria, with words broken into
syllables and “explosive”), past pointing (inability to touch finger to nose or heel to shin), dysmetria
(overshoot and then oscillate to target); moderate head tremor (titubation), intention tremor, disordered
ocular movement; ipsalateral impairment (direct or double-crossed); no paresis or significant reflex
abnormalities
-
lesions of nodulus and flocculus cause disturbance of equilibrium and positional nystagmus
lesions to anterior lobe increase shortening and lengthening reactions, increased tendon
reflexes, exaggeration of postural reflexes
lesion to cerebellar hemisphere causes ataxia, hypotonia (decrease in normal resistance) and
clumsiness of ipsilateral limb
Vermis – proximal and trunk coordination; projects to fastigial nuclei
Flocculolonodular lobes – balance and vestibular-ocular reflexes; projects to vestibular nuclei and
fastigial nuclei
Lateral hemispheres – motor programming for extremities; projects to dentate nucleus
Intermediate hemispheres – distal limb coordination; projects to interposed nuclei
Input from pontocerebellar fibers (cortex), climbing fibers (red nucleus, cortex, brainstem, spinal cord),
vestibular inputs, and spinocerebellar pathways, mossy fibers
Blood supply from posterior and anterior inferior cerebellar arteries (PICA/AICA) and superior cerebellar
artery
Truncal ataxia/cerebellar gait – lurching, unsteady, and wide-based ataxic gait in which the person
appears inebriated, may have difficulty sitting without support; associated with dysfunction of the
entire cerebellum or lesions limited to its median lobe (vermis); vertigo, nausea, vomiting
(usually bilateral, but may fall or sway towards side of lesion)
Appendicular ataxia – ataxia of movements of extremities; lesion of intermediate and lateral
hemispheres (may have no signs if unilateral)
Scissors gait – steps are abnormally short and appear effortful, with the knees remaining in close
contact (seen also in MS)
Parkinsonian gait – stooped posture, flexion at the hips elbows and knees, decreased mobility,
short and shuffling steps, difficulty with initiation and stopping
Dysmetria – disordered measuring of distance/control of range of voluntary, coordinated movements in
muscular acts, tested with the finger to nose test
* Cerebellar disease and ataxia (intention tremor)
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Spastic hemiparesis – the affected arm is held flexed and immobile against the body and the leg is moved
forward stiffly and in a semi-circle, sometimes with the toe dragging
Muscle tone marked by flaccidity, rigidity/cogwheeling, spasticity, and posture retention
Slow saccades, nystagmus, vertigo (loss of suppression of vestibulo-ocular reflex), nausea, vomiting,
scanning or explosive speech, headache (frontal, occipital, upper cervical)
Tonsil herniation can compress medullary respiratory centers
Causes of acute ataxia in adults – toxin ingestion, ischemia or hemorrhagic stroke (vertebrobasilar artery)
Causes of chronic ataxia in adults – brain metastases, chronic toxin exposure (e.g., alcohol), MS,
degenerative disorders of cerebellum, or pathways
- also Dilantin and barbiturate intoxication, Wernicke-Korsakoff, autosomal dominant
progressive neurodegenerative diseases
Causes of acute ataxia in children – accidental drug ingestion, varicella-associated cerebellitis, migraine
Causes of chronic ataxia in children – cerebellar astrocytoma, medulloblastoma, Friedreich’s ataxia,
ataxia-telangiectasia
See Blumenfeld Figures 15.1, 15.2, 15.3 (A-C), Hendelman Figure 52
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CEREBROVASCULAR DISEASE
Any abnormality of the brain resulting from the pathological process of the blood vessels, including
lesion/rupture of the vessel wall, occlusion of the lumen by thrombus or embolus, altered permeability of
the vascular wall, and increased viscosity or other change of the quality of the blood; risk factors include
age, hypertension, heart disease, hyperlipidemia, diabetes, smoking, obesity, family history; also may be
migraines, sickle-cell disease, vasculitis
Rule-out migraine, seizure, CSF flow obstruction, genetic, toxic/metabolic (e.g., hypoglycemia),
infection/inflammation (e.g., encephalitis, MS), movement disorder (e.g., chorea, dystonia, tic disorder),
psychogenic
Infarct – area of cerebral necrosis due to vascular insufficiency
Ischemic – lack of adequate blood flow
Thrombus – solidified blood within a vessel
Thrombosis, cerebral – occlusion of a cerebral blood vessel by a thrombus that usually occurs within a
vessel (e.g., vertebral, basilar, carotid stenosis); most common cause of CVA; usually in morning
Sagittal sinus thrombosis – associated with hypercoagulability (e.g., pregnancy, post-partum), causing
elevated ICP, infarct, seizure (may see empty delta sign with contrast)
Embolism – sudden blocking of an artery by a thrombus fragment or other intra-arterial or intracardiac
material or air, septic, fat, cholesterol; tends to lodge at bifurcations, branchings, and curvatures
(atrial, myocardial, valvular; patent foramen ovale); associated with pain
Hemorrhage/hematoma – bleeding from vessel leakage or rupture; most often from hypertension,
affecting cerebral cortex, basal ganglia, thalamus, pons, cerebellum
- epidural – blood between the skull and dura, by rupture of the middle meningeal artery due
to fracture of temporal bone; lens-shaped biconvex; likely to be fatal
- subdural – blood in the subdural space resulting from rupture of bridging veins, exposing the
cortex to blood product and mass effect; crescent shaped (goes from hyperdense to hypodense
over time); headache, chronic pain, inattention, insomnia, nausea, vomiting, diplopia, ataxia
- subarachnoid – tracks into sulci; from arterial aneurysm rupture (berry 80%), AVM (1/3 at
junction of ACA and ACommA, also bifurcation of MCA, junction of internal carotid, and
PCommA); laceration of vessels (traumatic); severe headache (“worst ever”), can be
associated with meningismus, nuchal rigidity, vomiting, fever, diplopia, confusion, collapse,
initial focal signs, hypertension, blood in CSF and xanthochromia (yellow discoloration of
CSF due to the presence of blood that has begun to undergo hemolysis/deterioration and
release of hemoglobin), elevated ICP; often occurs during exertion/sex; death is common
because as little as 100ml can produce coma from increased intracranial volume
- cerebral/hypertensive/intracerebral/intraparenchymal – blood within the brain, frequently
associated with hypertension, in basal ganglia, thalamus, cerebellum, and pons (mainly from
penetrating branches of MCA, PCA, and basilar arteries); trauma, typically associated with
missile wounds, depressed skull fractures, and shear injuries to deep blood vessels, causes
frontal-temporal contusions; lobar hemorrhage from amyloid angiopathy causing vascular
fragility
- extracranial – inner ear, subcutaneous tissues, raccoon eyes, subgaleal (“goose egg”),
cephalohematoma (newborns)
- cerebellar – occipital headache, gait ataxia, dysarthria, lethargy
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Aneurysm – frequent rupture in the AcoA, PcoA, and middle cerebral bifurcation (90% in anterior region
circle of Willis); risks factors include hypertension, smoking, alcohol; signs include headache,
lethargy, photophobia and phonophobia, fever, meningismus/nuchal rigidity (stiff neck), Kernig’s
sign (pain in hamstrings when knees straight and hips flexed), Brudzinski’s sign (flexion at neck
causes hips to flex)
saccular/berry – have neck and dome, usually carotid and branches
fusiform – main vessel becomes dilated
Stroke/apoplexy/cerebrovascular accident (CVA) – the sudden onset of neurological dysfunction as the
result of a cerebrovascular event; risk factors are age, hypertension, high cholesterol, diabetes,
cigarette smoking, positive family history, cardiac disease, migraine, drug abuse; most common is
ischemic (thrombotic or embolic etiology), and also hemorrhagic (blood leaks from a weakened
vessel because of aneurysm or vascular malformation), also neurological (encephalitis, tumor,
epilepsy, multiple sclerosis), metabolic (hypoglycemia, hypercalcemia), pulmonary embolism,
myocardial infarction, pneumonia, or diabetic ketotic coma; can be progressive or completed
(non-progressive); symptoms include unconsciousness, syncope, dizziness, vertigo, aphasia,
dysarthria, seizures, incontinence, confusion; cell death from over accumulation of excitatory
glutamate
- Carotid (typically progresses for up to 18 hours)
1) ACA – contralateral lower extremity paresis; bilateral infarct yields mutism, apathy,
psuedobulbar palsy
2) MCA – contralateral hemiparesis/upper extremity paresis, hemisensory loss, aphasia, hemiattention
- Vertebrobasilar (typically progresses for 2-3 days)
1) Basilar – cranial nerve palsy with contralateral hemiparesis (no cognitive impairment),
internuclear opthalmoplegia; coma, locked-in syndrome if total occlusion
PCA – contralateral homonymous hemianopsia, alexia without agraphia
2) Vertebral – lateral medullary (Wallenberg’s) syndrome (dysarthria, dysphagia, ataxia)
Transient ischemic attack (TIA) – a sudden, onset of focal cerebral neurological dysfunction
attributable to blood vessel disease which resolves in less than 24 hours; most carotid TIAs last 3-5
minutes and vertebrobasiliar 10-12 minutes; indicative of CVD and ~5% will develop a stroke within
a year if untreated, treatment usually endarterectomy and aspirin/antiplatelet therapy
Carotid – contralateral hemiparesis, hemianopsia, hemisensory loss, aphasia, ipsalateral
monocular blindness (amaurosis fugax) due to ophthalmic artery first branch of ICA
Vertebrobasilar – vertigo, vomiting, tinnitus, paresthesia or numbness, dysarthria, dysphagia,
transient global amnesia, drop attacks, nystagmus, ataxia, cranial nerve abnormalities
Arteriosclerosis – thickening and hardening of smaller arteries associated with chronic hypertension,
major risk factor for stroke
Artherosclerosis – buildup of fatty deposits on arterial walls, associated with MI; most often affect MCA,
ACA, ophthalmic artery
Vasculitis – inflammation or vasospasm causing narrowing of vessels
Vascular malformations:
1) Arteriovenous Malformation (AVM) – congenital vascular abnormality of direct connection
between artery and vein that bypasses normal capillaries
2) Cavernous malformation – abnormally dilated vascular cavity lined by only one layer of vascular
endothelium
3) Capillary telangiectasias – small regions of abnormally dilated capillaries (rarely hemorrhage)
4) Venous angiomas – dilated veins (no clinical symptoms)
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5) Hemangioma/cavernous angioma – a vascular malformation that resembles a neoplasm
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Transient neurologic signs from TIA, migraine, seizure, cardiac arrhythmia, hypoglycemia; also AVM,
cyst of third ventricle, hypo/hyperkalemia, MS, encephalitis, medication, toxin, chorea, dystonia,
tics, panic attacks, narcolepsy, trigeminal neuralgia
Transient loss of consciousness from syncope (vasovagal hypotension)
Lacuna – ischemic infarction, generally less than 5mm, from occlusion of distal branches of arteries,
associated with hypertension and arteriosclerosis
Lacunar syndromes:
1) Pure motor dysarthria, or ataxic hemiparesis – posterior limb of internal capsule (lenticulostriate
MCA, anterior choroidal ICA, perforating PCA), ventral pons (penetrating basilar)
2) Pure sensory stroke – ventral posterior lateral (VPL) thalamus (thalamoperforator PCA)
3) Sensorimotor – posterior limb of internal capsule and thalamus (thalamoperforator PCA or
lenticulostriate MCA)
4) Basal ganglia – hemiballismus (lenticulostriate MCA, anterior choroidal ICA, thalamoperforator
PCA, Heubner’s ACA)
Medications: aspirin, t-PA, heparin
Thrombolytic therapy – acute treatment of ischemic stroke that uses agents to dissolve clots obstructing
flow through the cerebral arteries
Endarterectomy – surgical revascularization procedure in which the carotid artery is opened and plaque
removed
Embolization – intervention neuroradiological method to close vessels feeding arteriovenous
malformations prior to resection, treat aneurysms not surgically accessible, and close cavernous
fistulas; may also be performed when uncontrolled bleeding follows a head or neck injury
Hachinski ischemia scale – assesses risk factors, clinical signs, and historical variables associated with
cerebrovascular disease, used to determine the likelihood of vascular causes as the source of
cognitive impairment in dementia
Contusion – a bruise without cerebral hemorrhage
Luxury perfusion – transient phenomenon seen after cerebral infarction in which there is an
enhanced capillary blush and early venous filling on angiography
Sentinel bleed – leakage of small amounts of blood that may occur intermittently before a larger
hemorrhage
Steal phenomenon – diversion of blood flow from vascularized tissue to tissue deprived of blood
flow due to proximal arterial obstruction or a vascular abnormality
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CLINICAL PSYCHOLOGY
Cognitive-Behavioral
1. Beck’s Cognitive Theory – negative (helpless, unlovable), distorted, illogical statements
(automatic thoughts) involving the cognitive triad about the self, world and future (work to
distance and neutralize); includes arbitrary inference, selective abstraction, overgeneralizations,
magnification and minimization, personalization, dichotomous thinking
2. Ellis’ Rational Emotive Therapy (RET) – irrational thoughts lead to maladaptive behaviors,
challenge beliefs
3. Stimulus control – narrowing (restrict target behavior to limited set of stimuli), cue strengthening
(link behavior to cues), competing responses (eliminate responses that block desirable behaviors
and encourage responses that block undesirable behavior)
4. Stress inoculation – cognitive preparation (education), skills acquisition (learn and rehearse),
practice (application); good for aggression, impulsivity, anger
5. Paradoxical intention – encourage what is feared to circumvent anticipatory anxiety (e.g.,
insomnia)
Client-Centered (Rogers) – unconditional positive regard, empathy, and genuineness allow for
congruence and self-actualization
Psychoanalytic Theory
1. Freud’s Traditional Psychoanalysis – ego defense mechanisms keep unacceptable impulses from
reaching consciousness; reaction formation (OCD), displacement (phobia); steps of confrontation,
clarification, interpretation, working through
a. Id – unconscious, functions under pleasure principle and biological drives (selfpreservation, libido, aggression)
b. Ego – conscious, functions under reality principle
c. Superego – conscience, from internalization of societal and parental restrictions
2. Jung’s Analytic Psychology – extroversion vs. introversion, personal unconscious (repression)
and collective unconscious (archetypes); dream interpretation, association, transference analysis
3. Adler’s Individual Psychology – pathology (neuroses, psychoses, delinquence) results from
maladaptive and defensive attempts to overcompensate for feelings of inferiority; goal to replace
“mistaken style of life”; use dream interpretation, resistance, transference, role-play
4. Neo-Freudians – relationships throughout lifespan
Sullivan
a. Parataxic distortion – act toward people currently as if significant others from past
b. Second parataxic mode – person sees causal connections between unrelated events
c. Prototaxic mode – discrete unconnected momentary states (before language
development)
Horney – parental behaviors (indifference, overprotection, rejection) causes child to experience
basic anxiety (helplessness, isolation in hostile world); defend against anxiety though movement
toward others, movement away from others, movement against others
Fromm – focus on effects of societal structures and dynamics on personality; styles include
receptive, exploitative, hoarding, marketing, productive
5. Ego Analysts (Anna Freud, Hartmann) – ego defenses to resolve conflicts; ego autonomous
functions to adapt; pathology when ego loses autonomy from id; use re-parenting
6. Object Relation (Mahler, Winnicott, Kernberg, Fairbairn, Kohut) – insight into repeated
relationships through original mother-child relationship; internal representations of self and others
(introjects); use re-parenting (Kohut – narcissism when self-love not satisfied by parent)
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Transactional analysis (Berne) – simplify client’s understanding of unhealthy interactions to let adult ego
take control and integrate three ego states (child, parent, adult)
Personality
1. strokes – recognition of others and how transactions occur at social and covert levels
2. scripts – life plan
3. life positions – “I’m okay/not okay”, “You’re okay/not okay”
Transactions
1. complementary – original communication met with appropriate response
2. crossed – original communication elicits inappropriate ego state
3. ulterior – confusion because one of communicators gives dual message
Gestalt Therapy (Perl)– want integration of whole through awareness and integration of self and
environment; overcome boundary disturbance; want consistency of self (actualization, growth, awareness)
and self-images; “I” statements, dream analysis, empty chair technique, here-and-now
Boundary disturbances include introjection (assimilate without understanding), retroflection
(substitution of self for environment), deflection (avoidance), confluence (indistinct boundary
between self and environment), isolation
Existential Psychotherapy – individual and ultimate concerns of existence (death, isolation,
meaninglessness, responsibility); neurotic anxiety from evading of normal anxiety
Reality Therapy (Glasser) – pathology from inability to meet basic needs (survival, belonging/affiliation,
power, fun, freedom); from work with delinquent adolescents; want to replace failure id with success id;
Schools Without Failure program
Solution-Focused Therapy – move from complaint narrative to solution narratives, ask questions
(exception, scaling, formula tasks, miracle, skeleton key)
Family Therapy
1. Systems Theory – want to change from closed to open (accepting of outside influence); includes
wholeness (interrelated), non-summative (whole greater than sum), equifinality (same results for
all), equipotentiality (one cause can lead to different results), homeostasis (try to maintain status
quo), negative feedback (correct deviations), positive feedback (create deviations)
2. Communication/Interaction Therapy – encourage positive communications; includes double-bind
communication, metacommunication, symmetrical or complementary communication,
pseudohostility
3. Bowen’s Extended Family Systems Therapy – interlocking constructs of differentiation of self,
triangulation, nuclear family emotional system, family projective process, emotional cutoff,
multigenerational transmission process, sibling position/birth order, societal regression; use
genograms and triangulation models
4. Minuchin’s Structural Family Therapy – look at family as whole and subsystems; boundaries can
be enmeshed or disengaged; conflict, triangulation, detouring, stable coalition; therapist
restructures (enactment, reframing, blocking), joins to model, creates a family map
5. Haley’s Strategic Family Therapy – restructure through paradoxical interventions, reframing,
circular questioning
6. Object Relations Family Therapy – psychodynamic principles; insight is core for family change
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Group Therapy - Adler, Burrow, Moreno, Yalom
Balance between developmental level, gender, intelligence, stability, size
Stages – hesitancy, dependence on leader, concerned with structure; hostile and critical
communication; cohesion and trust, disclosure
Role of leader – knowledgeable about group dynamics, manage conflicts, encourage
participation, handle transference and countertransference
Benefits – sense of hope, learn social skills, universality, sharing, cohesiveness, support
Cultural/Ethnic Considerations
Etic approach – look at culture from outside using universally accepted means of investigation
Emic approach – study a culture from inside to see as own members do (preferable)
1. African American – more emotional, nonverbal, concrete
Cross’s Model of Psychological Nigrescence – pre-encounter, encounter, immersionemersions, internalization, commitment
2. Latino – patriarchal, rigid family and sex roles
Cuento therapy – Spanish folktales
3. Native Amerian – importance of elder tribal members, legends; non-directive, open, accepting
Network Therapy – therapist serves as catalyst
4. Asian American – family and social roles well defined and rigid, therapy not encouraged
5. Gay/Lesbian
McLaughlin’s 8 Stages of Homosexual Id Formation – isolation, alienation and shame,
rejection of self, passing as straight, consolidating a self id, acculturation, integration of self
and public id, pride and synthesis
Berry’s acculturation model – integration, assimilation, separation, marginalization
Wrenn’s cultural encapsulation – define world in terms of own beliefs and stereotypes, minimizing and
ignoring cultural variations, unaware of biases, counseling dogmatic
Hall’s communication styles – high-context (nonverbal information) vs. low-context (verbalizations
stressed and elaborate codes)
Minority Identity Development Model – conformity (to dominant culture), dissonance, resistance and
immersion, introspection, synergistic articulation and awarness
Helms’ Identity Development for Whites – parallel, regressive, progressive, and crossed interactions;
limited contact, disintegration, reintegration, pseudo-independence, immersion-emersion,
autonomy
Crisis intervention – formulation, implementation, termination
Brief psychotherapy (<25 sessions) – primary problem focus, therapeutic alliance
Good predictors of therapy outcome – high intelligence, openness, low defensiveness, high ego strength,
high anxiety tolerance, moderate therapy expectations
2/3 improve with therapy versus 1/3 of controls; 80% better off than controls
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CRANIAL NERVES (CN)
I
Olfactory
Sensory
II
Optic
Sensory
III
Oculomotor
Motor
Parasympathetic
IV
Trochlear
Motor
V
Trigeminal
Sensory
Motor
VI
Abducens
Motor
VII
Facial
Sensory
Motor
Parasympathetic
VIII
Vestibulocochlear
Sensory
IX
Glossopharyngeal
Sensory
Motor
Parasympathetic
X
Vagus
“wandering”
Sensory
Motor
Parasympathetic
XI
Spinal accessory
Motor
XII
Hypoglossal
Motor
Smell
Anosmia
Vision (acuity, color, fields, extinction)
Anopsia
(covered in myelin, so susceptible to CNS illnesses like MS)
Eye movement (reaction to light, lateral inward,
eyelid), eye opening
Pupillary constriction and accommodation (Edinger-Westphal)
Dilated pupil “blown”, ptosis, outward deviation,
diploplia
Eye movement (up and down, inward/oblique)
Diploplia (vertical)
Face light touch, hot/cold, corneal reflex, jaw reflex
(ipsalateral; 3 branches – ophthalmic, maxillary, mandibular)
Masticatory movements (face and head, mucous
membranes of nose and mouth, cornea and conjunctiva,
innervates meninges)
Decreased sensation in face, severe pain (neuralgia/tic
douloureux), jaw weakness, asymmetric chewing
Eye movement (lateral movements, outward/abduction)
Diploplia (horizontal), deviation of eye inward
Taste (anterior 2/3 tongue)
Facial movements/strength, expression, eye closing
Salivation (superior) and tearing (lacrimation)
Bell’s palsy, hemifacial spasm, loss of taste
(UMN – forehead spared, neighbor effects (opposite LMN))
Hearing (hearing test, caloric/water), position and
movement of head
Deafness, tinnitus, disequilibrium, vertigo,
spatial disorientation
(covered in myelin)
Tongue (posterior 1/3), tonsils, pharynx (gag reflex),
middle ear
Swallowing
Salivation (inferior)
Spasms of pain in posterior pharynx
Pharynx and larynx (ambiguus), esophagus, external ear,
chemo/baroreception for heart, visceral for
thoracic and abdomen (dorsal X)
Speech (“ah”), swallowing (movement of larynx and pharynx)
Cardiovascular, respiratory, GI
Hoarseness, poor swallowing, loss of gag reflex
Neck and shoulder (trapezius and sternocleidomastoid)
muscles, viscera
Wasting of neck with weakened rotation, inability to
shrug
(ipsalateral weakness and head turns away from lesion)
Tongue muscles (movement, tremor, wasting,
wrinkling)
Wasting of tongue with deviation to side of lesion on
protrusion
(UMN contralateral, LMN ipsalateral)
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Twelve paired nerves arising from the brainstem that innervate muscles of and receive sensory
information from the head
Sensory/Afferent (Pure I, II, VIII) (more dorsal)
Visceral (general and special visceral): VI, IX, X (solitary nucleus)
General somatic: V, VII, IX, X
Special somatic: VIII
Motor/Efferent (Pure III, IV, VI, XI, XII) (more ventral)
Somatic motor (general somatic): III, IV, VI, XII
Branchial motor (special visceral): V, VII, IX, X, XI
Parasympathetic (general visceral): III, VII, IX, X
Mixed: V, VII, IX, X
Without primary sensory nuclei in brainstem: I (Olfactory sulci), II (Optic chiasm)
Midbrain: III, IV, (V)
Pons: V, VI, VII, VIII
Medulla: (V), (VII), (VIII), IX, X, XI, XII
Have 3 motor columns and 3 sensory columns in brainstem
Oculomotor palsy (III) - pupil constriction, ptosis (drooping or closure of the eyelid), paresis of
adduction; susceptible to PcommA aneurysm; diabetic infarction (often with contralateral
hemiparesis from ipsalateral midbrain lesion)
PERRL/PERRLA – pupils equal, round, reactive to light, and accommodating (CN III functioning)
Trochlear palsy (IV) – exit crossed and lateral (only nerve that does) and susceptible to compression
from cerebellar tumors and shear injury from head trauma
Abducens palsy (VI) – susceptible to downward traction injury by elevated ICP (often with contralateral
hemiparesis from ipsalateral pons lesion)
Bell’s palsy (VII) – hemifacial weakness; often with hyperacusis (abnormal acuteness of hearing)
Bulbar Palsy (IX, X, XI) – dysarthria, dysphagia, hypoactive jaw and gag reflexes, respiratory impairment
Cranial nerve palsies (ipsalateral palate paralysis and facial hypalgesia) with alternating hypalgesia
(contralateral body anesthesia) and ipsalateral ataxia from medullary lesion (Wallenberg’s)
Taste (CN VII and IX) through ventral posterior medial (VPM) nucleus of thalamus, projecting to
postcentral gyrus adjacent to tongue somatosensory area and into parietal operculum and insula
Hearing (CN VIII) through medial geniculate nuclei (MGN) of thalamus, projecting to primary auditory
cortex on Heschl’s transverse gyri (hearing loss can be conductive or sensorineural)
Vision through lateral geniculate nucleus (LGN) of thalamus; medial longitudinal fasciculus (MLF)
connects oculomotor, trochlear, abducens, and vestibular nuclei (supranuclear pathways;
connection of CN VI and contralateral CN III; III, IV and VI essential for eye movement/
conjugate gaze; also input from paramedian pontine reticular formation (PPRF)
Schwannoma’s on VIII and V
Trigeminal neuralgia associated with herpes zoster (shingles)
Dysphagia – impaired ability to chew or swallow food or liquid due to impairment in
corticobulbar tracts or lesions of V (trigeminal), VII (facial), IX (glassopharyngeal),
X (vagus), or XII (hypoglossal) cranial nerves; prominent component of bulbar palsy
Dysphonia – an impairment of sound generation from the larynx; may result in breathiness,
hoarseness, or harsh voice quality
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Face: sensation by V, movement and expression by VII
Taste: VII and IX primarily
Sensation from meninges: V and X
Viscera: IX and X, speech from nucleus ambiguus (also incorporating XI)
Larynx and pharynx: IX, X, XI
Oral nucleus: V, VII, IX, X (spinal trigeminal, interpolar)
Bulbar laughing and crying – VII, IX, X, XII
See Sidman & Sidman 1120A, 1122A, 1134A, Blumenfeld Figure 2.22
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CRANIUM AND VENTRICLES
Ventral – belly
Dorsal – back
Rostral – beak
Caudal – tail
(90 degree shift at brainstem)
Foramina – hole allowing cranial nerves, spinal cord, blood vessels to enter and leave cranial cavity
Foramen magnum – the opening in the base of the skull (occipital bone) where the brain stem becomes
the spinal cord; cervicomedullary junction is where the spinal cord meets the medulla
Fossae – compartments of the cranial cavity divided by ridges of bone
Anterior fossa – contains frontal lobes
Divided by lesser wing of sphenoid bone
Middle fossa – contains temporal lobes
Divided by petrous ridge of temporal bone and meninges
Posterior fossa – contains cerebellum and brainstem
Meninges – the three membranes enclosing the brain and spinal cord and lining the skull and vertebral
canal (PAD from in to out)
1)
pia (closest to brain)
1a)
subarachnoid space – CSF and major arteries (weblike)
2)
arachnoid (middle)
arachnoid and pia = leptomeninges
2a)
subdural space – bridging veins and dural venous sinuses
3)
dura (furthest from brain) – strongest layer that includes falx cerebri and tentorium
cerebelli;
periosteal outer layer fused to meningeal inner layer, except for
i.
Falx cerebri – dural sheet separating the two cerebral hemispheres
ii.
Tentorium cerebelli – the portion of the dura covering the posterior fossa,
attached to the falx, separating the cerebellum from the occipital and temporal
lobes (“tent”; midbrain seen through tentorial notch)
3a)
epidural space – middle meningeal artery (supplies dura)
Ventricles, cerebral – cavities of the brain filled with CSF, lined with ependymal cells
a) two lateral (anterior/frontal, body, atrium, posterior/occipital, inferior/temporal; touching
caudate nucleus and thalamus, CC on top) connect to third by
b) the Foramen of Monro, formed by thalamus and hypothalamus, connecting to the fourth by
c) the Aqueduct of Sylvius/cerebral aqueduct, formed by cerebellum on top and pons and
medulla below
Cerebral Spinal Fluid (CSF) – fluid produced by choroid plexus at posterior part of lateral ventricle,
enters 3rd ventricle via the Foraminae of Monro, drains into the 4th ventricle via the Aqueduct of
Sylvius (at midbrain), then into the subarachnoid space via the Lateral foramina of Luschka and
Midline foramen of Magendie, then reabsorbed by arachnoid granulations and emptied into the
great dural venous sinuses (normal adult volume 150cc, 500cc produced per day); CSF collection
cisterns; alterations may reflect nervous system impairment (e.g., bacterial meningitis, myelitis,
MS, subarachnoid hemorrhage) or germ-cell proteins (chorionic gonadotropic, alpha-fetal
proteins)
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Choroid Plexus – epithelial tissue in ventricular system that secretes CSF, a major component of
the blood-brain barrier, found in body of lateral ventricles (not anterior horn) and roof of third
ventricle and roof of fourth ventricle
Cerebral aqeduct/Aqeduct of Sylvius – canal draining CSF from third to fourth ventricle through
the midbrain; common site of obstruction causing childhood hydrocephalus
Foramen of Monro – opening on both the left and right side that connects the third ventricle to
the lateral ventricles
Foramina of Luschka – two lateral opening openings between the fourth ventricle and
subarachnoid space
Foramen of Magendie – the opening between the fourth ventricle and the subarachnoid space
Cisterns – widening of subarachnoid space to form large CSF collections
Macro Cisterna Magna – posterior fossa space receiving CSF from foramens of Magendie and Luschka
CSF reabsorbed through arachnoid villi (if blocked leads to communicating hydrocephalus) in dural
sinuses through hydrostatic/hydraulic pressure in one-way form
Blood-brain barrier – capillary endothelial cells are linked by tight junctions, lipid-soluble substances (O2
and CO2) pass; barrier interrupted in circumventricular organs [e.g., median eminence and
neurohypophysis (pituitary release regulation), pineal (melatonin release)]
- vasogeneic edema – excessive extracellular fluid
- cytotoxic edema – excessive intracellular fluid
Intracranial pressure (ICP) – pressure within the cranial vault; increase results from increased volumes of
CSF, blood, or brain tissue; symptoms include headache, altered mental state (irritability,
depressed alertness and attention), nausea, projectile vomiting, papilledema (engorgment and
elevation of optic disc), visual loss, diplopia, Cushing’s triad (hypertension, bradycardia, irregular
respiration); treated with steroids, mannitol, hyperventilation (vasoconstriction), shunt
Normal pressure <20 cm H2O or <15 mm Hg
Cerebral Perfusion Pressure = Mean arterial pressure – Intracranial pressure
Low CSF – headache worse while standing
High CSF – headache worse when lying down
Herniation, brain – abnormal protrusion of the brain through a natural opening due to increased
intercerebral pressure
- central – downward displacement of brainstem
- subfalcine – cingulated gyrus and other brain structures herniated under falx cerebri; can
occlude ACA and lead to infarcts
- tonsillar – protrusion of the cerebellar tonsils through the foramen magnum, which exerts
pressure on the medulla; often fatal
- transtentorial/uncal/temporal – downward displacement of medial structures through the
tentorial notch (over bone) by a supratentorial mass, which in turn exerts pressure on the
brainstem; triad of “blown” pupil (CN III - unresponsive), hemiplegia (usually contralateral,
ipsalateral called Kernohan’s), coma; compression of PCA can cause infarcts
Ventriculostomy – operation for the treatment of hydrocephalus to establish free communication
between the floor of the third ventricle and the underlying interpeduncular cistern
See Blumenfeld Figures 5.1, 5.2, 5.4, 5.11, 5.18, 12.3, Hendelman Figure 20A
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DEMENTIA
Generalized loss of cognitive functions (including memory impairment and at least one other impairment)
resulting from cerebral disease occurring in clear consciousness (i.e., absence of confusional
state/delirium) causing significant impairment in functioning; does not suggest progressive course or
irreversibility
I. AIDS dementia – from HIV entering the brain and causing diffuse, multifocal destruction of
white matter and subcortical structures, micronodules throughout brain; characteristic features
include: apathy, social withdrawal, impaired concentration and memory (learning and recall),
psychomotor slowing, impaired fluency, and executive dysfunction; may have visual
hallucinations, delusions, delirium; tremors, impaired repetitive movement, imbalance, ataxia,
hypertonia; Kaposi’s sarcoma lesions; in late stages may develop myoclonus or parkinsonism
Sidtis & Price AIDS Dementia Complex Staging Scheme (1997)
1) Stage 0 (normal)
2) Stage 0.5 (equivocal/subclinical) – gait and strength normal, may show mild motor and
cognitive signs not causing significant impairment
3) Stage 1 (mild) – functional, intellectual, or motor impairment, can walk without
assistance
4) Stage 2 (moderate) – only able to perform basic activities of self-care, may need prop for
ambulation
5) Stage 3 (severe) – major intellectual incapacity and/or motor disability
6) Stage 4 (end stage) – nearly vegetative, nearly mute, paraparetic/paraplegic with double
incontinence, intellectual and social skills rudimentary
II. Alcoholic dementia – cognitive decline associated with chronic alcohol abuse of 15-20 years;
includes executive dysfunction, decreased interest, poor personal hygiene, poor judgment,
decreased cognitive efficiency, poor attention and recent memory, and flattened affect; associated
with enlarged ventricles, frontal cortical atrophy and thinning of cerebral cortex
III. Alzheimer’s disease (#1 - 50%) – marked by
1) senile/amyloid/neuritic plaques in cortex and hippocampus [enlarged, degenerating
axonal endings (dystrophic neuritis) surrounded by a core of extracellular amyloid,
protein core with beta-amyloid and ApoE; associated with dementia severity]
2) neurofibrillary tangles (intracellular accumulation of tau proteins – most highly correlated
with dementia due to synapse loss) due to loss of presynaptic muscarinic cholinergic
neurons in nucleus basalis of Meynert/substantia innominata and also septal nuclei,
nucleus of the diagonal band; additional loss of NE, SE, Somastostatin, and vasopressin;
also granulovacular bodies and atypical dendritric arborization; cortical atrophy with
hypometabolism in posterior parietal temporal regions; risk factors are being female (2x
more), TBI, thyroid disease; medications to increase postsynaptic muscarinic Ach and
NMDA include tacrine, donepezil (Aricept), rivastigmine, galantamine, Namenda;
Carphologia/carphology/floccillation – lint picking or aimless plucking at clothes frequently
accompanied by chewing movements
Autosomal dominant transmission (3 possible alleles, one form each parent):
1. Chromosome 21 (Down’s syndrome – mutation of Amyloid Precursor Protein, early onset
familial)
2. Chromosome 1 (mutation of presenilin 2 genes, early onset),
3. Chromosome 14 (mutation of presenilin 1 genes, early onset)
4. Chromosome 19 (encodes ApoE, E4 allele increases and E2 allelle decrease, late onset familial)
5. Chromosome 12 (encodes alpha 2-macroglobulin, plays role in amyloid deposition, late-onset)
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IV.
V.
VI.
VII.
VIII.
IX.
X.
3) Areas affected
i. medial temporal lobes (amygdala, hippocampal formation, entorhinal cortex)
ii. basal temporal cortex (lateral posterior cortex, parieto-occipital cortex, posterior
cingulate gyrus)
iii. frontal lobes
4) Stages
i. 1-3 years: deficits in memory (new learning and explicit), visuospatial skills
(construction, disorientation), and language (empty speech, WFD/anomic
aphasia); may show indifference and irritability
ii. 2-10 years: deficits in memory (more severe recent and remote – intrusions and
FP), visuospatial skills (more severe construction, disorientation), language
(fluent aphasia, impaired comprehension, relatively preserved repetition),
acalculia, ideomotor apraxia, delusions (20-35%), overall decreased cognition;
indifference and irritability; restlessness and pacing; EEG slowing, may see
cerebral atrophy, hypometabolism/hypoperfusion
iii. 8-12 years: echolalia, palilalia, or mutism; cognition severely impaired, apathy,
limbs assume rigid and flexed position; urinary and fecal incontinence; EEG
diffuse slowing; diffuse cerebral atrophy, hypometabolism/hypoperfusion, death
often from pneumonia or urinary tract infection with sepsis
Axial dementia – loss of recent memory due to impairment of midline (axial) brain structures
which may include thalamus, hippocampus, fornix, mammillary bodies, and hypothalamus (e.g.,
Korsakoff’s)
Cortical dementia – dementia characterized by a loss of higher cortical function such as aphasia,
apraxia, agnosia, amnesia, acalculia, visuospatial deficits, deficits in judgment with relatively
normal neurological exam and intact motor functions, gait, posture, speech; associated with
neocortex and hippocampus (e.g., Alzheimer’s disease, Pick’s, FLD)
Creutzfeldt-Jakob Disease (CJD) – a rare, subacute cerebral degeneration transmitted by prions
(no DNA or RNA) and characterized by a rapidly progressive dementia; associated with varying
degrees of myoclonus, ataxia, derangement of posture and movement, disturbance of vision, EEG
abnormalities (runs of sharp waves/periodic complexes), and seizures; generally affects those
over 65 and course is usually fatal within 6 months; biopsy reveals subacute spongiform
encephalopathy; autosomal dominant pattern (chromosome 20)
Dementia of the Alzheimer’s Type (DAT) – dementia that behaviorally appears to be
Alzheimer’s Disease without pathological verification
Dementia paralytica/neurosyphilis/general paresis – nervous system manifestation of syphilis
typically appearing 15-30 years after initial infection that consists of executive dysfunction and
typically begins with personality change and apathy; other deficiencies include poor personal
hygiene, poor judgment, mood swings, progressive intellectual decline, attention and memory
impairment, and wandering, can see psychosis; involves frontal lobe atrophy, meningeal
thickening, and vascular lesions; diagnosed through CSF; Argyll-Robertson pupils (accommodate
but do not react); currently rare because of treatment
Dementia pugilistic (“Punch Drunk”) – condition characterized by forgetfulness, psychomotor
slowning, dysarthria/slurring, and wide-based gait that occurs in boxers; common flattened affect
and parkinsonian extrapyramidal signs of pyramidal and cerebellar dysfunction; may have
seizures, paranoia, euphoria, depression; associated with cerebral atrophy, thinning of CC,
depigmentation of substantia nigra, neurofibrillary tangles
Dialysis dementia – subtle personality change, speech impairment, and cognitive impairment that
may develop following extensive hemodialysis; begins by resolving day after dialysis but
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XI.
XII.
XIII.
XIV.
XV.
XVI.
XVII.
XVIII.
XIX.
XX.
XXI.
XXII.
progresses to general cognitive impairment, asterixis (rapid contraction followed by slow
extension), mutism, myoclonus, and possible seizures; may be related to high levels of aluminum
Frontal Lobe/Frontotemporal Dementia – dysexecutive syndrome (perseveration, forced
utilization, disinhibition, apathy, inability to shift attention), mood/personality/behavioral changes
usually first (disinhibition, impulsivity, lack of concern, stereotypy, witzelsucht laughter);
reduced speech (abulia, mutism); altered eating (hyperphagia); average onset 55 years; autosomal
dominant pattern (chromosome 17), tau pathology, TBI; poor executive functions and verbal
fluency
Lewy-body dementia – a Parkinson Plus syndrome that appears like DAT, with a combination of
parkinsonian extrapyramidal signs (masked face, bradykinesia, resting tremor, postural reflex
abnormalities, gait impairment) and dementia with delusions, visual hallucinations, and
fluctuating mental status/confusion; cortical (not basal ganglia) neurons and substantia nigra
contain Lewy bodies (eosinophilic intracytoplasmic ubiquitin positive inclusions) but not
neurofibrillary changes or plaques (or else AD); use antiubiquitin staining; after age 50; rapid
decline; fluctuating attention, variable memory deficits, poor memory retrieval, deterioration in
verbal functions and visuospatial skills
Multi-infarct dementia (#2 – 10-15%) – a vascular, arteriosclerotic dementia arising from
repeated small cerebral infarctions (etat lacunaire), associated with physical
impairments/psychomotor retardation including paresis, clumsiness, rigidity, and reflex
abnormalities; gait disturbance, pseudobulbar palsy with dysarthria, focal neurological deficits;
depression; emotional lability; there is usually abrupt onset followed by step-wise deterioration;
EEG focal slowing; operationalized using the Hachinski ischemia scale
Pick’s Disease (lobar atrophy) – idiopathic, progressive dementia associated with severe atrophy
of the frontal lobes and anterior temporal lobes; neuronal loss in cell layers 1-3 and Pick’s bodies
in cytoplasm (dense argentophilic intraneuronal inclusions causing a mild increase in neuron
size); personality change is often the initial behavioral manifestation (disinhibition, restlessness,
stereotyped behavior), aphasia with stereotyped verbal output may be a prominent feature,
memory is relatively spared and visuospatial function relatively preserved earlier on; hyper oral
tendencies (Kluver-Bucy syndrome)
Presenile dementia – occurring before age 60-65
Primary progressive aphasia – aphasia without initial dementia or memory impairment;
degeneration in the left temporal lobe from perisylvian cortex
Semantic dementia – characterized by selective impairment in semantic memory with relative
sparing of nonsemantic language components and perceptual and spatial skills, thought to result
from focal cortical degeneration predominantly affecting the temporal poles
Senile dementia – occurring after age 60-65
Subcortical dementia – dementia due to damage of basal ganglia, thalamus, or brainstem
characterized by slowed cognition/psychomotor retardation (bradyphrenia), memory retrieval
disturbance, visuospatial abnormalities, disturbance of mood/affect (apathy, loss of initiative),
poor fluid thinking, difficulties with complex intellectual tasks, speech or motor system
abnormalities (tremor, dystonia, dysarthria, choreoathetosis, stooped/hyperextended posture, poor
coordination), and absence of aphasia, apraxia, and agnosia (e.g., HD, PD, PSP)
Toxic and metabolic dementias – abrupt onset, short course, acute confusional state; can be due to
genetics, hypoxia, endocrine disease, medications, metals, nutritional deficiencies, drug
intoxication
Vascular dementia – resulting from cerebrovascular disease from repeated cerebral infarction,
single vascular insult, or chronic ischemia; risk factors include hypertension, heart disease,
diabetes, hyperlipidemia, smoking
Vasculitis dementia – caused by inflammation of the cranial arteries, associated with systemic
illnesses such as giant cell arteritis and lupus
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Common causes:
>65 – AD, MID
21-65 – AIDS, drug and alcohol abuse, head trauma, MS and other demyelinating diseases
Reversible causes – medication, depression, hypothyroidism, electrolyte imbalance (calcium, magnesium,
sodium), B12 deficiency, other metabolic abnormalities, subdural hematoma, normal pressure
hydrocephalus
Sundowning – increased confusion during the late afternoon and early evening hours that is often
present in patients with dementia or acute confusional states
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DEVELOPMENTAL DISORDERS
I. Craniospinal Deformities
Neural tube – the embryonic tube that develops into the spinal cord and brain
A. Neural tube defects (3rd-4th gestational week) – from ectodermal layer (take folic acid)
I.
