1 Structure and Function of the Neurologic System Chapter 14.
ALTERATIONS IN NEUROLOGIC FUNCTION
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Transcript of ALTERATIONS IN NEUROLOGIC FUNCTION
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)