Emotion
Role of amygdala in emotion:
 Involved in:
o Recognition of threat-related stimuli
o Acquisition of fear-condition responses
 Fast responses
o Automatic processing
 AMY responses larger in LH response to fearful faces
Relationship of Amyg and hippo:
 Fear conditions – neural w/ noxious stimulus…condition fear
resp to neutral stimulus
o Disassociation b/w hippo and amyg:
 Damage only amyg: no fear conditioning but
the experience is remembered
 Damage only hippo: fear condition but
experience is forgotten
o Don’t need cerebral cortex
 Fear conditioning without CS and NS pairing:
o Experiment “instructed fear” …told participants that a stimulus would be paired
with a shock
 Activates fear network (Amygdala, insula, striatum, anterior cingulate,
premotor cortex)
 Skin conductance response
Relationship of Amyg to memory:
 Sometimes: amyg increase = retention of declarative info improves
o not always true though
 example memories of 9/11 inaccurate
 effects of recall on info storage in LTM
Does amyg respond to other emotions? – 19 slide 8
 Task irrelevant sad probe images during simple target detection task
 Yes?
Effect of mood on amyg activity:
 Mood disorders = biased perception and memory for sad events
 Mood manipulation Experiment:
o Prior to run either happy or sad movie clip
o Amyg activation by sad distractors is greater when mood is also sad
o Mood effect on sad distractors = large in both hemisphers
o Mood change specially modulated response to sad distractor
o Sad distractors enhanced by sad mood in:
 Ventromedial prefrontal cortex
 Anterior cingulate gyrus
 Retrosplenial cortex LH
 Insula
 Posterior regions
Can you override amyg activation?:
 Oxytocin- neuropeptide underlies social interactions (attachment and social
recognition)
o Reduces fear response
4 hypothesizes:
1) RH
a. Emotion processed predominantly in RH
2) Valence
a. Processing neg emotions = RH dominant
b. Processing pos emotion = LH dominant
3) 1 network
a. all emotions are processed by a set of brain regions
b. not specific to a respective emotional category
4) Localist
a. Processing of different emptions corresponds to
activation in distinct brain networks
Constructionist Approach:
?????????
Emotional Face Processing:

Amygdala and
orbitofrontal cortex receive visual informal from:
o cortical regions (face sensitive regions in fusiform gyrus
and posterior superior temporal sulcus
o faster magnocellular pathway directly from the early visual
cortex
o subcortical collicular-pulvinar pathway (just to amyg)

amyg and OFC reciprocally connected and send feedback projects to visual areas
including fusiform gyrus and STS
Role of amyg damage on face perception
 face identification intact
 impairment of fearful face identification (NOT sad face though)
Development
Development Requires:
 Input
 Behavior
 Experience
Infancy Structural Changes
 1st 2 years cranial fissure closes
 changes in white and grey matter
o due to methylation
Sensitive Periods
 development periods where experience affects developmental outcome
 multiple periods—why? Develops at different rates?