Upper neural tube closure defects
A. Anencephaly – vault of skull absent, absence of cerebral hemispheres, diencephalon, and
midbrain (brain masses), face grossly abnormal
B. Cranium bifidum (fusion defects) and encephalocele – skin-covered brain, meninges, or
CSF protrudes through skull defect; MR, ataxia, CP, and epilepsy associated with
hydrocephalus
C. Dandy-Walker malformation – cerebellum and medulla fail to develop; associated with
hydrocephalus, MR, agenesis of CC, craniofacial deformities, macrocephaly, Klippel-Feil
syndrome, DeLange syndrome
D. Arnold-Chiari malformation – deformation of brain stem and cerebellum, displaced
downward; associated with psychomotor retardation, hydrocephalus, spina bifida,
myelomeningocele
II.
Lower neural tube closure defects
Spina bifida – a developmental anomaly characterized by defective closure of the bony
encasement of the spinal cord, so that the cord and meninges may protrude through
A. Spina bifida occulta – abnormal fusion of spinal umbar vertebra without involvement of
the spinal cord tissue, often asymptomatic; may be associated with lipoma, congenital
dermal sinuses, dimples
B. Spina bifida cystica – spinal defect that includes a cystic-like sac, which may or may not
contain the spinal cord; MR, paraplegic; may be due to folic acid deficiency, recessive
genetic abnormality, radiation, toxins
1. meningocele (no spinal cord protrusion) – meninges and skin protrude through
spine defect to form CSF-filled bulge; associated with gait impairment, kidney
and bladder problems
2. myelomeningocele/meningomyelocele (spinal cord protrusion) – rudimentary
spinal cord and meninges because nerve roots fail to separate from the
epithelium and protrude into sac; associated with hydrocephalus, meningitis,
Arnold-Chiari; associated with maternal use of anti-epileptics (Tegretol,
Depakote)
III.
Other
A. Hydranencephalus – cerebral hemispheres replaced by CSF cystic sacs, enlargement of
head, hydrocephalus; may be due to vascular occlusion causing necrosis
B. Porencephaly – symmetrical cavities in the cortex, cystic lesion, associated with MR,
epilepsy; may be due to trauma, vascular occlusion, infection
B. Enlargement of the head:
1) Hydrocephalus – frontal bossing, eyes turned down, prominence of scalp veins, separation of
cranial sutures, thinning of scalp, “cracked-pot” sound on percussion of skull
2) Macrocephaly – large head with relatively normal ventricles but enlarged brain, seen in late TaySachs disease, Alexander disease, and spongy degeneration of infancy
3) Megalocephaly – an unusually large head or a progressive enlargement of the bones of the head,
face, and neck
C. Craniostenoses/Craniosynostosis – a condition in which the cranial sutures fuse prematurely, resulting
in deformity of skull growth and can cause developmental delay and learning disability and affect
psychosocial development if not treated
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D. Microcephaly/nanocephaly – an abnormally small head, forehead narrow and recedes sharply, occiput
flat, lumbering gait, extremely low intelligence, lack of communicative speech, usually associated with
MR
E. Combined cerebral, cranial, and somatic abnormalities
F. Rachischisis (Dysraphism) – disordered fusion of dorsal midline structures
G. Chromosomal abnormalities
1) Down’s syndrome (trisomy 21) – (most common for MR) associated with moderate mental
retardation (impaired language, sequential processing, motor delays), epicanthal folds, open
mouth, short stature, abnormal palmar crease and fingerprints, increased risk for congenital heart
defect, ear infections, leukemia, seizures; associated with increasing maternal age at time of
conception, early Alzheimer’s Disease (30s and 40s)
2) Fragile-X syndrome – (second most common overall for MR, most common inherited form of
MR) excessive trinucleotide (CGG, >200) repeat in defective gene
a. Males (2x more than females) – increased head circumference and weight, elongated
face, enlarged testicles, dysfluent, apraxic speech, echolalia, palilalia, hyperactivity,
ADHD, LD, mood disorder, repetitive/stereotyped movements, autism, PDD; IQ declines
over time
b. Females – often lack dysmorphic features seen in males, frontal lobe deficits, attention
deficits, shy, behavioral abnormalities less common than in males
3) Rett’s syndrome – a progressive syndrome affecting females in which the infant develops
normally until approximately one year of age when the course changes to one of progressive
dementia, truncal ataxia, epilepsy, autism, acquired microencephaly, and clumsiness of the hands;
associated with “hand washing” movements
4) Prader-Willi/Prader-Labhart-Willi Syndrome (monosomy 15 from father) – obese, voracious
appetite, short stature, hypogonadism, aggressive, repetitive skin picking, OCD, decreased
sensitivity to pain, hypotonia, hypometria, MR, language deficits
5) Angelman Syndrome (monosomy 15 from mother, “happy puppet”) – born appearing normal but
drift off developmental course, severe MR (limited speech but gesture), microcephaly, epilepsy
80%, stereotyped involuntary and jerky-ataxic voluntary movements, smiling face, paroxysms of
unprovoked laughter, hyperactive; misdiagnosed Rett’s, autistic
6) PKU (chromosome 12) – autosomal recessive amino acid metabolism disorder (aminoacidurias),
prevents metabolism of phenylalanine (too high) to tyrosine (too low; due to deficiency in hepatic
phenylalanine hydroxylase) and synthesis of dopamine and melanin; when untreated associated
with severe MR, decreased attention and responsiveness, seizures, spasticity, hyperactive
reflexes, tremors, psychiatric manifestations, excema, fair complexion; treatment diet leads to
short stature, low weight, anemia, hypoglycemia; even treated have DHD symptoms and below
average IQ
7) Williams syndrome/infantile hypercalcemia (deletion on chromosome 7) – disorder of
metabolism producing a characteristic “elfin” facial appearance, elastic properties of aorta, skin,
and other organs (supravalvular aortic stenosis), motor delays, mild to moderate MR (reading,
visuospatial/NVLD), talented in music and verbal fluency
8) Klinefelter syndrome (XXY) – males with eunuchoid appearance, excessive height, wide
armspan, sparse facial and body hair, high-pitched voice, enlargement of the mammary gland,
small testicles; associated with mild MR, LD, dyslexia; high incidence of psychosis, asthma,
diabetes
9) Turner syndrome (XO, XO/XX – have only 45 chromosomes) – females with short stature,
webbed neck, wide set eyes, triangular face, broad chest, low set hairline, low ears, delayed
sexual development, mild MR, NP pattern consistent with NVLD, math difficulty, social deficits,
impaired facial recognition, anxiety/depression
10) XYY syndrome – a chromosomal abnormality resulting from nondysjunction of the sex
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chromosomes that lead to cerebral migrational abnormalities and maturational delays;
extremely tall, severe acne, increased activity and aggressiveness, delayed speech acquisition
11) Lesch-Nyhan syndrome – rare, X-linked metabolic disorder resulting in impaired enzyme
involved in making nucleotide bases of nucleic acids; leads to hypotonia then hypertonia at
around 6-9 months of age; compulsive and self-injurious behavior (e.g., self-mutilating lips),
extrapyramidal involvement, spasticity, hyperuricemia, choreoathetosis, and tremor develop;
speech delayed and dysarthric, MR; many symptoms not observed until 2-6
12) Tay-Sachs disease – an autosomal recessive genetic disorder (chromosome 5) of lipid
metabolism; characterized by poor visual fixation and an increased startle response shortly after
birth, followed by delayed psychomotor development and motor regression, with death usually
occurring between ages 3-5 years; primarily affects Jewish children of Ashkenazic descent
13) Patau syndrome (trisomy 13) – microcephaly and sloping head, lowset ears, cleft lip and palate,
impaired hearing, severe mental retardation, death in early childhood
14) Edwards syndrome (trisomy 18) – slow growth, seizures, severe mental retardation, lowset ears,
mottled skin, clenched fist with third finger over index finger, death in early infancy
15) Cri-du-chat syndrome (deletion of short arm of chromosome 5) – abnormal cry like a kitten,
severe mental retardation, epicanthal folds, moon face
16) Antimongolism (monosomy 21)
17) Ring chromosomes – mental retardation with variable physical abnormalities
18) Leukodystrophies – group of genetic disorders that involve destruction of CNS (also PNS) white
matter, and optic nerve, cerebellum, spinal cord demyelination; may not manifest until young
adulthood, continuous physical and mental decline (ALD, MLD)
19) Adrenal Leukodystrophy (ALD) – X-linked, recessive disorder, usually produces neurological
symptoms and adrenal insufficiency in boys 5-15, then mania, gait impairment, dementia by
demyelination; adrenal hormone replacement and “Lorenzo’s oil” does not alter disease course
20) Duchenne muscular dystrophy – X-linked, begins with weakness of the thighs and shoulders and
progresses to being wheelchair bound and respiratory insufficiency; absence of dystrophin in
muscle; associated with mild MR
21) Early onset dystonia – associated with DYT1 gene, usually confined to Ashkenazic Jews
22) Friedrich’s/hereditary spinal ataxia – autosomal recessive chromosome 9, excessive GAA
repeats; progressive gait ataxia; emotional lability may be present, speech may be affected but
cognition unaffected
II. Neuromigrational Disorders (NMD) (phakomatosisectodermal)
A. Tuberous sclerosis – autosomal dominant pattern of inheritance with variable penetrance and
expression (chromosome 9 or 16) in which there are sclerotic masses (tubers) in the cerebral
cortex, subtle hypopigmented areas on skin, scaly lesions on trunk, periungal fibromas of fingers,
adenoma sebaceum/facial angiofibromas (nodules on face appearing in adolescence), tumors in
organs (retinal, renal, cardiac), mental retardation, and intractable epilepsy; progressive dementia
B. Neurofibromatosis – characterized by developmental changes in the nervous system, muscles,
bones, and skin; usually late teens/early 20s
1. Type I (peripheral - von Racklinghausen’s disease) - genetic condition (chromosome 17)
marked by café au lait spots, neurofibromas of peripheral nerves, and Lisch nodules (iris
– pathognomonic), also cerebral tumors, optic glioma; associated with ADHD, LD, lower
IQ
2. Type II (central - familial acoustic neuroma) – genetic condition (chromosome 22)
marked by bilateral acoustic neuromas that impair hearing until deaf; meningiomas;
mental impairment only if compress critical brain regions
C. Sturge-Weber (encephalo-trigeminal angiomatosis) – autosomal dominant with variable
penetration; port wine stains in facial region of trigeminal nerve (nevus flammeus),
cerebrovascular malformations/calcification accompanied by atrophy of one hemisphere;
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associated with MR, LD, epilepsy, behavioral disturbance, focal physical deficits dependent on
site of lesion
D. Ataxia-Telangiectasia – autosomal recessive condition (chromosome 11) that interferes with
DNA repair, associated with immunodeficiency (reduced IgA/IgE); first manifested by chronic
sinus and respiratory tract infections, then lymphomas and neoplasms, progressive ataxia,
cognitive impairments, dilated vessels on conjunctive, nose bridge, cheeks
E. Heterotopia/Focal/Cortical dysplasia – abnormalities of cortical cytoarchitechture, with
disordered neuromigration/layering and displaced islands of gray matter appearing in the
ventricular walls or white matter, caused by aborted cell migration; frequently results in MR,
associated with LD and epilepsy
F. Lissencephaly (agyria – no gyri, smooth; pachygyria – few gyri, coarse) – arrest of cell migration,
associated with agenesis of CC, microencephaly, epilepsy, growth and severe developmental
retardation, early death; face has prominent forehead, short nose, protuberant upper lip, small jaw
G. Polymicrogyria – development of many small gyri due to focal necrosis, associated with LD,
severe MR, epilepsy
H. Holoprosencephaly – neuromigrational disorder with craniofacial abnormalities that develops
during the fifth-sixth week of gestation; cortex forms as a single undifferentiated (hemi)sphere, in
part or total; typically severe MR
I. Megaloencephaly – large head (>2 SD above mean) involving increased neurons and glia,
associated with MR
J. Schizencephaly/schizoencephalic porencephaly – abnormal divisions or cavities of the brain,
including clefts in parasylvian region and pre-/postcentral gyri, associated with hydrocephalus,
MR, motor handicap
K. Agenesis of the corpus callosum – associated with spina bifida, facial and ocular deformities,
microencephaly, megaloencephaly, hydrocephalus, Dandy-Walker, Leigh syndrome, epilepsy,
MR, neuropsychological deficits (VS, syntactic)
L. Cerebellar agenesis – portions of the cerebellum, basal ganglia, or spinal cord absent or
malformed
III. Disorders due to Infection/Intoxication
Prenatal infection  severe MR, convulsions, microcephaly, and hydrocephalus
Maternal infections with psychological consequences  syphilis, toxoplasmosis, rubella
(low birth weight, meningoencephalitis, psychomotor retardation, MR,
cataracts/retinopathy, abnormality of heart and major blood vessels), cytomegalovirus
(enlargement of spleen and liver, retarded growth, damage to visual and auditory
systems, microcephaly, MR), chicken pox, herpes simplex, hepatitis, mumps
IV. Nutritional Disorders
Protein/lipid deficiencies associated with myelination disorders
A. Kwashiorkor – protein deficiency
B. Marasmus – calorie deficiency
V. Maternal DNA Disorders
A. MELAS – mitochondrial encephalomyelopathy, lactic acidosis, strokelike episodes;
childhood mtDNA disorder associated with cognitive decline or MR
B. MERRF – myoclonic epilepsy and ragged-red fibers; childhood mtDNA disorder associated
with cognitive decline or MR
C. Progressive ophthalmoplegia – mtDNA disorder with retinitis pigmentosa, short stature,
cardiomyopathy, endocrine abnormalities
Fetal hydantoin syndrome – craniofacial abnormalities and limb defects, usually from maternal phenytoin
use
Neimann-Pick
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DISCONNECTION SYNDROMES
Commissure – white matter fiber tract that connects the two cerebral hemispheres and transfers
information from one hemisphere to another; the largest is the corpus callosum connecting
cortical regions, followed by the anterior commissure connecting olfactory structures and lateral
parts of the temporal lobe, and the hippocampal commissures
Commissurotomy/corpus callosotomy/split-brain procedure – surgery to separate the hemisphere
and isolate/decrease severity of generalized tonic-clonic seizures;
immediately after respond to letters and simple commands, mildly akinetic; see left neglect,
right-ear dominancy in dichotomous listening tasks, inability to name objects in left hand but can
pick up with left hand if named, right constructional apraxia, spatial acalculia, cannot crossreplicate hand postures, difficulty naming points touched on left side of body; also right-sided
verbal anosmia (inability to name smell), double hemianopia, hemialexia
Disconnection syndrome – any disorder in which cortical areas that normally work in conjunction become
isolated, involving interruption of information transfer, usually because of white matter lesions
(Geschwind)
Conduction aphasia – fluent but paraphasic, impaired repetition, relatively intact
comprehension
* lesion in arcuate fasciculus
Sympathetic apraxia in Broca’s aphasia – apraxia of command movements of left hand
* disconnect of left language area and motor association cortices from right motor
association cortices/corpus callosum
Pure word deafness – can hear and identify nonverbal sounds but loss of verbal
comprehension, speech is normal
* left temporal lobe/Wernicke’s or connection between temporal lobes
Pure word blindness (alexia without agraphia) – loss of ability to read; seen with right
hemianopia, color anomia
* lesion to left visual cortex and connection of dominant language areas and right visual
cortex via splenium of CC
Agraphia without alexia (disconnections of language from motor functioning)
Pure word mutism – lose capacity to speak but oral and reading comprehension and
writing intact
* dominant frontal lobe lesion separating Broca’s area from subcortical motor centers
Anterior cerebral artery syndrome – left limbs have normal spontaneous movement but
cannot respond to verbal or written requests because of disconnect between left
language centers and right motor centers
* stroke or ACA leads to infarction of frontal lobes and anterior CC
Ideomotor apraxia, particularly left-sided ideomotor apraxia to verbal commands
Internuclear opthalmoplegia – disconnect CN III and VI
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DISEASES
Acute intermittent porphyria (AIP) – autosomal genetic disorder of porphyrin metabolism causing
abdominal pain, psychosis and quadriparesis (urine red)
Addison’s disease – hyposecretion of aldosterone and cortisol (from adrenal gland), leading to weakness,
drowsiness, weight loss, lowered temperature, suspiciousness, irritability, depression
African trypanosomiasis – African sleeping sickness transmitted by tsetse fly, associated with dementia
Amyotrophic lateral sclerosis (ALS/Lou Gehrig’s) – confined to voluntary motor system, affects upper
motor neurons (spasticity and weakness) and lower motor neurons (wasting and twitching/
fasciculations of muscles); often begins focally in muscle groups; average 2-4 year survival; can
be caused by toxin in cycad nut (primary lateral sclerosis UMN, spinal muscular atrophy LMN);
chromosome 21
Anorexia nervosa – slowed reaction time, impaired STM, retrieval deficits, decreased vigilance
Anoxia/Hypoxia – lack of oxygen supply to tissue resulting from circulatory deficiency (ischemia due to
hypotensive shock, cardiac arrest, vasospasm, and cardio-thoracic surgery) or deficiency in red
blood cells (anemia due to CO poisoning, cyanides, or anesthesia overdose) most greatly affects
watershed areas, including hippocampus, then primary visual/occipital and visual association
cortices, also basal ganglia, cerebellum, some frontal regions; cognition affected at 75% arterial
oxygen, unconsciousness at 50% arterial oxygen, death at 30-40% arterial oxygen; cognitive
deficts included impaired anterograde memory, executive dysfunction, apperceptive agnosia
(visual synthesis of objects), visuospatial deficits; affective changes due to damage of medial
temporal and frontal lobes; permanent damage at 3-5 minutes; CO poisoning may spare
perisylvian arc; cyanosis (dark slate blue color of the mucous membranes, lips, nail beds, and skin
due to deficient blood oxygenation)
Anton’s Syndrome – denial of cortical blindness (anosognosia), confabulation may be present, intact
papillary reflexes
* bilateral occipital lobe lesions
Arboviruses (Arthropod-Borne viruses) – typically occur from May to October in northern hemisphere;
includes Eastern and Western Equine Encephalitis and California Encephalitis
B12 deficiency – megaloblastic anemia causing CNS demyelination with subacute combined degeneration
of spinal cord; associated with mood disturbance, psychosis, and reversible dementia
Balint’s syndrome – elements in visual field cannot be perceived as whole despite variable
perception of elements; associated with field cuts, aphasia, neglect
- inability to voluntarily look into periphery (psychic paresis of gaze)
- apraxia of ocular searching movements
- failure to touch/grasp object under visual guidance (optic ataxia/apraxia – impaired depth
perception)
- disturbance in spatial attention (difficulty with periphery)
- simultanagnosia (piecemeal perception)
* usually bilateral, dorsal parietal, posterior-lateral occipital, or inferior lesions;
occasionally unilateral; due to MCA-PCA watershed infarct
Benign familial chorea – autosomal dominant inheritance, but nonprogressive, no cognitive or emotional
decline
Binswanger’s disease – periventricular subcortical demyelination (white matter degeneration) from
uncontrolled, chronic hypertension, associated with dementia (primarily temporal-occipital
regions)
Brain abscess – collection of pus from infection spreading from middle ear or sinus, congenital heart
disease, spread of infection, entry of bacteria following penetrating head injury; symptoms
similar to meningitis, including restlessness, progressive headache, fever, and focal neurological
signs; diagnose with CT (lumbar puncture can spread); treat with antibiotics, aspiration/drainage
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Bulbar palsy – dysarthria, dysphagia, and hypoactive gag reflex due to damage of CN IX, X and XI;
not central, so no cognitive changes
Capgras syndrome – psychiatric delusion in which a familiar person is perceived as an impostor or double
(similar to neurologic reduplicative paramnesia)
Carbon monoxide (CO) poisoning – damage centered in globus pallidus of basal ganglia, also cortex,
hippocampus, cerebellum, fornix, CC; disorientation, headache, dizziness, fainting;
affects attention, memory (verbal memory associated with fornix), processing speed, EF;
may have delayed personality alteration, mental deterioration, incontinence, gait disorder,
mutism with frontal release signs and masked face
Cerebral amyloid angiopathy – dementia through multifocal recurrent hemorrhages and white matter
ischemic disease; often familial
Cerebral Palsy (paralysis) – motor system impairment from cerebral injury, including MR, seizures,
vision and hearing impairments, toe walking, LD, language disorders, hyperactivity,
psychological problems, pseudobulbar palsy, or other neurologic complications; subtypes
include:
~spastic/pyramidal (70%) - clumsy movements, hyperactive deep tendon reflexes,
clonus, Babinski sign; limb growth arrest, related to prematurity and necrosis
(periventricular necrosis)
~extrapyramidal (15%) - choreathetosis/writhing, involvement of larynx, pharynx
and diaphragm, related to low birth weight and anoxia damaging basal ganglia
~hypotonic/atonic
~mixed
Cytomegalovirus (CMV) – a herpes virus that is a common cause of intrauterine infection, associated
with congenital malformations and growth retardation; seen as an independent virus, with
Guillain-Barré syndrome, or AIDS
Chronic Fatigue Syndrome (CFS) – complaints include sore throat, muscle pain; marked by slow
processing speed and impaired working memory, also poor concentration, impaired learning,
WFD; diagnosis of exclusion; associated with chronic Epstein-Barr, neurasthesia
Chronic Obstructive Pulmonary Disease (COPD) – disease with poor expiratory airflow, may cause
chronic hypoxia, resulting in cognitive decline
Combined system disease – disorder associated with either pernicious anemia or with vitamin B12
deficiency without anemia, manifested by subacute myelopathy, dementia, posterior spinal
column dysfunction, and peripheral neuropathy
Cushing’s disease – a disorder associated with increased adrenocortical secretion of cortisol (adrenal
gland), caused by ACTH-dependent adrenocortical hyperplasia or tumor; psychiatric
manifestations are common, “cushingoid” appearance of moon-shaped face and truncal obesity,
acne, easy bruisability, ruddiness and purple skin striae, poor healing, hypertension, diabetes,
immunosuppression, osteoporosis, amenorrhea; memory loss, emotional lability, depression,
somatic delusions
Cysticercosis – infection with the larval form of porcine tapeworm; cysts in muscles, eyes, CNS; seizures,
headache, nausea, vomiting; symptoms may not show for 4-5 years, may resemble brain tumor,
may cause chronic meningitis or arachnoiditis, may cause obstructive hydrocephalus and
increased intracranial pressure; leaves calcifications throughout brain (“brain sand”); most often
seen in Central America
Degenerative disorders of the nervous system – disorders with insidious onset, no laboratory marker
(clinically diagnosed), gradually progressive; diffuse areas of brain affected, certain groups of
neurons degenerate, no associated inflammation, associated with characteristic cytoplasmic
inclusions; includes AD, PD, ALS, HD
DeLange syndrome – NVLD
Diabetes Mellitus– cognitive deficits associated with poor control of glucose level (hyperglycemia);
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associated with polyuria (frequent urination), polydipsia (excessive thirst) and polyphagia
(excessive hunger); apathy, confusion, mental dullness; deficits in working memory,
verbal learning, memory, information processing, see psychomotor slowing; increase risk for
stroke, dementia and infection; have distal symmetrical polyneuropathy in glove and stocking
pattern; causes increase in blood levels of fatty substance leading to atherosclerosis; sexual
dysfunction; onset in childhood may affect intellectual functioning
- Type I poor development of insulin (associated with autoimmune disease, <30 years)
- Type II developed resistance to insulin (being overweight, lack of exercise, >30 years)
Encephalitis – brain inflammation from infection, usually of viral origin; most common is herpes
simplex, varicella-zoster, and cytomegalovirus
Encephalomalacia – morbid softness of the brain usually caused by vascular insufficiency or trauma
Encephalopathy – nonspecific diffuse brain impairment, usually resulting from a systemic condition;
behaviorally characterized as a confusional state
End Stage Renal Disease (ESRD) – kidney failure, affecting balance of bodily fluids and electrolytes and
metabolization of hormones; leads to uremia; most often caused by diabetes mellitus and
hypertension; lethargy, decreased concentration, personality change, confusion, decreased mental
alertness, impaired memory, sensory perception deficits, diminished perceptual-motor
coordination, sexual dysfunction, leg cramps, headaches, nausea, with anemia; treated with
dialysis or transplant
Episodic dyscontrol syndrome/intermittent explosive disorder – a reaction to frustration characterized by
loss of self-control and striking out in rage disproportionate to stimulus; neurologically associated
to lesions in ventromedial structures including portions of the frontal cortex, hypothalamus, septal
nuclei, (i.e., “septal rage”), and amygdala
Extrapyramidal syndrome – a syndrome of akinesia, rigidity, tremor, akathisia, and buccolingual
dyskinesia (i.e., choreoathetoid movements of the mouth, jaw, and tongue) resulting as a side
effect from neuroleptic medication, developing acutely (versus after longterm use in tardive
disorders)
Failure to thrive – syndrome in which growth for a child is significantly below expectation; malnutrition
primary component; deficits in cognitive, social, and emotional functions develop later
Fetal alcohol syndrome – syndrome resulting from ethanol exposure during the first trimester;
characterized by microcephaly, impaired coordination, decrease birth size, and facial
abnormalities, with a high frequency of mental retardation, tremors
Fibromyalgia – chronic disorder characterized by widespread musculoskeletal pain, fatigue, and tender
points; may be associated with sleep disturbance, morning stiffness, irritable bowel syndrome,
and anxiety; high diagnostic overlap with chronic fatigue (most common in middle aged females)
Folic acid/folate deficiency – sensory and reflex abnormalities, depressed mood; impaired memory,
abstract reasoning, construction; increased stroke risk
Foster-Kennedy syndrome – frontal lobe tumor compressing ipsalateral optic nerve, causing optic
atrophy, and intracranial pressure causing contralateral papilledema of optic nerve
Functional disorder – a disorder without a known physiological or structural etiology, often used to refer
to a psychiatric or psychological disorder that impairs functioning
Gerstmann Syndrome – agraphia, acalculia, finger agnosia, R-L disorientation; associated with
contralateral visual field cut, alexia, anomia, more severe aphasia
*dominant inferior parietal lobe/angular gyrus lesion
Gilles De La Tourette syndrome – combination of vocal and multiple motor tics that develop by age 18
and last more than one year; autosomal dominant inheritance, four times more common in boys,
onset usually in late childhood (average 7), tics, grunting, snorting, coprolalia, associated with
ADHD and OCD, can treat with dopamine (D2) antagonist or clonodine; chromosome 18
* basal ganglia dysfunction
Guillain-Barré syndrome (acute inflammatory demyelinating polyneuropathy) – a post-infectious (often
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upper respiratory tract infection; post-lyme disease; campylobacter jejuni - diarrhea) autoimmune
disease of peripheral myelin associated with paresthesias in the distal extremities and leg
weakness, areflexia, bulbar palsy; most common demyelinating disease of the peripheral nervous
system; have elevated protein in CSF; not marked by cognitive impairment; lasts several weeks
Hallervorden-Spatz syndrome (HSS) – rare, hereditary recessive, degenerative disorder marked by
reduction in myelin sheaths of globus pallidus and substantia nigra and accumulation of iron
pigment; symptoms include progressive rigidity beginning in legs, choreoathetoid movements,
dysarthria, dystonia, and emotional and mental deterioration (visuospatial and memory); no
treatment; death usually before 30
Hepatic dysfunction – associated with elevated levels of ammonium, increased GABA activity; ~5% with
cirrhosis develop encephalopathy; may exhibit motor symptoms, lethargy and asterixis;
encephalopathy characterized by triphasic brain waves; treated with benzodiazepine receptor
antagonists (e.g., flumazenil)
Herpes simplex encephalitis – viral brain infection caused by HS1, most common cause of serious
nonepidemic encephalitis, with a course generally of 1-2 weeks; marked by fever and alteration
of consciousness, associated with headache, personality change (Kluver-Bucy syndrome), speech
difficulties, and seizures; predilection for inferior and medial surfaces of the frontal and temporal
lobes (limbic area; entry through the olfactory pathway); see hemorrhagic necrosis, inflammatory
infiltrates, and cells containing intranuclear inclusion; memory impairment (amygdala and
hippocampus) and complex partial seizures often occur; treat with antiviral (acyclovir); 70%
mortality
Horner’s syndrome – drooping of the eyelid (ptosis), constriction of the pupil (miosis), deficient
sweat secretion (anhidrosis), and flushing of the affected side of the face caused by
paralysis of the cervical sympathetic nerves, due to deficient NE; found in cluster headache,
cervical spinal cord injury, apical lung tumor, lateral medullary syndrome (Wallenberg’s)
Human immunodeficiency virus (HIV) – RNA retrovirus (information stored as RNA but copied into
DNA) that destroys white blood cells (type of lymphocyte), HIV-1 more common than HIV-2;
depresses immunity through disabling/destroying helper T-cells (CD4+) – usual count 8001300/microliter, healthiest have greater than 500, significantly compromised when below 200
(called AIDS); causes excessive production of antibodies by B lymphocytes; immediate
symptoms similar to mononucleosis, including rash, swollen lymph nodes, discomfort, eventually
leading to weight loss (wasting), fatigue, diarrhea, anemia, thrush (fungus in mouth); develop
opportunistic infections [e.g., Kaposi’s sarcoma – purple/brown patches, non-Hodgkins’
lymphoma, vaginal years infection, cryptococcal meningitis, pneumonia, toxoplasmosis,
tuberculosis, mycobacterium avium complex (treatable), cryptosporidium (GI infection),
progressive multifocal leukoencephalopathy, cytomegalovirus encephalitis, cancer of cervix and
rectum]; neuronal damage through chronic activation of macrophages and microglia, increasing
production of cytokines
- Cognitive findings include poor attention and concentration, fatigue, slowed processing
speed, mild memory problems
- Antiviral drugs [AZT, ddI, d4T, 3TC, protease inhibitors (prevents protease from making new
copies of HIV) – best in combination] for direct treatment (delay, not cure), also treat
opportunistic infections
Hypertensive encephalopathy – a rapidly evolving syndrome of severe acute hypertension characterized
by headache, nausea, and vomiting, and may include acute visual disturbances, seizure, stupor,
and coma, may be accompanied by neurologic signs; associated with cerebral edema and
punctuate hemorrhages rather than infarction and diffuse hemorrhage associated with chronic
severe hypertension
Hyperthyroidism – excessive activity of the thyroid gland due to immunological reaction (Grave’s
disease), thyroiditis, toxic thyroid nodules (adenomas), or toxic multinodular goiter (Plummer’s
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disease); characterized by increased metabolism, goiter, and disturbances in the autonomic
nervous system and in creatinine metabolism; behavioral symptoms include emotional lability,
anxiety, restlessness, nervousness, confusion, insomnia, fatigue, tachycardia, palpitations, heat
intolerance, inappropriate temper outbursts, and euphoria; weight loss, tremor, excessive
sweating, frequent bowel movements, eye changes (puffiness, irritation, tearing, sensitivity to
light); usual onset 30s-40s, 7-10 times more common in women; slower reaction time, impaired
motor functioning, mild deficits in attention, memory, complex problem solving
Hypoglycemia – diminished blood glucose that may lead to tremulousness, cold sweats, piloerection,
hypothermia, anxiety, hunger, dizziness, palpitations, depression, blurred vision, headache, and
possibly seizures and coma; can be accompanied by confusion, hallucinations, and bizarre
behavior
Hypothyroidism/myxedema – decreased or absent thyroid hormone, characterized by lethargy, apathy,
cognitive impairment (slow mentation, attention, memory, visuospatial), ataxia, dysarthria, and
nystagmus; cold intolerance, depression, excited confusion, carpal tunnel, hair loss, constipation;
hallucinations, paranoia, delirium when severe; can lead to basal ganglia calcification and
parkinsonism or chorea-like symptoms; “hung up” deep tendon reflexes; in children can lead to
cretinism; seen with chronic lack of iodine; common cause is autoimmune reaction due to
Hashimoto’s thyroiditis; in adults need to rule-out dementia
Internuclear ophthalmoplegia (INO) – medial longitudinal fasciculus (MLN) syndrome (dorsal brainstem
lesion), causing disconnect of third and sixth nerves, with nystagmus of abducting eye and failure
of adducting eye to cross midline (characteristic of MS, brainstem strokes, thiamine deficiency,
lupus); no ptosis or dilation as seen in CN III palsy
Klüver-Bucy syndrome – behavioral disturbances following bilateral anterior lobe ablation in monkeys
(limbic - bilateral amygdala), characterized by placing objects in mouth, loss of normal fear,
visual agnosia, placidity, hypersexuality, and hyperphagia
Korsakoff’s syndrome/disease – cognitive deficits including amnesia (anterograde and retrograde memory
deficit), disturbance of orientation, confabulation (anosognosia for amnesia), lack of insight, poor
memory for temporal order, impaired source monitoring, metamemory motivational
difficulty/apathy, poor spontaneous conversation, and psychosis; adequate immediate memory;
arises from B1 (thiamine) deficiency, usually preceded by Wernicke’s encephalopathy; often
secondary to alcohol abuse
*hemorrhages in midline encephalon (dorsomedial nucleus of thalamus related to
anterograde memory impairment; damage to mammillary bodies)
Kuru – a chronic, rapidly progressing, fatal nervous system disease caused by priors and characterized by
prominent ataxia, dysarthria, tremulousness, with dementia in late stages; shows severe cerebellar
loss, spongiform change, and prion-amyloid plaques; found among the Fore people of New
Guinea, had been transmitted through cannibalism
Lateral medullary/Wallenberg’s syndrome – dysarthria, dysphagia, ataxia, opposite palate decviation;
most common brainstem infarction
Leukoaraiosis – diffuse white matter change seen in older people but not always associated with dementia
Leukodystrophy – disturbance or degeneration of white matter of the brain associated with metabolic
defects (e.g., Fabry Disease, metachromatic leukodystrophy)
Leukoencephalitis – inflammation of the white matter of the brain
Leukoencephalopathy – disease affecting the white matter of the brain (e.g., progressive multifocal
leukoencephalopathy associated with AIDS)
Leukomalacia – morbid softening of the white matter due to necrosis, commonly seen following anoxic
event
Limbic encephalitis – progressive dementia from remote neoplasm (paraneoplastic), characterized by
agitation, confusion, hallucinations, or seizures
Lyme disease – multisystem disease from bacteria borrelia burgdorferi/spirochete infection transmitted by
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deer ticks, clinically manifested by “bull’s eye rash” (erthema migrans) and flu-like symptoms,
lymphocytic meningitis, painful radiculoneuritis, cranial neuritis/facial palsy, headaches; may
involve memory impairment and difficulty with complex cognitive functioning, irritability and
depressed mood; treat with IV ceftriaxone
Malignant hyperthermia – chromosome 19 autosomal disorder; precipitated by general anesthesia or
muscle relaxant succinylcholine
Marchiafava-Bignami disease – rapidly progressing degeneration/demyelination of the corpus callosum
that is associated with cognitive deterioration, emotional disturbances, confusion, hallucinations,
tremor, rigidity, and seizures; typically affects middle-aged alcoholics who drink excessive
amounts of red wine; progresses from dementia to coma to death in a few months
Meige’s syndrome – cranial dystonia; responds to botulinium injections
Meniere’s disease – vertigo, fluctuating or stepwise progressive hearing loss, tinnitus, and nystagmus
associated with salt restriction or diuretics
Meningitis – inflammation of the meninges, within the subarachnoid space; symptoms include fever, stiff
neck (nuchal rigidity), vomiting, headache, backache, photophobia, nausea, altered mentation
(lethargy, malaise, confusion, coma); chronic meningitis (syphilis, tuberculosis, fungi, parasite)
can lead to dementia, seizures, cranial nerve palsies, can have focal neurological deficits (hearing
loss, hemiparesis, dysphasia, hemianopsia) and hydrocephalus
- Aseptic/lymphocyte-predominant – nonbacterial meningitis; etiology may be inflammatory
response, viral, or idiopathic
- Bacterial – presents with meningismus, somnolence or mild confusion common, associated
with CSF obstruction and seizures; evolves rapidly; diagnosed through CSF evaluation
(increased leukocytes/white blood cells), treated with high dose antibiotics; causes include E
Coli, influenza, pneumonia
- Cryotococcal – opportunistic infection from yeast Cryptococcus, often present in
immunocompromised individuals; basilar meninges commonly involved, leading to
presentation of headache, cranial nerve involvement, CSF obstruction, and increased
intracranial pressure; typically chronic and leads to death
- Mollaret – recurrent aseptic meningitis of obscure origin
- Tuberculous – inflammatory response in basal cisterns affecting circle of Willis and causing
infarcts
- Viral – typically self-limited and treated symptomatically; headache and nuchal rigidity;
lymphocytic pleocytosis with normal CSF glucose; usually no associated change in mental
status (from herpes simplex, postinfection, herpes zoster, transverse myelitis, enteroviruses,
mumps, measles, varicella)
Meningoencephalitis – inflammation of both the brain and meninges, often viral in origin (e.g., herpes
simplex); symptoms include confusion, fever, headache, seizures, focal neurological signs
Metachromatic leukodystrophy (MLD) – an autosomal recessive metabolic disorder characterized by
myelin loss and accumulation of metachromatic lipids in the white matter and associated with
general cognitive impairment and psychosis
Mild Cognitive Impairment (MCI) – transitional states between nomal cognition and mild dementia,
including subjective memory complaint and corroboration on memory tests within context of
intact general cognitive abilities and ADLs; evolves to dementia (AD) at a rate of 10-15% per
year (normal is 1-2%); more rapid decline predicted by Apo E4, atrophic hippocampi; may give
cholinesterase inhibitors, anti-inflammatory, anti-oxidant
MPTP toxicity – toxin through synthetic heroin-like meperidine causing parkinsonism from damage to
dopamine in substantia nigra pars compacta
Muscular dystrophy – (MR with Congenital and Duchenne)
Myasthenia gravis – an autoimmune neuromuscular disorder associated with decreased post-synaptic
nicotinic acetylcholine receptors at the neuromuscular junction, initially characterized by
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drooping eyelids (ptosis), diplopia, weakness with repetitive effort, and impairment in speech and
swallowing (nasal speech); normal pupil; Tensilon test temporarily reverses ocular and facial
weakness through cholinesterase inhibition; treated with anticholinesterase thymectomy
(resection of thymus gland behind breastbone, associated with immune functioning); steroids,
plasmaphersis, or human immunoglobins deactivate Ach receptor antibodies (does not attack
cerebral Ach because those muscarinic)
Myotonic dystrophy – a slowly progressing, autosomal dominant disease (excessive trinucleotide repeats)
characterized by muscle atrophy and weakness, decreased vision, eyelid drooping, and slurred
speech, usually presenting in 20s; mental impairment
Neuroleptic malignant syndrome – muscle rigidity, fever, autonomic dysfunction, and encephalopathy
that occurs as an idiosyncratic reaction to neuroleptics, tricyclic antidepressants, lithium, cocaine,
or amphetamines, and antiparkinsonian drug withdrawal; muscle protein released into blood and
causing renal failure; high mortality rate
Neurosyphilis – begins as syphilis from persistent treponema pallidum infection, presentation resemble
meningitis, symptoms in early stage include fatigue, irritability, personality change, forgetfulness,
and tremor, in late stage includes impaired memory and judgment, confusion, disorientation,
seizures, psychosis, dysarthria, myoclonus, skin lesions, poor motor control; treat with antibiotic
(penicillin)
Niacin deficiency – vitamin deficiency syndrome consisting initially of confusion, impaired memory,
apathy, and irritability; seen in alcoholics and others with poor diets
Panencephalitis – inflammation of the entire brain, resulting in gray and white matter lesions, typically
viral in origin
Parinaud’s syndrome – lesion compressing dorsal midbrain and pretectal area leading to impaired vertical
(up) gaze, large, irregular pupils that do not react to light, eyelid abnormalities, and impaired
convergence/convergence-retraction nystagmus; caused by pineal tumors and hydrocephalus (in
children may see “setting-sun sign” with eye inward and downward)
Pellagra – niacin deficiency causing dementia, dermatitis, and diarrhea (3Ds)
Pernicious anemia – combined system disease from B12 deficiency, leading to anemia, dementia, and/or
spinal cord impairment
Phakomatosis – inherited disorders involving organs of ectodermal origin (the nervous system, eyeball,
retina, and skin), including tuberous sclerosis, neurofibromatosis, and Sturge-Weber syndrome
Poliomyelitis – polio caused motor neuron virus infecting anterior horn (motor) cells of spinal cord and
lower brainstem; not associated with cognitive impairment
Post-concussion syndrome – persistence of symptoms seen after mTBI, including dizziness, headache,
poor concentration/attention, and sensory abnormalities; insomnia, fatigue, short-term memory
deficits, affective disturbance (anxiety, irritability, depression), phonophobia, photophobia,
hypochondriacal concern, sleep problems
Posterior fossa disease – due to ischemia/basilar artery; crossed findings (face on one side, body on
other), bilateral weakness and sensory loss, vertigo, ataxia, dysarthria, diplopia
Postinfection encephalomyelitis – caused by measles, varicella, rubella, and other viral illnesses;
associated with dementia
Primarily mitochondrial myopathies – from deficiency of lipid storage enzymes and cytochrome
oxidase, causing weakness and exercise intolerance, short stature, epilepsy, lactic acidosis
Progressive Bulbar Palsy (Fazio-Londe Syndrome) – lower motor neuron disease, with age of onset from
childhood to adolescence, involving progressive paralysis of facial, lingual, pharyngeal,
laryngeal, and ocular muscles; death within months to years
Progressive Multifocal Leukoencephalopathy – demyelinating disorder caused by viral infection
(papovavirus), lesions usually in subcortical regions, first symptoms usually loss of arm/leg
strength and loss or coordination or balance; NV more affected than V (usually 3-6 months till
death)
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Pseudobulbar Palsy – spastic weakness of the muscles of the face, pharynx, and tongue (dysarthria,
dysphagia) from bilateral lesions of the corticobulbar tracts (frontal, not brainstem); often
accompanied by involuntary laughing or crying; often with hyperactive reflexes and Babinski
sign; associated with arteriosclerosis and ministrokes
Pseudodementia – a potentially reversible psychiatric condition that resembles dementia (e.g.,
depression); symptoms may evolve more quickly and fluctuate under differing environmental
conditions; cognitive deficits associated with depression are in the areas of sustained effort and
concentration, motor speed, reaction time, processing speed, performance accuracy, flexibility,
and abstract thinking; perceptual tests, speech, memory, and incidental learning generally intact;
go on to develop dementia at 3-6 times the rate of normal controls
Pseudotumor cerebri – elevated intracranial pressure/edema with no mass lesion causing generalized,
bilateral headache; see small or “slitlike” ventricles; may compress CN VI; common in
adolescent females, particularly with menstrual abnormalities, obesity; may have papilledema;
treated with acetazolamide or shunt, diuretics, steroids
Rabies – viral disease of CNS, 15 days – 1 year incubation time; begins with anxiety, fever, headache,
paresthesia at bite site, then delirium, seizures, nuchal rigidity, paralysis, excitability, spasms of
neck, esophagus, pharynx; pre-treat with vaccine
Raynaud’s – idiopathic trophoneurosis, with paroxysmal spasm of digital arteries producing pallor or
cyanosis of fingers or toes, occasionally resulting in gangrene; common in young women
Reduplicative paramnesia – a confabulation consisting of a false belief in the duplication of people or
places
Reflex sympathetic dystrophy (RSD) – a syndrome of ANS dysfunction characterized by vascular
instability, often manifested by limb pain and swelling; can be triggered by stroke, TBI,
peripheral nerve injury, and myocardial infarction
Sarcoidosis – granulomatous disease resembling TB; may affect any organ, but most common in skin,
lymphatic glands, or bones of hands
Schilder Disease – diffuse sclerosis
Scrapie – a transmissible, degenerative, prion disease of sheep and goats
Sheehan’s syndrome – postpartum pituitary necrosis usually caused by deliveries complicated by
hypotension; symptoms include failure of lactation, no regular menses, sexual and generalized
indifference, easy fatiguability, bitemporal hemianopsia or superior quadrantanopia; leads to
secondary adrenal insufficiency
Sickle cell disease – a genetic disorder of hemoglobin named for the abnormal crescent shape of the red
blood cell; may be associated with cognitive delay, disordered consciousness, seizures, and
meningitis
Small vessel disease – lacunar infarction of lenticular striate, thalamoperforates, paramedian perforating
branches (basal ganglia, pons, internal capsule); symptoms include pure motor hemiparesis (pons)
pure sensory stroke (thalamus), dysarthria, clumsy hand (pons), ataxic hemiparesis (pons)
Sotos syndrome - NVLD
Spinocerebellar atrophy – from trinucleotide repeats
Subacute Sclerosing Panencephalitis (SSPE) – possibly associated with measles, develops in children,
myoclonus present, see behavioral and personality change, dementia, periodic complexes on EEG
Susac’s syndrome – retinal arteriolar occlusions, sensorineural hearing loss, multifocal brain lesions along
corpus callosum; may appear like MS
Syndenham’s chorea (rheumatic chorea, “St. Vitus’ Dance”) – disorder associated with rheumatic fever
and streptococcal infections and PANDAS, affecting ages 5-15, more in females; tics, Tourette’s,
ADHD, dystonia, impulsivity, obsessive-compulsive
Systemic lupus erythematosus (SLE) – a generalized collagen vascular disease characterized by skin
eruptions, neurological manifestation (3 S’s: stroke, seizures, psychosis), lymphadenopathy,
fever, chorea; produces CNS changes in 5% initially, later up to 75%
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Tardive dyskinesia (TD) – a nonreversible, involuntary movement disorder resulting from dopamine
hypersensitivity after long-term neuroleptic therapy, often involving the tongue, jaw, and facial
expressions; risk of a TD increases with age and medication dosage
Temporal arteritis (giant cell arteritis) – vasculitis (enlarged and firm) affecting temporal arteries,
including those supplying eye; headache in temporal lobes, may have jaw pain chewing, malaise,
fever, weight loss; may lose vision; affects elderly
Tetnus – affects the motor unit of the peripheral nervous system; early symptoms include restlessness,
localized stiffness and soreness, low-grade fever, hemorrhage at wound, irritability, insomnia,
headache, late symptoms include nuchal rigidity, lockjaw (trismus), risus sardonicus (sardonic
expression), dysphagia; treat with antibiotics; mortality 25-75%
Thalamic syndrome/Déjérine-Roussy syndrome – severe contralateral pain from parietal/primary sensory
cortex, due to infarct of thalamus; allodynia (conversion of benign pain to unbearable
pain), hyperapthia (testing for Babinksi produces severe pain), superficial persistent
hemianesthesia, mild hemiplegia, mild hemiataxia, variable astereognosis, and choreathetoid
movement in the limbs of the paralyzed side
Top-of-the-basilar Syndrome – a condition from emboli that pass through the termination of the basilar
artery and occlude the thalamoperforant arteries, consists of visual, oculomotor, and behavioral
abnormalities without significant motor dysfunction; peduncular hallucinosis; memory
impairment is common with infarction of the medial thalamus; apraxia of eyelids
Toxic-metabolic encephalopathy – a condition associated with systemic disorders of metabolism or
intoxication that is commonly characterized by altered mental status, with course commonly
