ALTERATIONS IN
NEUROLOGIC FUNCTION
Aging and the Nervous System
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Decreasing Neurons
Memory Impairment
Decreasing Sensory and motor function
Decreasing Arterial blood flow
Neurotransmitter changes
Fibrosis of meninges
Medications
Coma: alterations in arousal
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Structural locations
– Supratentorial, infratentorial, subdural,
extracerebral, intracerebral
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Pathologic causes
– Infectious, vascular, neoplastic, traumatic,
congenital, degenerative, metabolic
– All systemic diseases that cause CNS
dysfunction are considered to be
metabolic
Basic causes
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Anything that increases intracranial
pressure
Damage from hypoxia, hypoglycemia
drugs, or toxins
Lesions or metabolic disorders that
damage the RAS
– Everything that goes to the cortex MUST
pass through the thalamus via the RAS
Clinical Manifestations of
Cerebral Dysfunction
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Alterations in Levels of Consciousness
indicate cortical dysfunction
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Automatism
Confusion/Disorientation
Delirium/Lethargy
Stupor/Deep stupor
Coma
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Light coma, coma, deep coma
Objective score—Glasgow Coma Scale
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Used to give prognosis after head injury
– Eye opening
– Best verbal response
– Best motor response
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Score > 11
Score 3--4
1-4
1-5
1-6
85% have good recovery
85% die or remain
vegetative
Assess specific functions
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Language and speech--L hemisphere
– Dysarthria
– Dysphonia
– Aphasia
Breathing may be hemispheric or
brain stem controlled
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Hemispheric Patterns
– Post hyperventilation apnea
– Cheyne-Stokes respiration
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Brain Stem Patterns
– Central neurogenic hyperventilation
– Apneusis
– Cluster breathing
– Ataxic breathing
– Agonal gasps
Cranial nerves assess non-cortical
function
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I
Olfactory
II
Optic
III, IV, VI Control movement of eyes
V
Motor & sensory to temporal and
masseter muscles
VII
Taste, muscles of facial expression
VIII
Hearing and balance
IX, X Taste, swallowing, gag reflex
XI
Flexors of neck, ability to shrug
XII
Tongue muscles
Motor disruption may locate
hemisphere and level
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Purposeful (normal)
Inappropriate/not purposeful
– Disruption of corticospinal system
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Absent/unresponsive
– Cortical shutdown
– Thalamic disruption
– Spinal cord lesions
Higher levels usually inhibit lower
levels
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Decorticate rigidity--arms flexed
– damage above the midbrain
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Decerebrate rigidity--exaggerated extension
– damage to midbrain
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Extensor in arms, flexion in legs
– Pons dysfunctional
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Flaccid--no response
– Lower pons/upper medulla damaged
Upper motor neuron vs lower motor
neuron
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Muscle stretch reflexes (deep tendon
reflexes)
– LMN disease results in no reflexes of affected
area only, flaccid paralysis, muscle atrophy
– UMN disease initially areflexic, progressing to
hyperreflexic, with spasticity as lose upper
inhibition; minimal muscle atrophy
Seizure Disorders
Relatively common (10% incidence)
– Peak ages 1-10 years and > 60 years
Look for underlying cause of xs neuronal discharge
– head trauma with dura injury is predisposing factor
Epilepsy is recurrent, spontaneous seizure pattern
Primary epilepsy is usually idiopathic
patient < 20 years old
Secondary epilepsy has known trauma, infection, etc
Seizure Disorders--Classification
Table 16-9
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Partial—conscious throughout
– simple—lasts < 1 minute
– complex—lasts 1-3 minutes
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Generalized— involve entire cerebral
cortex and diencephalon
– lose consciousness, bilateral , symmetric
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Specialized epileptic syndromes
Types of generalized seizures
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Absence seizures (petit mal)—go vacant for a
few seconds
Tonic-clonic seizures (grand mal)
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incontinence, tongue biting, postictal phase with no memory
of seizure
last 3-5 minutes, unconscious for another 30+ minutes
– Increased HR, BP, body T, WBC count
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fever convulsions—tonic-clonic seizures in children < 3 yrs
Status epilepticus
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Continuous seizure activity of 20+ minutes
– neurologic emergency with 22-25% mortality
– IV diazepam; phenobarbital
– IV dextrose, ventilation support as needed