o In vision: for acuity vs face perception and for dorsal vs ventral stream
development—slide 30 day 19
Teratogens:
 Agents that can cause defects to the central nervous system
o Agenesis: Organ doesn’t development
o Genesis: Organ develops abnormally
 Agents Examples:
o Lead
o Alcohol
o Mercury
o Rubella
o Thalidomide
 Timing determines the extent of damage
o Later damage = limited to specific cellular components
o Most vulnerable 2 - 8 gestation weeks
 Either sudden embryo abortion or infant dies @ birth
o 1-2 weeks: zygote division period
 damage = prenatal death
 not susceptible to teratogens
o 3 -7 weeks: embryonic period
 major structural abnormalities
o 8 - 36 weeks: fetal period
 physiological defects
 minor structural abnormalities
Experience Dependent Plasticity:
 when brain is exposed to unprimed experiences, new synapses form


development through these new synapses…acquisition of new skills (like driving)
can occur anytime but synaptic formation will be greatest if it occurs earlier in
development
Experience Expectant Plasticity:
 brain is primed (through evolution) to expect experiences
 expected experiences activate particular synapses
o normative development
o likely involves synaptogenesis and pruning process
 limited to early periods of development
Visual Acuity- slide 6 20
 40x worse in newborns than adults
 due to immature retinas (not so much optics of lens and eye)
o poor acuity is true regardless of distance
o ganglion cells need time to develop
 cones to elongate and migrate to fovea (start off sparsely packet and
short/stumpy)
 color vision poor as well
Grating Acuity – slide 8 20
 reaches adult like levels @ 4-6
Congenital Cataracts
 proteins clump --> cloudy lens
 only light input, no pattern
 can be surgically removed
o still requires correct lenses for 20/20 vision
Acuity Recover :
 1 hour of input:
o acuity of a normal 6-week-old
o dependent upon experience
 cover 1 eye for bilateral…it will not recover
 1 month of input:
o acuity improves, eventually catches up w/ normal development
 only if removal occurs by 9 months
 1 year of input:
o acuity falls within normal limits
o development happens faster than normal babies…does not surpass them
though
o in unilateral recovery dependent on patching stronger eye
o if surgery occurs after 2 months: this recovery = NOT TRUE
 overall: rapid improvement
Bilateral vs Unilateral Cataracts
 faster improved in bilateral
o need competition between eyes


ocular dominance columns require competitive input to function
properly
 stronger eye will take over neural tissue of weak eye
 effect of pruning
o balance restored by patching stronger eye
in bilateral…global motion sensitivity is compromised more
Timing of Cataract Surgery
 healthy input is crucial until 10 yrs old
o fast and early treatment is essential if cataracts develop before 10
o this is after reaching adult levels at 7
Ways Visual Experience can affect Later Development:
1. prevent deterioration of existing neural networks
2. Reserving neural networks for later refinement
3. Allowing a developmental trajectory to start from an optimal place
4. Allowing recovery from earlier deprivation, possibly via the recruitment of alternate
pathways
5. Allowing the refinement of previously established structures
Language Milestones
 Babbling – 6 months
 Word Comprehension – 9 months
 First word – 10 -13 months
 2-3 words – 18 -24 months
 girls tend to reach these milestones before boys
o large variability across individuals
Vocab Development Stages
 Early Stages
o Slow, may take months to learn 30 new words
 By 18 months
o 50 word vocab
 By 6 years
o Learn 10 new words a day (18 month – 6 yr)
o 14,000 word vocab
 By 18 years
o Up to 20 new words a day (6 -18 yrs)
o 60,000 word vocab
Mills Ex
 vocab development drives lateralization
 ERPs of known vs unknown words in 13-17 month olds and 22 month olds
o younger = bilateral
o older = lateralized

LH asymmetry due to age maturation or vocab size? - Divide 13-17 into high and low
comprehenders – 32 20
o P100: only high comprehenders have LH asymmetry
o N200:
 no asymmetry yet
 only high comprehenders show reliable known v unknown effect in more
anterior electrode sites
 refinement of network underlying the process
Effect of Vocab on LH asymmetry
 tested 19-22 month olds
o dominant and non-dominant languages
o each language, known and unknown words
 By 20 months early brain responses show LH lateralization for known spoken words
 In younger babies, larger vocabs had earlier appearance in LH asymmetry for known
words
o Also true with bilingual: dominant lateralized earlier than non-dominant
language
Hemispherectomy data
 Epileptic Children w/ seizers causing cell death
o Remove 1 hemisphere
o Allows up to compare for language
 After LH removal, RH takes over language functions—for kids who already developed
language functions in LH
 Motor Control issues—for kids who already had language functions in LH
o RH secondary and somatosensory cortex takes over LH motor behavior…too
much competition for speech to establish good representation
o Plasticity required for fine grained motor control needed for speech no longer
available @ the ages kids had surgery
LH Lesions
 More Delays w/ expressive language