fluctuating and symptoms worse in evening; common cause of confusional states in the elderly
Toxoplasmosis – an opportunistic infection with the parasite Toxoplasm gondii, from cat feces or
undercooked meat; can be congenital or acquired, most commonly presents with AIDS; CT
usually shows ring enhancing lesions associated with brain abcesses, common in basal ganglia;
associated with general subacute encephalopathy and language impairment; marked by fever,
altered mentation, seizures, focal signs, hemiballismus
Tuberculosis – intracerebral masses; seen in immune comprised people, common in India
Uremia – clinical syndrome due to renal failure, characterized by nausea, vomiting, headache, hiccough,
weakness, lethargy, apathy, dimness of vision, seizures, hallucinations, coma; encephalopathy
characterized by triphasic brain waves; affects attention, psychomotor speed, immediate recall,
mental flexibility
Varicella-Zoster – human herpes virus that causes chickenpox (varicella), becomes latent in cranial nerve
and dorsal-root ganglia, and later reactivates to produce shingle (zoster) and postherpetic
neuralgia (CN III, V, VII); treat with antiviral (acyclovir) and analgesic
Velocardiofacial syndrome - NVLD
Von Economo’s disease/encephalitis – postencephalic parkinsonism
Weber’s syndrome – midbrain arterial thrombosis damaging CN III and corticospinal tract
Wernicke’s disease – an acute phase of the Wernicke-Korsakoff syndrome that involves ataxia,
confusional state, and eye movement abnormalities/third and sixth nerve palsies (nystagmus, gaze
paresis) (“ACE”); patients are disoriented, apathetic, amnestic, and unable to engage in
meaningful conversation; etiology is B1 (thiamine) deficiency leading to periaqueductal petechial
hemmorhage
Wernicke-Korsakoff syndrome – a syndrome seen in chronic alcoholism or malnutrition associated with
B1 (thiamine) deficiency; it is characterized acutely by Wernicke’s disease (nystagmus, ocular
paresis, ataxia) and chronically by Korsakoff’s disease; often impairments on visual-perceptual
and frontal executive tasks; may fail to demonstrate release from proactive interference; marked
by confabulation, retrograde and anterograde amnesia, lack of insight, meager content in
conversation, apathy
* lesions in the diencephalon (dorsomedial thalamus, mammilliary bodies, periventricular
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gray matter), midbrain, cerebellum (vermis)
West syndrome – an encephalopathy of infancy characterized by infantile spasms/myoclonic seizures,
arrest of psychomotor development, mental retardation, and hypsarrhythmic EEG (high voltage
slowing and multifocal spikes)
Wilson’s Disease/hepatolenticular degeneration – an autosomal recessive disorder (chromosome 13)
resulting from a defect in copper metabolism; low ceruloplasmin leading to excessive copper
accumulation; includes an involuntary movement disorder (basal ganglia – tremor, rigidity,
dysarthria, akinesia, dystonia, ataxia,“wingbeating tremor”) and hepatic (liver)
insufficiency/cirrhosis; copper deposition in the cornea often leads to a pigmented copper ring
(Kayser-Fleischer ring - pathognomonic) at the outer margin of the cornea; initially presents with
personality/mood changes/psychosis and progresses to dementia; peak onset teens-20s
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DISORDERS OF CONSCIOUSNESS
AAA – Alertness (pontomesencephalic reticular formation, intralaminar thalamic nuclei, cortex),
Attention (with addition of frontoparietal cortex), Awareness
Consciousness – state of awareness of both self and environment, implying fully responsiveness to
stimuli; involves both arousal and content
Concussion – mild traumatic brain injury characterized by at least a brief loss of consciousness
(<30 minutes), brief post-traumatic amnesia (<24 hours), any loss of memory for events
surrounding accident, any alteration in mental states at time of accident, or focal neurological
deficits (that may or may not be transient)
Confusional state/delirium – condition involving alterations in level of arousal/consciousness, difficulty
staying alert, disturbance of attention, and impairment in the logical stream of thought; associated
with disturbance in sleep-wake cycle, disorientation to time and place, rambling or incoherent
speech, illusions, visual hallucinations, agitation, and change in psychomotor behavior; onset is
rapid, course is short, fluctuating course with worse at night (sundowning); etiologies include
metabolic disturbances, toxic exposure, medications, infection, trauma, increased intracerebral
pressure, focal stroke, or seizures; may show impairments in attention, memory, language
comprehension, and visuospatial functions
(confusion  reduced alertness and psychomotor activity
delirium  overactivity, sleeplessness, tremulousness, hallucinations, convulsions)
Lethargy – state of being awake but drowsy, inactive, and indifferent to external stimuli
Stupor – an unconscious state from which the patient can be partially aroused but cannot reach a fully
wakeful state of awareness
Coma – a state of unconsciousness and decreased responsiveness/unarousability associated with
neurologic injury, most often to bilateral damage in the reticular activating system in the upper
pons and midbrain, but also diffuse, bilateral damage to cortex and bilateral lesions of thalamus
(intralaminar and midline); no sleep-wake cycle; may see doll’s eyes; coma not present if cold
water to the ear produces contralateral nystagmus (indicate that the cerebral hemispheres are
intact)
Due to tumor, hemorrhage, thrombosis, embolism, fracture, concussion, subdural hematoma
(dilated pupils), brain abscess, hypertensive encephalopathy, meningitis, hydrocephalus,
alcohol/barbiturate (hypothermia, hypotension) and opium intoxication (constricted pupils), CO
poisoning (cherry-red skin), anoxia, cardiopulmonary arrest, hypoglycemia, hypothyroidism,
hypoadrenalism, diabetic coma (extracellular fluid deficit), thiamine deficiency, uremia, hepatic
coma (jaundice), hypercapnia, infection, heat stroke, epilepsy
Glasgow Coma Scale assesses ability to open eyes, utter words, and follow commands
Minimally conscious/responsive state – the inability to interact consistently with the environment even
though some environmental awareness exists (e.g., selective visual tracking, intermittent
nonreflexive motor activity)
Persistent vegetative state (PVS) – condition of profound nonresponsiveness in the wakeful state that is
caused by brain damage, characterized by nonfunctioning cerebral cortex, absence of discernible
adaptive responses to external environment, akinesia, mutism, and inability to signal in any way;
EEG is isoelectric or show abnormal slowing
Brain death – absence of cerebral functions, absence of brainstem functions (electrocerebral silence)
Locked-in syndrome/coma vigil – complete paralysis due to bilateral lesions of motor pathways
(corticospinal tract) and lower cranial nerves (impaired horizontal eye movement through CN VI)
in the inferior, ventral portion of the pons or medulla, usually from occlusion of a basilar
artery branch; vertical eye movement remains possible, cognitive function in unimpaired, and
EEG is normal; can be caused by Guillain-Barre or myasthenia gravis
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Twilight state – transient impaired consciousness in which the patient may perform certain acts
involuntarily without subsequent memory for those acts; may be seen in recovery from general
anesthesia
Transient loss of consciousness without other focal features – most common cause cardiogenic syncope;
related to cardiac output, temporary reduction of blood flow to the brain, a decrease in essential blood
component, or other factors, including psychological factors (e.g., anxiety)
Coma stimulation – systematic, repetitious sensory stimulation administered to shorten coma or improve
arousal level
Purposeful response to stimuli Brainstem reflexes sleep-wake cycle
Brain death
No
No
No
Coma
No
Yes
No
Stupor,obtundation,lethargy Yes, at times
Yes
Variable
PVS
No
Yes
Yes
Akinetic mutism,abulia,catatonia Yes, at time
Yes
Yes
Locked-in syndrome
No
Yes (vertical eye mvmnt) Yes
Status epilepticus
Variable
Variable
Variable
Dissociation,somatiform Yes, at time
Yes
Yes
EEG
flat
various patterns
various patterns
various patterns
various patterns
normal
seizure activity
normal
Pupils
Toxic/metabolic – normal
Midbrain lesion or transtentorial herniation – “blown”
Pontine lesion – small, responsive
Opiate overdose – pinpoints
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DRUG USE/EXPOSURE
Alcohol – at moderate levels have impaired visual-motor skills, integration of sensory stimuli, and
information processing; at higher levels results in sedation, CNS depression, stupor, coma; after sudden
alcohol cessation can have delirium tremors (DTs) lasting up to a week, associated with agitation, tremor,
excessive dreaming, confusion, and hallucinations, associated with risk of status epilepticus
Amphetamines – CNS stimulant lasting longer than cocaine, excessive DA through blocked reuptake and
release, causes euphoria and increased vigilance; can lead to hallucinations, psychosis, hyperkinetic
movement disorder (e.g., dystonia, chorea), stroke, seizure; withdrawal leads to depression, REM rebound
Cocaine – CNS stimulant, excessive DA through blocked reuptake and release, blocks reuptake of NE
and 5-HT, causes euphoria and increased vigilance; high doses cause rapid motor activity, rambling
speech, impaired judgment, paranoid and psychotic behavior, agitation, irritability, anxiety, stroke,
seizure; withdrawal leads to depression, REM rebound; reduce alpha waves in frontal and temporal
regions, general atrophy; cognitive deficits in psychomotor speed, visuospatial deficits, memory,
concentration, planning, inhibition (consistent with DA depletion)
Glue sniffing – impaired attention, memory, visuospatial functioning, complex cognition, naming,
reading, writing, manual dexterity, processing speed; see diffuse atrophy of cerebral hemispheres and/or
brainstem
Marijuana (THC) – affects THC receptors in cortex, basal ganglia, hippocampus, and cerebellum; calms,
reduces nausea and vomiting, elevates mood; associated with impaired memory, sustained attention,
executive functions
Phenylcyclidine (PCP) – central analgesic, depressant, hallucinogen; blocks reuptake of DA, NE, 5-HT,
prevents glutamate from activating NMDA receptor; high doses causes positive and negative symptoms
of schizophrenia; overdose with mucle rigidity, vertical nystagmus, sterotypies, blank stare, unresponsive,
violence, seizure, “wide awake coma”
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DYSARTHRIA
Speech disorder resulting from disturbances of neuromuscular control of the speech
mechanisms/articulation, related to paralysis, weakness or incoordination of the respiratory muscles,
larynx, tongue, lips, and jaw; origin can be peripheral (e.g., facial paralysis, loss of teeth) or central (e.g.,
basal ganglia or cerebellar disease); characterized by slurring, breathiness, wetness, or straining;
consistency differentiates it from inconsistent apraxia of speech
-
-
-
Ataxic – impaired articulation and prosody characterized by slurred speech and scanning speech,
patient may appear inebriated
* cerebellar lesions
Flaccid – hypotonia and weakness in the speech muscles
* damage to the motor units of the cranial or spinal nerves
Hyperkinetic – abnormal rhythmic speech associated with involuntary movements (e.g.,
choreaform, athetoid, ballistic)
* basal ganglia and subthalamic nucleus lesions
Hypokinetic – characterized by speech monotone and reduced range of speech
* basal ganglia lesions
Spastic – characterized by slow speech that further deteriorates with rapid fatigue
* upper motor neuron lesions
Unilateral upper motor neuron – mild motor speech disorder resulting from weakness of the
tongue and lower facial muscles; symptoms frequently diminish or resolve completely
* acute upper motor neuron lesions
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ENDOCRINE SYSTEM
1. Steroid hormones (e.g., sex hormones)
2. Amino acid derivatives (e.g., epinephrine)
3. Peptide hormones (e.g., insulin)
Pituitary gland – the “master gland” of the endocrine system; under direct control of the hypothalamus;
bound by sella turcica (anterior and posterior clinoid process); blood supply from ICA (inferior
and superior hypophysial arteries); surgically reached through sphenoid sinus (transsphenoidal
approach)
A) Anterior (adenohypophysis) – Rathke’s pouch (pharynx) – controlled by releasing
inhibitory factors from arcuate nucleus, periventricular nucleus, medial preoptic nucleus, and
paraventricular nucleus that travel down the median eminence via a hypophysial portal
circulatory system
1) adrenocorticotropic hormone (ACTH) – stimulates the adrenal cortex (on top of kidney)
to produce corticosteroid hormone (cortisol, aldosterone) for maintaining blood pressure,
electrolyte balance, glucose mobilization
*Cushing’s disease (↑ cortisol), Addisons (↓ cortisol and aldosterone)
2) growth hormone (GH) – causes the liver, kidneys, and other organs to produce
somatomedins (insulin-like growth factors) for growth of bones and tissue
*dwarfism or giantism in children, acromegaly in adults
3) prolactin – causes the mammillary glands to produce milk; dopamine
4) thyroid-stimulating hormone (TSH) – stimulates the thyroid gland to produce thyroxine
and triiodothyronine, promoting cellular metabolism
*hyperthyroidism/hypothyroidism (rare – usually local to thyroid)
5) luteinizing hormone (LH) – sex and genesis hormones
*hypogonadism, infertility
6) follicle-stimulating hormone (FSH) – sex and genesis hormones
*hypogonadism, infertility
B) Posterior (neurohypophysis) – released by supraoptic and paraventricular nuclei
1) oxytocin – milk letdown, uterine contractions
2) vasopressin (also called arginine vasopressin (AVP) or antidiuretic hormone (ADH)) –
kidney water retention; plays role in memory consolidation
*diabetes insipidus by deficieny or insensitivity (diluted urine)
*defiency in multiple hormones called panhypopititarism
Pituitary adenoma – benign anterior epithelial tumor, usually diagnosed because of hormonal
irregularities (prolactin secretion most common); if undetected, may compress the optic chiasm,
causing bitemporal hemianopsia or superior quadrantanopsia; dopaminergic agonists (e.g.,
bromocriptine, cabergoline) inhibit prolactin release and somastostatin analogue octreotide
inhibits growth hormone release; dexamethasone suppression test
Pituitary apoplexy – tumors with hemorrhaging leading to headache, meningeal signs, cavernous
syndrome, visual loss, hypotension, depressed level of consciousness
Pituitary gland connected to bottom of hypothalamus via pituitary stalk, just under optic chiasm
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Hypothalamus – HEAL: Homestasis, Endocrine control, Autonomic control, Limbic mechanisms
part of the diencephalon, integrating the peripheral autonomic mechanisms, endocrine activity,
and many somatic, homeostatic functions (e.g., water balance, temperature regulation, sleep, food
intake, development of secondary sex characteristics); forms the inferior and lateral walls of the
third ventricle; controls pituitary gland; mammillary bodies form posterior portion; median
eminence releases neurons to anterior pituitary
1) Periventricular area (from telencephalon) – most autonomic control
2) Medial hypothalamic area – preoptic, anterior (supraoptic), middle (tuberal), posterior
(mammillary)
3) Lateral hypothalamic area
1. Suprachiasmatic nucleus (SCN) regulates circadian rhythms, has receptors for
melatonin
2. Ventral lateral preoptic area releases GABA that inhibits histamenergic neurons
in tuberomammillary nucleus for nonREM sleep
3. Lateral hypothalamus important in appetite stimulation (lesion leads to weight
loss)
4. Medial/ventromedial hypothalamus inhibits appetite (lesion leads to obesity;
involves leptin and Ob receptors)
5. Anterior hypothalamus – thirst (lesion to lateral hypothalamus reduces water
intake); heat dissipation (lesion causes hyperthermia)
6. Posterior hypothalamus – conserve heat
Autonomic fibers through medial forebrain, dorsolateral brainstem, periaqueductal gray matter
Subiculum of hippocampus  fornix  mammillary bodies
Mamillary bodies  mammillothalamic tract  anterior thalamus  cingulated gyrus
Amygdala  stria terminalis or ventral amygdalofugal pathway  hypothalamus
Mammillary bodies – paired, spherical masses located on the basal surface of the posterior hypothalamus;
part of the pathway from the hippocampus (via the postcommissural fibers of the fornix) to the
anterior nucleus of the thalamus (via the mammillothalamic tract), projecting to the anterior
cingulated gyrus; implicated in amnesia associated with Korsakoff’s syndrome
Medial forebrain bundle – a fiber system in the lateral hypothalamus that connects the hypothalamus with
the midbrain tegmentum and the limbic system; it carries fibers from norepinephrine and
serotoninergic cell groups in the brainstem to the hypothalamus and cerebral cortex and
dopaminergic fibers from the substantia nigra to the caudate nucleus and putamen
Thyroid and Parathyroid gland – cellular differentiation, growth, metabolism
Thyroid – cacitonin, parathyroid – parathyroid hormone
Pancreas – secretes digestive enzymes into small intestines and secretes insulin (decrease) and
glucagons (increase) to regulate blood sugar level (hyper- and hypoglycemia)
Adrenal glands – sit on top of kidney
1. Cortex – secretes corticicosteroids (e.g., cortisone) that reduce inflammation but raises blood
pressure and suppresses immune system (hypercortisol - Cushing’s disease); aldosterone
controls minerals in extracellular fluid (hypo both – Addison’s)
2. Medulla – secretes epinephrine (adrenaline), responding to stressors such as fright, anger,
caffeine, low blood sugar
Gonads – males androgens (e.g., testosterone), females estrogen and progesterone
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Pineal gland – located near the center of the brain, stimulated by nerves from eyes, secreting melatonin
when dark (associated with 5-HT), promoting sleep, controlling biological clock, circadian
rhythms, depressing activities of gonads, affecting thyroid and adrenal functions (SAD – too
much melatonin)
Overactivity of hypothalamic-pituitary-adrenal axis in response to stress causes overproduction of
corticotrophin-releasing factor (CRF), contributing to depression
See Blumenfeld Figures 17.3, 17.4
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ETHICAL PRINCIPLES OF PSYCHOLOGISTS AND CODE OF CONDUCT (APA, 2003)
INTRODUCTION AND APPLICABILITY
Preamble and 5 General Principles are aspirational goals.
10 Ethical Standards are enforceable rules of conduct; the fact that a given conduct is not specifically
addressed does not mean that it is necessarily ethical or unethical; lack of awareness or misunderstanding
is not itself a defense to a charge of unethical conduct.
APA may take action against member after conviction of a felony, expulsion or suspension from an
affiliated state psychological association, or suspension or loss of licensure. If sanction less than
expulsion, in-person hearing not guaranteed. Ethics code not intended to be a basis of civil liability.
Reasonable means the prevailing professional judgment of psychologists engaged in similar activities in
similar circumstances, given the knowledge the psychologist had or should have had at the time.
If the Ethics code establishes a higher standard of conduct than is required by law, psychologist must
meet the higher standard. If ethical responsibilities conflict with law, regulations, or governing legal
authority, make known commitment to the Ethics code and take steps to resolve the conflict in a
responsible manner. If conflict unresolvable, may adhere to law, regulations, or governing authority in
keeping with basic principles of human rights.
PREAMBLE
Goals are the welfare and protection of the individuals and groups with whom psychologists work and the
education of members, students, and the public regarding ethical standards of the discipline.
GENERAL PRINCIPLES
1. Beneficence and Nonmaleficence – strive to benefit and do no harm, resolve conflicts, alert to misuse
of their influence, aware of own ability
2. Fidelity and Responsibility – establish relationships of trust, act professionally and responsibly, clarify
roles and obligations, manage conflicts that could lead to exploitation/harm, consult, ethical compliance
of colleagues, volunteering/pro bono
3. Integrity – promote accuracy and honesty in the science, teaching and practice
4. Justice – access to psychological services, do not condone unjust practices
5. Respect for People’s Rights and Dignity – respect, privacy, confidentiality, self-determination, cultural
and individual differences, eliminate biases
ETHICAL STANDARDS
1.
Resolving Ethical Issues
1.01
Misuse of psychologists’ work – take steps to correct or minimize
1.02
Conflicts between ethics and law, regulations, or other governing legal authority
1.03
Conflicts between ethics and organizational demands
1.04
Informal resolution of ethical violations
1.05
Reporting ethical violations
1.06
Cooperating with ethics committees
1.07
Improper complaints
1.08
Unfair discrimination against complainants and respondents
2.
Competence
2.01
Boundaries of competency – including new technology
2.02
Providing services in emergencies
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3.
4.
5.
6.
7.
2.03
Maintaining competence
2.04
Bases for scientific and professional judgments
2.05
Delegation of work to others – avoid multiple relationships, competence of others
2.06
Personal problems and conflicts
Human Relations
3.01
Unfair discrimination
3.02
Sexual harassment
3.03
Other harassment
3.04
Avoiding harm
3.05
Multiple relationships
3.06
Conflict of interest
3.07
Third-party requests for services – identify who is the client
3.08
Exploitative relationships – do not exploit persons over whom they have supervisory,
evaluative, or other authority
3.09
Cooperation with other professionals
3.10
Informed consent – if legally incapable, provide appropriate explanation, seek assent,
obtain permission from legally authorized person
3.11
Psychological services delivered to or through organizations; interruption of psychological
services
Privacy and Confidentiality
4.01
Maintaining confidentiality
4.02
Discussing the limits of confidentiality – including email and fax
4.03
Recording – obtain permission
4.04
Minimizing intrusions on privacy
4.05
Disclosures
4.06
Use of confidential information for didactic or other
Advertising and Other Public Statements
5.01
Avoidance of false or deceptive statements
5.02
Statements by others – responsibility for such statements; do not compensate employees of
the media, paid advertisements must be identified as such
5.03
Descriptions of workshops and non-degree-granting educational programs
5.04
Media presentations – do not indicate that a professional relationship has been established
5.05
Testimonials – do not solicit testimonials from current therapy clients or others vulnerable
to undue influence
5.06
In-person solicitation – do not engage uninvited in-person solicitation
Record Keeping and Fees
6.01
Documentation of professional and scientific work and maintenance of records
6.02
Maintenance, dissemination, and disposal of confidential records of professional and
scientific work
6.03
Withholding records for nonpayment
6.04
Fees and financial arrangements
6.05
Barter with clients/patients – only if not clinically contraindicated, not exploitative
6.06
Accuracy in reports to payor and funding sources
6.07
Referrals and fees – payment to be based on service provided, not referral
Education and Training
7.01
Design of education and training programs
7.02
Descriptions of education and training programs
7.03
Accuracy in teaching
7.04
Student disclosure of personal information – do not require except if clearly identified in
admission/program material or information necessary to obtain assistance for personal
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problems judged to be preventing training or professional related performance in a competent
manner or posing threat to students or others
7.05
Mandatory individual or group therapy
7.06
Assessing student and supervisee performance
7.07
Sexual relationships with students and supervisees – don’t
8.
Research and Publication
8.01
Institutional approval
8.02
Informed consent to research
8.03
Informed consent for recording voices and images in research – unless naturalistic
observation or includes deception and consent obtained during debriefing
8.04
Client/patient, student, and subordinate research participants
8.05
Dispensing with informed consent for research – anonymous questions, naturalistic
observations, or archival
8.06
Offering inducements for research participation – avoid
8.07
Deception in research
8.08
Debriefing
8.09
Humane care and use of animals in research
8.10
Reporting research results – do not fabricate data, correct errors
8.11
Plagiarism
8.12
Publication credit
8.13
Duplicating publication of data
8.14
Sharing research data for verification
8.15
Reviewers – respect confidentiality of and proprietary rights
9.
*Assessment
9.01
Bases for assessment – clarify impact on limited information, explain sources of
information on which based conclusions and recommendations
9.02
Use of assessments – proper application, valid and reliable instruments, limitations of test
results and interpretations
9.03
Informed consent in assessments – implied because routine (e.g., educational,
organizational), or is to evaluate decisional capacity
9.04
Release of test data – test data refers to raw and scaled scores, responses to tests questions
or stimuli, and notes and recordings concerning client statements and behaviors; with release,
provide test data to client or other person identified in release (no longer just those qualified
to interpret); may refrain from releasing test data to protect a client or others from substantial
harm, or misuse or misrepresentation of data or test
9.05
Test construction
9.06
Interpreting assessment results – indicate limitations
9.07
Assessment by unqualified persons – only for training with supervision
9.08
Obsolete tests and outdated test results
9.09
Test scoring and interpretation services – valid selection, interpretation, third party
observation
9.10
Explaining assessment results
9.11
Maintaining test security – test materials refers to manuals, instruments, protocols, and test
questions or stimuli and does not include test data
10.
Therapy
10.01
Informed consent to therapy
10.02
Therapy involving couples or families – clarify who is patient
10.03
Group therapy
10.04
Providing therapy to those served by others
10.05
Sexual intimacies with current therapy clients/patients – don’t
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10.06
10.07
10.08
10.09
10.10
Sexual intimacies with relatives or significant others of current therapy
clients/patients – don’t
Therapy with former sexual partners – don’t
Sexual intimacies with former therapy clients/patients – don’t for at least 2 years and only
in the most unusual circumstances
Interruption of therapy
Terminating therapy
General Guidelines for Providers of Psychological Services
Aspirational but minimal guidelines to improve the quality, effectiveness, and accessibility of
psychological services (self-regulation in the public interest)
Includes acceptable qualifications to establish desirable levels of service, background and
application differences, life factors
1. Providers of Psychological Services – psychologist must have doctorate from regionally
accredited institution or other school using organized, systematic program; others must have
qualifications and supervision commensurate with responsibilities
2. Psychological Services
3. Psychological Service Unit
4. Users – direct user, institution or organization, third-party purchasers
5. Sanctioners (family, court, school, employer, government)
Guidelines
1. Providers – within expertise and competence, responsibility, supervision, maintain
knowledge, respecialization, innovation
2. Programs – service unit composition responsive to client needs, avoid violations of rights,
conform to legal statutes, inform, consult, therapy procedures, avoid use of privileged
information for personal gain
3. Accountability – promotion of human welfare, pro bono services, evaluation of services
Specialty Guidelines for the Delivery of Services by Clinical Psychologists (also for Counseling, School,
and I/O)
For educational purposes and to facilitate continued development of the profession
Clinical Psychologist must have doctorate from regionally accredited institution or other school using
organized, systematic program plus doctoral and post-doctoral training; others must have qualifications
and supervision commensurate with responsibilities
Standards for Education and Psychological Testing
General and non-technical criteria regarding the evaluation of tests, acceptable practical use, and effects
of test use
General Principles
1. Validity – different types of validity, rationale, justifiable interpretation, sample, biases,
adjustments, statistical equations
2. Reliability and Errors of Measurement – best to report imprecision estimates (e.g., CI)
3. General issues – revalidation/rationalized changes, consultation for different test takers,
alternative explanations
Standards
1. Technical Standards for Test Construction and Evaluation
2. Professional Standards for Test Use
3. Standards for Particular Applications (e.g., employment)
4. Standards for Administrative Procedures
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 manuals should list needed qualifications, rationale, research, recommended uses, cautions
against misuse
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Guidelines for Diverse Populations (Ethnic, Linguistic, Cultural)
Multicultural assessment involving socioeconomic and political factors, work to reduce prejudice and
discrimination
Relevant factors: generations/years in country, English fluency, extent of family support, community
resources, level of education, change in social status, intimate relationships with different people, stress
related to acculturation
Specialty Guideline for Forensic Psychologists
Aspirational, professional practice issues (not minimum qualifications)
Issues include no services on contingency fee, recognizing conflicts and dual relationships, limits
of confidentiality, need of waiver if information to be used for other purposes, do not
provide services without counsel (except pro se), not for criminal proceedings (unless
defendant introduces mental condition), keep to role, avoid detailed public statements
Licensure
To protect the public, to qualify individuals – determine standards for admission and monitor
performance, assesses basic knowledge of psychology
Legal Aspects
Malpractice
1. Professional relationship and established legal duty of care
2. Demonstrable breach of “standard of care” (from experts, legal statutes, professional articles,
third-party payers)
3. Patient suffered harm or injury
4. Breach of duty was proximate cause
Damage
a. Compensatory – loss due to injury
b. Nominal – cannot be monetarily translated
c. Punitive – to punish reckless or malicious acts
(Civil suit – “preponderance of evidence”)
Causes
1. Sexual and other dual relationships (mostly men older than clients) – 43%
2. Lack of competence – practicing outside of expertise, failure to treat effectively, misuse of tests,
practicing while impaired, failure to warn – 42%
3. Breach of confidentiality (most frequently occurring ethical dilemma) – 10%
4. Improper financial agreement – altering diagnosis to meet insurance-reimbursement criteria –
15%
Risk Management – be familiar with ethical and legal standards, keep records, monitor high risk
clients, evaluate if to take on litigious clients
Subpoena
1. Validity check
2. Contact client
3. If consent or waive, release; if not, contact attorney
4. Can seek guidance from court or motion to quash/protective order
Testimony – assert doctor-patient privilege until court ordered
Court Order – must comply to avoid contempt
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Terms
Insanity – legal term referring to lacking substantial capacity to appreciate the wrongfulness of
the act or behave according to the requirements of the law
Competence to Stand Trial (Dusky v. US) – as the result of a medical condition, lacks sufficient
ability to consult with a lawyer to a reasonable degree of rational understanding and to
understand proceedings (psychological abilities and impairments)
Fact Witness – testify about something directly observed (not opinion)
Expert Witness – has superior knowledge to offer opinions and testify on hypothetical scenarios
Guardianship – responsible for another’s necessities
Guardian ad litem – adult appointed by court for representation in a civil legal proceeding (e.g.,
minor)
Insurance companies not covered by HIPPA (Health Insurance Privacy and Portability Act)
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FRONTAL LOBE THEORIES
I. Norman and Shallice – controlling and monitoring activities
1. Autonomic Contention Scheduler (ACS) – automatic and direct priming of stored knowledge by
stimuli in environment or conceptual thought
2. Supervisory Attention System (SAS) – conscious awareness of what we know that set priorities
for action; can override ACS; what is damaged in frontal lobe dysfunction
II. Goldman-Rakie – primate working memory; firing of prefrontal neurons when delay between
stimulation and recall; linked spatially
III. Fuster – Temporal Processing Model; action sequences tend to be goal related/conceptually driven, so
related to each other both by time and common goals (cross-temporal contingencies)
IV. Stuss and Benson – behavioral/anatomical theory
1. Dorsolateral prefrontal cortex – sequencing, forming mental sets, integrating behaviors
2. Ventromedial prefrontal cortex – drive, motivation, will
V. Luria – problem-solving deficits by impaired programming and regulation of behavior (SAS)
VI. Damasio – Somatic Marker Theory; modulation of decisions; patients with ventromedial frontal
lesions have diminished galvanic skin response
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GAIT
1. Spastic – stiff-legged, sometimes with scissoring of legs and toe-walking, decreased arm swing
* corticospinal (UMN, MS)
2. Ataxic – wide-based, unsteady, staggering
* cerebellum/cerebellar vermis (alcohol, infarct)
3. Frontal – slow, shuffling, “magnetic”; can bicycle lying down
* frontal (hydrocephalus, tumors, diffuse subcortical white matter disease)
4. Vertiginous – ataxic, fall on Romberg
* cerebellar, vestibular nuclei, semicircular canals (alcohol, infarct)
5. Parkinsonian – slow, shuffling, narrow based, stooped forward, decreased arm swing, poor initiation,
en bloc turning, retropulsion
* substantia nigra or other basal ganglia (Parkinsonian syndromes, use of neuroleptics)
6. Dyskinetic – dancelike (choreic), flinging (ballistic), or wringing (athetoid) movements
* subthalamic nucleus or other basal ganglia (Huntington’s infarct, use of levodopa)
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HEADACHE
Supratentorial dura innervated by CN V
Posterior fossa dura innervated mainly by CN X
1. Vascular
a. Migraine
i. aura associated with vasoconstriction, headache associated with inflammatory
reaction of vasodilation (15%)
ii. provoked by certain foods (tyramine, nitrate, phenylthylamine, MSG), stress (and
relaxation after stress), eye strain, menstrual cycle, change in sleep, barometric
changes, medication (vasodilators); (80%)
aura involves blurring, distortions, or fortification scotoma (visual loss bordered by zigzagging
lines); often unilateral; may have nausea, vomiting, photophobia, phonophobia; usually lasts 30
minutes – 24 hours, relief with sleep;
~5% men and ~15% women, peak age 42, 75% positive family history, greatest Caucasians, then
African Americans, then Asians; complicated may include transient focal neurologic deficits
(sensory, motor, visual, brainstem, eye movement);
Acute medications include anti-inflammatory, anti-emetic, triptans (5HT agonist), ergot
derivative, prophylactic medications include beta-blockers, tricyclics, calcium channel blocker,
valproate (anti-epileptic), methysergide, caffeine, autogenic treatment, thermal biofeedback
b. Cluster (histamine headache) – pain behind eye with autonomic symptoms (tearing, eye
redness, flushing, sweating, congestion, Horner’s syndrome); REM sleep may precipitate; 5x
more common in males, occurring 1/10 of migraines, lasting 30-90 minutes; similar treatment to
migraines, also lithium, inhaling oxygen
c. Basilar – ataxia, vertigo, dysarthria, diploplia, nausea, vomiting, possible memory impairment
(temporal lobes)
d. Hemiplegic – hemiparesis, hemiparesthesia, aphasia accompanies, fortification scotoma; may
become risk factor for stroke; familial type autosomal dominant on chromosome 19
2. Tension– steady, dull ache; may be familial; associated feeling with brain tumor
3. Other – acute trauma, intracranial hemorrhage, cerebral infarct, carotid or vertebral artery dissection,
venous sinus thrombosis, post-ictal, hydrocephalus, pseudotumor cerebri, low CSF pressure, toxic
or metabolic derangement, meningitis, epidural abscess, vasculitis (temporal/giant cell arteritis),
trigeminal or occipital neuralgia, neoplasm, disorders of eyes, ears, sinuses, teeth, joints, scalp
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HISTORY
Neuropsychology – the study of the relation between brain function and behavior
Approaches:
American (actuarial)
Statistical
Standardized
Normative data
Protocol
Russian (clinical)
Clinical
Non-standardized
Individual differences
Hypothesis testing
Localization of functioning 3000-1700 BC
Almaceon (500 BC) – located mental processes in the brain
Hippocrates (460 BC) – brain the organ of intellect and controlled senses and movements contralaterally
Plato (427 BC) – brain seat of rationality
Aristotle (384 BC) – brain cooled blood
Herophilus (300 BC) – localization in ventricular chambers (Cell Doctrine)
Galen (130) – intellect in substance, not ventricles; theory of “psychic gas”
Vesalius (1514) – brain diagrams; brains similar in structure but vary in size across animals
Descartes (1596) – mind-brain problem (“dualism”); pineal gland as “seat of soul”
Gall (1758) – studied cortex, fibers; connected left frontal brain damage and aphasia; phrenology
(functional brain localization as reflected by shape of the skull) to evaluate personality
Bouillaud (1825) – studied loss of speech associated with frontal lesions; contralateral control
Dax (1836) – studied left lesion with aphasia and right hemiplegia; papers published by son
Auburtin (1861) – continued with Bouillaud’s cause
Flourens (1800s) – brain functions as a whole, equipotentiality; antiphrenology
Munk (1881) – ablation of occipital cortex of dogs
Vogt, Campbell, Brodmann (late 1800s) – cytoarchitectonic maps
Ribot (late 1800s) – distinction between anterograde and retrograde memory; Ribot’s law (more recently
formed memories lost first)
Lashley (late 1800s-early 1900s) – move toward holism; mass action and equipotentiality theory that
memory impairment does not depend on localization of lesion but amount of tissue damaged,
amnesia considered inability to activate memory traces, not loss of memory engram
(also Marie, Head, Goldstein)
Hughlings-Jackson (1830-1910s) – hierarchical organization; homonculus
Broca (1863 – patient Leborgne) – localization of language, dominance in left hemisphere; ‘aphemia’ as
inability to speak despite intact vocal mechanisms and normal comprehension
Wenicke (1860-70s) – localization of language and connectionism
Benedikt (1865) – applied the term agraphia to writing disorders, focusing on connection of agraphia to
aphasia
Ogle (1867) – noted agraphia and aphasia separate
Galton – father of testing movement
Meynert – sensory localization; described brain structures and function
Fritsch & Hitzig (1870) – produced contralateral movement through brain stimulation
(excitability, movement, localized)
Bartholow (1874) – first electrical stimulation of human cortex
Lichtheim (1885) – recognized seven syndromes/aphasia based on hypothetical deficits and
lesion location
Wernicke-Lichtheim model – a brain-based model of language function in which normal function is
associated with an underlying neural pathway that includes input/output functions with clear
interrelationships between other cortical language areas; aphasias could be predicted and
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explained by reference to where in the pathway damage occurred;
model of language processing based on acoustic (A) and articulatory motoric (M)
representations and impulses leading to and from concept (C) formation;
proposed writing disorders similar to disorders of speech
Cattell – individual differences in behavior; crystallized and fluid intelligence
Dejerine (1891-2) – identified first callosal syndrome and alexia without agraphia
Liepman – described apraxias
Osler (1913) – term ‘neuropsychology’ first used
Scoville & Milner (1918) – removed bilateral hippocampi of H.M. (1954), rendering amnestic
Spearman (1927) – two-factor theory of intelligence, g (general) and s (specific)
Monez & Lima (1935) – frontal lobotomies
Penfield (1930s) – mapped sensory and motor regions
Lashley (1936) – ‘neuropsychology’ enters nomenclature
Piaget – periods of intellectual development: Sensorimotor (0-2), Preoperational (2-7), Concrete
operations (7-11), Formal operations (11+)
Wechsler (1939) – published Wechsler-Bellevue Intelligence Scale
Neilson (1946) – writing is closely associated with speech but functionally and anatomically separate
(like Ogle); three types of apraxic, aphasia, and isolated (Exner’s area)
Goldstein (1948) – primary agraphia resulted from disruption of motor act, secondary agraphia resulted
from speech disturbance
Kluver (1957) – neuropsychology becomes a recognized field
Guilford (1959) – model of intelligence based on factor analysis
Geschwind (1965) – connectionism, alexia
Vygotsky – cultural historic theory
Luria – brainstem responsible for regulating cortical tone (arousal); posterior cerebral cortex responsible
for receiving, organizing, and storing visual, auditory, and tactual stimuli (input); anterior
cerebral cortex responsible for emitting motor responses, formulating intentions, planning and
evaluating behavior (organization and planning)
RAS sensory and motor areas single modality secondary association areas intermodality
integration prefrontal regions (does not take into account parallel/non-hierarchical processing)
Golden – standardized Luria’s Neuropsychological Investigation
Goodglass – study of language and aphasia
Mishkin – interaction between amygdala and hippocampus in recognition memory, independence of these
structure in associative learning, cortical disconnection
Pribram – hologram model of memory
Zangwill – equipotentiality
Kaplan – Boston Process Approach
Jackson – neglect
Posner, Heilman, Mesulam, Bisiach – attention and neglect
Lissauer – agnosia 2-stage model, apperceptive and associative
Brain – neglect
Neurosurgery: Horsley-Clarke (stereotaxic device), Scoville (H.M.), Milner (epilepsy surgery), Sperry
(split brain studies)
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HUNTINGTON’S DISEASE
Progressive, autosomal dominant disorder (chromosome 4, excessive trinucleotide CAG repeats >36
increased risk, >39 HD; anticipation in successive generations; 50% of children will get) that produces
basal ganglia lesions [mostly caudate nucleus, some putamen; deficient glutamate decarboxylase leads to
too much glutamate and too little GABA primarily (50% in corpus striatum), then decreases cholinergic
activity and increases dopaminergic activity], under-inhibition of thalamus, and damage to frontal cortex
and CC
Glutamate and other excitatory amino acids excessively stimulate NMDA receptors lead to excitotoxicity
through excessive calcium flow (apoptosis)
Characterized by:
1) first psychiatric symptoms [personality change (depression, anxiety, OCD, impulsivity,
mania), psychosis]
2) second choreiform movements, dyskinesia (involuntary jerking, dystonic posturing, facial
frowning, grimacing, smirking; rigidity in young adults)
3) dementia (attention, memory storage and retrieval, EF, anomia – NO aphasia, apraxia,
agnosia as in cortical dementias)
4) other: abnormal eye movements including slow saccades, impaired smooth pursuit,
sluggish optokinetic nystagmus; slow voluntary movements; motor impersistence; gait
abnormality; slurred speech, difficulty swallowing
onset usually 30-50 but can be in childhood (tend to have more CAG repeats, less chorea,
more rigidity, faster progression), 15 year survival, more common in those of northern
European ancestry; treat chorea with anti-dopaminergic; UHDRS study group uses Stroop,
Symbol Digit, Verbal Fluency
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HYDROCEPHALUS
An abnormal increase in CSF within the skull that is marked by dilatation of the cerebral ventricles and
enlargement of the skull, either from increased production or decreased absorption of CSF or obstruction
of flow or reabsorption, may or may not be associated with elevated pressure; symptoms include nausea,
vomiting, headache, imbalance and gait apraxia (from stretching of corticospinal tract in internal capsule,
“magnetic gait”), incontinence, and slowed response, limited vertical gaze (Parinaud’s syndrome); with
elevated ICP may see Cushing’s triad (hypertension, bradycardia, irregular respiration); commonly occurs
secondary to obstruction of CSF pathways from tumor or meningeal disease or, in children, from
cytomegalovisus or toxoplasmosis
-
-
-
-
communicating hydrocephalus – from disease of subarachnoid space that traps CSF in fourth
ventricle so not reabsorbed by arachnoid villi or from overproduction of CSF (e.g., choroid
plexus papilloma)
noncommunicating/obstructive hydrocephalus – from obstruction in the ventricular system
preventing passage of CSF from brain into spinal canal (often from aqueductal stenosis, or
brainstem or posterior fossa tumor)
hydrocephalus ex vacuo – enlargement of cerebral ventricles due to atrophy or loss of
adjacent tissue
normal pressure hydrocephalus – enlargement of ventricles associated with inadequacy of
subarachnoid spaces (not due to brain atrophy); usually seen in older age; associated with
dementia (aphasia), incontinence, gait apraxia (“wet, wacky, wobbly”); usually treat with
shunt
advanced infantile hydrocephalus – pressure on midbrain, scalp veins distended, “sunset
eyes” deviated downward, (Parinaud’s syndome - paralysis of upward gaze); associated with
vomiting and poor feeding
Shunt – plastic tube inserted surgically between a cerebral ventricle and the abdomen to divert excessive
CSF of hydrocephalus away from the brain
Common causes in children: neural tube defect (e.g., spina bifida, myelomeningocele), Dandy-Walker,
(Arnold Chiari), aqueductal stenosis, intraventricular hemorrhage
Affects brain development by stretching or destroying CC, affecting white matter tracts, disruption of
myelination
More right hemispheric impact (PIQ<VIQ, visuospatial<language)
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LEARNING DISABILITY MODELS
1a. Pennington’s neuropsychological model
a. primary – core symptoms universal, specific, persistent
b. correlated – same etiology affecting different brain systems (e.g., those with autism don’t
always hve MR)
c. secondary – consequences of primary or correlated symptoms
d. artifactual – associated but not causally related
1b. Pennington’s functional domains
a. phonological processing – dyslexia; left perisylvian region (including Wernicke’s and
Broca’s)
b. executive functions – ADHD; prefrontal region
c. spatial reasoning – math, handwriting; posterior right hemisphere
d. social cognition – autism spectrum; limbic, orbital, right hemisphere
e. long-term memory – amnesia; hippocampus, amygdala
2a. Rourke’s neuropsychological model – LD is a disorder of information processing from dysfunction in
neural systems
a. phylogenetically lower to higher centers
b. posterior cortex to anterior cortex
c. right-left dysfunction
2b. Rourke’s syndromes of developmental neurocognitive processing disorders
a. verbal processing disorder – disruption of language skills in auditory or visual modality;
left hemisphere
b. nonverbal processing disorder – disruption of ability to perceive or produce nonverbal
information, may also be associated with affective disorders; right hemisphere
c. attention deficit disorder – disruption of arousal-attention-concentration; right
hemisphere, bifrontal, and/or reticular activating system
d. insight/judgment/comportment disorder – do not learn rules of socially acceptable
behavior and decision-making strategy, stimulus-bound and concrete; frontal networks
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INTELLIGENCE
Spearman “g” (general factor) plus “s” (specific factors)
Thurstone’s primary mental abilities
Sternberg Triarchic Model – analytic, creative, practical
Vernon & Eysenck – neural efficiency of brain (i.e., processing speed)
Cattell – crystallized (increases until 60s) and fluid intelligence (peaks in late adolescence; includes
reasoning, abstraction, and concept formation)
Used to be ratio of mental age/chronological age, now derivation score (SS)
Impact on heredity (more for verbal than nonverbal)
Identical twins together = .85
Identical twins apart = .67
Fraternal twins together = .58
Siblings together = .45
Siblings apart = .24
Biological parent together = .39
Biological parent apart = .22
Adoptive parent = .18
Heritability estimate = .45 for children, .75 for adults (greater influence of genetics with age)
IQ + SES 30% variance; also home environment, nutrition, schooling, toxic exposure
Flynn effect – tendency for standardized test scores of a population to rise over time,
IQ scores of ~3 points per decade
Stable over life span .70-.90
WAIS-III :
VIQ increase until mid-50s and then declines slightly
PIQ peaks in mid-20s and then declines rapidly and steadily
VIQ practice effects 2-3 points, PIQ 9-10 points
V>P in MS, AD, Schizo, depression, bipolar, alcoholic, high SES
P>V in delinquent, sociopathy, LD, bilingual, illiterate, autism, low SES
DS most sensitive to brain impairment; OA and PA lowest reliability
AD: VCI>POI>WMI>PSI
Within group differences exceed between group differences
Brain reserve capacity – a theory of residual cognitive function which proposes that the greater the brain
reserve, as inferred by premorbid IQ or education, the higher the threshold for developing
cognitive impairment following injury
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LEARNING
1.