Can result in hypoglycemia, hypotension, dysrhythmias
If goes > 1 hour, cerebral hypotension, breakdown of
blood brain barrier, cerebral edema
Alterations in Cerebral
Homeostasis
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Cerebral edema
– Most often caused by hypoxia, cerebral
ischemia, fluid/electrolyte imbalance,
meningitis, trauma
– Peaks 36-48 hours after trauma
– Leads to increased intracranial pressure
– Blood vessels distorted, brain tissue displaced
and eventually may herniate
Types of cerebral edema
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Vasogenic (#1)
– Increased permeability of of capillaries
after injury
– BB barrier damaged
– Starts at site of injury, spreads to white
matter of same side
– Edema --> increased pressure -->local
ischemia--> vasodilatation-->more edema
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Cytotoxic (metabolic edema)
– poisoning of active transport systems
– Cells lose K, gain Na
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Ischemic edema
– Follows infarction
– Both vasogenic and cytotoxic
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Interstitial edema
Increased Intracranial Pressure
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Cerebral edema #1 cause
– Tumors, trauma (bleeding, edema), obstruction
to CSF flow
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Closed system, fluid is incompressible
Must have a decrease in contents to protect
brain
– CSF forced out of cranium
– Vasoconstriction and compression of vessels
provide early compensation
Progression of Pathophysiology
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Reduced cerebral blood flow causes increased
sympathetic activity
– Vasoconstriction, increased BP
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Brain becomes hypoxic and hypercapnic
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Lowered LOC
Cheyne-Stokes breathing
Dilated, sluggish pupils
Bradycardia
Build up of CO2 leads to respiratory acidosis--> cerebral
vasodilatation--> more edema
Herniation of brain compresses low P compartment
Clinical signs of increased ICP
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Altered level of consciousness is most
sensitive indicator
Classic triad
– Headache, papilledema, vomiting (often
projectile)
Hyperthermia, motor/sensory changes,
altered speech, seizures
Coma when both hemispheres or brainstem
stop functioning
ACQUIRED BRAIN INJURY
Traumatic Injuries
Definition
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Any insult caused by an external physical
force
may produce a diminished or altered state of
consciousness
can also result in the disturbance of behavioral
or emotional functioning
may be either temporary or permanent and cause
partial or total functional disability or
psychosocial maladjustment
Concussion
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Most common type of traumatic brain
injury
Caused when the brain receives trauma
from an impact or a sudden momentum or
movement change.
– The blood vessels in the brain may stretch and
cranial nerves may be damaged
– Direct blows to the head, gunshot wounds,
violent shaking of the head, or force from a
whiplash type injury
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Skull fracture, brain bleeding, or swelling
may or may not be present
– may or may not show up on a diagnostic
imaging test
– can cause diffuse axonal type injury resulting
in permanent or temporary damage
– blood clot in the brain can occur
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It may take a few months to a few years for
a concussion to heal
Diffuse Axonal Injury
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Caused by shaking or strong rotation of the
head, as with Shaken Baby Syndrome, or
by rotational forces, such as with a car
accident
Injury occurs because the unmoving brain
lags behind the movement of the skull,
causing brain structures to tear
– tearing of the nerve tissue disrupts the brain’s
regular communication and chemical
processes
Shaken Baby Syndrome
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Blood vessels between the brain and skull
rupture and bleed
Accumulation of blood causes cerebral
edema and increased intracranial pressure
Signs: Irritability, changes in eating
patterns, tiredness, difficulty breathing,
dilated pupils, seizures, and vomiting
Contusion
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Bruise (bleeding) on the brain caused by
direct impact
• Signs are those of a mild concussion
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Coup-Contrecoup Injury
• Contusions that are both at the site of the
impact and on the complete opposite side of
the brain
Second Impact Syndrome (Recurrent
Traumatic Brain Injury)
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A person sustains a second traumatic brain injury
before the symptoms of the first traumatic brain
injury have healed
– Loss of consciousness is not required
– Second impact is more likely to cause brain swelling
and widespread damage.
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Long-term effects of recurrent brain injury can be
muscle spasms, increased muscle tone, rapidly
changing emotions, hallucinations, and difficulty
thinking and learning.