o Biggest delays if lesion is more posterior
o Language functioning lower end of average range
RH Lesions
 More delays w/ comprehension
 Also issues w/ gestures and in discourse
Detecting Differences by 7
 Nearly impossible to detect difference in RH/LH and anterior/posterior
4 major themes of Language Organization
1) LH specialization: linguistic tasks
a. After 5-7 LH not distinguishable from RH lesions
2) Left Frontal Specialization: expressive language (Broca’s Hypothesis)
a. Turns out to be irrelevant if it’s left or right frontal lesion
3) Left Temporal Specialization: receptive language (Wernicke’s Hypothesis)
a. After 5-7 LH not distinguishable from RH lesions
4) RH specialization: some discourse functions
a. Slower development for RH lesion patients in using complex syntax
Spatial Cognition
 Left: issues w/ encoding parts and details of spatial patterns
 Right: pattern integration
 Both produce some evidence of hemifeild neglect
Rey-Osterrieth Figure
 Jumbled up image
 Reproduce image by breaking down into units (do one sections, fill in details, go to next)
 Pulls apart different visuospatial skills:
o copying v memory
o attention to detail v global form
o attention to left v right image
Rey-Osterrieth Figure Results
 copying: both lesions had accuracy issues
 memory: RH stroke kids had more issues w/ detail and elements than LH
o as they get older this issue is resolved
 placement: LH kids show more deficits
o as they age, the issue is resolved
Williams Syndrome:
 Cause: detection of genes in chromosome 7
o Ex: Gene for Elastin
 Protein in cellular tissues of arteries
 Absence likely accounts for cardiovascular issues
 Up until 20 yrs ago was diagnosed by physical and psychological anomalies
o Now diagnosed by FISH (fluorescent in situ hybridization)
Incidence of WS:
 1 out of every 20,000 to 50,000 have it – extremely rare
 equal representation in men and women
Characterization of WS:
 facial abnormalities
 severe intellectual impairment
 uneven cog prof
 low visuospatial skills
 atypical brain activation
WS includes:
 moderate mental retardation
o evident in higher order con
 hypersensitive to sound
 gregarious personality
 affinity for music
 relatively preserved auditory and verbal memory
 elfin appearance
 hypercalcemia
 cardiovascular anomalies
Elfin:
 broad puffy eyes
 small pig nose
 broad nasal bridge
 full cheeks
 prominent lips and ears
 wide mouth
 small widely spaced teeth
 face typically narrows as one ages
Cardiovascular Abnormality aortic stenosis:
 narrowing of the aortic walls
 other atrial systems affected
Hypercalcemia:
 feeding disturbances
 chronic ab pain
 vomiting and all that fun shit
Hyperacusis:
 sensitivity to sound
 young: easily startled
 older: hear things other ppl don’t…hella sensitive
WS activity:
 super active
 easily distracted
Hypotonia:
 younger
 low muscle tone
 delays in motor development
Hypertonia:
 older
 high muscle tone
WS brain abnormalities:
 reduction of volume – 20% smaller
o white matter
o grey tracts in right occipital lobe
o greater loss occipital
posterior
 temporal limbic area, superior
cerebellum, frontal lobe, and
 abnormal auditory cell
neuronal size in temporal
o hyperconnectivity of
partial than anterior
temporal areas,
most grey matter = fine
packing density and
lobe
auditory cortex
o relatively spared auditory functions
o hyperacusis
WS Cognitive Profile:
 development milestones = later
o walking
o eating – hypercalcemia
o talking
o 2 3 word utterance
 after this, language development proceeds more rapidly
 outplaces kids with DS
WS Language Strengths:
 more advanced than expected*
 word development
 phonological (sound) processing
 auditory short and working memory
 verbal fluency
 can produce embedded clauses in elicited speech
WS Language Issues:
 development of semantics
 pragmatic language
 comprehension of nonliteral language
 complex syntax in receptive language (embedded clauses)
WS Facial Processing (general idea):
 spend hella time focusing on faces
 local, not global
 used for identification, not recognition
 slower processing, only slightly less accurate
WS Facial Processing Similarities w/ Typical:
 typical right fusiform activation is intact
 no difference in amygdala activation
WS Facial Processing Differences w/ Typical:
 structures w/ greater activation to faces in WS:
o frontal, middle temporal
o hippocampus
o thalamus
 structures w/ greater activation to faces in
normal ppl:
o left fusiform gyrus
o cuneus
o occipital
Amygdala Activation in WS:
 heightened = positive social stimuli
 absent/low = negative social stimuli
Autism general:
o impaired social relatedness and language development, presentation of unusal,
repetitive, or stereotypical behavior
o many diagnostic criteria doesn’t appear until 2…later diagnosis = later treatment
ASP Prevalence/Incidence:
o Until recently, ASD was an extremely rare developmental disorder
 relatively stable at 4 in 10,000
 1 in 68 (14.6 per 1,000) school-aged children (March,2016)
o Much more frequent in males
 Ratio of roughly 3.9 affected males to 1 affected female
o If the true risk of a condition increases over a short period of time, it implies
changes in nonheritable risk factors – changes in genetic risk factors take
generations to impact trends.