2.
3.
4.
Perceptual – changes within the sensory system
Stimulus-response – connections between sensory and motor systems
Motor – changes within the motor system
Relational – among individual stimuli
Hebb’s Rule (1949) – if a synapse is repeatedly active at the same time the post-synaptic neuron fires,
changes will take place in the structure or chemistry of the synapse to strengthen connection; cell
assembly within neuronal loop reverberates (STM) and ultimately creates lasting structural change (LTM)
Lomo (1966) – long-term potentiation occurs when postsynaptic cell is depolarized at the same time it is
stimulated; NMDA receptors (through calcium channel and protein kinasis enzymes) only open when
glutamate in cleft; weak synapses become strengthened through associative LTP; generally found in
hippocampus but also prefrontal cortex, piriform cortex, entorhinal cortex, motor cortex, visual cortex,
thalamus, and amygdala; increases AMPA receptors (through sodium channel); pre-synaptic changes
through nitric oxide synthase
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LIFESPAN DEVELOPMENT
Birth Defects
1. Genetic Factors
a. Recessive Genes – sickle-cell anemia, Tay-Sachs, cystic fibrosis, PKU, some DM
b. Chromosomal Abnormalities – sex-linked (Turner, Klinefelter, Fragile X) or autosomal
(Down’s)
2. Teratogens – substances that cross the placenta
a. Alcohol – facial deformities, retarded growth, heart defects, MR, hyperactive, irritable
b. Narcotics – neonatal abstinence syndrome, LBW, small head, SIDS, childhood academic
problems
c. Cocaine – miscarriage, early delivery, stillbirth, small for gestational age, SIDS, seizures,
LBW, small head, exaggerated startle, increased tone and motor activity, impaired fine
motor coordination, auditory impairments, high-pitched cry, sleep and feeding problems,
difficult to comfort in childhood, developmental delays, difficulties with speech and
language development, poor peer interactions, behavioral and attentional problems
d. Nicotine – placental abnormalities, miscarriage, premature rupture of membranes, SIDS,
LBW, prematurity, perinatal death, respiratory disease, deficits in learning and behavior,
emotional and social problems
e. Heroin – miscarriage, low birthweight, prematurity, intrauterine growth retardation
f. Stimulants – lethargy, tremor, increased intraventricular hemorrhage
g. Lead – MR, LBW
3. Maternal Conditions
a. Rubella – when in 1st trimester, heart defects, blind, deaf, MR
b. HIV/AIDS– smaller, 35-60% transmit if untreated, only 1/3 survive to age 8 with AZT
and antibiotics
i. Infant – high illness, inflammatory responses, oral candidiasis
ii. Kid – immunological abnormalities, cognitive and physical delays
c. Malnutrition – worst in 3rd trimester (low protein restrains brain growth, NT), stillbirth,
miscarriage, LBW, MR
d. Stress – miscarriage, painful and preterm labor, LBW, hyperactive, irritable, irregular
feeding, sleeping, bowel movements, crying
4. Birth Complications
a. Anoxia – MR, CP, delayed development
b. Herpes simplex 2 – death, brain damage, blind
Childhood Psychopathology
Risk factors – severe marital discord, low SES, overcrowding, parent criminality, maternal
psychopathology, child placed outside the home (2% one factor, 21% with four or more)
Resiliency factors – reduced stress, easy temperament (sociability), stable support (e.g., Kauai)
Newborn Perception
Vision – 1/10 of adult at birth, complete by 6 months; 2-5 days attend to faces, know Mom at 1 month;
limited color at 2 months, some depth perception 4-6 months
Audition – hear last month in utero; at birth almost at level of adults in intensity; localization present at
birth, disappears at 2-4 months, reappears later; at 3 months can differentiate consonants, voices, know
Mom
Taste & Smell – prefer sweet and avoid unpleasant; 8-10 days prefer Mom’s milk
Pain – increases in the first 5 days
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Developmental Milestones
3 months – bring object to mouth
4 months – roll from stomach to back
5 months – sit on lap, reach, grasp
6 months – sit alone, stand with help
8-9 months – crawl, creep
9-10 months – pull self to standing
10-11 months – stand alone, walk with help
12 months – first steps
13-14 months – walk
15 months – creep up stairs, scribble, use cup
18 months – run clumsily, walk stairs with help, use spoon
24 months – go up stairs alone, kick ball, turn pages, 50% toilet trained
30 months – jump, hand-eye coordination
36 months – tricycle, dresses alone
Cognitive Development Theories
1. Piaget’s Constructivism – sequential stages involving maturation interacting with environment;
equilibrium
a. Sensorimotor (0-2) – object permanence, causality, symbolic/representational thought
b. Preoperational (2-7) – symbolic/semiotic function; limited by precausal/transductive
reasoning (magical thinking), animism, egocentrism, lack of conservation (irreversibility
and centration)
c. Concrete (7-11) – mental operations, conservation (horizontal decalogue: numbers,
liquid, length, width, volume), reflective self
d. Formal (11+, but not all adults attain) – abstraction, relativism, hypothetical-deductive
reasoning, systematic testing, renewed egocentrism (Elkind – personal fable, imaginary
audience)
2. Vygotsky – social and cultural
- interpersonal and intrapersonal/internalization
- zone of proximate development (scaffolding, temporary aides), pretend play
3. Bronfenbrenner’s Ecological Model – child in context
- microsystem (family, school), mesosystem (microsystems interacting), macrosystem
(environment/society), exosystem (environmental influences on microsystems)
4. Information Processing – maturation and experience
- acquisition, generalization, increase storage capacity, process- and task-specific abilities
Age and Memory
No decline in remote LTM, span, sensory
Declines in recent LTM (encoding), working memory (processing efficiency), episodic memory
Declines dependent on task and person for semantic, procedural, metamemory
Language
Prelinguistic
1 month – cry (1st hunger, anger and pain; then fussy)
6-8/12 weeks – coo
4 months – babble
6 months – lallation
8 months – distinct own language sounds
9 months – echolalia
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12 months – expressive jargon
9-14 months – babble narrows to own language sounds
Linguistic
12-24 months – holophrastic speech (1 word)
18-24 months – telegraphic speech (2-3 words)
27 months – prepositions and pronouns (300-400 word vocabulary)
30-36 months – most rapid vocabulary growth (1000 words)
2.5-5 years – complex and grammatical sentences (50 new words/month)
6-7 years – metalinguistic awareness (language as communication tool)
Language and Thought
Linguistic Relativity Hypothesis (Whorf) – language determines thought
Nativist View – language and thoughts independent
Piaget – language development dependent on thought
* most likely bi-directional
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LIMBIC SYSTEM
A group of brain structures that includes the hippocampus, amygdala, dentate gyrus, cingulate gyrus,
septal areas, and parts of the diencephalon (thalamus, hypothalamus), associated with autonomic and
neuroendocrine functions, motivation, emotion (behavioral changes), appetite, recent memory
(consolidation into LTM), and olfaction
HOME = Homeostasis, Olfaction, Memory, Emotions and drives
(hypothalamus)
(hippocampus) (amygdala)
1) Limbic cortex – parahippocampal gyrus, cingulate gyrus, medial orbitofrontal cortex, temporal
pole, anterior insula
2) Hippocampal formation – dentate gyrus, hippocampus, subiculum (between the parahippocampal
gyrus and Ammon’s horn; archicortex)
3) Amygdala
4) Olfactory cortex (paleocortex)
5) Diencephalon – hypothalamus, thalamus (anterior nucleus, mediodorsal nucleus, internal
medullary lamina, habenula), mammillary bodies
6) Basal ganglia – ventral striatum (nucleus accumbens, ventral caudate and putamen), ventral
pallidum
7) Basal forebrain – provides major cholinergic (Ach) innervation to the neocortex and medial
temporal lobes, including septal area, diagonal band of Broca, nucleus accumbens septi, olfactory
tubercle, substantia innominata [nucleus basalis of Meynert (AD)], bed nucleus of stria
terminalis, preoptic area
* lesion often due to ACommA aneurysm, leading to anterograde amnesia and deficits seen in
frontal lobe lesions
8) Septal nuclei – lateral septal nucleus receives input from hippocampus, outputs from the medial
septal nucleus (Ach)
9) Brainstem
Amygdala – emotion, mediation of defense; basolateral nuclei (cortical connections), corticomedial nuclei
(olfaction, appetite), and central nuclei (autonomic control via hypothalamus and brainstem) and
bed nucleus of stria terminalis (connection to hypothalamus and septal area; ventral
amygdalofugal pathway to forebrain and brainstem)
Cingulate gyrus – “satisfaction center”; arch-shaped cortical gyrus lying above the corpus callosum,
lesions often produce akinesia
Cingulum – bundle of association fibers in the white matter under the cingulate gyrus
Cingulotomy – surgery that sections the cingulum, to treat chronic pain or control OCD
Septum – “pleasure center”; inhibits emotionality; lesions cause septal rage syndrome
Entorhinal cortex – anterior portion of the parahippocampal gyrus on the medial surface of the
temporal lobe; major input and output relay between association cortex and hippocampal
formation relays; involved in odor processing and memory; greatly affected in DAT
Fornix – the efferent tract of hippocampus and subiculum arching over the thalamus to synapse on
structures in the rostral telencephalon and diencephalon (hypothalamus); about half of the fibers
terminate in the mammillary body, rest to lateral septal nucleus and anterior thalamic nucleus
Hippocampus – part of the limbic system located in the medial temporal lobe, important for learning and
memory consolidation, episodic/contextual memory; connection to association cortex via
perirhinal and parahippocampal cortex, connected to entorhinal cortex (Brodmann’s area 28);
common seizure focus; three-layered cortex (archicortex/archipallium), broader anteriorly;
immediate memory retained even with damage
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Inputs from entorhinal cortex via CA (cornu ammonis/Ammon’s Horn) (CA4 closest to
dentate gyrus and CA1 closest to subiculum); output via subiculum
1. Perforant pathway via dentate gyrus to granule cell, mossy fibers to CA3, CA3 and CA1
through fornix, Schaffer collaterals to CA1; longterm potentiation (synaptic plasticity) though
increased glutamate and protein synthesis
2. Alvear pathway via CA1 and CA3
Hippocampal system – parahippocampal gyrus, uncus, hippocampal formation, dentate gyrus,
fasciolus, indusium griseum/supracollosal gyrus, fimbria, and fornix; input from entorhinal
cortex, output from subiculum to entorhinal cortex
-
Papez’ Circuit (James Wenceslaus Papez) – circuit proposed to control emotions and emotional
expressions : hippocampus/amygdala (Alvear pathway)  fornix (recall and anterograde memory) 
mammillary bodies  mamillothalamic tract  anterior thalamus  cingulated gyrus  hippocampus
(via parahippocampal gyrus and entorhinal cortex)
Amnesia (loss of declarative memory, consolidation of new memories), from bilateral medial
diencephalic lesions
See Blumenfeld Figure 2.24, 18.2, 18.4, 18.6, 18.7, 18.8, 18.9, 18.13, Hendelman Figures 75, 77B, 80
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MEMORY
the acquisition and retention of information; dependent on encoding, consolidation, retrieval, forgetting
(temporal lobe – hippocampus, parahippocampus, amygdala, neocortex)
Mnestic – pertaining to memory
I.
II.
III.
IV.
V.
VI.
A. Anterograde – the ability to learn and recall new information (hippocampus and
amygdala)
B. Retrograde – the ability to recall information that had been previously stored or learned,
involving both a retrieval deficit and loss of previously stored information (mammillary
bodies, thalamic nuclei, interconnecting pathways)
A. Declarative/explicit – experiences, facts or events that can be consciously recalled
(hippocampus, amygdala, medial thalamus, temporal lobes, prefrontal cortex)
i.
Episodic – memory that is context specific and often autobiographical, preserving the
temporal and spatial features of past events (associated with contextual encoding
deficit)
ii.
Source – memory for the circumstances in which an episodic memory is
formed; source amnesia may be related to frontal lobe pathology
iii.
Semantic – memory that is context-free, reflecting general knowledge of symbols,
concepts, and the rules for manipulating them; impairments commonly observed in
acute confusional states, moderately severe dementia, or focal lesions affecting
linguistic functions
B. Nondeclarative/implicit – a range of memory types in which performance is altered
without conscious mediation, including procedural memory (skills not verbalized or
consciously inspected, such as motor learning; corpus striatum), priming, and classical
conditioning; this is operationally defined regarding change in performance such as savings
or priming (basal ganglia, substantia nigra, ventral thalamus, premotor cortex)
A. Primary – the content of immediate consciousness
B. Secondary – recall of information that is no longer in consciousness
A. Short-term – retention of information over brief periods (e.g., span)
B. Long-term – retention of information over long intervals
C. Remote – retention of information or distant events
A. Registration/Sensory – holds large amounts of information very briefly; information
retained through reverberating neural networks (associated with LTP)
B. Immediate – the capacity to maintain information in conscious awareness
C. Recent – the ability to form new memories; includes orientation to time and place
Sensory – the first stage of memory processing in which a perceptual record is stored
A. Echoic – sensory memory for auditory material that is of relatively large capacity but
limited duration (2-3 seconds)
B. Iconic/eidetic – sensory memory for visual material that is of relatively large capacity but
limited duration (250-300 milliseconds)
Working Memory (Baddeley & Hitch) – a limited capacity memory system that provides temporary
storage to manipulate information/workspace to process information, including Central
Executive System, Phonological (dorsal)/Articulatory (ventral) Loop (with both short-term store
and rehearsal mechanisms) and Visuospatial Sketchpad
*dorsolateral prefrontal association cortex
Prospective – memory for plans, appointments, and actions anticipated to occur in the future; includes
timely completion and memory for the intention
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Topographical – memory for spatial layout
Encoding specificity principle – principle that the retrieval of an event is a function of the overlap
between the context of the learning and that of the retrieval; memory is facilitated when
information available at encoding is present at retrieval
Dual code theory – memory theory that concrete words can be represented by an imaginal code and
verbal code whereas abstract words give rise only to a verbal code
Ribot’s law (of regression) – the principle that the vulnerability of memory loss to neurological insult is
an inverse function of the age of those memories, resulting in a temporal memory loss gradient;
memories most recently acquired are most vulnerable to loss following neurological insult or
disease, but also present in normal aging
Primacy effect – the tendency for words presented earlier in a series to be better recalled when using a
free recall task; may be decreased by rapid stimulus presentation or using words with similar
meaning
Recency effect – the tendency to recall items from the end of a list in a free recall task; the absence of a
recency effect may indicate interference due to problems with attention
Serial position effect – the tendency to more readily recall items presented at the beginning (primacy
effect) and toward the end (recency effect) in a free-recall task
Proactive interference/inhibition – decreased learning of new information on account of the effects of
previous learning; greater for information that is semantically related
Retroactive interference/inhibition – impairment in recall of previously learned information due to the
learning of new information
Release from proactive interference – improved memory performance for stimulus words following a
shift in semantic category
Encoding – process by which the cognitive system builds up a stimulus representation into memory
(e.g., translation of auditory input into semantic stimulus, like a bell ringing)
Elaboration – memory process in which the products of initial encoding are enriched by further
processing
Distractor task – a task administered as part of some memory task to prevent rehearsal
Clustering – grouping similar items together during recall
Priming – a form of nondeclarative/implicit memory in which prior exposure to a stimulus exerts an effect
on a subsequent stimulus detection or identification; neocortical task
Incidental learning – learning that occurs without volitional effort; tested with tasks the subject is
unaware will have later memory recall assessed
Spacing effect – enhanced memory for repeated items when the repetitions are separated by other events
Storage deficit – a memory deficit resulting from impaired consolidation
Cued recall – memory recall in which information about items to be recalled is provided
Retention – the persistence of information over time
Recognition – memory that is assessed through discrimination of target items presented earlier from
distractor items not previously administered
Memory decay – the loss of recently learned information as a function of time
Forgetting – the loss of information over time
Savings technique – an approach to assessing retention in which a task is first learned to a specific level
and the amount of savings is determined by amount of time/number of trials needed to later
relearn the task to the same level
Metamemory – knowledge about the nature and contents of one’s own memory
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Registration of information – sensory organs, primary cortex, association cortex
Short-term memory/working memory – parietal and prefrontal cortex
Encoding and consolidating information – limbic system (thalamus)
Storage of information – cerebral cortex
Retrieval of information – prefrontotemporal network
Caudate  habit learning
Cerebellum  classical conditioning
Amygdala  conditioned fear
Amnesia associated with hippocampus, hippocampal projections to the fornix and septum, dorsal medial
thalamic nuclei (poor consolidation)
Pattern of Memory Impairment:
1) Medial Temporal lobe – from anoxia, limbic encephalitis, CVA, AD, epilepsy/surgery (e.g., H.M.)
- insight present, confabulation absent, deficits in retrograde and declarative memory
2) Diencephalon – from infarction of thalamic arteries, trauma, tumor, Wernicke-Korsakoff
- insight absent, confabulation present, deficit in retrograde memory, sensitive to proactive
interference, anterograde amnesia
3) Frontal lobe – from CVA, tumor, surgery, aneurysm (AcoA)
- insight usual, confabulation often present, deficits in retrograde and contextual memory,
attentional deficits, proactive interference
Memory components (Moscovitch)
1) nonfrontal neocortical – perceptual and semantic modules mediating performance on itemspecific, implicit memory
2) basal ganglia – mediates performance on sensorimotor procedual tests
3) medial temporal/hippocampal – mediates encoding, storage, retrieveal on explicit episodic
memory (things that are associative/cue dependent)
4) central-system frontal lobe – mediates performance on strategic explicit and rule-based tests
Double dissociation from domain specificity and information encapsulation; output is shallow and
assigned meaning and relevance by central systems
Memory tests can be associative (cue sufficient for retrieval), strategic (provides start of memory search),
procedural (sensory-motor skills), or item-specific (can look at accuracy and speed with
repetition)
1) perceptual input modules and perceptual repetition priming – anatomically localized
2) conceptual repetition effects and semantic records – mediated by interpretive central-system
structures (deficient in AD)
3) hippocampal component – hippocampus, parahippocampal gyrus, entorhinal and perirhinal
cortices, mammillary bodies, DM thalamus, cingulated cortex, fornix; associated with level of
processing
4) frontal lobes – impairments associated with deficits in organization and strategic processing
5) procedural implicit tests – sensorimotor skills retained if no damage to basal ganglia
Aging causes decline of frontal lobe memory functions associated with strategic processing
Transient global amnesia (TGA) – a sudden, acute amnesia that is typically benign and resolves within 24
hours, appearing to involve subcortical structures affected by ischemia of PCA or partial seizures;
migraine; patients are disoriented and cannot form new memories but may carry out complex
behaviors and recall basic personal information; associated with anterograde and retrograde
amnesia but preservation of immediate memory, often precipitated by events associated with
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sudden body changes (e.g., cold shower, sex, strong emotional experience)
Topographical amnesia – specific loss of memory for places
Hysterical/psychogenic amnesia – memory loss of non-neurologic origin arising from emotional
disturbance
Broken record syndrome – tendency to repeat associated with dense amnestic state
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METALS
Lead – longterm exposure associated with learning and behavioral disorders and lowered IQ, poor
attention and memory, impaired EF, visuospatial deficits, impaired coordination; fatigue,
headache, poor emotional control; peripheral neuropathy is common in adults; primarily
involving the hippocampus; also CNS, kidneys, reproductive system, blood
Mercury – acute exposure, if does not result in death from respiratory, GI, or renal dysfunction,
associated with encephalopathy of cerebellum, basal ganglia, primary visual cortex, spinal cord;
motor slowing, clumsiness, tremor, paresthesia, visual and hearing defects, agitation; longterm
exposure associated with depression, slowing, impaired STM
Aluminum – dialysis dementia, marked by stuttering and dysfluent speech, myoclonus and difficulty
swallowing, concentration and memory problems; may be related to other dementias
Manganese – drowsiness, dizziness, sleep disturbance, emotional lability, apathy; slowing, parkinsonan
symptoms
Heavy metal poisoning – poisoning from metals having higher atomic numbers than calcium in the
periodic table of elements
Chelation – treatment for heavy metal poisoning using substance for which the toxin has a chemical
affinity
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MOTILITY
1) large motor neurons – from anterior horns of spinal cord and motor nuclei of brainstem to skeletal
muscles; lesions result in loss of voluntary, automatic, postural, and reflexive movement
(paralysis)
2) upper motor neurons (corticospinal/pyramidal, corticobulbar, and others) – motor cells in the
cerebral cortex near the rolandic fissure connected to spinal motor neurons through pyramidal
tract in medulla
3) brainstem nuclei that project to spinal cord, including pontine nuclei, medullary reticular nuclei,
vestibular nuclei, and red nuclei, subserve posture and particularly highly automatic and repetitive
movement
4) basal ganglia and cerebellum control muscle tone, posture, and coordination by connection with
the corticospinal system via the thalamocortical fibers and premotor cortex
5) other parts of cerebral cortex, including premotor and accessory motor areas, involved in
planning, programming, and acting out voluntary/purposive movement, and nervous system
concerned with tactile, visual, and auditory sensation
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MOTOR NEURONS
Lower motor neuron (LMN) – cell bodies and tracts that innervate muscle; lesions are associated with
weakness, decreased muscle tone and stretch reflexes, hypoactive deep tendon relex (DTR),
fasciculations (involuntary muscle twitching that is typically a sign of muscle denervation),
muscle atrophy, flaccidity (loss of muscle tone); abnormal nerve conduction studies; no Babinski
Upper motor neurons (UMN) – the primary motor output pathway that originates in the precentral gyrus,
passes through the medullary pyramids, and descends the spinal cord as the corticospinal tract,
synapsing with lower motor neurons in the spinal cord; lesions associated with hemiplegia or
hemiparesis; whole groups of muscles affected, atrophy slight and due to disuse, “long tract
signs” of hyperrelexia/clonus/hyperactive deep tendon reflex (DTR), spasticity/increased tone,
Babinski, normal nerve conduction studies; can see facial weakness with sparing of forehead and
neighbor effects; decrease in autonomic arm swing
Corticospinal – motor tracts from primary motor cortex to spinal cord nuclei in the ventral horns;
pass through pyramidal medulla; lesions lead to spasticity, shortening and lengthening reaction,
increased tendon reflexes (hyperreflexia), clonus, positive Babinski sign, and paralysis of
voluntary movement (corticospinal impulses normally inhibit muscle tone)
Corticobulbar – motor tracts from primary motor cortex to cranial nerve nuclei in the brainstem
Pyramidal motor system – principal motor output cells of the neocortex consisting of pyramidal-shaped
neurons that typically have long axons, originating in the precental gyrus, pass through the
medullary pyramids, and descend the spinal cord as the corticospinal tract; consisting of upper
and lower motor neurons that guide purposeful and voluntary movement lesions produce
hemiplegia or hemiparesis
Extrapyramidal motor system – a functional unit consisting of physiologically similar structures,
including the basal ganglia (all five sections) and their connections to each other and the
thalamus; modulates movement and maintains muscle tone and posture, dysfunction results in
involuntary movement disorders; observe rigidity (substantia nigra), tremor, chorea, athetosis and
dystonia (striatum), and bradykinesia
Hyporeflexia – depressed activity in tendon reflexes associated with dysfunction of the reflex arc;
unilateral suggestive of radiculopathy (lesion of nerve root) and bilateral suggestive of peripheral
neuropathies (non-lesional)
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MOVEMENT DISORDERS
Involuntary disorders resulting from impairment of the extrapyramidal motor system that are present
while awake but not asleep
1) Tremor – repetitive, rhythmic movements from activation of agonist and antagonist muscles
a) action/postural – most common, fast, most evident when limbs and trunk actively maintained
(e.g., arms held extended); includes essential/familial/benign/senile, nervous, and
physiological tremors; caused by lithium and anticholinergics, suppressed by alcohol;
relieved with beta-adrenergic antagonist/beta-blockers, thalamotomy or thalamic stimulation
b) resting – slower, evident when extremities supported against gravity, commonly seen in PD
(pill rolling); gone during full relaxation and sleep
c) intention/ataxic – slowest, side to side movement elicited by attempting to touch target,
increasing as approach target
* cerebellar
d) rubral – slow head and trunk titubation; associated with MS, brainstem infarcts
* superior cerebellar peduncle; red nuclei
2) Dyskinesia – impairment of voluntary movement involving an excess of movement, including
persistent eccentric posture, twisting of limb; non-rhythmic, divided by speed and size
a) choreoform – involuntary, intermittent, jerky, rapid movements, usually in hands, often
blended into normal movements (e.g., “piano playing”); subsides during sleep; commonly
seen in HD, benign familial chorea, Sydenham’s chorea (rheumatic from strep A), systemic
lupus erythematosus, gravidarum (during pregnancy), levodopa use
* basal ganglia dysfunction
b) athetosis – involuntary slow, regular, twisting, writhing movement of tongue, face,
extremities, or whole body, more prominent distally (e.g., HD, Wilson’s, antipsychotics,
levodopa); can be associated with mental retardation
* striatum/putamen
c) ballismus – intermittent, violent flinging actions, usually unilateral (hemiballism), greater in
arms than legs
* contralateral subthalamic nucleus lesion leading to decreased inhibition of thalamus;
treated with dopamine antagonist
d) choreoathetosis – combined choreic (jerking) and athetoid (writhing) movements seen in
Huntington’s disease, Cerebral palsy, and with neuroleptics
* subthalamic nucleus
3) Abnormal tone
a) spasticity – increase muscle tone associated with increasing resistance that suddenly
disappears with massive movements; e.g., “clasp-knife” rigidity with lengthening and
shortening reactions; from upper motor neuron lesions
b) flaccidity – decreased muscle tone and hyporeflexia (LMN lesion)
c) plastic rigidity – muscle resistance present and increased throughout entire range of passive
movement; e.g., “lead pipe”
i)
cogwheel – combination with resting tremor
ii)
gegenhalten – semi-voluntary resistance to passive movement; associated with FLD
and dementia
d) hypotonia – decrease in tone; from cerebellar or peripheral dysfunction
e) dystonia – distorted positions of limbs, trunk, or face held for periods of time, treated with
botulinum toxin injections (interferes with presynaptic release of ACH at neuromusulcar
junction); may be seen with dopamine antagonists, such as antipsychotics (levodopa) or antiemetics
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Torticollis – neck muscles
e.g., spasmodic torticollis – contraction of neck with head flexed and drawn towards
the contracted side, with face rotated over other shoulder
ii)
Blepharospasm – spasmodic blinking and intermittent involuntary eye closure
associate with other dystonic contractions of head and neck
iii)
Spasmodic dysphonia – laryngeal muscles
iv)
Writer’s cramp
f) myotonia – increased muscular irritability and contractility with delayed muscle relaxation
4) Myoclonus – fast, bilateral and symmetrical, jerking movements from alternating muscle contractions
and relaxation (from lesion in cortex, cerebellum, basal ganglia, brainstem, or spinal cord; from anoxia,
uremia)
a) startle myoclonus – in Jakob-Creutzfeld and AD
b) myoclonic epilepsy – variant of petit mal, no LOC
c) intention myoclonus – from anoxic brain damage
d) palatal myoclonus – markedly rhythmic and notably persistent movement of palate during
sleep
* lesion of central tegmental tract
e) asterixis/“liver flap” – rapid, sporadic contraction followed by slower return to extension;
tested by extending arms with palms facing forward (motioning “stop”) and seeing flapping
tremor of hands; seen in toxic or metabolic encephalopathies, particularly hepatic failure, and
confusional states
5) Tics – an involuntary, brief, stereotyped movement resembling a purposeful movement because it is
coordinated and involves muscles that are normally synergistic, involving an urge to perform and sense of
relief after (urges also in restless leg syndrome and akathisia)
a) motor – face and shoulders/neck usually
b) vocal – grunts, coughing, howling, barking, obscenities (coprolalia)
i)
Bradykinesia – abnormal slowness of movement associated with movement initiation difficulty, includes
slowness of speech, chewing, and swallowing
* increased inhibition from basal ganglia to thalamus
Hypokinesia – decreased movement
* lesions to frontal lobes, subcortical white matter, thalamus, reticular formation, basal
ganglia
Akinesia – absence of movement associated with PD, abulia, catatonia
*corticospinal, corticobulbar, lower motor neuron, muscular
Akathisia – fidgety, pace
Astasia-Abasia – inability to stand (astasia) and walk (abasia) despite normal ability to move legs when
seated or lying down; considered a psychogenic gait
Automatism – simple, repetitive motor acts that are not mediated by conscious intention
Decerebrate posturing/rigidity – bilateral, marked, rigid extension of the legs with internal rotation and
extension of the arms, produced by bilateral midbrain lesions that extends to the upper brainstem
near the red nucleus
Decorticate posturing/rigidity – bilateral, marked, rigid flexion of the arms to the chest and of the legs and
extension of ankle and knee, produced by bilateral dysfunction of the cortex; lesions may involve
gray and white matter, internal capsule, or thalamus bilaterally
Steppage – because of impaired position sense, raise legs excessively
* posterior spinal cord degeneration (tabes dorsalis)
Synkinesia/motor overflow – involuntary movement of a muscle group during the execution of voluntary
movements that involves a different muscle group; may be seen with athetosis, in which distant
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muscles contract, or with diffuse brain damage, in which there is movement of the contralateral
hand during fine-motor movements
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Speed (slow  fast BRD ACB TM)
bradykinesia/  rigidity  dystonia  athetosis  chorea  ballismus  tics  myoclonus
hypokinesia
(tremor slow or fast)
Ventromedial tract – axial musculature, maintaining posture
Dorsolateral tract – distal musculature, control of voluntary movements
Extensor – muscle that, when contracted, causes limb extension or straightening
Flexor – muscle that, when contracted, causes limb to bend or flex
Dorsiflexion – backward bending and turning upward of the hand/finger or foot/toes
Hoffman sign – a pincher flexion movement of the index finger and thumb elicited by flexion of third or
fourth finger, a sign of hyperreflexia that may occur with upper motor neuron disease (or anxiety)
Ca++ triggers contraction, energy extracted from ATP
Palsy – partial paralysis or paresis
Diplegia – bilateral paralysis of corresponding extremities
Hemiplegia – paralysis on one side of the body that is cause by brain injury; the degree of paralysis is
often incomplete (hemiparesis) and the arm is usually weaker then the leg
Paraplegia – paralysis of both legs
Quadriplegia – paralysis of all four limbs resulting from injury to the brainstem or cervical spine
Paresis – partial or incomplete paralysis; generally used to describe focal deficits associated with
upper motor neuron lesions
Dysarthria hemiparesis – pure motor hemiplegia and dysarthria without sensory abnormalities or
cortical signs
* contralateral corticobulbar and corticospinal tracts in internal capsule or ventral pons
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MULTIPLE SCLEROSIS (MS)
Demyelinating, autoimmune disease characterized by multi-focal chronic inflammatory lesions (sclerotic
plaques from astrocytes and gliosis) in the white matter that block or distort normal transmission of nerve
impulses; are disseminated (i.e., separated in time and space, last at least 24 hours, occur in intervals
greater then 1 month, and involve different parts of the CNS); lesions found in spine, optic chiasm
(central scotoma), periventricular white matter (high intensity abnormalities)
Categories include relapsing-remitting, primary progressive, secondary progressive, progressive-relapsing
Clinical presentation includes numbness and weakness, optic neuritis/retrobulbar neuritis (unilateral or
bilateral vision loss, scotoma, color desaturation), intranuclear opthalmoplegia (INO), Marcus Gunn pupil
(pupil paradoxically dilates when a light is shined in the eye, CN II), acute/transverse myelitis, vertigo,
seizures, ataxia, paresthesia, psuedobulbar palsy, diplopia, hemiplegia, trigeminal neurologia (CN V),
bladder dysfunction, spasticity, dysphagia, spinal cord 3-I’s (incontinence, impotence, impairment in
gait/tandem gait), Charcot’s triad (horizontal nystagmus, dysarthria, tremor), Lhermitte’s sign (electrical
sensation), scanning speech; severe fatigue, sensitive to heat, stress
Usually detected by IgG/Albumin in CSF > in serum, oligoclonal bands, myelin basic protein
Evoked response/potential tests reveal interruptions in visual, auditory, or sensory pathways
Twice as frequent in females, usual onset 20-40, more prevalent away from equator – disease acquisition
believed to occur before age 15, genetic variability (25% monozygotic twins), immunological influence;
may be slow acting virus, delayed reaction to common virus, or autoimmune reaction in which the body
attacks self
Mood sequelae and cognitive changes resembling those with frontal and subcortical lesions: depression,
personality change; language skills generally spared (mild naming and word generation problems),
impaired memory retrieval but relatively intact recognition, impaired attention (span, tracking), impaired
executive functions, slowed processing speed, motor impairment (thus VIQ>PIQ); higher suicide rate
(x7.5); cognitive impairment most associated with total lesion area but also physical impairments,
duration, enlarged ventricles, CC atrophy, periventricular demyelination, cerebral hypometabolism
Looks like Lyme disease, AIDS, Guillain-Barre, leukodystrophies (Adrenal LD, Metachromatic LD),
infections, toxins attacking CNS myelin (Marchiafava-Bignami from degeneration of CC from homemade
wine, Chronic toluene exposure), lupus
Flare-ups treated with corticosteroids/ACTH, Interferon (naturally occurring protein that suppresses the
immune system; side effects including flu-like symptoms, anemia, depression), but no cure
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NEGLECT SYNDROME
Failure to attend, respond to, report, or orient to novel visual, auditory, or tactile stimuli presented in the
hemispace contralateral to a brain lesion that cannot be attributed to primary sensory or motor deficits
(typically when right/nondominant hemispheric lesion) or memory deficits; attributed to impairment of
“top-down” process; often due to CVA, tumor, seizures; evaluated with tests such as line bisection,
cancellation test, draw a clock; DA med may help (Jackson 1867, Brain 1941)
* mostly right parietal/frontal cortex lesion (overseeing spatial distribution of attention); also cingulate
gyrus, thalamus, basal ganglia, reticular formation
Inattention
- Sensory neglect – deficit in awareness contralateral to lesion, not involving cortical systems
- Extinction to double simultaneous stimulation (Masking) – failure to report contralateral
stimulation when simultaneous stimulatation; can be both forward and backward if not
simultaneous
- Defective vigilance – contralateral stimulation failed to be detected after repeated stimulation
- Allesthesia/Allochiria – when touch on side contralateral to lesion is referred to ipsalateral side
(first stage in recovery)
- Exomethesthesia – a rare form of allesthesia in which somatosensory stimulus location is
identified off the body and in external space
Intentional (Motor) Neglect
- Akinesia – failure to initiate movement
- Hemiakinesia – failure to use an extremity contralateral to a cerebral lesion, typically seen with
right cerebral injuries
- Motor extinction – contralateral akinesia with simultaneous bilateral limb movement
- Hypokinesia – initiation of activity after long delay
- Bradykinesia – slowness of movement
- Motor impersistence – inability to sustain an act (testing includes sticking out tongue and keeping
eyes closed)
- Allokinesia – incorrect limb moved or limb movement that occurs contralateral to intended
movement
Spatial Neglect
- Spatial agraphia
Personal Neglect
- Asomatognosia – denial of one’s own body part (usually only on left side – hemiasomatognosia)
- Autotopagnosia – inability to recognize or localize parts of own body (finger agnosia)
- Dressing apraxia
Memory and Representational Deficits
- Anterograde – inability to recall stimuli perceived in contralateral hemispace
- Retrograde-representational – inability to recall contralateral-sided details
- Anosognosia – denial of illness
- Anosodiaphoria – inappropriate lack of concern over deficits
1) Parietal component – (inferior parietal lobe) key role in spatial attention associated with motor output;
trouble disengaging
2) Frontal component – (frontal eye fields, inferior frontal gyrus, dorsolateral) converting plan and
intention into specific motor sequence
3) Limbic component – (cingulate gyrus; anterior global, posterior differentiated) motivation and effort
4) Subcortical component – (thalamus, striatum, superior colliculus, mesencephalic reticular formation,
posterior limb of internal capsule) trouble with engaging
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Representational Hypothesis
Bisiach’s Representative of Approach – loss of spatial representation of external world;
not supported by cuing of left hemispace
Attentional Hypothesis
Heilman’s Unilateral Akinisia – hypoarousal to new sensory information
Posner’s Covert Orienting – disengage, shift, engage model of attention
Mesulam’s Attention Network – domain-specific impairment of spatial impairment by
damage in one or more components of distributed network
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NERVOUS SYSTEM
Central Nervous System (CNS) – brain and spinal cord
Peripheral Nervous system (PNS) – a system of afferent and efferent neurons that connect the CNS with
the sensory receptors, muscles, and viscera of the body
1. Somatic – voluntary sensory, skeletal motor, skin
2. Autonomic Nervous System (ANS) – involuntary; involved in the maintenance of internal
body functions and behavior; regulates smooth internal organs/muscles (viscera); involved in
emotions, stress reactions, and rage expressions; regulates 4 ‘F’s (feeding, fighting, fleeing, sex);
regulated by hypothalamus and limbic system
- Parasympathetic – “rest or digest”: pupil constriction, bronchoconstriction, cardiac
deceleration, digestion, salivation, intestinal vasodilation (C1-C8, S2-S4; releases
acetylcholine)
- Sympathetic – “fight or flight”: pupil dilation, bronchodilation, cardiac acceleration,
piloerection, glucose release, systemic vasoconstriction; involved with visceral functions and
conservation and restoration of energy (T1-L2; releases neuroepinephrine)
White matter pathways: known as tracts or bundles in CNS; cross-hemispheric called commissure
Fasciculus – a nerve fiber bundle
Lemniscus – sensory fiber bundle in the medulla and pons that relays discrete or epicritic
functions
Nucleus – a group of nerve cell bodies inside the nervous system; when outside the nervous system or
PNS called a ganglion
Axons in PNS known as peripheral nerves
Afferent Arrives (sensory – dorsal/posterior nerve root)
– alar plate; receive axons from dorsal root ganglia
Efferent Exits (motor – ventral/anterior nerve roots)
– basal plate; contains cell bodies of axons that innervate muscles
Divided by sulcus limitans
Bell-Magendie law – separation into sensory and motor
31 pairs of spinal nerves (CTLSC):
Cervical (C1-C8), Thoracic (T1-T12), Lumbar (L1-L5), Sacral (S1-S5), Cauda equina/Coccygeal
Brachial plexus  arm (cervical enlargement), lumbosacral plexus  leg (lumbosacral enlargement)
Spinal cord ends at L1-L2; lesion in C causes quadriplegia
Lumbar puncture – technique for obtaining CSF (between L4-L5)
Spinal cord – gray matter on inside and white outside in horn shape (H), separated by fasciculus proprius;
alpha motorneuron from CNS to periphery
Corticospinal tract (descending) – begins in primary motor cortex of the precentral gyrus and goes
through cerebral white matter, forming the corona radiata and then posterior limb of the internal capsule,
traveling through cerebral peduncle in midbrain to reach spinal cord; 70-90% (lateral) cross over at
pyramidal decussation at junction between medulla and spinal cord, 10-30% (anterior) cross in spinal
cord through anterior commissure; moving from anterior to posterior lateral position
(above – contralateral; below – ipsalateral; meeting of upper and lower motor neurons)
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Ascending Pathways (to thalamus or cerebellum), including Lissuer’s tract:
- Posterior white column pathway (dorsal column/medial lemniscus) –
joint/kinesthetic/proprioception (position from receptors in the muscles, tendons, and
viscera), vibratory/pressure sense, fine touch (VPL thalamus); lower limbs represented
medially by fasciculus gracile and upper limbs represented laterally by fasciculus cuneatus;
cross over in medulla
- Anterolateral pathway (Spinothalamic tract) – pain and temperature laterally (posterior horn),
crude touch and pressure anteriorly (VPL thalamus); immediately cross over in spine via
anterior commissure and become internal arcuate and then medial lemniscus (legs represented
most laterally)
- Spinocerebellar pathway (Clarke’s column) – muscle tone, joint position and movement
sensation to cerebellum (unconscious registration) via nucleus dorsalis (trunk and limbs) and
external cuneats nucleus (arm and neck) to inferior cerebral peduncle
- Trigeminal tract – somesthetic (pain, temperature, touch, and pressure) for head (VPM)
With age, most likely to lose vibration sense but loss of position sense more obvious;
pain and temperature sensations usually preserved
Tabes dorsalis – destructive lesion in posterior roots (PNS)
B12 deficiency – lesions in posterior white columns (CNS)
See Sidman & Sidman 717A, 742A, 745A, 808A
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NEUROIMAGING/NEURORADIOLOGY
Arteriography – radiographs
Computerized Tomography (CT) – x-ray imaging technique using ionizing radiation, measures tissue
density, good in detecting acute hemorrhage/blood (immediately hyperdense) and mass effect
[white – most dense (bone), black – least dense (air); white brain matter darker than grey brain
