ALTERATIONS IN NEUROLOGIC FUNCTION

Aging and the Nervous System

Decreasing Neurons Memory Impairment Decreasing Sensory and motor function Decreasing Arterial blood flow Neurotransmitter changes Fibrosis of meninges Medications

Coma: alterations in arousal Structural locations

– Supratentorial, infratentorial, subdural, extracerebral, intracerebral

Pathologic causes– Infectious, vascular, neoplastic, traumatic,

congenital, degenerative, metabolic– All systemic diseases that cause CNS

dysfunction are considered to be metabolic

Basic causes 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

Alterations in Levels of Consciousness indicate cortical dysfunction – Automatism– Confusion/Disorientation– Delirium/Lethargy– Stupor/Deep stupor– Coma

Light coma, coma, deep coma

Objective score—Glasgow Coma Scale

Used to give prognosis after head injury– Eye opening 1-4– Best verbal response 1-5– Best motor response 1-6

Score > 11 85% have good recovery Score 3--4 85% die or remain

vegetative

Assess specific functions

Language and speech--L hemisphere– Dysarthria– Dysphonia– Aphasia

Breathing may be hemispheric or brain stem controlled

Hemispheric Patterns– Post hyperventilation apnea– Cheyne-Stokes respiration

Brain Stem Patterns– Central neurogenic hyperventilation– Apneusis– Cluster breathing– Ataxic breathing– Agonal gasps

Cranial nerves assess non-cortical function

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

Purposeful (normal) Inappropriate/not purposeful

– Disruption of corticospinal system Absent/unresponsive

– Cortical shutdown– Thalamic disruption– Spinal cord lesions

Higher levels usually inhibit lower levels

Decorticate rigidity--arms flexed– damage above the midbrain

Decerebrate rigidity--exaggerated extension– damage to midbrain

Extensor in arms, flexion in legs– Pons dysfunctional

Flaccid--no response– Lower pons/upper medulla damaged

Upper motor neuron vs lower motor neuron

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

Partial—conscious throughout– simple—lasts < 1 minute– complex—lasts 1-3 minutes

Generalized— involve entire cerebral cortex and diencephalon– lose consciousness, bilateral , symmetric

Specialized epileptic syndromes

Types of generalized seizures

Absence seizures (petit mal)—go vacant for a few seconds

Tonic-clonic seizures (grand mal) 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 fever convulsions—tonic-clonic seizures in children < 3 yrs

Status epilepticus

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

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

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

Cytotoxic (metabolic edema)– poisoning of active transport systems– Cells lose K, gain Na

Ischemic edema– Follows infarction– Both vasogenic and cytotoxic

Interstitial edema

Increased Intracranial Pressure Cerebral edema #1 cause

– Tumors, trauma (bleeding, edema), obstruction to CSF flow

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 Reduced cerebral blood flow causes increased

sympathetic activity– Vasoconstriction, increased BP

Brain becomes hypoxic and hypercapnic– 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 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

• Any insult caused by an external physical forcemay produce a diminished or altered state of

consciousnesscan also result in the disturbance of behavioral

or emotional functioningmay be either temporary or permanent and cause

partial or total functional disability or psychosocial maladjustment

Concussion 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

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

It may take a few months to a few years for a concussion to heal

Diffuse Axonal Injury 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

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

• Bruise (bleeding) on the brain caused by direct impact• Signs are those of a mild concussion

• 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)

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. 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

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)

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

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)

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 Generally can make a good recovery

Severe Brain Injury (< 8) 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 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 If awaken, often left with permanent

physical, cognitive, or behavioral impairments

Vegetative State 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

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

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 Cognitive impairment

– Thinking skills, especially memory Longer lengths of time spent in a

vegetative state Severe behavior problems- Psychosis,

depression, restlessness, combativeness, hostility

Muscle movement disorders

Anoxic Brain Injury

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

3rd most common cause of mortality in US– increased risk for African Americans, women– major cause of disability in adults

Risk factors– 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

Sudden, nonconvulsive, focal loss of neuron activity

Neural insult from decreased blood flow– Thrombotic strokes– Embolic strokes– Hemorrhagic stroke

Thrombotic strokes

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 All neurologic deficits clear within 24

hours– Reversible ischemic neurologic deficits persist

longer but do clear eventually

80% of patients will have another episode within 1 year unless treated

Embolic strokes

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

Least common cause (10%) – Hypertension, aneurysms, bleeding into

tumors, anticoagulation medication, head trauma

Signs and Symptoms

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 Dizziness, stumbling, loss of

balance/coordination Severe headache with no known cause

• 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

Get the patient on oxygen, consider clot busting drugs

Ischemic cascade Ischemic core develops

– CBF < 20% normal (50 ml/100 g brain tissue/minute is normal)

Ischemic penumbra (transitional zone)– CBF 20-50% of normal– Cells in this zone may be saved

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 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

Severely decreased quality of life– 60% are home-bound, 30% need assisted living

(15% need a nursing home)