ASD Why the rise in incidence/prevalence?
 Changing diagnostic criteria over time
 Lack of rigor in clinical diagnoses
 Overdiagnosis in young toddlers?
 Increase in frequency of diagnosis
 Change in method of classification in public health and education
 New etiology/etiologies?
Behavioral symptomatology
 qualitative impairment in social interaction (at least two symptoms)
o limited awareness/interest in the needs, distress, or presence of others
o emotionally removed
o cant share activities
o don’t understand social convention
o impaired empathy
o limited social skills
o awkward/stereotypical response
 qualitative impairments in communication (at least one symptom)
o issues with language comprehension/expression
o no pretend play  impaired communication skills
 restricted repetitive and stereotyped patterns of behavior, interests and activities (at
least two symptoms)
o preoccupied with specific areas of interest
o needs everything to be the same
o stereotypic body movements or abnormal posture
 Gaze perception:
o Don’t tend to look at others’ eyes
o But – can use direction of gaze as an attentional cue
 Face perception:
o Is atypical in individuals with AUT:
o
o
o
o
o
don’t show an “inversion effect”
Process faces on the basis of individual features, not as a whole unit
Weaker @ recognizing or discriminating face identity
poor at discriminating different facial expressions
Reduced fusiform gyrus activity:
 may be bc they spend less time fixating on eyes
Language ASD:
 Symptom that typically leads to diagnosis is delay or absence of speech onset
o This affects age at diagnosis
 Echolalia – repetition of overheard speech
o AKA telegraphic speech
 Neologisms—word inversion
 Deficits in social perception have negative consequences for language learning
 Deficits in joint attention
Early brain development ASD:
 Smaller head/brain size at birth (Courchesne et al 2003)
 Larger head/brain size from infancy to early childhood, ~10%
 Followed by disordered pruning processes, so that brain size is smaller by adolescence
 Unknown cause: maybe genes that control timining for growth and pruning are fucked,
maybe neurotrophins and neuropeptides are fucked
 Both gray matter & white matter affected
 Frontal cortex is site of greatest changes
White matter connectivity ASD:
 less well-developed long-range fiber tracts (hypoconnectivity)
 Involves long-range connections between temporal and frontal cortices (arcuate &
uncinate fasciculi) and limbic system
o Disruptions in language
development?
o Reduced integration of functions?
Cognitive Development ASD:
 Cognitive profile of ASD is uneven
 Higher the intelligence, less autistic
 Visuospatial skills approach typical levels
 Numerical skills at typical levels
 Attentional vigilance can exceed typical
levels
 Deficits in communication & social
behaviors
 Issues with higher level conceptual processes
Treatment approaches: EARLY INTERVENTION = BETTER OUTCOMES
 Intensive one-on-one intervention
 Involves operant and classical conditioning techniques – applied behavioral analysis
o Aimed directly at the behavioral symptoms





Teaching, reinforcing social engagement
Imitation of social engagement
Teaching, reinforcing language use and expression
Extinction, substitution of stereotypies
Target high risk groups
Cognitive Development in DS WS ASD
Disease
Profile
Receptive
Language
Expressive
Language
Visuospatial
skills
Numerical
skills
Face
Perception
Social
Cognition
Vigilance
Exec
Functioning
below
Musical/
auditory
memory
N/A
DS
flat
below
below
below
below
N/A
N/A
N/A
WS
Uneven
uneven
Slight
below
below
below
ASD
Slight
below
below
below
typical
above
N/A
N/A
N/A
Slight below
typical
below
N/A
below
above
below
Stroke Lecture/Textbook
Blood Flow Importance:
 Delivers oxygen, glucose, & nutrients via arteries
 Removes carbon dioxide, lactic acid, metabolites via veins
o So, without it, cells will die!