matter]; expressed in Hounsfield Units (HU = 0 for water); contrast adjusted by window and
level; with iodine contrast makes areas of increased vascularity and breakdown of blood-brain
barrier hyperdense
Spiral CT angiography (CTA) – rapid injection of intravenous contrast used with helical
(continuous) CT to obtain three-dimensional images of blood vessels
Doppler ultrasound – technique of measuring speed of sound through different media, to measure flow
and lumen diameter of large blood vessels, revealing the degree of vessel stenosis, helping to
identify CVD
Electrical stimulation mapping – technique for identifying cortical sensory, motor, and language areas by
applying electrical current directly to the exposed brain
Electrodermal activity – reflects autonomic nervous system functioning, providing a measure of
emotional response (conductance level, galvanic skin response)
Electroencephalogram (EEG) – brain waves recorded with scalp or depth electrodes, determined by
electric potential differences between two points (axonal membrane voltage);
usually 23 points, 10-10 system has 64 points; left-odd, right-even
- Contingent Negative Variation (CNV)/expectancy wave – a slow, negative potential shift in the
EEG that occurs in anticipation of a stimulus following a warning or alerting signal, occurring
maximally over the frontal lobe
Evoked potentials (EP) – electrophysiological responses representing summated, discrete electrical brain
discharges elicited by sensory stimulus or other event along ascending pathway to cerebral cortex
(auditory, motor, somatosensory, visual), determining hemispheric specialization; lasts in the
hundreds of milliseconds
1) exogenous sensory potentials – modality specific sensory processing
2) endogenous/event-related potentials (ERP) – reflect task in which engaged
Functional Magnetic Resonance Imaging (fMRI) – MRI with identified areas of blood flow change
through K+ ions;
Dynamic/perfusion (movement), Diffusion (early ischemia), Blood oxygen
level-dependent (BOLD; changes in regional blood flow)
Magnetic Resonance Angiography (MRA) – imaging technique that visualizes cerebral vasculature
without catheter or contrast medium; detects direction and speed of blood flow with movement of
protons between radio frequencies (venous flow measured through MRV)
Magnetic Resonance Imaging (MRI) – computerized imaging technique that excites protons to emit
electromagnetic signals, with information gained by time required to return to resting state; in T1
white matter is white, gray matter is gray, bone, CSF and air black, abnormalities black (identify
anatomy), in T2 white matter is dark grey, gray matter is light gray, bone and air black (low
water), CSF and abnormalities white (like negative) (detecting pathological changes); also have
proton density/first echo image; MRI better than CT for contrast resolution and old hemorrhage
but inferior for spatial resolution and acute hemorrhage; can do three-dimensionally with
magnetic gradient coils; gadolinium for contrast of inflammation or neoplasms, making areas of
increased vascularity and breakdown of blood-brain barrier hyperdense
UBO – unidentified bright object; this term is applied to hyperintense white matter foci from T2weights MRIs, and may reflect white matter pallor, ischemia, infarction, or plaques
Pixel – the smallest discrete part of a digital image display, commonly used in MRI/fMRI
(“picture element”)
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Magnetic Resonance Spectroscopy (MRS) – noninvasive chemical identification
Magnetoencephalography (MEG) – technique similar to EEG measuring magnetic signal of brain and
allowing for 3-D localization (SQUID)
Myelography – contrast introduced into CSF through lumbar puncture
Nuclear magnetic resonance (NMR) – the absorption or emission of electromagnetic energy from a static
magnetic field after excitation; commonly applied to spectroscopy
Neuroangiography – view vasculature with radioactive contrast; good for artherosclerotic plaques and
other vessel narrowing, aneurysms, AVM (through femoral artery and aorta)
Plain Film – used to evaluate structure of skull, facial bones, sinus
Pneumoencephalography (PEG) – radiological imaging technique preceding CT and MRI; involves
injection of air or oxygen into lumbar subarachnoid space to view ventricles, subarachnoid space,
and structures between ventricles and meninges
Positron emission tomography (PET) – images metabolic and physiological functions of the brain;
measures glucose uptake (85-90% of brain activity), uses radioactivity; high grade neoplasms
have increased metabolism whereas low grade neoplasms have decreased metabolism
Quantitative EEG (QEEG) – a method of quantifying EEG into discrete frequency
Regional cerebral blood flow (rCBF) – the measurement of blood flow within a given brain region,
usually based on oxygen turnover rate; not necessarily an indicator of brain metabolism
Single Photon Emission Computed Tomography (SPECT) – a functional neuroimaging technique using
radioisotope tracers to measures perfusion/blood flow; can detect ictal state of seizure; less
expensive and more widely available than PET
Ultrasonography – use sound waves; useful in pediatrics before fontanelles close, otherwise for vascular
lesions in head or neck
Wada test – a technique used to assess cerebral language lateralization and memory function that involves
administration of an anesthesia (sodium amytal, sodium amobarbitol, brevitol) to a single brain
hemisphere at a time via the femoral to carotid artery, leading to ACA and MCA, medial
temporal lobe perfused by PCA but ACA/MCA perfusion inhibits most of cortex, white matter
and CC; 98% of right-handers and 70% of left-handers show speech disturbance with left
hemisphere injection (with 15% of left-handers and ambidextrous showing bilateral speech
disturbance, but nonduplicative errors)
Ring-enhancing lesion – a cerebral lesion seen on neuroimaging (CT or MRI) with a contrast medium as a
bright circular spot surrounded by dark areas; seen in toxoplasmosis, brain abscess, and
metastatic carcinoma
Stereotaxic guided surgery – a surgical technique in which the patient is placed in a stereotaxic apparatus
before an MRI scan, allowing for precise determination of brain regions; commonly used for
intracranial electrode implantation (epilepsy), pallidotomy (PD), removal of disease tissue, and
biopsies
Stereotaxic radiosurgery – a minimally invasive technique of creating lesions with a gamma knife and
modified linear accelerator; currently used to treat poorly accessible AVMs and brain cancer
with brain stimulation, negative responses (disruption of functions) more common than positive responses
SeeBlumenfeld Figures 4.12-4.15, Tables 4.3, 4.4
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NEUROLOGICAL EXAM
1) Mental Status – appearance, awareness and alertness and attention/concentration (AAA), orientation,
memory (recent and remote), language (spontaneous speech, comprehension, naming, repetition,
reading, writing), visuospatial skills, calculation, left-right orientation, finger agnosia, agraphia,
praxis, neglect, construction, sequencing, frontal release signs, logic, abstraction, insight and
judgment, thought process (hallucinations/delusions), personality, mood
2) Cranial Nerves
3) Motor System – muscle mass, tone, strength, extraneous and involuntary movements, tremor
Lower Motor Neuron – muscle weakness, atrophy, fasciculations (muscle twitch/
quivering movements), hyporeflexia, decreased tone
Upper Motor Neuron – muscle weakness, hyperreflexia/spasticity, increased tone
Muscle strength:
5 – full strength
4 – weak but able to resist somewhat
3 – unable to resist but able to move against gravity if joints appropriately positioned
2 – can move joint but gravity needs to be eliminated
1 – just slight movement
0 – no movement
4) Reflexes – deep tendon, superficial, cortical
Postural reflexes – mechanisms that alter muscle tone in response to position change
Frontal release signs (see below)
Reflexes:
5+ - sustained clonus (vibratory contractions in response to stretch)
4+ - few beats of clonus/reduplication of reflex
3+ - hyperactive/brisk
2+ - normal active
1+ - hypoactive but activity can be elicited with reinforcement
0 - absent
5) Coordination, Gait, and Station – abnormal if ataxia, dysdiadochokinesia (abnormal alternating
movements); Romberg test; tandem gait (heel to toe – truncal ataxia), forced gait (e.g., all heel, all
toe), gait apraxia (can do only lying down)
6) Sensation – pain, temperature, vibration, joint position (tactile: graphesthesia, stereognosis, extinction
of double simultaneous stimulation)
Tests:
Babinski – movement of great toe upwards instead of downwards on stroking sole of foot, may include
fanning of smaller toes or silent/no response abnormal (usually see downward plantar response)
*corticospinal tract injury (UMN)
Lhermitte’s sign – electric-like sensation from the neck down the body when the head is flexed forward,
increasing tension on demyelinated fibers; seen most frequently in MS but also associated with
cervical spinal cord irritation, injury, degeneration, and tumors
Romberg – stand with feet together and eyes closed, see if sway or fall, suggestive of impairment in
proprioceptive or vestibular systems
*spinal cord posterior column impairment
Hoover’s sign – the absence of the reflexive downward movement in a supposedly paretic leg when the
nonparetic leg is lifted when lying down; sign of psychogenic paresis or malingering
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Frontal release signs – pathological reflexes commonly associated with diffuse cerebral impairment but
originally described in association with lesions of the frontal lobe; abnormal in non-infants
- grasp – abnormal, involuntary grasp of fingers stroking the palm across its width or the
fingers lengthwise
- snout – abnormal pursing of the lips when the upper lip is tapped
- rooting – abnormal puckering or pursing of the lips elicited by rubbing or scratching on or
near the corner of the mouth
- suck
----------- palmomental reflexes – a reflex elicited by scraping the palm with a sharp object, causing
reflexive contraction of the ipsalateral muscle in the chin; occurs frequently in healthy older
adults
- glabellar reflexes/Meyerson’s sign – inability to inhibit eye-blinking when tapped above the
bridge of the nose; this response usually extinguishes after a few taps (seen in PD, frontal
lobe disease, or diffuse cerebral disease; in schizotypal disorders there may be an absence of
any eye-blink response)
Soft neurologic signs – nonspecific signs suggestive of neurologic impairment that occur frequently in the
normal population (e.g., synkinesia/motor overflow), or mild or subtle findings in a neurologic
examination
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NEUROPSYCHOLOGICAL EVALUATION
Social history
Present life circumstances
Medical history, current medical status and medications
Circumstances surrounding the examination
Observation
ORIENTATION AND ATTENTION
I. Awareness
1. Awareness Interview – evaluates orientation and apperception of deficits
II. Time
1. Temporal Orientation Test – negative numerical values assigned to errors, starting at 100, below 95
significant
2. Time Estimation – estimate passage of one minute, up to 21-22 second error average
3. Discrimination of Recency – which of 2 cards most recently presented, verbal and picture formats
(associating mostly frontal functioning)
a. left damage – more difficulty verbal
b. right damage – more difficulty pictorial
III. Place
IV. Body Orientation – disorientation of personal space (autopagnosia) associated with left frontal
1. Personal Orientation Test – touch own and examiner named body part, name touched body part,
imitate touch, touch according to schematic, name seen and felt objects
a. left damage – greater difficulty following verbal directions
b. right damage – more likely to ignore left side of body or left presentation
V. Finger Agnosia – most evident middle three fingers, involves left angular gyrus or right hemisphere
1. Finger Localization – identified what one finger touched in view and not in view, identify two
fingers touched
2. Tactile Finger Recognition (Halstead Reitan) – identify finger touched by number
VI. Right-Left Orientation
1. Right-Left Orientation Test – own or examiner’s body; right-sided lesions makes difficult to
reverse and do on examiner
2. Standardized Road-Map Test of Direction Sense – traces a dotted path and verbally describes
pathway taking; reflects mostly left frontal damage, with difficulty in mental rotation
3. Laterality Discrimination Test – speeded task of laterality judgment and spatial perception (i.e.,
pictures of right or left side of body)
VII. Space
1. Distance estimations – associated mostly with right occipital lesions
2. Mental Transformations In Space – associated with parietal lobe lesions
3. Mental Re-orientation – associated with right posterior lesions (e.g., Puppet Test)
4. Space Thinking – is second picture same or opposite
5. Spatial dyscalculias – misplacement or neglect of number placement, rows
6. Topographical orientation – from revisualization of familiar routes (bilateral posterior lesions)
7. Topographical Localization – locate prominent cities on country map (bilateral posterior lesions)
8. Fargo Map Test – US geography and areas of personal familiarity
9. Route finding – way around familiar objects or learn new routes (e.g., Rivermead)
VIII. Reaction Time – finger pressing after an auditory or visual signal; also found on CPT tests;
slowed in TBI, MS, attentional disorders, depression, elderly
IX. Vigilance – the ability to monitor the environment over extended periods for infrequent target stimuli,
sustain and focus attention
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1. Continuous Performance Test (Conner’s; Gordon Diagnostic System game-like)
X. Short-term Storage Capacity – attention span/span of apprehension and processing ability
1. Digit Span Forward (Memory span) – often expressed as 7+2
2. Point Digit Span – does not require speech for response
3. Letter span – slightly less than for numbers
4. Hebb’s Recurring Digit Test – digit series with every third repeated, see how quickly learn
repeated sequence
5. Knox Cube Imitation Test – visuospatial attention span on four blocks
6. Corsi Block Tapping Test – from nine blocks spread on board; certain sequences repeated and
learning of repeated sequence evaluated (e.g., WMS Spatial Span; based on Recurring Digit Test)
7. Sentence Repetition – span of meaningful verbal material and linguistic cnstruction, of increasing
length
8. Silly Sentences
9. Target Test – sequence tapped out on nine black dots (for children, from Halstead-Reitan)
XI. Working Memory – ability to temporarily hold and manipulate information in short-term memory/
immediate memory and operations performed simultaneously (mental tracking)
1. Digit Span Backward – associated with left hemisphere damage and visual field defects
2. Reversing serial order – spelling and common sequences
3. Mental Control (WMS) – serial subtraction, alphabet, count forward by 3’s
4. Sequential Operations Series – alphabet reversal, serial subtractions
5. Alpha Span – recall lists of unrelated words in alphabetical order
6. Alphanumeric Sequencing – alternate letters and numbers
7. Letter-Number Sequencing – greatly influenced by education
8. N-Back Test – when stimulus is same as one present “n” steps back
9. Paced Auditory Serial Addition Test – divided attention (average correct 72% at slowest, 45% at
fastest)
10. Stroop Tests – concentration focused and inhibition/suppression of habitual response (also low in
depressed and anxious patients)
11. Brief Test of Attention – auditory divided attention, counting numbers and disregarding letters
XII. Complex Attention
1. Digit Symbol-Coding (DS) – psychomotor performance; sensitive to brain damage
2. Symbol Digit Modalities Test – visual scanning, tracking, and motoric speed assesses; symbols
are printed and numbers to be written (reverse from WAIS DS); discriminates dementia and
depression (allows for spoken response)
3. Trail Making Test – sequencing, divided attention and flexibility (originally part of the Army
Individual Test Battery)
4. Color Trails – non-alphabetic, number and color alternative to TMT
5. Everyday attention
6. Test of Everyday Attention/Memory – map searching, telephone directory, lottery number
broadcast
7. Dichotic Listening (words or music; Broadbent) – indicator of language lateralization and
evaluates divided attention and vigilance; usually there is a right ear advantage because of left
hemisphere dominance
PERCEPTION
(Reitan-Klove Sensory Perceptual Examination assesses visual, auditory, and tactile imperception; part of
Halstead Reitan, subtests below)
VISUAL
XIII. Visual Inattention/Neglect – neglect is typically of left field due to right hemispheric lesion, usually
parietal, also frontal; left lesion slower than right
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1. Line Bisection Tests – requires the marking of the center of horizontal lines; exacerbated if lefthanded, if line longer
2. Cancellation tasks – cross out targets interspersed with foils (e.g., Visual Search and Attention)
3. Test of Visual Neglect – cross out scattered lines
4. Bells Test – track the order of cancellation of bells
5. Balloons Test – cross out balloons from circles when few and then when many
6. Letter cancellation tests
7. Star Cancellation
8. Ruff 2 & 7 Test – discriminates between similar and dissimilar distractors
9. Visual Search and Attention Test – four trials of letters, symbols, and letters and symbols with
color distraction
10. Picture description tasks
11. Picture Scanning – point out major items in the picture (Behavioral Inattention Test)
12. Reading tasks – for example, four-word phrases
13. Indented Paragraph Reading Tests – lines with varied indentations
14. Writing Techniques – copying sentences and phrases
15. Drawing and copying tests – clock, complex figure
16. Spatial representation – ask to describe familiar locale
17. Behavioral Inattention Test – 6 conventional subtests and 6 behavioral subtests, including
telephone dialing, setting time, map navigation, coin sorting
18. d2 Test: Concentration Endurance Test – cancellation test that assesses sustained attention and
visual scanning (d with two quotation marks)
XIV. Visual Scanning
1. Counting dots – track pattern of counting
2. Visual Scanning Test – tracking of letters and numbers
3. Visual Search – search matching checkerboard grids with two black squares
XV. Color Perception (visual-visual, verbal-verbal, visual-verbal)
1. Testing for accuracy of color perception – cards printed with different colored dots forming
recognizable figure against background of contrasting dots (e.g., Dvorine and Ishihara)
2. Farnsworth’s Dihotomous Test for Color Blindness – align 16 colored caps by closeness in hue
3. Neitz Test of Color Vision – geometric design in muted color within gray dots, discriminates
even for color blind
4. Color-to-Figure Matching Test – check accuracy of coloring in common figure
5. Discriminating between color agnosia and color anomia – color in picture, determine pictures
wrongly colored, matching appropriate object color, point to named color, write name of color
shown
XVI. Visual Recognition
1. Angulation – most associated with right hemispheric functioning
2. Judgment of Line Orientation – match angular relationships; men score slightly better (right
parietal)
3. Unusual views of pictures objects – identify familiar objects under distorting conditions
4. Perceptual Speed – match target to one from group of five (similar to Symbol Search)
5. Face Recognition – recognition of unfamiliar faces with memory component; deficits associated
with spatial agnosia and disturbance and dyslexia; right temporal lobe
6. Test of Facial Recognition – recognizing and matching different views/lighting of same person;
deficits in PD; right posterior lesion
7. Recognition of facial expression of emotion – associated with frontal and right functioning
8. Figure and design recognition – designs from memory
9. Visual Form Discrimination – match target set of stimuli from four choices, then memory testing
XVII. Visual Organization – of ambiguous, incomplete, fragmented, or distorted visual stimuli
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1. Incomplete visual stimuli tests – least vulnerable to effects of brain damage (e.g., Picture
Completion)
2. Gestalt Completion Tests – incomplete silhouette picture on which the subject must impose
perceptual completion for identification; right hemispheric functioning
3. Closure Speed – identification of 24 degraded object pictures
4. Gollin Figures – picture series of line drawing from sketch to full figure
5. Chimeric Figures – figures created with differing stimuli in each hemifield or quadrant (e.g., deer,
elk, moose)
6. Visual Object and Space Perception Battery (VOSP) – first test vision with “X”s, then incomplete
objects and silhouettes (incomplete letters, distorted or angled or nonreal silhouettes), then space
perception (dot counting, position discrimination, number location, block counting); right and left
lesion findings, right worse than left
7. Fragment completion – shown a complete stimulus and then asked to identify that stimulus in a
fragmented form
8. Fragmented visual stimuli – reorganization of disarranged pieces (e.g., Object Assembly)
9. Hooper Visual Organization Test – cut-up objects that need to be identified (average at least
24/30); right-sided lesions give fragmented or part responses, left-sided lesions make more
naming errors; also have multiple choice format to reduce anomic errors
10. Ambiguous visual stimuli – developed as personality tests (e.g., Rorschach)
11. Motor-Free Visual Perception Test (MVPT) – multiple-choice test of visual perception assessing
spatial relationships, visual discrimination, figure-ground, visual closure, and visual memory
XVIII. Visual Interference – recognition tasks with distraction, analyzing figure-ground relationship
1. Hidden Figures/Embedded Figures – outline simple figure hidden in complex one; multiple
choice format (i.e., Closure Flexibility)
2. Overlapping Figures Test (Poppelreuter) – name as many figures that can see; posterior lesion
affects ability to perceive more than one object at a time or shift gaze, anterior lesion causes
perseverated or confused responses
3. Picture search – objects or part thereof at unusual angles in picture scene
AUDITORY
XIX. Auditory Acuity – can test by altering speaking volume
XX. Auditory Discrimination – repetition, discriminate similar sounding words
1. Phoneme Discrimination – tape-recorded task of half identical and half similar pairs of nonsense
words
2. Wepman’s Auditory Discrimination test – identical and similar one-syllable word pairs
3. Sound Blending and Incomplete Words (WJ-III) – ability to synthesize sounds in familiar words
presented whole and in syllables; also identify heard word missing phoneme(s)
4. Speech Sound Perception Test (Halstead Reitan) – test nonsense syllables with prefix and suffix
including “ee”; form questioned because 58/60 have correct answer in 2nd or 3rd (of 4) positions;
cutoff at 7 failures; most sensitive to left-sided lesions
XXI. Auditory Comprehension – requiring yes or no response
1. Putney Auditory Comprehension Screening Test – 60-item set with half true, half false
statements; can respond verbally or nonverbally; useful in locked-in syndrome and advanced MS
XXII. Nonverbal Auditory Reception – recognition, discrimination, and comprehension of nonsymbolic
sound patterns (e.g., music, tapping, animal noises); usually associated with aphasia and bitemporal lobe
lesions, sometimes just right lesions
1. Seashore Rhythm Test – discriminate between like and unlike pairs of musical beats; cutoff at 5-6
errors; sensitive to attention and concentration
2. Testing for amusia – for rhythm, pitch, timbre, melody, harmonics; melody difficulties most
likely to occur with right temporal lesion; rhythm recognition either hemisphere (e.g., Benton)
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3. Recognition of emotional tone in speech – read neutral sentences in different tones; associated
with right hemisphere (e.g., Emotional Perception Test, Prosodic perception task)
4. Sound Recognition – ability to recognize familiar environmental sounds (auditory object
recognition)
TACTILE
XXIII. Tactile Sensation – assessment of pain and pressure in hands; Von Frey hairs widely used;
Pressure Aesthesiometer
XXIV. Tactile Inattention – tactile extinction/suppression most associated with right parietal damage,
often with visual or auditory inattention; evaluated by single and double simultaneous stimulation
1. Face-Hand Test – double simultaneous stimulation; not much improvement with eyes opened
2. Quality Extinction Test – after becoming familiar by sight and touch with different textured
surfaces, need to identify blindfolded what touched to both hands
XXV. Tactile Recognition and Discrimination (cortical)
1. Stereognosis – recognition of objects by touch; usually associated with contralateral lesions,
although right hemispheric lesions can cause bilateral impairment (e.g., Tactile Form Perception
– sandpaper)
2. Graphesthesia/skin writing – ability to identify letters and numerals that are traced or written onto
the skin (e.g., palm, fingers); test both hands and across the hands
3. Fingertip Number-Writing Perception – use pencil to write number on fingertip; average person
does best on middle three fingers on left hand
4. Two-Point Discrimination – determine if being touched with one or two points on caliper with
varying distance between, usually on palm of hand, starting with dominant or non-damaged side
XXVI. Olfaction – women tend to be better than men; varies across cultures (e.g., Smell Identification
Test)
MEMORY
VERBAL
XXVII. Verbal Automatisms – such as the alphabet, days of the week, months of the year, counting to 20;
in nonaphasic patients may reflect attentional disturbance or fluctuation in consciousness in acute
conditions, severe and diffuse damage associated with dementia in nonacute conditions; even one error
reflective of impairment
XXVIII. Letters and Digits
1. Brown-Peterson Technique/Auditory Consonant Trigrams – short-term memory of three
consonants following distraction of counting backward with alterating time delay; assessing
divided attention (the ability to attend to more than one stimulus at a time or to multiple elements
or operation within a task) and processing speed
XXIX. Increased Testing Span
1. Supraspan – strings of eight or more random numbers
2. Telephone Test
3. Serial Digit Learning – 8 or 9 digits (depending on education) read until correctly repeated twice,
up to 12 trials
XXX. Words – memory of word lists, phrases, sentences, or passages; can be familiar-unfamilar,
concrete-abstract, low-high imagery, low-high association/meaningfulness, ease of catgerization, lowhigh emotional charge, structural dimensions (e.g., rhyming)
1. Brief word learning tests – three or four words stated and repeated by patient, asked to be recalled
5 minutes later (e.g., MMSE); can cue by category or offer recognition choice to differentiate
retrieval from storage problem; may or may not have distractor, may or may not be told will be
asked for later
2. Benson Bedside Memory Test – list of eight words read four times, then free recall, categorycued recall, and multiple choice; most acquire at least 7 words, recall 6 spontaneously
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3. Auditory Verbal Learning Test (AVLT – Rey) – five trial presentation of 15 words, followed by
distractor list; then immediate and delayed recalls, recognition; track repetitions and intrusions;
young adults get 6-7 words first trial, 12-13 fifth, lose 1-2 words after interference, no more loss
to delay, 1 error in recognition; discriminates new learning/learning slope, interference, rate of
forgetting, retrieval, and recognition; sensitive to left temporal lobe impairment (forgetting)
4. California Verbal Learning Test (CVLT) – five trial presentation of 16 words falling into four
categories, followed by distractor list; then immediate and delayed free and cued recalls,
recognition, forced-choice; track repetitions and intrusions; discriminates new learning/learning
slope, organization, interference, rate of forgetting, false positives, retrieval, and recognition;
sensitive to left temporal lobe impairment (forgetting), frontal lobe functioning (organization,
repetitions); Alzheimer’s have poor learning curve, forget and have intrusions and false positives
whereas Huntington repeat, retrieval deficits but recognize
5. Consortium to Establish a Registry for Alzheimer’s Disease (CERAD) Word List Memory – 10
unrelated words, three learning trials, read by patient, has free recall and recognition
6. Hopkins Verbal Learning Test – 12 words in three semantic categories, three learning trials, recall
and recognition
7. Interference Learning Test – looks at effects of interference in higher functioning people; 20
target words (white cards) mixed with 24 distractors (blue cards); varied concrete and abstract,
partially categorizable nouns; MS source errors
8. Selective Reminding (SR) – use word list but only repeat words in learning if missed on last
presentation; continues until three perfect trials, two perfect trials at 12 presentations, or 12
presentations; only words recalled twice in a row assumed to be in longterm storage (consistent
longterm retrieval, then would be associated with retrieval deficit)
a. Free and Cued Selective Reminding – 16 items, uses category cues at acquistion and
retrieval to enhance recall (i.e., visual identification to category)
b. Double Memory Test – similar to previous but 64 items
9. Word List (WMS) – 12 unrelated words read four times, interference list, immediate and delayed
recall, recognition
10. Verbal Paired Associates (WMS) – most recent version has 8 hard paired words, repeated four
times, recall, and recognition (does not have mismatched pairs in recognition, making recognition
task too easy); variants include number of trials to learn
11. Logical Memory (WMS) – story memory test in which one story read once and another read
twice, with delayed recall and recognition
12. Babcock Story Recall Format – first story read twice and reported and delayed recall, then second
story read twice and reported and delayed recall; expect interference from first to second story
13. Story sets – varied in familiarity and difficulty (e.g., Rivermead Behavioural Memory Test,
CogniSyst Story Recall Test)
14. Cowboy Story – from 1919; on average recall 8/27 units
15. Story Memory Test – multiple presentations (up to 5 trials until has 15 points) and four-hour
delay
VISUAL/NONVERBAL – problems related to association with constructional ability, visual and spatial
functions, integration of verbal elements; best to rely on recognition tests
XXXI. Visual Recognition Memory – recognition overcomes physical limitation to produce; does not
discriminate right from left hemisphere; more false alarms with right lesion
1. Recurring Figures Test – eight presentations of 20 cards with geometric or nonsense figures, 8
repeating, need to determine which seen before (total score 56)
2. Continuous Recognition Memory Test – six presentations of 20 cards with drawings of flora and
fauna in six, 8 repeating, need to determine which seen before
3. Continuous Visual Memory Test – seven presentations of cards with abstract designs, 7 repeating,
need to determine which seen before, recognition trial
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4. Faces (WMS) – 24 faces with immediate and delayed recognition; schizophrenics perform poorly
5. Family Pictures (WMS) – report on family portraits (who, what, and where) with four of six
family members; problem that cannot get descriptive points if misname character, confusion of
yard and picnic scenes, affected by verbal ability
XXXII. Visual Recall: Design Reproduction – associated with extrahippocampal right temporal lobe
1. Visual Reproduction (WMS) – cards drawn immediately and delayed; can also do recognition,
discrimination, and copy; relatively simple and can be verbally encoded
2. Complex Figure Test (Rey) – copy, immediate, delay, recognition; inclusion of short-term recall
may give higher delay score than if delay only; look at organizational strategy impact; right lesion
more impoverished, left lesion poorer organization
3. Benton Visual Retention test – three-figure format, sensitive to unilateral neglect; two recall
administrations, then copy, delay; scored by omissions, distortions, perseverations, rotations,
misplacements, and size errors; compared with IQ; mostly distortion errors; assess perception,
motor, visual and verbal conceptualization, and immediate memory
4. Bender Visual Retention Test – 2 or 3 geometric designs are presented for 5 or 10 seconds, then
drawn from memory
5. Brief Visuospatial Memory Test – scored in terms of accuracy and location
6. Graham-Kendall Memory for Designs Test – 15 geometric designs are presented for 5 seconds,
then drawn from memory
XXXIII. Visual Learning – rate, efficiency, retention
1. Biber Figure Learning Test – 10 target items of two geometric figures with five learning and
recall trials, immediate recall, delayed recall and recognition, 30 distractors
2. Visual Spatial Learning Test – need to recognize 7 of 15 nonsense designs and correctly place on
6x4 grid
3. Diagnostic Workup for Cerebral Disease – nine simple geometric designs produced by five lines,
use wooden sticks to reproduce, allow up to six trials to learn all, with delay
4. Heaton Figure Memory Test – use WMS cards showing all four designs up to five times until 15
points reached, with four-hour delay
5. Ruff Light Trail Learning Test – need to learn 15-step pathway through circles connected by
lines, must find by trial and error, up to 10 trials to do correctly twice
6. Shum Visual Learning Test – Chinese characters shown in five trials each with recognition
(distractors remain the same across trials), then interference and recognition
7. Hidden Objects – need to find previously hidden objects (e.g., pen, keys, watch) with varying
delay
XXXIV. TACTILE
1. Tactual Performance Test (TPT - Halstead) – three blindfolded administration trials (dominant
hand, nondominant hand, and both times summed), recall drawing (memory and location); older
slower; expect trial 2 to be quicker even with nondominant hand; have lesser item forms
2. Tactile Pattern Recognition – four pieces of twisted wire to be matched over increasing delays;
those with commissurotomy did better with left hand
REMOTE MEMORY
XXXV. Recall of Public Events and Famous Persons
1. News events test – free recall, multiple choice, forced choice, recognition and if true, when
occurred (e.g., Events Questionnaire, Famous Events Test)
2. Famous people tests – name by free recall, semantic and phonemic cuing, and multiple choice,
pairing of young and old pictures (e.g., Famous Faces Test, Old-Young Test)
3. President’s Test – six most recent presidents, testing verbal and visual naming and sequencing;
sequencing related to right hemisphere
XXXVI. Autobiographical Memory
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1. The Crovitz Test – describe personal experience associated with ten common nouns and estimate
time of occurrence; scored in terms of specificity in time and place and richness of detail; can ask
from specific time in life
2. Autobiographical Memory Interview – to determine retrograde amnesia
a. Incidents Schedule asks three questions from three time blocks, given prompts, scored
based on clarity and specificity
b. Semantic Memory Schedule asks three questions from four time blocks about names,
dates, and places
COMPREHENSIVE MEMORY TESTS
XXXVII. Memory Batteries
1. Wechsler Memory Scale – originally Memory Quotient, now Index scores
A. Indices: Auditory (LM & VPA) and Visual (Faces & Fam Pict) Immediate and Delayed,
Auditory Recognition Delayed, Immediate total, General (delayed and recognition total),
Working (LN & Spat Span)
B. Optional: Information and Orientation, Word Lists, Visual Reproduction, Mental Control,
Digit Span
2. Camden Memory Tests – includes Pictorial Memory (easy foils), Topographic Memory (similar
foils to photos), Paired Associate Learning, Short Recognition Memory for Words and Short
Recognition Memory for Faces (similar to Warrington RMT)
3. Randt Memory Test – designed for longitudinal studies; seven parts (general information,
incidental learning, SR word recall, digits, word pairs, paragraph, drawings) taking about 20
minutes; telephone interview for 24-hour recall
4. Memory Assessment Scales – assesses attention and STM, learning and immediate memory, and
delayed memory; verbal and nonverbal
5. Denman Neuropsychological Memory Scale – assess verbal and nonverbal memory (includes
RCFT and musical tone differentiation)
6. Rivermead Behavioural Memory Test – for moderate to severe impairment; developed for
practical application, monitoring changes, and face validity; includes remembering a name
associated with a photo, a hidden belonging (frontal lobe), appointment, newspaper article,
delivering a message
(E version doubles amount of material to make more difficult; also children’s version)
7. Learning and Memory Battery (LAMB) – information processing focus, with scores for initial
trial, total trial, and retention
8. Colorado Neuropsychology Tests – assesses implicit and explicit memory through Memory Cards
(“Concentration”), Tower of Hanoi, Repeat (Pattern Sequence), Mirror Readings, Priming,
Recall, Recognition, Paired Association, Temporal Order, Digit and Visual Span
XXXVIII. Paired Memory Tests – to discriminate verbal and nonverbal processing
1. Russell’s Version of the WMS – consisting of Logical Memory and Visual Reproduction,
determine percent retained
2. Warrington Recognition Memory Test (RMT) – immediate recognition of 50 words and 50 faces;
right lesion impaired only faces, left lesion more impaired words
3. Doors and People – recognition of doors, visual recall of shapes, name recognition, recall of
occupation associated with person in photo
4. Memory Test for Older Adults – for ages 55+, includes Word List and Geometric Figure
5. Three words-Three shapes test – bedside test of copying 6 stimuli, presented up to five times until
5/6 items correct, delayed testing
XXXIX. Memory Questionnaires
1. Memory Functioning Questionnaire – 64 7-point rated questions, including frequency of
forgetting, retrospective function, and mnemonic usage; depressed score better (higher)
2. Inventory of Memory Experience – remote and recent personal experiences, 7-point rating
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3. Subjective Memory Questionnaire – rate self on memory and frequency of problems, 5-point
ratings
4. Memory Assessment Clinics Self-Rating Scale – assesses Ability to Remember and Frequency of
Occurrence of problems, 5-point scale
5. Memory Questionnaire – have 5 divisions into Attention/Prospective memory, Retrograde
memory, Anterograde memory, Biographic/Overload memory, and currently relevant memory;
TBI greatest difficulty attention, least impaired historic
6. Everyday Memory Questionnaire – 9-point scale in terms of frequency
7. Memory Symptom Test – compare current functioning to previous functioning; collaterals give
higher reports, not significantly correlated with memory test results
VERBAL FUNCTIONS AND LANGUAGE SKILLS
APHASIA – check spontaneous speech, repetition, comprehension, naming, reading, and writing
XL. Aphasia Tests and Batteries
1. Boston Diagnostic Aphasia Examination (BDAE) – 12 areas assessed with 34 subtests, taking up
to 4 hours, with main sections of Auditory Comprehension, Oral Expression, Understanding
Written Language, and Writing; includes Boston Naming Test; references classic, anatomically
based aphasia syndromes
2. Communications Abilities in Daily Living – naturalistic everyday communication, including
number usage, communication, social interactions, response to misinformation, nonverbal
communication, humor (such as by telephone and with real money)
3. Functional Communication Profile – 45-item inventory administered by clinician
4. Multilingual Aphasia Examination (MAE) – 7-parts assessing receptive, expressive and
immediate memory components of speech and language; includes Token Test and COWAT as
well as spelling
5. Neurosensory Center Comprehensive Examination for Aphasia – 20 tests of language plus 4 of
visual and tactile performance; low ceiling is problem for highly educated
6. Porch Index of Communicative Ability – verbal, gestural, and graphic subtests using same
common items (e.g., key, toothbrush); scores on accuracy, responsiveness, promptness,
completeness, and efficiency
7. Western Aphasia Battery – Aphasia Quotient, many items from BDAE, and Performance
Quotient (reading, writing, arithmetic, geture, construction, matrices) yielding Cortical Quotient
8. Boston Assessment of Severe Aphasia (BASA) – 15 subtests in 5 clusters of auditory
comprehension, praxis, oral-gestural expression, reading comprehension, gesture recognition,
writing, and visuospatial tasks
9. Communicative Abilities in Daily Living – assesses all forms of communicative ability, including
gesturing, pointing, writing, and drawing in aphasics
10. Frenchay Aphasia Screening Test – comprehension, expression, reading, and writing (also have
Dysarthria Assessment)
11. Pantomime Recognition Test – understanding of meaningful, nonlingual actions; pretended
handling of objects presented on videotape
12. Psycholinguistic Assessment of Language Processing in Aphasia – spoken and written language
13. Sklar Aphasia Scale – emphasizes functional communication skills, including formal testing,
interview, and checklist
XLI. Aphasia Screening
1. Aphasia Screening Test (Reitan-Indiana) – meant to be descriptive of problem area; four task
version includes copying figures, naming and spelling the figures, repeating a phrase
2. Token Test (MAE) – large and small different colored squares and circles; must complete simple
and multistepped, direct and grammatically atypical instructions
VERBAL EXPRESSION – confrontation naming, word knowledge, descriptions
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XLII. Naming – Confrontation naming to assess dysnomia; lesions of left posterior superior temporal lobe
and inferior parietal regions (angular gyrus) associated with semantic paraphasic errors, lesions of insula
and putamen associated with phonologic paraphasic errors; repetitive transcranial magnetic stimulation
over temporal lobe can facilitate picture naming; reflective of noun naming, but can also ask to describe
action (verbs and prepositions)
1. Boston Naming Test (BNT, from BDAE) – 60 pictures to be named (start at 30), semantic and
phonemic cuing, multiple-choice; associated with left hippocampal functioning, can also be used
to assess visual perception in right hemispheric functioning
2. Visual Naming Test – confrontation naming test part of MAE
3. Graded Naming Test – last ones very difficult, expected to be influenced by education, average is
20/30
XLIII. Vocabulary – good at assessing dominant hemisphere disease
1. Vocabulary (WAIS) – good hold test; those with right hemisphere damage may be verbose or
circumstantial (have multiple-choice variant for NP purposes)
2. Paper-and-pencil vocabulary tests – usually part of academic battery (e.g., Mill Hill Vocabulary
Scale, Gates-MacGinitie)
3. Nonverbal response vocabulary tests – point to picture of word read or shown
4. Peabody Picture Vocabulary Test (PPVT) – points to or gives number of picture of word read or
shown
5. Quick Test – vocabulary in situational context, pointing to picture with words associated; IQ
score can be derived, underestimating high end
XLIV. Discourse
1. Story telling – both content and language (e.g., Cookie Theft from BDAE)
2. Describing events – open-ended questions, describe day or plan
XLV. Verbal Fluency – associated with aphasia and frontal lobe damage, left anterior to Broca’s,
dorsalateral/striatal, also left or right superior medial, left parietal
1. Fluency of speech – depends on meaningful clustering, sentence structure; can be phonological or
semantic (at least 50 words per minute)
2. Controlled Oral Word Association test (COWA/COWAT) – FAS (MAE has CFL and PRW
norms)
3. Category fluency – semantic; less difficult than letter fluency, AD more impaired on this than
letter (temporal lobe)
4. Action fluency – verb generation; worse with dementia
5. Writing fluency – write as many words as can beginning with given letter, worst with left frontal
damage (e.g., Thurstone Word Fluency Test)
6. Quantity of writing content – more verbose with right hemisphere damage (e.g., Thematic
Apperception Test)
7. Quality of writing – spelling, capitalization, orthographic skills, planning, grammar, syntax,
organization (e.g., Cookie Theft); AD less functor words, more implausible details, more spelling
errors
8. Speed of writing – copying and from dictation; more slowing the longer the task
Languagage processing
1. Speed and Capacity of Language-Processing Test (SCOLP) – evaluates Speed of Comprehension
and Spot-the-Word Vocabulary, with discrepancy yielding degree of probable cognitive
impairment
ACADEMIC SKILLS
XLVI. Reading – for reading ability and comprehension
1. Gates-MacGinitie Reading Tests – vocabulary and comprehension, timed and untimed
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2. SRA (Science Research Associates) Reading Index – multiple choice, assessing Picture-Word
Association, Word Decoding (fill in blank), Phrase Comprehension (sentence completion),
Sentence Comprehension (target meaning), Paragraph Comprehension
3. National (American) Adult Reading Test (NART/NAART), American NART (AMNART) –