Levels of brain injury
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Assess using Glasgow Coma Scale
– Provides an evaluation of initial level of injury
– There may be no correlation between the
initial Glasgow Coma Scale score and a
person’s short or long term recovery, or
functional abilities
Mild Traumatic Brain Injury (13-15)
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Loss of consciousness is very brief, usually
a few seconds or minutes, or does not
occur—the person may be dazed or
confused
Testing or scans of the brain may appear
normal
Mild concussion, contusions
Symptoms of mild traumatic
brain injury
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Headache, Nausea
Memory problems, Decreased speed of thinking
Decreased concentration and attention span
Depression, anxiety, mood swings
Fatigue, Sleep disturbances, Irritability
Sensitivity to noise or light
Balance problems
Moderate Traumatic Brain Injury
(9-12)
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A loss of consciousness lasts from a few
minutes to a few hours
– All problems of mild trauma may last for days
to weeks
– Confusion lasts from days to weeks
– Physical, cognitive, and/or behavioral
impairments last for months or are permanent
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Generally can make a good recovery
Severe Brain Injury (< 8)
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Prolonged unconscious state or coma lasts days, weeks,
or months
Categorized into subgroups
– Coma
– Vegetative State
– Persistent Vegetative State
– Minimally Responsive State
– Akinetic Mutism
– Locked-in Syndrome
Coma
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State of unconsciousness from which the
individual cannot be awakened
– responds minimally or not at all to stimuli
– initiates no voluntary activities
– Cerebral cortex and lower areas are not
working
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If awaken, often left with permanent
physical, cognitive, or behavioral
impairments
Vegetative State
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Arousal is present, but the ability to interact with the
environment is not (cortex is gone)
– Eye opening can be spontaneous or in response to
stimulation
– General responses to pain exist, such as increased
heart rate, increased respiration, posturing, or sweating
– Sleep-wakes cycles, respiratory functions, and
digestive functions return
Persistent Vegetative State (PVS) is a term used for a
Vegetative State that has lasted for more than a month
Minimally Responsive State
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Severe traumatic brain injury, but no
longer in a Coma or a Vegetative State
– Primitive reflexes
– Inconsistent ability to follow simple
commands
– An awareness of environmental stimulation
– May last for years before some recovery
ACQUIRED BRAIN
INJURIES
Non-traumatic
Symptoms
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Damage is diffuse, not focal, and at
cellular level
– mild, moderate, or severe impairments in one
or more areas
– cognition, speech-language communication;
memory; attention and concentration;
reasoning; abstract thinking; physical
functions; psychosocial behavior; and
information processing
Brain functionalities are more severely
affected than in trauma
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Cognitive impairment
– Thinking skills, especially memory
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Longer lengths of time spent in a
vegetative state
Severe behavior problems- Psychosis,
depression, restlessness, combativeness,
hostility
Muscle movement disorders
Anoxic Brain Injury
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Anoxic Anoxia- Brain injury from no
oxygen supplied to the brain
Anemic Anoxia- Brain injury from blood
that does not carry enough oxygen
Toxic Anoxia- Brain injury from toxins or
metabolites that block oxygen in the blood
from being used
Hypoxic Brain Injury
Brain receives some, but not enough oxygen
– critical reduction in blood flow or blood pressure.
– Airway obstruction, near-drowning, strangulation,
electrocution
– Trauma to the head and/or neck or chest
– Heart attack, stroke, arteriovenous malformation
(AVM), aneurysm, intracranial surgery
– carbon monoxide poisoning
– Infectious disease, meningitis, intracranial tumors,
metabolic disorders
Cerebral Vascular Disorders:
Stroke
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3rd most common cause of mortality in US
– increased risk for African Americans, women
– major cause of disability in adults
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Risk factors
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smoking (50% increase in risk)
obesity, high BP, sleep apnea
DM (2.5-3.5 increase in risk)
impaired cardiac function (esp atrial fibrillation )
Definition
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Sudden, nonconvulsive, focal loss of
neuron activity
Neural insult from decreased blood flow
– Thrombotic strokes
– Embolic strokes
– Hemorrhagic stroke
Thrombotic strokes
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Attributed to local arteritis and
atherosclerosis
Signs are usually slowly progressive
(stroke in evolution) over several hours
Transient ischemic attacks are partial
thrombotic strokes or the result of
vessel spasm
Transient Ischemic Attacks
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All neurologic deficits clear within 24
hours
– Reversible ischemic neurologic deficits persist
longer but do clear eventually
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80% of patients will have another episode
within 1 year unless treated
Embolic strokes
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Thrombus outside of brain breaks
loose and migrates into cerebral
vessels
– L atrial fibrillation, valve disease, fat, air
– Obstruction is usually at a bifurcation
– Follow on strokes are common, because
source of clot usually remains
Hemorrhagic stroke
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Least common cause (10%)
– Hypertension, aneurysms, bleeding into
tumors, anticoagulation medication, head
trauma
Signs and Symptoms
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Sudden numbness or weakness—esp face,
arm, leg, and usually one sided
Seeing double/change in visual field
Changed level of consciousness
– Confusion to coma
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Dizziness, stumbling, loss of
balance/coordination
Severe headache with no known cause
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Signs may spontaneously regress, become
more severe, or remain unchanged
– Thrombotic strokes tend to be slowly
progressive
– Embolic strokes are often followed by more
strokes as embolus breaks down and moves
– Hemorrhagic strokes usually most extensive
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Get the patient on oxygen, consider clot
busting drugs
Ischemic cascade
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Ischemic core develops
– CBF < 20% normal (50 ml/100 g brain
tissue/minute is normal)
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Ischemic penumbra (transitional zone)
– CBF 20-50% of normal
– Cells in this zone may be saved
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Ischemic cells lose ATP and swell up
– Respond by increasing intracellular Ca and
releasing xs glutamate
– Glutamate excites surrounding neurons to
produce lethal levels of nitric oxide
Prognosis
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Nearly 1/3 of all stroke victims die within 3 weeks
– Comatose have worst prognosis
– Hemorrhagic strokes have higher mortality and
poorer recovery
– Most recovery occurs within the first 2 months
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Severely decreased quality of life
– 60% are home-bound, 30% need assisted living
(15% need a nursing home)