Stroke:
 Cerebrovascular accident - “brain attack”…need for rapid response
 Interruption in the blood flow to the brain.
Stroke Symptoms:
 Sudden numbness of the face, arm, or leg, especially on one side of the body
 Sudden confusion, trouble speaking or understanding speech
 Sudden trouble seeing in one or both eyes
 Sudden trouble walking, dizziness, loss of balance or coordination
 Sudden severe headache
Circle of Willis:
 Circle of communicating arteries formed at the base of the brain by the carotid and
basilar arteries
 if one of the main arteries is occluded, the distal smaller arteries that it supplies can
receive blood from the other arteries (collateral circulation).
“Watersheds” of major arteries:
anterior cerebral artery:
o extends upward and forward from the internal carotid artery.
o supplies the frontal lobes, the parts of the brain that control logical thought,
personality, and voluntary movement, especially the legs.
o Stroke in 1 anterior cerebral artery results in opposite leg weakness and sensory
loss.
o If both anterior cerebral territories are affected, profound mental symptoms
may result including:
o disinhibition and dysfunction of executive functions
o aphasia if left lateralized
o left hemifield neglect if right lateralized.
middle cerebral artery:
 the largest branch of the internal carotid.
 supplies a portion of the frontal lobe and the lateral surface of the temporal and
parietal lobes, including the primary motor and sensory areas of the face, throat, hand
and arm of the contralateral side of the body.
 If left lateralized can result in aphasia
 if right lateralized left hemifield neglect.
 artery most often occluded in stroke.
lenticulostriate arteries:
 Small, deep penetrating arteries…the branch from the middle cerebral artery.
 Occlusions of these vessels are referred to as lacunar strokes.
o The cells distal to the occlusion die, but since these areas are very small, often
only minor deficits are seen.
o When the infarction is critically located, however, more severe manifestations
may develop, including paralysis and sensory loss because it induces cell death in
the basal ganglia.
o Within a few months of the infarction, the necrotic brains cells are reabsorbed
by macrophage activity, leaving a very small cavity - a lacune.
o About 20% of all stokes are lacunar and have a high incidence in patients with
chronic hypertension and in the elderly.
posterior cerebral arteries:
 stem in most individuals from the basilar artery but sometimes originate from the
ipsilateral internal carotid artery.
 supply the temporal and occipital lobes of the left cerebral hemisphere and the right
hemisphere.
 occlusion of the posterior cerebral artery = usually an occipital lobe infarction leading to
an opposite visual field defect.
 Depending on the location of the occlusion and may also include contralateral
hemiplegia and a variety of other symptoms, including color blindness, failure to see toand-fro movements, verbal dyslexia, and hallucinations.
 Deep infarctions can result in contralateral sensory loss and hemiparesis due to
involvement of thalamus & internal capsule.

Stroke associated with posterior arteries is less frequent than with anterior or middle
arteries.
External carotid arteries:
 supply the face and scalp with blood.
Internal carotid arteries:
 supply blood to the anterior three-fifths of cerebrum,
except for parts of the temporal and occipital lobes.
The basilar arteries:
 supply the posterior two-fifths of the cerebrum, part
of the cerebellum, and the brain stem.
 Any decrease in the flow of blood through one of the
internal carotid arteries brings about some
impairment in the function of the frontal lobes.
o results in numbness, weakness, or paralysis on
the side of the body opposite to the obstruction of the artery
 Occlusion of one of the vertebral arteries can cause many serious consequences,
ranging from blindness to paralysis.