phonetically irregular words; used to estimate premorbid IQ (with no language impairment),
correlates with education and social class, underestimates high IQ
4. Wide Range Achievement Test (WRAT) Reading – letter reading and recognition and words;
used to estimate premorbid IQ
5. Kaufman Functional Academic Skills Test (K-FAST) Reading – reading as related to everyday
activities (e.g., signs, labels)
6. Gray Oral Reading Tests – increasingly difficult reading passages, followed by comprehension
questions; rate also assessed
XLVII. Writing – qualitative aspects; right lesions repeats elements and may show neglect/inattention,
left lesions have spaces disrupting continuity; writing to command, dictation, and copying (e.g.,
micrographia in PD); organization, vocabulary, grammar, spelling, mechanics
XLVIII. Spelling – need to take into account education and history of LD/dyslexia
1. Wide Range Achievement Test (WRAT) Spelling
2. Johns Hopkins University Dysgraphia Battery – evaluates nature of spelling errors
3. Boder Test of Reading-Spelling Patterns – oral reading and spelling to dictation
IL. Knowledge Acquisition and Retention
1. Information (WAIS) – good hold test; culturally specific and variable
CONSTRUCTION
DRAWING
L. Copying – look at accuracy, perseveration, omissions, errors (e.g., closure, angles); frontal more
disorganized, parieto-occipital poor spatially; left smaller, detail-oriented, right omit details
1. Bender-Gestalt Test – 9 drawings arranged into configurational wholes, look for organization and
errors; can also have delayed recall; by age 12 most do all correctly (parietal lesions)
2. Benton Visual Retention Test – three forms, copy and then recalls
3. Complex Figure Test (Rey, Taylor, Medical College of Georgia) – errors and organizational
approach (quantity and quality)
4. Copying Drawings – 15 line drawings
LI. Free Drawing – left lesions have fewer details, perseverate, trouble sequencing, right lesions show
left-sided visual inattention, more details, sketch over drawings
1. Human Figure
2. Bicycle
3. House
4. Clock face (free, fill in, copy) – errors most seen in Alzheimer’s, with improvement in copy
versus free
ASSEMBLING/BUILDING
LII. Two-dimensional Construction
1. Block Design (WAIS) – evaluates visuospatial organization, error as well as approach (trial-anderror versus gestalt)
2. Kohs Block Design – four colors, more difficult than BD
3. Stick construction – with right lesion copy drawing better, with left lesion copy stick model better
4. Stick Test – direct and rotational copies; left posterior lesions performed worst
5. Object Assembly (WAIS) – puzzles; most sensitive to right posterior lesions
LIII. Three-dimensional Construction (thought to be more sensitive to right hemisphere than 2-D)
1. Block construction
2. Test of Three-Dimensional Block Construction
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3. Paper Folding
CONCEPT FORMATION AND REASONING
CONCEPT FORMATION
LIV. Verbal Formats
1. Proverbs/Proverbs Test/California Proverb Test – translate concrete statement into abstract,
metaphorical meaning (Gorham has multiple-choice for aphasia)
2. Word usage tests – abstractly compare two or more words; affected by concrete thinking, aphasia,
learning disability, limited education
3. Similarities (WAIS) – associated with left temporal and frontal lesions
4. Luria’s method for examining concept formation – similarities, differences, categories, parts,
opposites, analogies
5. Stanford-Binet subtests – similarities, difference, abstract words, opposite analogies, verbal
relations
6. Cognitive Estimation Test (e.g., Biber) – assesses ability to generate effective problem-solving
strategy
LV. Visual Formats
1. Category Test – patterns/differences and recall; need flexibility working with complex and novel
problem solving and capacity to learn from experience; sensitive to general brain dysfunction
(Halstead, Children’s)
2. Brixton Spatial Anticipation Test – nearly identical items for which need to detect subtle
variations
3. “Twenty Questions” task – evaluate questions in terms of broadness-specificity (constraintseeking, pseudo-constraint seeking, and hypothesis testing)
4. Identification of Common Objects – 42 picture drawings that are first named by the subject and
then ask questions to determine which selected
5. California Twenty Questions Test – identify target item from 30 pictures, goal to ask as few
questions as possible
6. Raven’s Progressive Matrices/Coloured Progressive Matrices – visual pattern matching and
analogies of designs through spatial, design, and numerical relationships; right lesions have more
difficulty with abstract/visuospatial, left lesions have more difficulty with verbally
mediated/pattern determination; left lesions do better on colored format
7. Advanced Progressive Matrices – for adolescents and adults with above average intelligence
8. Matrix Reasoning (WAIS) – similar to progressive matrices
9. Pyramids and Palm Trees Test – picture and word recognition requiring grouping by similar
property or association
LVI. Symbol Patterns – completion of symbol patterns (e.g., letters, numbers)
1. Abstraction Subtest, Shipley Institute of Living Scale – meant to assess mental deterioration
(versus vocabulary being hold test)
LVII. Sorting
1. Kasanin-Hanfmann Concept Formation Test (Vigotsky) – need to determine sorting strategy of
22 blocks varying by color, size, shape, and height using correcting clues
2. Card Sorting – two sets of 32 cards, with one having 8 categories and other random words, asked
to group
LVIII. Sort and Shift
1. Color Form Sorting Test (Weigl-Goldstein-Scheerer) – 12 tokens or blocks coming in different
colors and shapes, asked to group in multiple ways
2. Object Sorting Test – use 30 familiar/household object, group in multiple ways
3. California Sorting Test (Delis-Kaplan EFS) – sort cards with printed words in multiple ways, by
meaning or perceptual property
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4. Wisconsin Card Sorting Test (WCST) – must deduce sorting strategies from feedback; frontal
lesions have more perseveration and loss-of-set errors (need similar abilities to Category Test)
5. Modified Card Sorting Test – WCST with cards that sharing more than one matching attribute
removed
6. Milwaukee Card Sorting Test – modified WCST with patient verbalizing strategy before sorting
REASONING
LIX. Verbal Reasoning
1. Comprehension (WAIS) – questions of common sense judgment/practical reasoning and
proverbs; not subject to practice effects
2. Stanford-Binet subtests – problem situations, verbal absurdities
3. Word Finding Test – guess meaning of nonsense word based on context
4. Word Context Test – guess meaning of nonsense word from clue sentences
5. Sentence Arrangement – individual words need to be arranged to form a sentence
6. Verbal Reasoning – brain teasers involving relative relationships (e.g., who had what amount of
money from four people)
LX. Visually Presented Material
1. Picture Completion (WAIS) – tell what important part is missing
2. Picture Arrangement (WAIS) – need to arrange cartoon pictures into sensible stories (lowest
reliability and stability in battery)
3. Picture Problems – find absurdity in picture
MATHEMATICAL PROCEDURES
LXI. Arithmetic Reasoning Problems
1. Arithmetic (WAIS) – assesses working memory
2. Arithmetic story problems – each questions has varied number of operations required to get to
answer; uses more reasoning than difficult math
3. Block Counting – count the total number of block in two-dimensional drawings of threedimensional block piles
4. Estimations/Cognitive Estimations – judgment for novel or unfamiliar information
LXII. Calculations (left hemisphere for knowledge of numbers and arithmetic rules, parietal lobes for
numerical magnitude and approximations)
1. Arithmetic (WRAT)
EXECUTIVE FUNCTION
Cognitive abilities necessary for complex goal-directed behavior and adaptation to environmental changes
and demands; includes attentional resources, planning, organization, anticipating outcomes, flexibility,
initiation, termination, and self-monitoring; associated with prefrontal cortex overseeing distributed
networks
LXIII. Volition – the capacity for intentional behavior, including motivation, self-awareness (physical
status, environment), and social awareness (Cookie Theft, Picture Arrangement)
LXIV. Planning – the identification and organization of steps and elements needed to carry out an
intention or achieve a goal (Picture Arrangement, Block Design, Complex Figure Test, Bender-Gestalt,
Trails)
1. Self-Ordered Pointing – point to novel stimulus on each trial, requiring monitoring of previous
choices (working and strategic memory)
2. Porteus Maze Test
3. Mazes (WISC)
4. Tower Tests: London, Hanoi, Toronto – goal to take most direct, fewest moves to move balls or
rings according to rules (e.g., color or size stacking allowances)
5. Everyday tasks – generating solutions (worse anterior damage), judging adequacy and
completeness of plans
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6. Script generation – sequencing of frequent activities
LXV. Purposive Action – ability to initiate, maintain, switch, and stop sequences of complex behavior in
an orderly and integrative manner
1. Tinkertoy Test – have 50 piece and at least 5 minutes to make whatever want, evaluated in terms
of complexity and number of pieces used
LXVI. Self-Regulation – productivity (slow), flexibility and shifting (perseveration, in contrast to
repetition seen in attentional problems)
1. Use of Objects and Alternate Uses Test – write as many uses as can for five common objects,
look at convergent and divergent thinking
2. Homophone Meaning Generation Test – generate different meanings for common words
3. Cognitive Bias Test – look at top picture and choose one of two below that like best, target-driven
behavior associated with stimulus-boundedness
4. Design Fluency – invent as many different abstract drawings, then trial limited to four lines;
review errors and perseverations
5. Five-point Test – make as many different figures by connecting dots
6. Ruff Figural Fluency Test – five trials, some with distraction, to make as many different figures
by connecting dots
7. Design Fluency Test – connect dots under differing instructions, some with distraction
8. Motor Regulation (Go/no-go) (Luria) – ability to inhibit a response after a particular response set
has been established (e.g., when one finger is presented (go sign) the subject is to display two
finger; when two fingers are presented (no-go sign) the subject is to display no fingers); sensitive
to frontal lobe damage; withholding responses
9. Behavioral Dyscontrol Scale – bedside test of motor control
10. Executive Control Battery – includes drawing sequences to command, imitate assymetrical hand
postures, alteration of motor sequences, responding to command under conflicting conditions
11. Frontal Assessment Battery – conceptualization, item generation, motor sequencing, sensitivity to
interference (conflict), inhibitory control (go/no-go), environmental autonomy (imitation or
utilization behavior)
12. Perseverance – motor impersistence related to right or bilateral damage
13. Alternating sequences tests (Luria Figures) – associated with frontal lobe functioning (e.g., m n m
n)
LXVII. Effective Performance – monitor, self-correct, and regulate delivery
1. Random Generation Task – generate 100 letters of alphabet in random order; look at redundancy
of letters and pairs and alphabetical sequences; can also do for numbers (Mental Dice Task)
LXVIII. Batteries
1. Behavioural Assessment of the Dysexecutive Syndrome (BADS) – used to predict everyday
problems; includes Rule Shift Cards, Action Program Test (get cork out of tube), Key Search,
Temporal Judgment (time estimation on tasks), Zoo Map (planning), Modified Six Elements
(planning across 6 test subject areas), Dysexecutive Questionnare (symptom checklist)
2. Delis-Kaplan Executive Function System (D-KEFS) – nine stand alone tests that are variations of
other established tests
3. Executive Function Route-Finding Task – subject to physically find way from starting point to
target point with five choice points and one change in floor; evaluates understanding, information
seeking, memory, error detection and correction, on-task behavior; lacking in structure
4. Behavioral Assessment for Vocational Skills – assemble wheelbarrow
MOTOR PERFORMANCE
LXIX. Apraxia – imitation and movement to command through intransitive gestures (blow kiss) and
transitive object use, real (suck on straw) and pantomimed (blow out match); associated with left
hemispheric damage
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1. Florida Apraxia Screening Test-Revised – 30 verbal commands to demonstrate gestures
2. Florida Action Recall Test – pantomime actions implied by drawings (e.g., spread butter on
bread)
3. Test for Apraxia
4. Luria’s fist-edge-palm
LXX. Motor Performance – assists in determining lateralization of damage
1. Finger Tapping Test – speed; men tap faster and slowing after 40
2. Purdue Pegboard Test – manual dexterity; each hand separately and then simultaneously insert
round pegs
3. Grooved Pegboard – manual dexterity; score time to completion each hand independently
inserting keyed peg
4. Hand Dynamometer – hand/grip strength, typically measured in kilograms
ESTIMATING PRE-MORBID IQ
1. Best performance method – identify highest test score of highest level of functioning in everyday tasks
and use as standard
2. Hold tests (Babcock, 1930) – tests considered to be relatively insensitive to brain damage (e.g., WAIS
Vocabulary, Information)
3. Reading tests – assumed to be overlearned and highly correlated with intelligence (e.g.,
NART/NAART, WRAT)
4. Actuarial methods – formulas using demographics (e.g., age, sex, race, education, occupation) for
regression-based estimation (e.g., Barona, Crawford, OPIE - demographics plus WAIS subtests)
ASSESSMENT BATTERIES
GENERAL
Wechsler (WAIS/WISC/WPPSI/WASI/WIAT)
WAIS-III:
Verbal IQ = Vocabulary, Similarities, Arithmetic, Digit Span, Information,
Comprehension
Performance IQ = Picture Completion, Digit Symbol-Coding, Block Deisgn, Matrix
Reasoning, Picture Arrangment
Verbal Comprehesnion = Vocabulary, Similarities, Information,
Perceptual Organization = Picture Completion, Block Design, Matrix Reasoning
Working Memory = Arithmetic, Digit Span, Letter-Number Sequencing
Processing Speed = Digit Symbol-Coding, Symbol Search
Optional – Object Assembly
<70 Extremely Low, 70-79 Borderline, 80-89 Low Average, 90-109 Average, 110-119
High Average, 120-129 Superior, >129 Very Superior
Kaufman (KBIT – Vocabulary and Matrices, KAIT – crystallized and fluid intelligence, K-SNAP –
neuropsychological functioning)
Stanford-Binet Intelligence Scales (2-23 years); limited floor, adaptive administration using Vocabulary
and Chronological Age to determine entry level
1st level: (g) general factor
2nd level: crystallized abilities, fluid-analytic abilities, short-term memory
3rd level: verbal reasoning and quantitative reasoning, abstract-visual reasoning, short-term memory
(modification of French Binet-Simon originally used in children with LD)
Wide Range Achievement Test (WRAT)
Woodcock-Johnson (cognitive, academic achievement, interest)
Shipley Institute of Living Scale – yields conceptual quotient from comparison of vocabulary and abstract
scores; originally developed for schizophrenics
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Multidimensional Aptitude Battery – similar to WAIS but multiple-choice
Snijder-Oomen Nonverbal Intelligence Test
Haptic Intelligence Scale for adult blind – modified version of WAIS
NEUROPSYCHOLOGY SPECIFIC
Halstead-Reitan Battery (MR) – core battery includes Category Test, Tactual Performance Test (TPT),
Seashore Rhythm Test, Speech Sounds Perception Test, and Finger Tapping (Halstead Impairment
Index, >0.5 indicative of impairment), and personality
Repeatable Cognitive-Perceptual-Motor Battery – alternate version for repeating tests subject to practice
effects
Halstead Russell Neuropsychological Evaluation – integrates HR, WAIS, WMS, plus additional tests (at
least 10 hours), yields Neuropsychological Deficit Score
Kaplan-Baycrest Neurocognitive Assessment (KBNA) – assesses Attention/Concentration, Declarative
Memory, Visuoconstruction/Visuoperception, Praxis, Language, Reasoning/Problem Solving,
Expression of Emotion
Repeatable Battery for the Assessment of Neuropsychological Status (RBANS) – assesses Immediate
Memory, Visuospatial/Constructional, Language, Attention, and Delayed Memory
Luria’s Neuropsychological Investigation – divided into specific functions associated with three principal
function units
1) maintenance of cortical tone (brainstem)
2) obtaining, processing, and storing information (posterior)
3) programming, regulating, and verifying mental activity (anterior)
Luria-Nebraska Neuropsychological Battery – five summary scales: Pathognomonic, Right Hemisphere,
Left Hemisphere, Profile Elevation, Impairment, plus qualitative categories
(0-normal to 2-brain injury)
Neuropsychological Assessment Battery – 36 tests falling into five modules in two equivalent forms
BNI Screen for Higher Cerebral Functions
Neuropsychological Screening Battery for Hispanics
WAIS NI (Neuropsychological Instrument) – provides modifications (e.g., no discontinue, multiplechoice) and additional scores
BATTERIES COMPOSED OF PREEXISTING TESTS
University of South Dakota
HIV+:
NIMH Core Neuropsychological Battery
Multicenter AIDS Cohort Study Battery
Neurotoxicity:
Agency for Toxic Substances and Disease Registry
California Neuropsychological Screening Battery
Pittsburgh Occupation Exposures Test
World Health Organization-Neurobehavioral Core Test Battery
European batteries
Dementia:
Tests
Addenbrooke’s Cognitive Examination (sensitive but not specific)
Arizona Battery for Communication Disorders of Dementia
Cambridge Cognitive Examination (sensitive and specific)
Cognitive Scales for Dementia
Colorado Neuropsychology Tests – computerized tests
Consortium to Establish a Registry for Alzheimer’s Disease (CERAD) – memory,
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language, praxis, general cognition
Dementia Assessment Battery
Dementia Rating Scale (DRS – Mattis) (identifies AD) – structured mental status exam;
Attention, Initiation and Perseveration, Construction, Conceptualization, Memory,
total score 144; uses screen and metric (two-step approach to evaluation designed to decrease
the total number of items administered, with a difficult screening item first administered; if
the difficult screen is passed, all earlier items given credit for, if not, administer metric items,
beginning easy and getting more difficult)
Fuld Object-Memory Evaluation (10 objects in bag named and tested over delays – no
confounding by education or culture)
Iowa Screening Battery for Mental Decline
Kendrick Cognitive Tests for the Elderly – assesses memory (4 cards with 6 items) and
speed of responding to differentiate dementia from depression
MicroCog – computer administered test of Attention/Mental Control, Memory,
Reasoning/Calculation, Spatial Processing, Reaction Time
Mini-Mental Status Examination (MMSE; Folstein)
MOANS (Mayo Older Age Normative Study) – normative data for WAIS-R, WMS-R and
RAVLT for individuals aged 55-97
Neurobehavioral Cognitive Status Examination (NCSE/Cognistat)
Neuropsychological Screening Battery
The 7-minute Screen
Severe Impairment Battery (SIB), Cognitive Capacity Screening Examination – for moderate to
severe impairment
Short Portable Mental Status Questionnaire
Telephone Interview for Cognitive Status
Very brief screeners (Memory Impairment Scales, Min-Cog – 3 words and clock
drawing)
Mental Status and Rating Scales
Alzheimer Disease Assessment Scale (ADAS) – language, memory, praxis, orientation
plus concentration, motor, appetite, mood, behavior, psychosis
Blessed Dementia Scale – informant report, mental status questions, mental status test;
also Information-Memory-Concentration, Orientation-Memory-Concentration
Brief Cognitive Rating Scale – mental status and semistructured assessment
Global Deterioration Scale
Pfeiffer Short Portable Mental Status Questionnaire – does not evaluate language or
visuospatial function
Observational Ratings
Behavioral Pathology in Alzheimer Disease Rating Scale
Geriatric Evaluation by Relative’s Rating
Neuropsychiatric Inventory (caretaker completes)
TBI:
Assessment of Individuals with Cognitive Impairment
San Diego Neuropsychological Test Battery
Evaluating Severity
Glasgow Coma Scale (GCS) – rating scale of responsiveness in three dimensions (eye
1-4, verbal 1-5, and motor 1-6) ranging from 3-15; in TBI 13-15 mild injury, 9-12
moderate injury, <8 severe injury
Galveston Orientation and Amnesia Test (GOAT) – 8 mental status questions, plus recall
of events before and after injury, to assess PTA; Normal 76-100, Borderline 66-75;
Impaired <66
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Rancho Los Amigos Scale: Levels of Cognitive Functioning/Expected Behavior –
1. no response, 2. generalized response, 3. localized response, 4. confused-agitated,
5. confused, inappropriate, non-agitated, 6. confused-appropriate,
7. automatic-appropriate, 8. purposeful and appropriate
Oxford Test and Westmead PTA Scale – for testing daily until PTA abates
Outcome
Glasgow Outcome Scale (GOS) – scale designed to assess functioning after TBI;
1 = death, 2 = persistent vegetative state (absence of cortical function), 3 = severe
disability (conscious but cannot complete all ADLs), 4 = moderate disability
(disabled but independent), 5 = good recovery (resumption of normal life)
Disability Rating Scale – assesses progress from coma, 0-30; eye opening, communication,
motor, self-care
Psychosical Consequences
Katz Adjustment Scales: Relative’s Form – social obstreperousness, acute psychoticism,
withdrawn depression
Mayo-Portland Adaptability Inventory – ability, adustment, and participation
Neurobehavioral Rating Scale – modification of Brief Psychiatric Rating Scale (BPRS)
Craig Handicap Assessment and Reporting Technique (CHART) – community
participation and handicap
Community Integration Questionnaire – telephone interview to evaluate community
integration
Craig Hospital Inventory of Environmental Factors (CHIEF) – frequency and magnitude
of perceived barriers and hindrances in environment interfering in lives of disabled
Neuropsychological Behavior and Affect Profile – personality and emotional changes
encountered after brain injury through self- or other-related questionnaires
Functional Independence Measure, Functional Assessment Measure – competence and
need for assistance in self-care, physical mobility, and other functions, plus cognitive and
psychosocial functioning
Right Hemisphere Disease:
Mini Inventory of Right Brain Injury
Epilepsy:
Behavior
A-B Neuropsychological Assessment Schedule – self-report
Epilepsy Foundation of America – living concerns
Liverpool Assessment Battery – health-related quality of life
Quality of Life In Epilepsy
Side Effect and Life Satisfaction – to evaluation those on medication
Washington Psychosocial Seizure Inventory – true-false questions to determine social
maladaption
TEST VALIDITY – validity dependent on consistency with history and examination, likelihood that
results make medical sense, individual situation, emotional status; tested usually through forced-choice
(probabilities can be calculated and memory can be demonstrated without awareness; also primacy and
recency memory effects, priming effects, and comparison of word span and digit span)
1. Test Of Memory Malingering (TOMM) – recognition memory test of 50 forced-choice pairs;
appears difficult but very easy, assesses effort
2. 21 Item Test – free recall and forced-choice word recognition of nouns previously read; identifies
negative response bias
3. Validity Indicator Profile – 100 nonverbal abstractions and 78 word definitions varying in
difficulty
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4. Victoria Symptom Validity Test (VSVT) – computerized 5-digit number recognition with easy
and hard foils
5. Rey 15-Item/3 x 5 Memory Test – items to be recalled redundant and actually easy (5 groups with
3 associated stimuli)
6. Hiscock-Hiscock Forced-Choice Recognition Tests – digit recognition tests to detect
exaggeration
7. Portland Digit Recognition Test – memory test of digits in forced-choice format
TESTS FOR CHILDREN
GENERAL
Infant and preschool tests to detect developmental delays and disabilities; low predictive validity, low IQ
correlation (focus on sensorimotor ability), low reliability (short attention span, easy fatiguability, poor
motivation)
1. Wechsler – WISC (VCI, POI, FDI, PSI) ages 6-16; WPPSI (VIQ, PIQ) ages 3-7
2. Bayley Scales of Infant Development-Second Edition – assesses mental and motor development
(standard scores) and behavioral development (observational rating by examiner) (1 month-2½ years)
3. Kaufman Assessment Battery for Children (K-ABC) – intelligence test (2½-12½ years),
Mental Processing divided into sequential and simultaneous processing (fluid) and
Achievement (crystallized); mostly visual to reduce effects of verbal ability, culture, gender bias
4. Stanford-Binet Intelligence Scales-Fourth Edition – intelligence test (2-18 years)
5. McCarthy Scales of Children’s Abilities – verbal, perceptual-performance, quantitative, memory, and
motor yielding General Cognitive Index (2½- 8½) (MR)
6. Slosson Intelligence Test
7. Gesell Developmental Schedules – behavioral observations in motor, adaptive, language, and personal
social functioning (4 weeks – 6 years)
8. Leiter International Performance Scale – for children with hearing or language impairment or nonEnglish speaking; match and sequence blocks with pictured stimuli (2-18)
9. System of Multicultural Pluralistic Assessment (SOMPA) – ages 5-11; to contradict minorities
being classified as MR on IQ alone (takes into account adaptive behaviors and culture) to derive
Estimated Learning Potential
10. Denver Developmental Screening Test (0-6.4) – observe personal-social, fine motor, language, gross
motor
NEUROPSYCHOLOGICAL
1. NEPSY – assesses attention and executive function, language and communication, sensorimotor
function, visuopatial function, and learning and memory (3-12)
ACHIEVEMENT
1. Peabody Individual Achievement Test (PIAT) – evaluates general information, reading recognition,
reading comprehension, spelling, and mathematics (5-18 years)
2. Wechsler Individual Achievement Test (WIAT) – measures oral expression, listening comprehension,
reading, spelling, writing, and arithmetic (5-19 years)
3. Wide Range Achievement Test (WRAT-3) – measures reading (word recognition and pronounciation),
spelling, and arithmetic (5-75 years)
4. Woodcock-Johnson Psychoeducational Battery, Tests of Achievement (WJ-III, ACH) – assesses
reading, writing, mathematics, and knowledge of science, social studies, and humanities
5. Keymath Diagnostic Arithmetic Test – arithmetic test (5½-15½ years)
6. Stanford Diagnostic Reading Test – assesses reading, particularly for low achieving students (grades 113)
7. Kaufman Test of Educational Achievement (KTEA)
MEMORY
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1. Wide Range Assessment of Memory and Learning (WRAML) – for learning and memory of verbal and
visual information (5-17)
2. Children’s Memory Scale – downward extensions of WMS (5-16)
3. Test of Memory and Learning (TOMAL) – 10 core and 4 supplemental scales (5-19)
LANGUAGE
1. Clinical Evaluation of Language Fundamentals-Third Edition (CELF-3) – receptive and expressive
language, listening to paragraphs, word association, rapid automatic naming (6-21)
2. Sequenced Inventory of Communication Development – receptive and expressive language (4 months
– 4 years)
VISUOSPATIAL
1. Test of Visual-Perceptual Skills – visual recognition of figures without need for motor response
2. Developmental Test of Visual-Motor Integration (VMI - Beery) – copy of increasingly complex
geometric figures, for children (2-15)
AUDITORY PERCEPTION
1. Auditory Discrimination Test
2. Lindamood Auditory Conceptualization Test
3. Goldman-Fristoe-Woodcock Test of Auditory Discrimination
MOTOR
1. Marching test – connect series of circles that are connected by lines, each hand separately and then
coordinated
ADAPTIVE
1. Vineland Adaptive Behavior Scale (0-18) – communication, daily living, socialization, motor
function (interview, classroom)
2. Adaptive Behavior Scale (3-17) – adaptive behavior and emotional adjustment (school and home
observation)
3. Columbia Mental Maturity Scale (3-12) – general reasoning ability, indicate drawing that does not
belong (CP, MR, brain damage, speech/hearing impairment)
4. Behavioral Assessment for Children
5. Child Behavior Checklist
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OCCUPATIONAL INTERESTS AND APTITUDE
1. Career Assessment Inventory – vocational interest inventory for high schoolers through adults,
including retraining for a new career
2. General Aptitude Test Battery – assesses job-related aptitudes for vocational and educational
counseling
3. Wonderlic Personnel Test – test of problem-solving ability with 50 multiple-choice and short-answer
items; provides rough estimate of IQ
4. Strong-Campbell Interest Inventory – occupational choice and satisfactions
5. Kuder Vocational Preference Record – interests
6. MacQuarrie Test for Mechanical Ability – assesses visuomotor and visuospatial ability, developed for
work settings
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OLFACTION
Bipolar olfactory receptor neurons in olfactory mucosa lead down olfactory tracts by unmyelinated axons
through cribiform plate to bulbs, projecting through mitral and tufted cells in glomeruli via lateral
olfactory stria directly to primary olfactory cortex (piriform and periamygdaloid, in the uncus at the end
of the parahippocampal gyrus) and amygdala, and secondarily to entorhinal cortex, hypothalamus,
hippocampus, orbitofrontal cortex, and dorsomedial thalamus; interhemispheric connection through the
anterior commissure
Olfactory bulbs vulnerable to shearing by the cribriform plate with head trauma
1) Quantitative abnormalities
a. anosmia/hyposomia – impaired sense of smell from nasal, neuroepithelial, or central
damage; when bilateral also can have ageusia (loss of taste)
b. hyperosmia (rare)
2) Qualitative abnormalities
a. dysosmia or parasomia – distortions or illusions (may be associated with depression)
3) Hallucinations/delusions – of central origin and associated with temporal lobe seizures (uncinate fits)
4) Higher-order loss of discriminations
a. olfactory agnosia – perceptually intact but cannot recognize
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PARKINSONISM
May be idiopathic, postencephalitic, from infarct of putamen or caudate, CO poisoning, toxic exposure,
substance abuse, multiple head trauma, drug induced, multisystem atrophy; may be lateralized; rule-out
hydrocephalus, frontal lobe lesions, diffuse subcortical disorders, dopaminergic antagonists (Haldol,
Compazine)
-
-
*akathisia – inner restlessness and continual leg movement
akinesia – decreased initiation of movement (e.g., facial expression, blinking)
* bilateral lesions in SMA or anterior cingulated gyrus
amimia – inability to express ideas through gestures/facial expressions
aphagia – difficulty chewing and swallowing
anteropulsion – appear to be continually falling and shuffling forward
*bradykinesia – slowness of movement
bradyphrenia – abnormal slowness of mentation
*cogwheel rigidity – muscle rigidity/resistance to joint movements resulting from lead pipe
rigidity/hypertonia combined with tremor (steady resistance is felt throughout the range of
movement)
decreased arm swing
dyskinesia from levodopa therapy
dystonia – slow, involuntary, arrhythmic muscle contraction that produce forced, distorted
posture; levodopa may produce
en bloc turning – turns are executed without the normal twist of the torso
*festinating gate – trot in bursts, get faster and faster, stops, then starts again
flexor rigidity – stooped
freezing – a temporary inability to move, more common in doorways, exits, and where there is a
change in floor pattern
gegenhalten/counterholding – variable resistance to passive movement, being unable to relax
muscles on command
glabellar reflexes/Meyerson’s sign – inability to inhibit eye-blinking when tapped above the
bridge of the nose; this response usually extinguishes after a few taps
*hypokinesia – abnormally diminished motor activity
hypokinetic dysarthria – decreased speech volume, imprecise articulation, accelerated speech rate
with words running together
hypometria – abnormally small movements (e.g., micrographia)
hypophonic voice – hurried, muttering quality
March á petis pas – progressively accelerating steps
masked face/reptilian stare – expressionless facial appearance in which there is a significant
decrease in spontaneous eye-blinking (hypomimia), may be confused with depression
micrographia
narrow based stance
palilalia (repetition of words at the end of an utterance, typically increased in speech and
decreased in volume)
on-off phenomenon – the tendency for anti-parkinsonian drug effects to suddenly wear off,
leaving the patient with decreased mobility, postural reflex loss
*postural/truncal instability
propulsive gait – progressively faster and smaller steps while walking, with risk to falling forward
*resting/pill-rolling tremor – rhythmic movement of wrist, fingers, and thumb; typically begins
unilaterally and not well responsive to dopamine therapy; anxiety and excitement increase, not
present during sleep
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-
retropulsion – if pulled back slightly, several backward steps are taken to regain balance
righting difficulty – difficulty to stand from sitting position
saccadic eye movement abnormal
shuffling and slow gait, small steps
small steps to turn
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PARKINSON’S DISEASE (also called Paralysis agitans)
Idiopathic progressive disease of mid- to later life; etiology unknown; basal ganglia disorder, up to 90%
deficit in nigrostriatal dopaminergic system (loss of melanin-containing cells in the substantia nigra pars
compacta, projecting to the putamen, deficient tyrosine hydroxylase, leading to deficit in conversion of
precursors into DOPA and then DA), excessive cholinergic activity; cell loss in caudate, Raphe nuclei and
locus coeruleus, over-inhibition of thalamus; includes positive symptoms (e.g., tremor) and negative
symptoms (e.g., bradyphrenia), no changes in reflexes; 15-40% dementia: executive dysfunction, varied
attention, memory retrieval problems, visuospatial deficits, slow processing, intact verbal skills;
depression in 25-60%; psychosis 10%; affects 1% over age 65; may see cytoplasmic inclusion of Lewy
Bodies in substantia nigra
May have greater bradykinesia, rigidity, and cognitive deficits, or more tremor
Also caused by toxins (MPTP – tainted heroin), free radicals (e.g., nitric oxide)
Levodopa/carbidopa increases dopamine (stimulates D2); may experience “On-Off” phenomenon and
freezing, can induce dyskinesia
Anticholinergics such as Cogentin or Artane
Amantadine increases DA release and anticholinergic and antiglutaminergic
DA agonsists (pergolide, bromocriptine, ropinole, pramipexole)
Pallidotomy – lesioning the medial globus pallidus (near internal capsule/putamen), by using
stereotaxically placed electrodes, to disrupt excessive cell excitation; reduces bradykinesia,
rigidity, and medication-related dyskinesias
Thalamotomy – lesioning of the ventral lateral (VL) thalamus with stereotaxically placed electrodes,
disrupting excessive excitation; reduces tremor
Deep Brain Stimulation (DBS) – constant high-frequency stimulation (100-180 Hz) is applied to thalamic
nuclei; for parkinsonism and chronic pain
Cell transplantation – fetal, adrenal medulla
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PARKINSON PLUS SYNDROMES
Disease exhibiting features of parkinsonism but distinct from Parkinson’s Disease, with usually
symmetrical symptoms and absence of resting tremor; poorer prognosis and do not respond well to
dopamine replacement therapy
1) Progressive Supranuclear Palsy (PSP; also Steele-Richardson-Olszewski) – idiopathic
degenerative disease characterized by subcortical dementia (memory loss, executive
dysfunction), parkinsonian features (extrapyramidal signs), imbalance/falling, loss of
volitional eye movement (vertical eye movement disorder gaze paresis – cannot look down;
doll’s eye maneuver preserved), loss of initiative, bradykinesia, extensor rigidity (hypererect),
apathy, slurred speech, dysphagia (trouble chewing and swallowing), pseudobulbar palsy
(masked face, facial and jaw jerking, exaggerated palatal and pharyngeal reflexes, drooling),
personality change/emotional lability (apathy, inertia), dissociated consciousness and ability,
wide-eyed stare, brainstem nuclear motor dysfunction; involves loss of neurons and gliosis in
area from brainstem to basal ganglia, including periaqueductal gray matter, superior
colliculus, subthalamic nuclei, red nucleus, palladium, dentate nucleus, vestibular nuclei, and
oculomotor nucleus (like HD and PD); does not respond well to dopaminergic and
anticholinergic medicines; typical onset in 50s-60s and 5-7 year progression to death
2) Cortico-basal ganglionic degeneration (CBGD)/corticostriatonigral degeneration – a
progressive disease of the basal ganglia characterized by apraxia, rigidity, dystonia,
myoclonus, cortical sensory deficits, alien hand (levitation or posturing of arm, particularly
when attention diverted or eyes closes), postural abnormalities, and supranuclear gaze palsy;
includes moderate generalized cognitive deterioration and executive functioning problems;
learning deficits can be compensated for by using semantic cues, poor free recall
3) Multisystem atrophy (MAS) – autonomic insufficiency with degeneration of the basal
ganglia, cerebellum, spinal cord, and peripheral sympathetic ganglia and loss of dopamine
from substantia nigra pars compacta
4) Olivopontocerebellar degeneration – characterized by parkinsonism and cerebral ataxia,
postural instability, action tremor, and dysarthria (no rigidity or bradykinesia); does not
respond to anti-parkinsonian drugs; deterioration in olives, pons, and cerebellum
5) Shy Drager syndrome – Parkinson symptoms and autonomic disturbance (impotence, urinary
incontinence, hypotension/dizziness on standing)
6) Striato-nigral degeneration – stiff, slow, gait disturbance, imbalance (usually NO tremor); do
not respond to L-dopa; damage mostly in striatum
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PSYCHOPATHOLOGY
Abnormal, or pathological, mental and behavioral conditions
MR
developmental cognitive impairment with IQ <70, at least two areas of adaptive functioning impaired,
<18 years old
Divisions:
a. mild (85%) – 50/55-70; educable up to 6th grade level
b. moderate (10%) – 35/40-50/55; trainable to 2nd grade level, require guidance/minimal
supervision, unskilled work
c. severe (3-4%) – 20/25-35/40; poor motor skills, limited communicative speech; assisted living
d. profound (1-2%) – <20/25; severe limitations in motor and sensory functions; require highly
structured environment and constant aid/supervision
Embryonic development 30% - Downs, toxins
Psychosocial 15-20% - mental disorder, deprivation
Pre- and peri-natal 10% - maternal malnutrition, anoxia, viral infection
Heredity 5% - Tay Sachs, fragile X, PKU
Medical condition 5% - malnutrition, lead poisoning
Unknown 30-40%
PDD
Autism – pervasive developmental disorder that appears before age 3 and is characterized by poor
social interactions, communication deficits (e.g., delayed spoken language, echolalia), and peculiar
behavior (e.g., stereotypic or ritualistic mannerisms) (need >2 social, >1 communication, >1 repetitive
and stereotyped behavior)
75% MR (most moderate), 4-5X more males, 50% mute, 20-35% epilepsy
Rule-out Rett’s, Angelman’s, Fragile X, PKU
poor verbal abilities, abstraction, receptive language worse than expressive
increased autonomic arousal, high 5HT
associated with genetics, maternal rubella, birthing complication
atrophy of cerebrum and cerebellum, associated with limbic and frontal system dysfunction, abnormal
brain lateralization
treat using operant techniques (Lovaas), anti-psychotic/anti-epileptic (stimulants contraindicated)
Rett’s – only girls, decelerated head growth after 5 months, psychomotor retardation, impaired language,
loss of hand skills, uncoordinated gait/trunk
Childhood Disintegrative Disorder – 2 years normal development followed by regression in motor skills,
play, social skills, adaptive behavior, language
Asperger’s – mild variant of autism characterized by social isolation and eccentric behavior, impaired
nonverbal communication, and clumsiness in speech articulation and gross motor behavior; impaired
social functioning, restricted behaviors/interests, NVLD
LD
Discrepancy between IQ and academic achievement, manifested by significant difficulties in the
acquisition and use of listening, speaking, reading, writing, reasoning, mathematical abilities, or social
skills, not entirely explained by visual, hearing, or motor impairment, emotional disturbance, MR, or
environmental factors
More common in males (males 4x more dyslexia), left-handers, family members with autoimmune
disease (testosterone related? Geschwind), 20-50% ADHD
Stuttering remits on own in 60% of cases
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NVLD – disorders consisting of motor and sensory integration deficits, poor visuospatial-organizational
ability, and difficulty with novel and complex situations; also may involve poor social perception and
social skills; problems with math, handwriting (coordination), and social cognition (right hemisphere)
ADHD
Associated with inattention, hyperactivity, and impulsivity before age 7; 4-9 times more common in boys
Neurochemical defect in dopaminergic and noradrenergic systems in prefrontal cortex
IQ several points lower, scores more variable
Associated with food allergies, lead, prenatal alcohol and nicotine exposure; genetics (60%)
Barkley’s behavioral disinhibition hypothesis – lack of ability to adjust activity levels to fit requirements
of different settings
Disruptive Behavioral Disorders
Conduct Disorder – violating rules and rights, aggressive, destructive, deceive/theft, rule violation
Childhood onset before age 10, adolescent onset after 10
Moffitt: “life course persistent” and “adolescent limited” types, distinguished by kinds of acts
Oppositional Defiant Disorder – negative, defiant, and hostile behaviors towards authority, more males
earlier then equal in puberty
Tourette’s – 1 vocal and > 1 motor tic, <18, treat with antipsychotic (too much DA); coprolalia is
utterance of obscenities
Attachment
Separation-Anxiety - >4 weeks, distress, fear, physical complaints (5-7 separation, 11-12 changes, >14
depression)
Reactive-Attachment - < age 5, pathogenic care (inconsistent caregiving); inhibited and disinhibited types
Delirium/Dementia
Delirium – disturbance in consciousness with cognitive changes or perceptual abnormalities;
problems in sleep-wake cycle, psychomotor activities, emotions; in young associated with fever or
medication, in elderly commonly seen post-surgery
Dementia – memory impairment with additional aphasia, apraxia, agnosia, or executive dysfunction;
impair social or occupational functioning and reflect a significant decline from previous functionings
(r/o MDD with intact recognition performance, procedural instead of declarative decline)
AD
Vascular – sudden onset, step-wise
HIV – attention, memory, slowness, frontal dysfunction, apathy, social withdrawal, ataxia, severe
depression/anxiety
PD (decreased DA) – resting tremor, masklike, loss of coordination, pill-rolling, bradykinesia, akathisia
HD (decreased GABA) – affective symptoms, impulsivity, athetosis, chorea, high suicidality
Drugs
Alcohol/sedative/hypnotic/anxiolytic withdraw – sweat, tachycardia/palpitations, tremor, insomnia,
nausea/vomiting, headaches, hallucinations, seizures, psychomotor agitation, anxiety
Delirium Tremens: disturbed consciousness and cognition, autonomic hypertension, hallucinations,
delusions, agitation, liver failure
Amphetamine/cocaine intoxication – dilated pupils, grandiose, euphoria, anger, paranoia, hallucinations,
tachycardia, sweat, nausea, vomiting, seizures
Amphetamine/cocaine withdraw – dysphoria, vivid and unpleasant dreams, insomnia/hypersomnia,
“crash”
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Cocaine (stimulant): seizure, hemorrhagic stroke, leukoencephalopathy/white matter lesions, elevated
body temperature, cardiac or respiratory arrest; associated with impaired concentration, memory, EF
Psychoactive: LSD, mescaline, psilocybin
Depression (NE, 5-HT low)
Major Depression – at least 5 symptoms; twice as common in females and adolescents in industrialized
countries; 15% die from suicide
Anaclitic: in infants deprived of maternal attention; withdrawal, weepiness, insomnia, decline in health
Dysthymia – at least 2 years
Seasonal Affective Disorder – thought due to abnormal regulation of melatonin secretions by pineal gland
Theory
1. Seligman’s Learned Helplessness – unexpected control/reduce expectancies, hopelessness,
attribute internal, global and stable
2. Beck’s Cognitive Theory – negative (helpless, unlovable), distorted, illogical statements
(automatic thoughts) involving the cognitive triad about the self, world and future (work to
distance and neutralize); includes arbitrary inference, selective abstraction, overgeneralizations,
magnification and minimization, personalization, dichotomous thinking
3. Ellis’ Rational Emotive Therapy (RET) – irrational thoughts lead to maladaptive behaviors,
challenge beliefs