Types of strokes:
 Ischemic strokes – temporary block in blood flow.
o 2 types, ebolitic (sudden, clot travels from somewhere else) and thrombitic
(slow gradual buildup of clot)
o acute, localized, non-permanent damage…fast recovery
o # of strokes vary
 Hemorrhagic strokes: “systemic hypoprofusion” – that’s a whole body lack of blood
flow.
o Severe impact
o Tend to occur more in white matter, thalamus, pons, cerebellum, caudate
nucleus
Stroke General Defects:
 Disinhibition
 Attention deficits
 Motor and sensory impairment
 Memory problems
 Deficits in abstract reasoning
 Lack of initiative
 Poor judgment
Deficits associated with RH stroke in adults:
 Emotional lability
 Contralateral motor & sensory deficits
 Visuospatial deficits
 Limits autonomy in self-care
o Less awareness of own limitations
o Often longer rehab time than LH stroke
Decficits LH strokes in adults:
 Depression
 Aphasias, alexias (difficulties reading), agraphias (difficulties
writing)
 Contralateral motor & sensory deficits
Cerebral venous thrombosis:
 An obstruction of the draining veins of the brain
 Results in edema (swelling) of vein and eventually surrounding neural tissue, as well as
increased intracranial pressure
 Can lead to hemorrhage
 This is what frequent airline travelers are at risk for – pressurized cabin usually coupled
with spending time at high altitude and/or dehydration and/or diarrhea
Cerebral venous thrombosis Risk factors:
 Having recently given birth
 Smoking and taking birth control pills
 Thrombophilia – genetic predisposition toward blood clots
 Long distance airline travel
Cerebral venous thrombosis impact:
 Headache
 Blurred vision
 Fainting or loss of consciousness
 Loss of control over movement in part of the body
 Seizures
 Coma
Aging
Cognitive changes:
 Increased crystalized intelligence
o Stored knowledge
o Habituation actions/problem solving
o *cognitive reserve against dementia
 decreased fluid intelligence
o new learning
o ability to solve abstract and complex new problems
o processing speed
 memory decline
o free recall
o intentional encoding
o working memory declines
preserved differentiation hypothesis:
 mental fitness prevents deterioration
brain changes:
 loss of size and weight
 flattening of cortical substances
 ventricles get larger
 white and grey matter deficiencies
 hippocampus, frontal lobes, and areas of temporal lobes are most vulnerable
o frontal most fucked
 ***occipital and somatosensory cortices preserved***
Physical changes:
 hypertension
 cardiovascular problems
Mild Cognitive Impairment
 age-related cognitive decline but not severe enough to be dementia
 memory impairment main cognitive issue
o encoding and recall
 hippocampal and brain atrophy worse than normal
 greater risk for developing dementia
Dementia
 behavioral syndrome
 acquired unusual loss of cognitive function
 decline in multiple cognitive areas—usually involving memory
Cortical vs subcortical:
 Cortical: predomiant grey matter loss in cortical regions
o AD
o Wilson’s Syndrome
o Pick’s
 Subcortical: predominant white matter loss or neuronal connections between cortical
area or grey matter loss below the cortex
o AIDs dementia
o Huntington’s
o Parkinson’s
o Progressive Supranuclear palsy
Progressive v Static:
 Progressive: disease associated with continuous cognitive decline…progression varies
o Vascular dementia = stepwise progression (strokes occur at different times)
 Static: cognitive decline occurs only when disease is present…otherwise dementia
progress plateaus
o Lead poisoning
Permanent v Nonpermanent: pretty self-explanatory:
Alzheimer’s Disorder:
 “Accelerated aging”
o if we lived long enough...AD would be inevitable

2x as common in females than men
o probably because women live longer
 no single cause
 less likely in educated people
o may be due to the cognitive reserve
Diagnosing AD
 requires behavior presentation of dementia and identification of neuropathic markers of
AD
 differicult to diagnose bc no singular test short of biopsy (people don’t want to submit
to that) and symptomology v similar to other types of dementia
o especially true in later stages
o leads to over diagnosis of AD
 process of elimination