4. Rehm’s Self-Control Model – attend to negative events and immediate outcomes, stringent selfevaluation, low self-reinforcement, high self-punishment
5. Psychoanalytic – anger turned inwards
6. Wolpe’s Classical Conditioning – low rate of response contingent reinforcement results in
neurotic depression
7. Bandura’s Self-Efficacy Model
Treatment
1. TCA – for “classic” depression, vegetative symptoms, worse in morning, moderate, anxiety
2. MAOI – for atypical depression, worse in late day, phobia, panic
3. SSRI – melancholic depression
Bipolar (NE high, 5-HT low)
Mania – elevated, expansive, or irritable mood at least one week, characterized by inflated self-esteem or
grandiosity, decreased need for sleep, increased motor activity, more talkative or pressured speech, flight
of ideas or racing thoughts, distractibility, increase in goal-directed activities, risk seeking
Bipolar I – manic and history of mania (1+ week), depression or mixed; F = M
Bipolar II – hypomanic (4+ days) and depression F > M
Cylothymic – at least two years with shorter swings and subclinical depression and mania
10-15% die from suicide, 10-15% with MDD develop BP I
* greatest genetic link, 65% identical twins, 14% fraternal twins
functional deficits in symptomatic patients
Anxiety
Presence of anxiety symptoms and avoidance
Agoraphobia – fear cannot escape; treated with interoceptive bodily sensations evaluation, flooding (in
vivo exposure with response prevention), antidepressants (TCA, imipramine)
Panic Disorder – treat with antidepressant (e.g., imipramine, MAOI)
Social Phobia – fear evaluation; treated with Cog-Be groups (exposure/flooding, cognitive restructing,
behavioral rehearsal), beta-blockers (propranol), MAOI (phenelzine), SSRI, SNRI
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OCD – male early onset, in adults M = F; treated with thought stopping and habituation, flooding, SSRI,
TCA (clomipramine); associated with overactive right caudate of basal ganglia, also cingulate and
orbitofrontal (hyperkinetic thoughts versus movements)
1. CBT Two-Factor Theory – anxiety response to previously neutral stimulus through classical
conditioning and negative reinforcement through compulsive rituals to avoid stimulus
2. Beck – anticipation of danger/harm, uncertainty of future events
3. Psychodynamic – ego and superego override libido in those disposed toward obsessional neurosis
(reaction formation and displacement)
Specific Phobia
1. Mowrer’s Two-Factor Theory – avoidance conditioning through classical conditioning and
negative reinforcement; use exposure and desensitization
2. Social Learning – vicarious
3. Psychodynamic – unacceptable sexual or aggressive impulses towards a person or object
unconsciously associated with feared object
4. Seligman – certain stimuli are biologically predisposed to be feared, adaptive
PTSD – >1 month of reexperience, avoidance, increased arousal; treat with exposure;
worse when delay onset, kids have “omen formation”; rape – cognitive processing; antidepressant
(e.g., imipramine) to help with flashbacks and nightmares
Acute Stress Disorder – lasting 2 days to 4 weeks, PTSD symptoms plus dissociative symptoms
(detachment, derealization, dissociative amnesia)
GAD – > 6 months, difficult to control, many somatic symptoms; treat with Cog-Be, SSRI/buspirone
Selye’s general adaptation model – Alarm, Resistance, Exhaustion (ARE)
Pure anxiety symptoms: apprehension, tension, trembling, excessive worry, nightmares
Pure depression symptoms: depressed mood, anhedonia, loss of interest, SI, decreased libido
Somatoform
Psychophysiological/psychosomatic disorder – a disorder with physical signs and symptoms that have a
psychological origin, typically affecting a single organ system innervated by the ANS; also applied to
common ailments presumed triggered by psychological stress
Somatization – the tendency for psychological discomfort to be expressed through bodily symptoms,
<30 years, 4 pain, 2 GI, 1 sexual, and 1 pseudoneurologic symptom
Conversion – changes in functioning suggestive of a physical/neurologic disorder without intentional
production of symptoms; appears to involve voluntary motor/sensory functioning [primary (block real
issue) and secondary gains (avoid unpleasant situation, gain support)]; suggestion of remission, hypnosis,
amytal interview
Factitious Disorder – voluntary production of symptom’s to assume patient role
a. Münchausen’s syndrome – a factitious disorder in which patients habitually present for hospital
treatment of an apparent acute illness, with apparent incentive to be in sick role (can be by proxy)
b. Ganser syndrome – a factitious disorder in which patients pretend to be insane, symptoms may
include amnesia, disturbance of consciousness, unusual behavioral acts, or hallucinations;
responses are often characterized by senseless or approximate answers to questions
Malingering – intentional production or gross exaggeration of symptoms motivated by external incentives
Hypochondriasis – morbid anxiety and fear about serious illness, misinterpret bodily symptoms
Undifferentiated – chronic fatigue, appetite loss, GI, genitourinary
Psychosis – altered mental state characterized by delusions, hallucinations, loosened associations, and
illogical thinking
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Schizophrenia
Kraeplin (1919) – Dementia Praecox
Blueler (1950) – association, affect, ambivalence, autism (4 A’s)
Schneider (1959) – 11 pathognomonic signs
Crow (1980) – positive and negative symptoms
> 6 months, > 1 month of 2 active symptoms, females have better prognosis
delusions, hallucinations, disorganized speech and thoughts (“word salad”, tangentiality), disorganized or
catatonic behavior, negative symptoms
Paranoid (coherent delusions, most familial)
Disorganized (not coherent themes, inappropriate affect, worst outcome)
Catatonic
Undifferentiated
Residual (attenuated positive symptoms, negative symptoms)
Delusions – persecutory, grandiose, reference, thought broadcasting, thought insertion
Frontal lobe dysfunction with hypometabolism associated with negative symptioms; includes abnormality
in the hippocampus, entorhinal and cingulated cortices, limbic area (dopaminergic projections of ventral
tegmental area); generalized atrophy; often have history of childhood social and cognitive dysfunction
preceding psychosis; deficient attention and EF, retrieval (retention normal), reaction time/processing
speed; pursuit abnormalities
48% identical twin, 17% fraternal twin, 10% sibling, 5.5% one parent, 46% both parents
increased DA, NE, and 5HT; decreased GABA and glutamate
Factors: in vitro viral exposure, pestivirus, influenza (born in winter – fraternal twin factor), double-bind,
high expressed emotion, diathesis-stress (Rosenthal), generational transfer (Bowen)
Schizophreniform Disorder – schizophrenic symptoms for < 6 moths
Brief Psychotic Disorder – symptoms < 1 month
Dissociative Disorder
Disruption in consciousness, identity, memory, or perception
Amnesia – inability to recall personal information, need to recall in controlled way
Fugue – psychogenic amnesia in which the patient wanders and may assume a new identity
Identity Disorder – two or more distinct identities/personality states; usually with history of severe abuse;
comorbid with self-mutilation, PTSD, suicidality, conversion
Depersonalization – detachment/estrangement, reality testing intact
Sleep D/O
Dyssomnia – narcolepsy, primary insomnia/hypersomnia, breathing-related, circadian rhythm
Parasomnia – nightmare, sleep terror, sleepwalk
Eating D/O
Anorexia – worse when late onset, male (biological correlate: hypothalamus/endocrine)
Bulimia Nervosa – alkolosis from vomiting, acidosis from laxatives; decreased endogenous opiods, 5HT,
NE
Cog-Be better than medication (antidepressant)
Minuchin – enmeshed family
30% sexually abused
Mental D/O due to General Medical Condition and Substance Induced
Types of personality change due to GMC: labile, disinhibited, aggressive, apathetic, paranoid,
unspecified/combined
Catatonic D/O due to GMC – TBI, CVA, encephalitis, metabolic conditions
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Hallucinogen Persisting Perception D/O – flashbacks persisting after discontinuation
Organically-based mood symptoms – substance induced (e.g., PCP, hallucinogens), endocrine diseases
(e.g., hypothyroidism), carcinoma of pancreas, viral illnesses, structural disease of brain
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Personality Disorders
Typically manifested in adolescence, chronic; associated with poor coping strategies, poor ego
functioning, low IQ, disorganized families
Cluster A (odd, eccentric): Paranoid, Schizoid (socially detached and restricted emotionality), Schizotypal
(reduced personal relations, cognitive/perceptual disturbance, eccentric behavior)
Cluster B (dramatic, emotional, erratic):
1. Narcissistic (Kernberg – defense from being thwarted as child; Kohut – arrested development)
2. Borderline (80% abused; Ego/Object relations – poor differentiation between self and object;
Kernberg – disposition toward aggression; Cognitive – anger from unrealistic expectation, poor
discrimination of wants and needs; DBT – includes CBT, social skills, group dynamics, selfsoothing exercises)
3. Antisocial (genetics, XYY, low-wave brain activity, lower levels of arousal and anxiety)
4. Histrionic
Cluster C (anxious, fearful): Avoidant, Dependent, Obsessive-Compulsive
Suicide
60-80% multiple attempts
MDD/BP, alcoholism, schizophrenia
50% have medical condition
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PSYCHOPHARMACOLOGY
The study of drug effects on behavior and their biochemical mechanisms of action
Psychoactive/psychotropic drugs – drugs capable of modifying cognition, emotion, behavior, or
other mental states
I. Antidepressants
1. Tricyclics – Imipramine (Tofranil), Clomipramine (Anafranil), Amitryptyline (Elavil), Doxepin
Action: NE and 5-HT
Uses: For somatic and vegetative symptoms, panic attacks, agoraphobia, OCD, chronic pain,
enuresis (Tofranil)
Side Effects: anticholinergic (dry mouth, blurred vision, pupil dilation, urinary retention,
tachycardia, nasal congestion, forgetfulness), skin rash, cardiotoxic, memory, confusion,
insomnia, tricyclic overdose (ataxia, agitation, impaired concentration, severe hypotension, fever,
arrhythmia, seizure), weight gain, fine tremor, blood dyscrasia, fatigue; interacts with sedatives,
anti-Ach, hypotensives
Withdrawal: headache, nausea, anxiety, nightmares, malaise, vomiting
2. MAO Inhibitors (MAOI) – Phenelzine (Nordil), Tranylcypromine (Parnate)
Action: NE (DA, 5HT)
Uses: atypical depression (e.g., reverse vegetative), hostility, anxiety, hypochondriasis
Side Effects: tremor, hypotension, dizziness, upset stomach, weight gain, headache, anticholinergic, blood dyscrasia, insomnia, skin rash; must avoid foods with tyramine (aged cheese,
alcohol, liver, banana, avocado) or will have hypotensive crisis (also barbiturate, amphetamine,
antihistamine); 5HT toxicity when taken with SSRI, including arrhythmia, nystagmus, tremors,
headache, confusion, irritability; OD includes ataxia, hypertension, hallucination, delusions,
convulsions
3. SSRIs – Fluoxetine (Prozac), Sertraline (Zoloft), Paroxetine (Paxil), Citalopram (Celexa),
Escitalopram (Lexapro), Fluoxamine (Luvox)
Action: 5-HT (SSRI)
Uses: depression, OCD, eating disorders, social anxiety
Side Effects: GI symptoms, sexual problems, headache, dizziness, insomnia, anorexia, anxiety,
tremor; less severe than tricyclics and less potentional for OD; 5HT toxicity syndrome from use
with MAOI (myoclonus, fever, diarrhea, agitated confusion, muscle rigidity, autonomic
instability)
4. Others – Serzone (with 5HT), Wellbutrin (with DA), Venlafaxine (Effexor), Cymbalta
Action: NE (SNRI)
Uses: depression, smoking, GAD
Side Effects: less anxiety and side effects than SSRIs
II. Mood Stabilizers
1. Lithium
Action: 5-HT, NE
Side Effects: hand tremor, GI, weight gain, fatigue, mild cognitive impairment, polyuria,
polydipsia, nausea; at toxic levels have vomiting, abdominal pain, diarrhea, severe tremor, slurred
speech, ataxia, seizures, coma; interacts with salt, caffeine, alcohol, diuretic; high relapse when
discontinue; contraindicated for cardiovascular, kidney, liver, thyroid, GI problems
2. Depakote/Depakene (valproic acid, sodium valproate, divalproex sodium)
III. Antipsychotics (neuroleptic) – 1st Phenothiazines (Chlorpromazine-Thorazine), Thioridazine
(Malleril), Haloperidal (Haldol), Clozapine (Clozaril), Risperidone/Risperdal, Geodon, Abilify, Seroquel,
Zyprexa
Action: DA (stimulate D2, stimulate or inhibit D1)
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Uses: positive symptoms, psychotic reactions
Side Effects: anticholinergic and extrapyramidal effects (Parkinsonian symptoms –
Haloperidal worst), tardive dyskinesia (twisting and extensor posturing; caudate; more in females
and elderly – decrease DA or increase GABA), akathisia, dystonia, orthostatic hypotension,
sedation, seizure, arrhythmia, neuroleptic malignant syndrome (like PD); risk of
agranulocytosis/white blood cell dyscrasia with Clozapine (works on DA and 5HT)
Withdrawal: Ach rebound, insomnia, nightmares, withdrawal-emergent syndrome (chorea, motor
impersistence, restlessness)
IV. Sedatives, Hypnotics, Anxiolytics – withdrawal associated with tremors, nausea, vomiting, paranoia,
hallucinations, delirium, seizures, decreased respiration; first suppresses inhibitory mechanisms, then
excitatory mechanisms (alcohol)
1. Benzodiazepines (-am) – Diazepam (Valium), Alprazolam (Xanax), Clonazepam (Klonipin),
Lorazepam (Ativan), Ytriazolam (Halcion), Chlordiazepoxide (Librium)
Action: GABA
Uses: anxiety, seizures, sleep, alcohol withdrawal, muscle spasms, CP (*most widely used
psychotropic class)
Side Effects: CNS depressant, sedation/drowsiness, confusion, disturbed sleep (decreased
sleep onset, REM, delta), hostility, depression, paradoxical excitement, increased
appetite, sexual dysfunction, slurred speech, ataxia, skin rash, disorientation in elderly,
psychomotor impairment, blood dyscrasia, anterograde amnesia, potential for withdrawal,
tolerance, dependence, cross-tolerance, rebound
Withdrawal: seizure, panic, stroke, depersonalization, hyperexcitation
2. Barbiturates (-al)– Thiopental (Pentothal), Amobarbital (Amytal), Secobarbital (Seconal)
Action: Reticular Activating System
Uses: acute agitation, anesthesia
Side Effects: agitation, depression, slurred speech, nystagmus, dizziness, irritable, impaired motor
and cognition, addictive, synergistic with alcohol, may have paradoxical excitement; beta waves;
OD with ataxia, respiratory depression
Withdrawal: REM rebound, nightmares, tonic-clonic seizures
3. Beta-blockers – Propanolol (Inderal)
Action: Beta-adrenergic
Uses: physical manifestations of anxiety (anticipatory)
Side Effects: GI, hypotensive episodes, sexual dysfunction, numbness, memory impairment
V. Opiods – Opium, Morphine, Codeine, Oxycodone, Heroin, Percodan, Demerol, Dilaudid, Darvon,
Methadone
Action: Enkephalin receptors and endorphins
Uses: sedation, pain relief, diarrhea, cough suppression
Side Effects: “rush” then drowsiness; pupil constriction (“pin-point”), decreased visual acuity,
perspiration, GI, constipation, nausea/vomiting, respiratory suppression; toxicity marked by slow
and shallow breathing, clammy, muscle rigidity, cataplexy, hypotension, decreased pulse,
convulsions, coma; possible visuospatial/visuomotor deficits; can see pulmonary edema, radial
nerve palsy; OD with hypoxia
Naloxone (Narcan) reverses effects
Withdrawal: autonomic hyperactivity (flu-like), dysphoria
VI. Psychostimulants – Amphetamines (dexamphetamine) (MDMA/Ecstacy), Methylphenidate (Ritalin),
Pemoline, (Cyclert), (Dexedrine), Focalin, Provigil (nicotine, strychnine, cocaine)
Action: Catecholamines (DA, NE, Epinephrine)
Uses: ADHD, narcolepsy, treatment resistant depression
Side Effects: anorexia, dry mouth, restlessness, insomnia, arrhythmia, mood fluctuation,
growth suppression, weight loss, abnormal movements (tics); prolonged use/overdose have
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teeth grinding, skin picking, paranoid states, hallucinations, tachycardia, anxiety, confusion,
convulsions, fever, cognitive impairment (attention, memory, abstraction), reduced REM
Withdrawal: depression, fatigue, somnolence, apathy; mood and anxiety symptoms may last for
months
VII.
Anticonvulsants – Tegretol (Carbamazepine) (can also be used as mood stabilizer for rapid
cyclers), Lamictal, Neurontin, Topamax, Trileptal
Action: 5HT
Side Effects: CNS (drowsiness, dizziness, confusion, ataxia, hyperreflexia, clonus, tremor), GI,
anorexia, blood dyscrasia (rare), anemia, rash, cardiovascular, dermatologic problems;
contraindicated for cardiac conduction abnormalities
VIII. Agents for Cognitive Deficit (Nootropics) – Cognex (Tacrine), Donepezil (Aricept),
Selegiline (Eldepryl), Rivastigmine (Exelon), galntamine, Namenda (NMDA), Estrogen, Ibuprofen,
Vitamin E & C, Nerve growth enhancers
Action: Cholinergic/Cholinesterase inhibitor
Side Effects: anticholinergic and extrapyramidal effects (Parkinsonian symptoms)
Aging impacts pharmacokinetics of drugs:
1) absorption – gastric pH, intestinal blood flow, GI motility, number of absorbing cells,
ingestion of other drugs
2) distribution – fat tissue (↑), body water, binding to plasma proteins (↓)
3) metabolism – decreased hepatic (liver) flow
4) excretion – renal (kidney) clearance problem with dehydration
See website www.psychmeds.info for list of most common medications
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REPORTS
1. Referral
2. Client data
3. Current concerns
4. Informant report
5. History
6. Review of previous reports
7. Observations
8. Tests administered
9. Test results and interpretations
a. General intellectual status
b. Achievement
c. Attention/Concentration
d. Executive Function
e. Learning/Memory
f. Language
g. Visuospatial ability
h. Sensorimotor function
i. Personality/Mood
10. Diagnostic summary
11. Recommendations with vocational implications
12. Appendix: Tests scores
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SEIZURES
A discrete clinical attack in which there is uncontrolled, excessive, and hypersynchronous discharge of
cortical neurons; half related to epilepsy, half to acute brain disorders (e.g., stroke, hypoglycemia);
approximately 5% of people will experience a seizure during their lifetime
Epilepsy – chronic brain disorder characterized by recurrent seizures; hypometabolism borders
epileptogenic zones
I. Partial: a focal seizure in which the EEG abnormality involves a single brain region
1. Simple – no change in consciousness/responsiveness, single manifestation (aura); can have
positive (e.g., hand twitching) or negative (e.g., impaired language) symptoms (typically 510”)
a. Motor - associated with temporal lobe seizures, has prominent ictal motor
automatisms (e.g., lipsmacking, turning of eyes or head or body, leg cycling,
fencing posture)
i. Jacksonian march – focal motor seizure progression that begins focally in one
part of the body and spreads systematically to adjacent areas; reflects spread of
epileptic activity through the sensorimotor homunculus (e.g., fingers, arm, then
face)
ii. Todd’s mono/hemi-paresis/paralysis – lasting from several minutes to 48 hours,
accompanying post-ictal muscle weakness; a previous focal deficit may worsen
or a new deficit may appear; often seen with stroke or tumor
b. Somatosensory/Sensory – unformed hallucinations in any sensory modality
c. Autonomic
2. Complex (psychomotor) – altered consciousness/impaired responsiveness (usually medial
temporal lobe or frontal lobe), typically 30”-2’, EEG 5-8 Hz; postseizure confusion (may
include aphasia, amnesia, fatigue, agitation, aggression, headache), complex symptomatology
(automatisms, subjective feelings, postural changes); déjà vu (inappropriate
familiarity)/jamais vu (the feeling that familiar places or things are suddenly unfamiliar),
depersonalization, hallucinations, illusions, size distortion (e.g., macropsia, micropsia),
epigastric aura, unpleasant odor, extreme fear or panic (amygdala)
- when basal ganglia involved, have contralateral dystonia/immobility and ipsalateral
automatisms
a. Temporal - interictal behaviors include (“opposite” to Kluver-Bucy symptoms;
Geschwind’s Syndrome), hypergraphia (excessive writing)
Left – schizophreniform: angry, paranoid, religiosity
Right – manic-depressive: obsessive, impulsive, elated, sad, emotional
Medial – nausea, déjà vu, fear, panic, unpleasant odor, autonomic phenomenon,
staring, oral automatisms, gestural automatisms
Lateral – vertigo, impaired hearing, auditory hallucinations, aphasia
b. Frontal – clustered, brief, minimal confusion, prominent motor automatisms,
vocalizations, bizarre, stereotyped
Dorsolateral – contralateral tonic-clonic activity, version/turning away from
side of seizure, aphasia
Supplemental motor – fencing posture, speech arrest, unusual sounds
Orbitofrontal and cingulate – elaborate motor automotisms, unusual sounds,
autonomic change, olfactory hallucination (orbitofrontal), incontinence (cingulated)
c. Occipital – visual hallucinations, contralateral eye deviation, rapid blinking or
eye flutter, field defects, ictal blindness; associated with migraine-like symptoms
d. Parietal – vertigo, contralateral numbness/tingling/burning, aphasia,
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hemineglect, deviation toward or away from side of seizure
II. Generalized: a seizure in which the EEG abnormality involves both brain hemispheres; no aura, no
focal semiology, no lateralized findings, immediate LOC; postictal amnesia, confusion, fatigue,
unresponsiveness; rarely from tumors, infarctions, or structural lesions
Primary – seizure onset arises from both hemisphere
1. Absence/petit mal – generalized seizure marked by a sudden blank stare and interruption
of ongoing activities, lose awareness, no postictal confusion, typically lasting less than
10”; automatisms, subtle clonic limb movements, and eye blinking often occur; usually
begins between ages 4-10 and is outgrown, others develop generalized; not associated
with cognitive impairment (frontal, amygdaloid-hippocampal, reticular-cortical); 3second spike and wave, 3-4 Hz; autosomal inheritance
2. Generalized tonic-clonic/grand mal – a generalized seizure (convulsion) with involuntary
muscle contraction associated with a sudden loss of consciousness and a generalized
tonic muscle contraction, followed by clonic jerks that increase in amplitude while
decreasing in rate, typically lasting less than 5 minutes; tongue biting or incontinence
may occur; produces metabolic and respiratory acidosis; lethargy and confusion are
common postictally, also amnesia and headache, lasting up to several hours; may occur
during withdrawal from alcohol, barbiturates, sedative-hypnotics; autosomal dominant
inheritance
3. Myoclonic – generalized seizures characterized by myoclonic jerks (i.e., sudden, brief,
muscular contraction), usually involving the arms and legs, and may lead to a fall; in
series or clusters, common after awakening; autosomal dominant inheritance
4. Atonic seizure/Drop attack – generalized seizure that results in sudden loss of motor tone
(akinetic)
Secondary – seizure begins as a focal or partial seizure and then spreads
Status epilepticus – a seizure lasting more than 30 minutes or repeated seizures without periods of
consciousness between them; generalized status tend to have sequelae of hippocampal sclerosis
 generalized convulsive status epilepticus – when longer than 2 hours has ~10% mortality rate
 nonconvulsive status epilepticus – marked by decreased alertness
 epilepsy partialis continua – continual seizure activity without loss of consciousness
Reflex epilepsy – associated with seizures that are precipitated by specific internal or external stimulation
(e.g., strobe lights, television, music)
Febrile – a generalized seizure associated with a rapid rise in body temperature; usually between 6
months-5 years; patients with temporal lobe seizures and history of febrile seizures are more
likely to have hippocampal atrophy and sclerosis
Benign focal epilepsy of childhood – most common type of partial seizure, centrotemporal spikes
i.
Rolandic epilepsy (nocturnal seizures) – benign focal motor epilepsy associated with centraltemporal EEG spikes that usually begins at 5-9 and remits by age 15, usually boys, autosomal
dominance with incomplete penetrance
ii.
Benign occipital epilepsy (visual symptoms) – often remits by puberty, inheritance
Continuous spike-wave discharges during sleep (CSWS) – during non-REM sleep, associated
with neuropsychological regression, includes partial motor and absence seizures
Landau-Klaffner syndrome – developmental epilepsy syndrome of acquired (global) aphasia following
normal development, involving temporal and temporal-parietal-occipital EEG abnormalities,
generalized seizures; often treated with steroids
Lennox-Gastant syndrome – childhood encephalopathy characterized by generalized seizures, diffuse
slow spike and wave EEG complexes, and high incidence of MR; cognitive impairments are
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exacerbated with antiepileptic medication
Uncinate seizure – a partial seizure originating in the uncus that is associated with hallucinations
of taste and (unpleasant) smell
Gelastic – laughing as ictal manifestation; associated with partial complex seizures and hypothalamic
hamartomas (fusiform and parahippocampal gyri)
Dacrystic – crying as ictal manifestation
Clinical Type
Somatic Motor
Jacksonian (focal motor)
Masticatory
Head and Eye turning
Auras
Somatosensory
Images, lights, patterns
Auditory
Vertiginous
Olfactory
Gustatory
Etiology:
-
-
Localization
Prerolandic gyrus
Amygdaloid nucleus
Supplementary motor cortex
Postrolandic
Occipital
Heshcl’s gyrus
Superior temporal
Mesial temporal
Insula
Infancy (0-2) – congenital CNS abnormality, birth injury, anoxia, metabolic disorders
(hypocalcemia, hypoglycemia, electrolyte imbalance, uremia, hepatic failure, hypoxia, PKU,
B6 deficiency), infections, toxemia, trauma, infantile spasms (West’s syndrome), febrile
convulsions
Childhood (2-10) – perinatal injury, congenital abnormality, CNS infection (e.g., meningitis),
thrombosis of cerebral arteries or veins, idiopathic
Adolescence (10-20) – idiopathic, trauma (50% 1st year, 80% within 4 years)
Adult (20-60) – alcohol/drug (barbiturate) withdrawal, trauma, neoplasm, idiopathic, vascular
disease, AVM, AIDS (cerebral toxoplasmosis)
Late life (60+) – cerebrovascular disease, stroke, tumor, neurodegenerative disease, trauma
EEG
Ictal – paroxysmal activity consisting of bursts of spikes, slow waves, or complexes
Post-ictal – low voltage activity (depression) followed by diffuse high voltage slowing; associated with
confusion and related to seizure severity
Inter-ictal – show specific abnormalities in 80%
15% nonspecific EEG changes (e.g., background slowing), 1-2% slow waves and/or spikes but no ictal
event
Sleep EEG more sensitive than waking
PET/SPECT
Hyperperfused ictal foci, hypoperfused post-ictally
Nociferous cortex – cortex associated with an epileptogenic lesion that impairs the functioning of
neuronal regions distant from the focus because of propogation of abnormal electrical discharges
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to induce:
breath deeply for 3 minutes (hyperventilation) – vasoconstriction
strobe (photic driving/stimulation)
sleep deprivation
after falling asleep
coughing, laughing
hormonal changes (menses, steroids)
insulin
kindling – may account for susceptibility to electrophysiological dysfunction in area opposite hemisphere
homologous to original site of discharge
Pseudoseizures – indicated by normal ictal EEG; emotional or psychological etiology, distinguished by
rare when sleeping or alone, gradual onset, crying ictally, occasional talking, asynchronous movements,
clear consciousness and recall, purposeful movement (e.g., side-to-side thrashing and pelvic thrusting,
alternating head movement – although may see in frontal partial seizures), may have directed violence,
infrequent urination and defecation, long lasting; risk factors include sexual abuse, epilepsy, psychiatric
disorder, head injury, modeled after other person, family discord/academic stress; 50% also have real
seizures
Other disorders that may look like seizures: rage attacks, cerebrovascular disturbances, panic disorder,
breath holding spells in infants, sleep disorders, migraine, metabolic disturbance
Forced normalization – psychiatric/psychotic disturbance after control of seizures
COGNITIVE FINDINGS
I. IQ – decline often associated with AED toxicity or status epilepticus; co-occurs with MR,
autism, cerebral palsy, LD
II. Language – expressive more impaired than receptive, naming difficulties, hypergraphia
III. Perceptual-motor skills – TPT and Bender-Gestalt impairments
IV. Attention – focal seizures have greater deficits in selective attention, generalized seizures
have greater deficits in sustained attention
V. Memory – may be related to pathology of temporal lobes, LTM more affected than STM
VI. Executive functions – frontal lobes affected by temporal/hippocampal discharge through
temporal-frontal pathways
VII. Motor Skills – overall slowing, including reaction time and psychomotor speed
Overall, affected by frequency of seizures, duration of disorder, history of status epilepticus, early onset,
poor seizure control
TREATMENT
I. Anti-epileptic drugs (AED) – need to check liver function and white blood count
1. phenobarbital (Luminal) – related to hyperactivity, irritability, sleep disruption
2. phenytoin (Dilantin) – high side effects, may lead to progressive deterioration, intoxication
includes nystagmus, ataxia, dysarthria
3. carbamazepine (Tegretol) – few cognitive side effects
4. Primidone (Mysoline)
5. diazepam (Valium)
6. valproic acid (Depakote) – minimal cognitive side effects
7. gabapentin (Neurontin)
8. lamotrigine (Lamictal)
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9. topiramate (Topamax)
Stevens-Johnson syndrome is allergic reaction causing leaky blisters on mouth, eyes, and skin
AED intoxication indicated by ataxia of gait, nystagmus, dysarthria, lethargy or stupor, dysmetria on heelshin test, tremor on finger-nose test
Note: may cause cognitive problems, including impaired attention, memory, motor speed, and processing
speed
II. Surgery
Focal resection (ablative): 80% seizure free in temporal lobectomies
(Vein of Labbé/superior anastomotic vein, connects middle cerebral vein and lateral sinus, marks
posterior limit for left temporal lobectomy to avoid post-operative language decline)
Corpus callosotomy (palliative): to control generalization, not frequency
Functional hemispherectomy – frontal and occipital poles spared
Multiple subpial transection – technique for brain areas involving language or primary sensorimotor
function (eloquent cortex), involving shallow cuts in the gray matter to disconnect horizontal
white fibers
III. Vagus nerve stimulator – pacemaker-like device implanted in left side of chest attached to left vagus
nerve (CN X) in carotid sheath; 3 seconds on, 5 minutes off
IV. Ketogenic diet – high fat diet producing acidosis; 1/3 experience seizure control
Functional adequacy – conceptualization of brain function that proposes that the residual function of the
tissue to be resected during anterior temporal lobectomy determines the degree of pre- to postsurgery memory change (i.e., how well tissue to be removed functions)
Functional reserve – conceptualization of brain function that proposes that the functional capacity of the
tissue contralateral to the area resected during anterior temporal lobectomy determines the degree
of pre- to post-surgery memory change (i.e., how well tissue remaining functions)
When pregnant, get vitamin K to improve blood clotting if on AED
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SENSORY LOSS
Brainstem – lesion in medulla causing loss of pain and temperature on same side of face and opposite side
of body, involving trigeminal tract
Thalamus (Déjerine-Roussy) – loss of sensation on opposite side of body, position most affected, may
feel pain
Parietal lobe – disturbance on opposite side of body, with loss of position sense, impaired localization of
touch and pain, elevation of 2-point threshold, astereognosis, tactile agnosia
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SLEEP
Wakefulness: Alpha (8-13 Hz) and Beta (>13 Hz) – low voltage, fast frequency
1-4 synchronized
Stage 1: Alpha, Theta (4-7 Hz), Beta
Stage 2: Theta with K-complex and sleep spindles (50%)
Stage 3: Delta (<4 Hz)
Stage 4: Delta (10-15%)
Parasomnias (sleepwalking, night terrors) occur in Stages 3 and 4
REM: “paradoxical sleep” with eye movement and faster brain activity but low muculoskeletal tone
(25%), desynchronized; lowest body temperature
Majority deep sleep first half of night, REM second half; REM and Stages 3 and 4 decline with age
Sleep generated and regulated by brainstem (medulla) through diencephalon and limbic system
NonREM: GABAergic cells of hypothalamus inhibit histaminergic activation and Ach
REM: GABAergic REM-on cells and REM-waking-on cells in pons activate phasic eye movements and
phasic muscle activity with inhibiting tonic muscle tone (glutamatergic REM-on cells)
Hypothalamic nonREM-on cells, nonadrenergic and serotonergic REM-off cells
Cognitive findings associated with poor sleep mostly in sustained attention/vigilance, coordination, and
emotional regulation, also memory retrieval and executive functioning
Sleep Disorders
1. Dyssomnias
A. Intrinsic
I. Insomnia
II. Narcolepsy – a condition of excessive daytime sleepiness involving brief “attacks” of
sleep preceded by little or no non-REM sleep; associated with cataplexy (abrupt
attacks of muscular weakness and hypotonia triggered by emotional stimuli), high
emotionality, sleep paralysis, hypnagogic and hypnopompic hallucinations; 90%
develop in adolescence to 25; associated with chromosome 6 when cataplexy,
histocampatibilty complex antigen
III. Sleep apnea – a breathing disorder of temporarily stopped breathing caused by upper
airway obstruction or a central disorder (decreased REM, increase Stage 1, CheynesStokes respiration); associated with frequent nighttime awakenings, daytime
sleepiness, impairments in attention and concentration, motor uncoordination,
depression, ADHD symptoms; hypoxia may cause memory and EF deficits
IV. Restless Leg Syndrome – from polyneuropathy, iron deficiency; treat with DA
V. Periodic limb movement (nocturnal myoclonus)
VI. Hypersomnias
B. Extrinsic – inadequate sleep hygiene, environmental sleep disorder, hypnotic, stimulant,
alcohol, and toxin dependency
C. Circadian – time zone change, shift work, delayed sleep phase
2. Parasomnias
A. Arousal disorders – sleep terrors, sleepwalking
B. Sleep-Wake transition disorders – rhythmic movement disorder, sleep talking
C. Parasomnias associated with REM – nightmares
D. Other – bruxism, enuresis
3. Medical/Psychiatric Disorders
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A. Psychiatric – psychosis, depression, alcoholism
B. Neurologic – dementia, PD, fatal familial insomnia (hyperactive ANS, endocrine
abnormalities, motor abnormalities, inattentiveness, amnesia, sequencing problems,
confusion; is a prion disease related to Creutzfeldt-Jakob, damages thalamus), epilepsy,
headaches
Shortened sleep latency due to alcohol and drug use, narcolepsy, sleep apnea, sleep deprivation
Prolonged sleep latency due to delayed sleep phase syndrome, inadequate sleep hygiene, restless leg
syndrome, acute schizophrenia, major depression, mania
Shortened REM latency due to depression, narcolepsy, sleep apnea, sleep deprivation rebound,
withdrawal from alcohol, hypnotics, tricyclic antidepressants
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STATISTICS
Inferential Statistics – generalizability based on random selection and independent observations
Independent Variable (IV) – treatment or intervention that is manipulated (x)
Dependent Variable (DV) – measured outcome (y)
Descriptive/Nonexperimental Research
Content analysis – categorical
Protocol analysis – thinking aloud (clearly defined, exhaustive, mutually exclusive)
Sequential analysis – to study complex social behaviors
Behavioral sampling
Time sampling – if the behavior is present at the time assessed
Interval recording – if occurred during given period, no clear beginning or end
Event sampling – each time occurs, for rare events or leaves permanent record
Situational sampling – across settings
Observational
Case study
Survey
Analog – artificial setting
Experimental Research
1) True experimental – randomized assignment, IV manipulated
2) Quasi-experimental – not-randomized (when single or pre-existing groups)
a)
Ex-post facto – assessing IV after applied (correlational)
b)
Developmental
A) Cross sectional
B) Longitudinal
C) Cross-sequential
Variability in DV due to
1) IV (experimental variance) – maximize
2) Systematic error (confounding, extraneous) – control through random assignment, hold
extraneous variables constant, match subjects, blocking (analyze), statistical control [e.g.,
ANCOVA (eliminate)]
3) Random error (fluctuations in subjects, conditions, measurements) – minimize
Threats to Internal Validity (causation)
1) Maturation – error is systematic, can use single-group time-series
2) History – systematic error (use ABA, multiple groups)
3) Testing – readminister (practice effects)
4) Instrumentation – keep measures consistent
5) Statistical regression
6) Selection – randomly assign
7) Attrition/mortality – may be biased
8) Interaction with selection (e.g., selection and history  volunteers)
Control through random assignment, matching, blocking, ANCOVA
Threats to External Validity (generalizability)
1) Interaction between testing and treatment
2) Interaction between selection and treatment
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3) Reactivity
i. Hawthorne effect – better performance because of attention
ii. Evaluation apprehension – act to avoid negative evaluation
iii. Demand characteristics – cued to expectations or purpose
iv. Experimenter expectancy – bias
4) Multiple treatment interference (order/carryover effects) – one level of IV affects another
(use counterbalancing)
Control through random selection, observational research, single- or double-blind,
counterbalancing, simple random sampling, stratified random sampling, cluster sampling
Single Subject Designs
A = baseline
B = treatment
1) AB – controls for maturation only
2) ABA/ABAB (reversal) – controls for maturation and history
3) Multiple baseline – across behaviors, settings, or subjects, with treatment never
withdrawn
Group Designs
1) Between-group – different levels of the IV across groups
2) Within-subjects – each subject receives all levels of the IV (repeated/nested); subject to
carryover effects, maturation, history, autocorrelation between pre- and post-tests
(increasing Type I error and decreasing Power)
3) Mixed design – within and between, can counterbalance
Factorial Designs – 2 or more IV, providing main and interaction effects
Null hypothesis: HO= IV has no effect of DV
Alternate hypothesis: HA= IV has effect of DV
Type I error – true HO rejected, alpha
Type II error – false HO retained, beta
Power = probability of rejecting HO when false (1-beta); greater with larger N, higher alpha, 1-tailed test,
greater difference between population means
Scales of Measurement
1) Nominal – unordered categories (e.g., sex)
2) Ordinal – ordered/rank (e.g., Likert)
3) Interval – successive points equally space but no zero (e.g., IQ)
4) Ratio – has absolute zero (e.g., time, weight)
Nonparametric Tests
Nominal:
X2 ( >5 per cell)
Ordinal:
Mann-Whitney U – for 2 independent groups (~t-test independent)
Wilcoxon Matched Pairs – for 2 correlated/matched groups (~t-test correlated)
Kruskal-Wallis – for 3+ independent groups (~one-way ANOVA)
Parametric Tests – *homoscedasticity (equal scatter), homogeneity of variance, normal distribution,
independent observations
To increase Power: ↑ alpha, ↑ N, ↑ ES, ↓ error, use powerful statistics, one-tailed if possible
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2 groups
T-test – comparison of two means (one sample or correlated samples df = N-1, independent samples df =
N-2)
ANOVA (3+ groups) (Parametric – interval and ratio)
Want F > 1; use regression if unequal group size; comparison of between to within group variance
One-way – 1 IV, independent groups (across groups)
Repeated Measures/Nested – 2+ correlated groups (across time)
Split-plot/Mixed – both independent and correlated groups (across group and time)
Factorial – 2+ IVs, main and interaction effects
Randomized Block – extraneous variable made IV
ANCOVA – combined regression to control extraneous variable
MANOVA – 2+ DVs
Post-hoc:
Fisher’s LSD – pairs and complex (highest Type I error, lowest Type II)
Scheffe’s S – pairs and complex (most conservative; lowest Type I error, highest Type II)
Tukey’s HSD – pairs, equal group sizes, more powerful
A priori:
Dunn-Bonferroni, trend analysis (linear and non-linear; e.g., drug dosage, level of anxiety), linear
contrasts, orthogonal component
Correlations (see in scattergram)
Assumed linearity, unrestricted range (heterogeneous), homoscedasticity
Pearson r – both interval or ratio; square (r2) to obtain percent of variability explained
Contingency – both nominal
Spearman Rank Order (rho) – both ordinal
Biserial – artificial dichotomy and interval or ratio
Point Biserial – true dichotomy and interval or ratio
Tetrachoric – both artificial dichotomy
Phi – both true dichotomy
Eta – both interval or ratio but relationship non-linear
Prediction
Multiple correlation/regression (R) – continuous or discrete predictor(s) for single discrete criterion,
linear relationship, error normally distributed with mean of zero; want high correlation with criterion but
low correlation between predictors (maximizes predictive power)
Line of best fit/least squares criterion (minimizing error); R2 = coefficient of multiple determination
Logistic Regression – continuous or discrete predictor for single discrete criterion, nonlinear relationship
( is quadratic)
Canonical Correlation – multiple predictors and multiple criteria
Discriminant Analysis – criteria nominal, for classification
Multiple Cutoff – minimum cutoff scores on a series of predictor
Partial Correlation – assess relationship between two variables with effects of another variable partialled
out
Trend Analysis – to examine trend of change (e.g., linear, quadratic, cubic, quartric)
Causal/Structural Equation Modeling
independent – exogenous, dependent – endogenous, independent and dependent – intervening
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Path Analysis – recursive (one-way causal flow), want insignificant findings for feasibility
LISREL – recursive and non-recursive, combines path analysis and factor analysis EQS
Receiver operating characteristic curve (ROC) – a curve derived from signal detection theory that plots
the probability of correctly detecting hits against false alarms; used in recognition memory tests
and binary outcome prediction (e.g., presence or absence of a lesion)
Item Discrimination
Item difficulty: index (p) indicates percent of subjects answered correctly (e.g., .80 = 80% correct);
greatest discrimination at p = .50 (highest for T/F is p = .75)
D (discrimination index) = U (upper scoring group %) – L (lowest scoring group %); want D>.35
Item Response Theory (latent trait or external criterion) – uses Item Characteristic Curve (ICC) involving
probability of correct reponse rate (% answered correctly against total test score, external criterion, or
latent trait); takes into consideration difficulty, discrimination, guessing; considerd sample-invariant;
equate across tests, use computer adaptive tests
Power tests – tests in which there is no time restriction or component
Speed tests – timed tests in which the dependent measure is the number of items completed within the
specified time limit
Reliability – the degree to which scores on a tests are systematic and free from measurement error
X (obtained score) = T (true score) + E (measurement error)
r = true score variability, already squared (e.g., r = .80 = 80% variance explained)
Reliability best when test longer, range of scores unrestricted (difficulty = .5), heterogeneity of
examinees, homogeneity of content
1) Test-retest (coefficient of stability) – subject to time sampling error, memory, and
practice
2) *Alternate forms (coefficient of equivalence) – subject to time and content sampling error
(good for stable traits and speeded tests)
3) Split-half (coefficient of internal consistency) – spuriously elevated on speeded tests
(Spearman-Brown Prophecy formula overestimates)
4) Coefficient alpha (coefficient of internal consistency; Kuder-Richardson 20 if
dichotomous) – inter-item consistency/average reliability, subject to content sampling
error and heterogeneity (conservative estimate)
5) Inter-rater (inter-scorer, inter-observer) – correlation of scores by two raters or percent
agreement (kappa - adjusted for expected level of chance agreement)
Reliable change index (RCI) – statistical measure for repeated assessments used to determine whether
changes present on follow-up testing or within expectations, taking into consideration test-retest
reliability, error, and practice effects
Validity
1) Content – measures what designed to measure, determined through agreement (e.g.,
achievement, mastery)
2) Construct – measures theoretical trait, determined through evidence accumulation
i. convergent validity – monotrait-heteromethod
ii. discriminant validity – heterotrait-mono/heteromethod
iii. factor analysis – intercorrelations between each test and each factor;
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variability = communality + specificity + error
a.
orthogonal – uncorrelated (varimax, quartimax, equimax); sum
of squared factor loadings = communality (accounted variability across
test; lower-limit estimate of reliability); in principal components,
orthogonal eigenvalues (squared) account for unique variability in each
factor; summing eigenvalues ~= # of tests
b.
oblique – correlated (quartimin, oblimin, oblimax)
iv. cluster analysis – classify into homogeneous groups, exploratory or confirmatory,
hierarchical or nonhierarchical
3) Criterion – the ability to predict specific variable behavior, as determined by the
relationship between predictor and criterion (e.g., SAT and college GPA), assessed
predictively or concurrently (face validity); rarely exceed .6
4) Incremental Validity (IV) – to increase decision making accuracy
Predictor determines whether a person is positive or negative,
criterion determines whether a person is true or false
IV = Positive Hit Rate [TP/(TP + FP)] – Base Rate [(TP + FN)/N]
e.g., success = 10/20 = 50% (BR), predicted 8/10 = 80%, IV = 80 – 50 = 30%
Raising predictor cutoff increases T and F negative, decreases T and F positives
Best when IV high, BR moderate, selection ratio low
5) Ecological validity – degree to which a measure predicts behavior in everyday
circumstances
Predictive accuracy – the probability that, given a specific test finding, a particular condition of interest
exists
Retrospective accuracy – the probability that, given a particular condition of interest, a specific test
finding will be obtained
Positive Predictive Power (PPP) = TP/(TP + FP)
Negative Predictive Power (NPP) = TN/ (TN + FN)
Sensitivity = TP/(TP + FN)
Specifity = TN/(TN + FP)
PPP best with high prevalence and high specificity
Sensitivity increases when true positive increased; decreases when false negatives increased
Specificity increases when true negatives increased; decreases when false positives increased
Sensitivity and specificity do not change just because of different population
Variance = average of the squared difference of each observation from the mean Σ(x - mean x) 2/n
Standard deviation (SD) = square root of variance
Standard Error of Measurement (measured scores) SEmeas = SDx (1-rxx)1/2
(CI around obtained score)
~ reliability
Standard Error of Estimate (predicted criterion scores) SEest = SDy (1-rxy2)1/2 (CI around predicted score)
~ validity
Standard Error of Mean – provides index of expected inaccuracy of sample means
Relationship between validity and reliability; reliability places a ceiling on validity
Predictor: rxy < (rxx)1/2
Predictor criterion: rxy < (rxx * ryy)1/2
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(e.g., if reliability .81, validity <.90)
Correction of Attenuation – estimates what a predictor’s validity would be if predictor and criterion
perfectly reliable
Correction for Guessing = R (# right answers) – (# wrong answers/# choices per answer – 1)
Reliability of difference scores – cannot be greater than average reliability coefficient; more highly
correlated, smaller reliability of difference score and larger SEmeas
Standard Score z = (x – mean x)/SD; mean = 0, SD = 1
Norm-referenced – percentile (non-linear transformation, ordinal, rectangular – maximizing change in
middle, minimizing at ends), z-score (linear transformation, same shape), T-score
Criterion-referenced – percent mastered or external criterion (expectancy table, gpa, % score)
Age and grade equivalent scores highly sensitive to minor changes in raw score, not representing equal
intervals
Deviation quotient – standard scores that express performance relative to the mean of a reference group,
can be derived from combination of scores (Tellegen & Briggs, 1967, for IQ)
Negative skew – most scores high because easy test, ceiling effects; mean<median<mode
Positive skew – most scores low because difficult test, floor effect; mean>median>mode
Use median when skewed or many outliers
Kurtosis – the degree to which a distribution of scores cluster around the mean
- leptokurtic more peaked than normal
- platykurtic flatter than normal
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TASTE/GUSTATION
Tip – sweet and salty
Back – bitter
Side – sour
Relays through nucleus of the solitary tract (CN VII, IX, X) in medulla, then to ventral posteromedial
(VPM) nucleus of thalamus, then primary gustatory cortex in anterior insula-frontal operculum, then
secondary gustatory cortex in orbitofrontal cortex
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TESTS OF EMOTIONAL FUNCTIONING AND PERSONALITY
Quality of Life: Satisfaction with Life Scale
Psychiatric Symptoms: Brief Psychiatric Rating Scale (BPRS); Structured Clinical Interview for DSM-IV
(SCID) for evaluation of adults
Projectives – when confronted with ambiguous or unstructured stimuli, people tend to project onto it their
own needs, experiences, and idiosyncratic ways of interacting with the world
Common to brain injured individuals:
- Constriction – responses reduced in size and quantity
- Stimulus-boundedness – reponses stick closely to stimulus
- Structure-seeking – search for guidance or structure
- Reponse rigidity – difficulty shifting, being flexible, and adapting to changes; perseverate
- Fragmentation – respond piecemeal; associated with concreteness and poor organization
- Simplification – poorly differentiated or detailed
- Conceptual confusion and spatial disorientation
- Confabulated responses – illogical or inappropriate compounding of otherwise discrete
percepts or ideas (not the same as memory confabulation)
- Hesitancy and doubt (perplexity) – uncertainty and dissatisfaction
1. Rorschach – interpretation or free association to black and colored inkblots
i. Formal Aspects – number and appropriateness (form quality) of response, content, use of
shape, color, shading and movement (determinants), location, relative size, and frequency of
use of identifiable parts/portions
ii. Content – appropriateness and usualness of perception, repetition and variation,
elaboration, emotional tone, evidence of thought disorder or special preoccupations
Right hemisphere damage – overelaborated, overincorporated, bizarre
Left hemisphere damage – perplexity, card rejection, concrete, unelaborated
TBI – fewer responses, idiosyncratic and poor forms, loose associations, repetitions and
perseverations (stereotypy), concreteness
2. Thematic Apperception Test (TAT) – storytelling to cards to assess thought content, emotions, and
conflicts/needs; beginning, scene, and outcome
Brain injury – fewer words and ideas, long delays, describe picture versus make up story,
respond to discrete elements, poor descriptions, misinterpretations, stereotypy
3. Drawing tasks
Objective Tests
I. Depression
1. Beck Depression Inventory – self report, 21 questions, 0-3 rating
2. Hamilton Rating Scale for Depression – filled out by observer or interviewer
3. Geriatric Depression Scale
4. Children’s Depression Inventory
II. PTSD
1. Penn Inventory for PTSD
III. Psychiatric evaluation
1. Millon Clinical Multiaxial Inventory (MCMI) – state and trait focused (i.e., Axis I and II);
compared against base-rate data
2. Minnesota Multiphasic Personality Inventory (MMPI) – elevations and profile; empirically
derived (empirical criterion keying distinguishing between groups)
1) Hypochondriasis (HS) – somatization; immature, self-centered, complaining, demanding
2) Depression (D) – depressed; pessimistic, withdrawn, slow, timid, shy
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3.
4.
5.
6.
7.
8.
9.
10.
11.
12.
13.
14.
15.
3) Hysteria (Hy) – conversion reaction; immature, egotistical, suggestible, friendly
4) Psychopathic Deviate (Pd) – antisocial; rebellious, resentful, impulsive, energetic,
irresponsible
5) Masculinity-Femininity (MF) – sexual problems
a) Male – fussy, idealistic, submissive, sensitive, effeminate
b) Female – aggressive, dominant, masculine
6) Paranoia (Pa) – paranoid; suspicious, hostile, rigid, distrustful
7) Psychasthenia (Pt) – OCD; worrying, anxious, dissatisfied, sensitive, rigid
8) Schizophrenia (Sc) – schizophrenia; confused, imaginative, individualistic, impulsive,
unconventional
9) Hypomania (Ma) – bipolar; energetic, enthusiastic, active, sociable, impulsive
0) Social Introversion (Si) – withdrawn; aloof, sensitive, inhibited, timid
With Harris-Lingoes Subscales
Validity
L-Scale (Lie) – personal virtue; conventional, rigid, self-controlled
F-Scale (Infrequency) – measures exaggeration; restless, changeable,
dissatisfied, opinionated
K-Scale (Correction) – if trying to present self in favorable way;
defensive, inhibited
Fb (Back Side Infreqeuncy)
VRIN, TRIN (Variable/True Response Inconsistency)
F(p) – psychopathology
S (Superlative)
5 Content Scales – fears, health concerns, type A, antisocial, negative treatment indicator
California Personality Inventory (CPI) – focuses on normal aspects of personality, more to predict
education and vocational achievement; clusters of Self (poise, self-assurance, ascendancy), Other
(socialization, responsibility, character), Intellect, Emotion
Personality Assessment Inventory (PAI) – no overlapping scale items, lower reading level
Profile of Mood States – descriptive adjectives to describe how felt in last week (anxiety,
depression, anger, activity, fatigue)
Sickness Impact Profile – physical, psychosocial, and independence scales
Symptom Check List-90 (SCL-90) – primary symptom dimensions
Brief Symptom Inventory – briefer form of SCL
Child Behavior Checklist (CBCL) – personality, social competency, amd behavior problem
assessment of child through parent or teacher ratings
Personality Inventory for Children – through parent questionnaire (5½-16)
Vineland Adaptive Behavior Scales – social and personal adaptive abilities in daily living (3-18)
Conner’s Rating Scales – for behavioral problems, as rated by parents and teachers (e.g.,
hyperactivity, conduct) (3-17)
Overt Aggression Scale – checklist determining verbal and physical and self- and other-directed
aggression
Edwards Personal Preference Schedule – reflects Murray’s 15 needs
16 PF – Cattell’s factored “primary source traits”
Neuroticism, Extroversion, Openness, Agreeableness, Conscientiousness (NEOAC)
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THALAMUS (“couch” or “bed”)
Sensory-relay nuclei located in the diencephalon, serving as the main relay center for sensory impulses
(all except olfaction) and cerebellar and basal ganglia projections to the cerebral cortex; lesions may
produce sensory deficits, aphasia, executive dysfunction, thalamic pain (burning sensation – treated with
antiepileptic), or memory impairments (retrograde and anterograde, medial - explicit, ventral - implicit)
3 regions divided by Y-shaped structure internal medullary lamina (has intralaminar nuclei) are Medial
(mediodorsal), Lateral and Anterior nuclear groups:
Midline thalamic nuclei
Thalamic reticular nucleus – receives inputs and projects back to thalamus, inhibitory
GABA
Medial geniculate body – to auditory areas in the temporal lobe (Heschl’s gyrus)
Lateral geniculate body – gives rise to optic radiations
Relay nuclei – VA and VL (motor), VPL (somatosensory; spinothalamic through medial
lemniscus), VPM (trigeminal; taste)
Association nuclei – DM (prefrontal), AN (limbic), and Pulvinar (visual) and LP (parietal)
(together part of extrageniculate optic pathway)
See Blumenfeld Figure 7.6, Table 7.3, Mesulum Figure 1-14
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TRAUMATIC BRAIN INJURY (TBI) AND RECOVERY
Brain injury caused by an external mechanical force such as a blow to the head, concussive forces,
acceleration-deceleration forces, or projectile missile; primary causes are MVAs, fall, and interpersonal
violence, but also industrial and sports (boxing, soccer); peak age 15-24, specifically in males, also 0-5
and elderly; see problems in attention, verbal retrieval, nonverbal functioning, emotional distress, fatigue
Open head injury – discrete, focal lesions, higher risk for seizures
Closed head injury – generalized/diffuse cerebral involvement (hyperemia – diffuse swelling)
Risk Factors:
- a single TBI doubles the risk for another, 2 TBIs increases risk 8 fold
- LD/ADHD
- Alcoholism/drug abuse
- Heart disease and hypertension
- Psychiatric illness
- Seizures
- Divorce
- Low SES/education
- unemployment
Neuropathology of closed head injury:
10) Diffuse axonal injury (DAI) – injury to brain tissue associated with rotational forces and
acceleration-deceleration, produced mechanically by shearing strains between brain tissue of
differing densities (breaking, shearing, or stretching of myelinated axons; may have brain
shifting/herniation) and neurochemically by released cytotoxic factors (e.g., free radical) and
changes in glucose transport and blood flow; prominently at the junctures between gray matter
and white fiber tracts; causes widespread or patchy damage to white matter and cranial nerves
11) Focal or subcortical contusion – injury associated with coup-contrecoup, depressed skull fracture
(protrusion of bony fragments into the dura and brain, causing laceration of the dura and
underlying cortex), rotational or inertial forces causing local abrasion (tearing hemorrhage,
swelling edema); areas susceptible include orbital frontal and inferior anterior temporal
12) Hypoxic-ischemic injury – due secondarily to physical/chest injury or obstructed airway, may
also have fat emboli from fracture, increased intracranial pressure from edema; impaired memory
due to hippocampal injury, white matter degeneration, and hydrocephalus (from disturbed CSF
flow)
13) Hemorraging – petechial (small spots of blood in white matter) and intracranial
Degenerative events:
1) anterograde/orthograde/Wallerian degeneration – degeneration of severed axon and myelin sheath
2) astrocyte activity – invade to remove debris, may seal or scar area
3) calcification – large deposits where neural degenertion takes place
4) chromatolyses – color dissolution (cell Nissel substance breaks down), so no stain uptake
5) gliosis/sclerosis – scarring associated with hyperplasia glial overgrowth/replacement of cell bodies
by glial cells
6) necrosis – localized death of individual or groups of cells
7) phagocytosis – removal of dead cells by mitochondria and astrocytes
8) retrograde degeneration – death of remaining axon, cell body, and dendrites after being severed
9) terminal degeneration – shrinkage/degeneration of terminals after axon severed
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10) transneuronal degeneration – death of neurons that innervate/are innervated by damaged or
destroyed neuron
11) free radicals – cytotoxic substances characterized by unpaired electrons in outer orbits released by
trauma; particularly toxic to neural tissue; oxidants (e.g., hydrogen peroxide)
12) cicatrix – scarring of the brain, consisting of both vascular and glial components
Associated Physiological events:
1) diaschesis – temporary loss of functioning produced by acute focal brain damage in an adjacent
region or region connected through fiber tracts
2) shock – cells everywhere show temporary depression when input removed (e.g., spinal)
3) edema – excessive water accumulation resulting in tissue swelling and increased intracranial
pressure
- vasogenic  accumulation in the extracellular space
- cytotoxic  impaired neural and glial membranes allow excess water to diffuse into cells
4) blood flow – decreased CO2, decreased flow, decreased metabolic activity; overall decereased
brain activity
5) neurotransmitter release – levels change
6) glucose uptake – decreased metabolic activity
7) changes in electrical activity – can be index of posttraumatic function
8) autoneurotoxicity – delayed tissue death following oxygen deprivation overexciting cell and
increasing release of glutamate
9) infection
10) epilepsy
11) obstructive hydrocephalus
Recovery and compensatory techniques – an alternate means of task performance when preferred
approach is more difficult or impossible
1. Spontaneous recovery – due to resolution/absorption of hematoma, decreased swelling,
normalization of blood flow, return of metabolic/electrolyte/neurochemical balance
2. Axonal growth – regeneration of neural elements (axonal or collateral sprouting)
3. Behavioral compensation – use of a new or different behavioral strategy
4. Collateral sprouting – the growth of collaterals of axons to replace lost axons or to innervate
targets that have lost other afferents
5. Denervation supersensitivity – the proliferation of receptors on a nerve or muscle when
innervation is interrupted that results in an increase in response (hypersensitivity) when residual
afferents are stimulated or when chemical agonists are applied, resulting in partial sparing or
restoration of function
6. Diaschesis (von Monakow) – recovery following temporary disruption of functioning in areas
adjacent or connected to the primary damage, so inhibited functions slowly reemerge (i.e.,
reestablishment of unimpaired neurological systems)
7. Disinhibition – removal of inhibitory actions of a system (by destruction or pharmacological
blocking)
8. Equipotentiality – nonlocationalization (Lashley)
9. Functional compensation – behavioral modifications
10. Functional reorganization – intact portions of the nervous system reorganize their inputs and
outputs after injury to take over lost functions subserved by damaged tissue
11. Hierarchical representation – function represented at several levels and damage at higher levels
releases lower ones from inhibition and leads to compensation (see with multiple sensory
damage)
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12. Nerve growth factor (neurotrophic) – a protein that may be secreted by glial cells that promotes
growth in damaged neurons and facilitates regeneration and reinnervation
13. Plasticity – neural and/or behavioral resilience through alteration in structure or function (cortical
reorganization)
14. Regeneration – process by which damaged neurons, axons, or terminals regrow and establish
their previous connections; more in PNS (do not see full cell regrowth)
15. Rerouting – process by which axons or their collaterals seek out new targets when their normal
destination has been removed
16. Silent synapses – a hypothetical synapse that is thought to be present but whose function is not
behaviorally evident until the function of some other part of the system is disrupted
17. Sparing – a concept that refers to a process that allows certain behaviors to survive brain damage
(Kennard principle – sparing of function following infant lesions)
18. Sprouting – growth of nerve fibers to innervate new targets, particularly if they have been vacated
by other terminals
19. Substitution – the idea that an unoccupied or underused area of the brain will assume functions of
a damaged area; could be redundant or duplicate (not popular theory) (Pavlov, Lashley, Bucy)
20. Transient collaterals – collaterals that at some time during development innervated targets that
they subsequently abandon as development proceeds
21. Vicaration – functions of damaged areas assumed by adjacent areas (not popular theory)
Variables affecting recovery – lesion size, age, sex (females less lateralized), handedness (left less
lateralized), intelligence (although absolute loss may be equal), personality (optimistic, extroverted, easy
going)
Secondary Impact Syndrome – a condition in which the second of two independent mild head
injuries/concussions over brief periods of time produces greater impairment than would be expected from
the cumulative effects of both injuries; typically follwing initial brain injury while still symptomatic;
observed in contact sports; rapid deterioration associated with loss of autonomic regulation of blood
vessel diameter, with increased blood volume causing increased intracranial pressure, diminished cerebral
perfusion, and brain herniation
Measuring severity:
1) Level of consciousness – alert, lethargic, stuporous, comatose
2) Glasgow Coma Scale – eye opening, motor response, verbal response (3-15)
 Mild (13-15) – loss of consciousness <20 minutes, post-traumatic amnesia <24 hours, no focal
neurological deficits, no focal radiological evidence of injury (~80% of nonfatal TBI)
 Moderate (9-12)
 Severe (3-8)
3) Glasgow Outcome Scale – good recovery, moderate disability, severe disability, persistent vegetative
state, death
4) Duration of LOC/coma
5) Duration of post-traumatic amnesia (PTA) – period of anterograde amnesia in which new memories
cannot be consistently made and recalled; best predictor of recovery; usually 4x length of coma
<5 minutes, 5-60 minutes, 1-24 hours, 1-7 days, 1-4 weeks, >4 weeks
very mild
mild
moderate severe very severe extremely severe
6) Oculovestibular response/“caloric testing” – automatic eye movements elicited by injecting ice
water into the ear of a comatose patient; no response predicts poor outcome
Cognitive deficits – often see bigger PIQ than VIQ decline (speed); greatest recovery in first 6-9 months;
social interaction and personality often greatest change
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1) mild – attention, verbal retrieval, emotional distress, fatigue, depression
2) moderate – headache, memory problems, difficulty with everyday living, frontal/temporal
damage
3) severe – cognitive, emotional, and exective dysfunction (also anomia, pragmatics), social
isolation, social dysfunction
Sensory changes – anosmia, vision (acuity, field, oculomotor, diplopia, photophobia), dizziness, poor
balance, hearing deficits (tinnitus)
Rehabilitation – activities designed to facilitate and maximize recovery of function following injury and
to maximize accommodation to functional disabilities and handicaps
Cognitive rehabilitation/remediation/retraining – any systematic program directed at modifying cognitive
function following acquired brain injury; the restorative approach reinforces previously learned
patterns of behavior, the compensatory approach establishes new patterns of cognitive activity for
impaired systems
Task analysis – a rehabilitation procedure in which the physical, cognitive, and social demands of a
complex task are analyzed to identify the source of breakdown to target interventions
Community re-entry – model of outpatient rehabilitation emphasizing the resumption of community roles
rather than restoration of specific skills
Goals of memory rehabilitation – completed through exercises, external aids, mnemonic strategies,
spaced retrieval, errorless learning, vanishing cues
1. restoration of damaged function
2. compensation for lost function
3. optimization of residual function
4. substitution of intact function
rehabilitation should include early stimulation, forced use, extensive and excessive practice, relevance to
daily life, include family members, continue training after plateaus, break down into simple components
According to the WHO:
Impairment – a loss or abnormality of structure or function at the level of tissue or organ that can lead to
disability
Disability – the restriction or inability to perform a skill or activity that results from pathology or
impairment and may turn into a handicap
Handicap – a disadvantage for an individual on account of a disability that prevents the fulfillment of
expected social roles
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VASCULAR SUPPLY
Only 25-50% have complete Circle of Willis – ring or arteries surrounding the optic chiasm and pituitary
stalk, consisting of the Anterior Connecting Artery and two Posterior Connecting Arteries;
can have alternative paths (anastomoses)
Fistula – an abnormal communication passage from normally separated regions
Vertebral – posterior
- Basilar artery – bifurcates to two PCAs
 PCA – supplies the thalamus, hypothalamus, posterior internal capsule, cerebral
peduncles, choroid plexuses of the lateral and third ventricles, temporal and occipital
lobes, midbrain (paramedian penetrating branches and long and short circumferential
pontine); produces contralateral homonymous hemianopia, sensory loss, hemiparesis,
thalamic aphasia, alexia without agraphia; occlusion of a branch can lead to cranial nerve
palsy or contralateral hemiparesis; total occlusion can lead to coma or locked-in
syndrome
Carotid - anterior
- Carotid Artery – bifurcates to form ICA and ECA (external)
 ICA (two branches) – bifurcates into ACA and MCA; ICA occlusion appears as MCA
plus ipsalateral ocular symptoms
 ACA – two main branches (pericallosal and callosomarginal arteries, plus
frontopolar and orbital) that supply blood to dorsolateral and mesial frontal
regions, medial parietal lobes, sensorimotor cortex for lower body, anterior basal
ganglia and internal capsule; typically produce lower extremity sensory loss and
weakness, grasp reflex, flat affect, impaired judgment, apraxia, abulia,
incontinence, motor impersistence, alien hand syndrome, pseudobulbar palsy;
bilateral occlusion causes apathy, confusion, mutism, spastic paraparesis
 MCA – superior (above Sylvian fissure: lateral frontal, Broca, face and arm),
inferior (below Sylvian fissure: lateral temporal, lateral parietal, occipital), and
deep (internal capsule and basal ganglia) (stem refers to all 3); damage
(infarct/ischemia) most common because of supply area; supplies temporal lobe,
thalamus, striatum, and insula (have gaze preference towards side of lesion); face
and arm sensorimotor cortex; hemiparesis, hemisensory loss, homonymous
hemianopsia; left - aphasia, right - neglect, anosagnosia, dysprosody
- ACommA (one) – connects the two ACA
- PCommA (two) – connects the PCAs to anterior supplies
- Thalamoperforator arteries (off PCA) – supplies thalamus and sometimes posterior limb of
internal capsule
- Recurrent artery of Heubner (off ACA) – supplies head of caudate, anterior putamen, globus
pallidus, and internal capsule
- Lenticulostriate arteries (off MCA) – small penetrating arteries supplying the lentiform nucleus
and striatum (basal ganglia and internal capsule); narrowing or rupture (lacunes) seen in
hypertension
- Anterior Choroidal Artery (off ICA) – supplies choroid plexus, hippocampus, amygdala, caudate
nucleus, thalamus, globus pallidus, putamen, and posterior limb of internal capsule
Anterior Communicating Artery Syndrome – anterograde amnesia, disorientation, confabulation, and
attentional and behavioral disturbances (distractibility, perseveration, and utilization behavior)
Middle Cerebral Artery Syndrome – face, arm and leg weakness, field cut, left – aphasia and
right – neglect
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Vertebrobasilar insufficiency – forgetful, poor concentration, attacks of transient global amnesia
Watershed zones – border zone of anastomoses (anatomical connection of one set of blood
vessels to another) between the territories of two major cerebral arteries; these areas as
well as contiguous distal branch territories of the arteries involved become infracted with
reduced supply of oxygen from hypotension, anoxia, or CO poisoning; see proximal arm
and leg weakness (“man in the barrel” syndrome, ACA-MCA), transcortical aphasia
(dominant, MCA-PCA), higher-order visual processing (nondominant, MCA-PCA)
Calcarine artery – feeds visual cortex
See Blumenfeld Figures 2.26, 10.3-10.9, 14.17-14.19, Table 10.1, Darby & Walsh Figures 2.29-2.35,
Goldberg Figure 10
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VENOUS DRAINAGE
Superficial veins drain into superior sagittal sinus transverse sinus sigmoid sinus jugular vein and
cavernous sinus superior petrosal sinus inferior petrosal sinus (or transverse sinus)  internal
jugular vein
Deep veins (anterior cerebral and deep middle cerebral) drain into internal cerebral veins  basal veins of
Rosenthal great vein of Galen
Great vein of Galen + inferior sagittal sinus  straight sinus/sinus rectus
Torcula (torcular Herophili) – meeting of superior sagittal (right), straight (left), and occipital sinuses
Inferior anastomotic vein of Labbe  transverse sinus
Superior anastomotic vein of Trolard  superior sagittal sinus
Superficial middle cerebral vein  cavernous sinus
All reach internal jugular veins
Sagittal sinus thrombosis – increased frequency in women pregnant and immediately post-partum, leads
to elevated ICP
Empty delta sign – dark region on imaging suggests filling problem
See Blumenfeld Figure 10.11
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VISION
Image from lens falls onto retina (hits sclera first), primary area fovea in which the center of gaze is
projected (greatest visual acuity and innervation of retinal neurons), surrounded by macula
Axons leave retina via optic disc to optic nerve (blind spot) past optic chiasm to optic tract then most
through lateral geniculate nucleus (LGN) of thalamus then optic radiations to primary visual cortex/striate
cortex; some through extrageniculate pathway from optic tract to brachium of superior colliculus/pretectal
area to pulvinar and lateral posterior thalamus to brainstem and association cortex (lateral parietal, frontal
eye fields)
Most information (magnocellular and parvocellullar) arrives at cortical layer 4 (4B – stria of Gennari, a
thin, myelinated tract running horizontally in the granular layer of the cortex) of primary visual cortex
(area 17) forming ocular dominance columns; ~25% devoted to analyzing information from fovea
Prestriate cortex – the visual association cortex adjacent to the primary visual (striate) cortex
Information processing by visual association cortex (areas 18 and 19) and higher-order association cortex
via dorsal “Where?” stream and ventral “What?” stream
Bitemporal hemianopsia – loss of outer halves of both visual fields from damage to crossing fibers at
optic chasm, usually associated with pituitary tumors
Photoreceptors:
Rods (120 million) – for gray and at periphery; low-level lighting (dopsin), low temporal resolution,
lower acuity
Cones (6 million) – for color and in center; high spatial and temporal resolution and detect colors
(rhodopsin); greatly represented in fovea
photoreceptors connect to inhibitory/excitatory bipolar cells (and horizontal) and then ganglion cells
forming optic nerve (M – gross and large movement, project to magnocellular layers; P fine detail and
color, project to parvocellular layers) (and amacrine) – center-surround inhibitory-excitatory contrast
pattern (on-center excited by light, off-center inhibited by light)
Photoreceptors and bipolar cells have passive conduction; ganglion cells have action potentials
Effective visual field – portion of the visual field in which letter recognition is possible
Diplopia – double vision
Scotoma – a discrete area of poor vision or blindness within the visual field, generally circular or oval
Papilledema – blurring of the margins of the optic disk resulting from increased intracranial pressure
Papillitis – inflammation of the optic nerve where it enters the eye; typical with MS
Pseudoachromatopsia – performance failure on color vision tests for reasons other than poor color vision
or discrimination (e.g., apraxia, neglect)
Scintillation – an illusion in which there are sparks, flashes of light, or glitterings in the peripheral visual
fields; associated with seizures or migraines
Size constancy – a perceptual process that allows a stimulus to be perceived as approximately the same
size despite variations in its proximity
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Visual field defects – areas of blindness or altered vision within the visual field; caused by lesions of the
retina, optic nerve and tract, lateral geniculate body, geniculocalcarine pathway, and striate
cortex of the occipital lobe
- Quadrantanopsia/quadrantanopia – defective vision or blindness in one quadrant of the visual
field; superior quadrantanopsia is associated with lesions of the contralateral temporal lobe,
inferior quadrantanopsia is associated with lesions of the contralateral parietal lobe
- Hemianopia/hemianopsia – loss of vision for one-half of the visual field or either one or both eyes
- Homonymous hemianopsia – hemianopsia affecting the analogous right or left halves of the
visual fields of both eyes
Meyer’s/Meyer-Archambault loop – fibers from lateral geniculate nucleus, over temporal horns of lateral
ventricles, into temporal lobes that forms part of the optic radiation; lesions produce contralateral
superior homonymous quadrantanopsia
Impaired blood flow in opthalmic artery due to emboli, stenosis, and vasculitis
Abducted – moving toward temple
Adducted – moving toward nose
Saccades – rapid, conjugate eye movements, bringing target of interest from periphery into center of
vision; governed by supranuclear centers; can be voluntary (700/sec) (frontal eye fields)
Smooth pursuit – smooth, steady, tracking movements stabilizing viewing of moving objects; governed
by pontine conjugate gaze centers; involuntary (100/sec)
Vergence – eye movements maintaining fixation by both eyes on target moving away or close (20/sec)
Nystagmus – rhymic eye movement with slow movement in one direction interrupted by fast
saccadelike movements in opposite direction; caused by lesions in the cerebellum, brainstem, or
vestibule; associated with alcohol, Dilantin, and barbiturate intoxication, ischemia of
vertebrobasilar artery, MS, Wernicke-Korsakoff, viral labyrinthitis, internuclear ophthalmoplegia
Optokinetic nystagmus – normal, involuntary rhythmic eye movement induced by looking at moving
stimuli, follow as long as can and then move in opposite direction; not present with parietal lobe
lesions (can be used to infer psychogenic blindness)
Photic stimulation – stroboscopic stimulation of light (1-20 per second) to elicit seizure, determine
malingered or hysterical blindness (EEG occipital detection), damage to geniculocalcarine
pathway between thalamus and occiptal lobe (evoked response unilaterally), or disease in optic
nerve (delay in evoked response usually occurring 20-30msec after)
Cerebral conjugate gaze center (frontal lobe eye fields) – pushed the eye to the opposite side
Pontine gaze center (pontine paramedian reticular formation-PPRF) – pulls the eyes to own side
Need ipsalateral CN VI (abducens) and contralateral CN III (oculomotor), connected through MLF for
conjugate lateral eye movement
Dysconjugate gaze – inability of both eyes to move together in alignment; the result is an uncoupling of
the fixation point, causing diplopia; caused by congenital disorders, injury to the brainstem or
cranial nerves that control extraocular muscles, or disease of extraocular muscles
Sunset gaze sign – an inability to look up, with the pupils appearing to be “setting” in the lower lid; may
accompany increased intracranial pressure
Gaze palsy – paralysis of gaze
- lateral gaze palsy – eyes typically deviate toward the side of the lesion and is associated with
acute lesions, more common and more severe after right than left cerebral injury
- vertical gaze palsy – eyes unable to move vertically, associated with damage to CN IV, the
tegmentum or PSP
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Frontal eye fields generate saccades in contralateral direction
Parieto-occipito-temporal cortex responsible for smooth pursuit in the ipsalateral direction
Basal ganglia modulates control of eye movement
Cerebral hemisphere damage leads to gaze preference toward side of lesion and away from side of
weakness (in seizures may also activate frontal eye fields and cause gaze towards weakness,
“wrong-way eyes”, also seen in thalamic hemorrhage and lesions of pons and tegmentum)
Motion blindness – bilateral lesions in posterior parietotemporal and occipital regions
Transient monocular/fleeting blindness (amaurosis fugax) – usually by emboli from carotid stenosis
blocking retinal arterioles (ICA)
Cortical (psychic) blindness – loss of vision due to occipital lobe damage or subcortical bilateral lesions
in optic radiation, most frequently from bilateral infarction of PCA; pupillary reflexes are
preserved, nystagmus not elicited, no visual evoked potentials, Anton’s syndrome common
Argyll-Robertson pupils – irregular, asymmetric, small pupils; accommodate but do not react (i.e., “like
prostitute”) to light; commonly from diabetic autonomic neuropathy and cataract surgery, syphilis
Pontine pupils – bilateral lesion of pons causing small pupillary size that are reactive to light
“Blown pupils” – lesion of efferent parasympathetic pathway from Edinger-Westphal nucleus to
constrictory muscle (CN III)
Illusions:
1) metamorphopsia – shape/size (micropsia, macropsia), form (dysmorphopsia), color,
movement distorted
*occipital or parietal occipital lobes, more often right sided
2) spatial – distorted perspective/depth
*lesions of tegmentum or brainstem (vestibular pathway)
3) palinopsia – persistence or reappearance of a recently viewed object
*associated with parietal and occipital lobe lesions
4) polyopia – perception of multiple images when viewing a single object
* usually parieto-occipital lesions
5) visual allesthesia – image is transposed from one field to the opposite, usually defective
field
6) oscillopsia – perception of back-and-forth movement of stationary object (due to
nystagmus)
7) visual synesthesia
8) erythropsia – unnatural coloring of visual field; with digitalis toxicity see yellowish halo
9) visual reorientation – environment appears tilted or inverted
10) cerebral akinetopsia – inability to perceive moving objects
11) Bonnet syndrome/Charles Bonnet hallucination – complex visual hallucinations in
elderly (usually) people without evidence of mental deterioration; associated with poor
vision
Vision Theories
Young-Helmholz trichromatic – red, blue, green receptor in retina
Hering’s opponent-process – red/green, yellow/blue white/black; excitation of one inhibiting the other; in
thalamus
Snellen chart – a test of visual acuity that contains a chart of printed letters of differing sizes
See Blumenfeld Figure 11.15
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