Sensory

Integration

Motor

CNSo Braino Spinal Cord

PNSo 31 SNso 2 ANso 12 CNs

The Lobes Frontal Temporal Parietal Occipital Limbic system

FRONTAL Personality, judgment, intellect, Broca’s speech area (motor) expressive aphasia

TEMPORAL Hearing, seat of memory, Wernicke’s (sensory) receptive aphasia

PARIETAL Sensation, numbers and calculation

OCCIPITAL Vision

LIMBIC SYSTEM Rage, extremes of emotion, sexual desire, “fifth lobe”

Cerebellum balance, general motors

Pons respiratory center

Medulla Oblongata cardiac and visceral organ pyramidal ducussation

Ascending Pathway conducts sensation conduction of pain Descending Pathway engage in motor function perspiration and pupil dilation

Cervical (8) C1-4 respiratory failure C1-8 quadriplegia

Thoracic (12) T1-12 paraplegia T6 and above autonomic dysreflexia (pounding headache, dilation of pupils, perspiration, and piloerection)

Lumbar (5) Sacral (5) Coccygeal (1) bowel bladder sexual sensation of lower extremities

SYMPHATETIC PARASYMPHATETIC

Neurotransmitter

AcetylcholineNE, E

Acetylcholine

Activity Hyperactive Hypoactive

Blood Pressure

Heart Rate

Respiratory Rate

Temperature

SYMPHATETIC PARASYMPHATETIC

Bronchi Dilation Constriction

Pupil Dilate Constrict

GIT

GUT

Genitalia Ejaculation Erection

Salivary glands

Thick, vivid secretion

Copious, water secretion

OLFACTORY smell a mild aroma (coffee granules)

OPTIC vision (snellen’s chart) OCCULOMOTOR movement of eyeball TROCHLEAR superior oblique (down gaze)

TRIGEMINAL ophthalmic (cotton wisp) maxillary (safety pins) mandibular (chewing) ABDUCENS lateral rectus (side gaze) FACIAL ant 2/3 rd of the tongue for taste movement of facial muscles

AUDITORY hearing and balance GLOSSOPHARYNGEAL post 1/3rd of the tongue gag reflex VAGUS ask the patient to swallow

20

SPINAL ACCESSORY shoulder shrug HYPOGLOSSAL tongue movement

LOC GCS (most sensitive) Orientation place Mood Language aphasia (E and R) Recent memory birthday General knowledge president? Calculation skills addition

EYE OPENING EYE OPENING RESPONSERESPONSE

SPONTANEOUSSPONTANEOUS

TO VOICETO VOICE

TO PAINTO PAIN

NONENONE

44

33

22

11

BEST VERBAL BEST VERBAL RESPONSERESPONSE

ORIENTEDORIENTED

CONFUSEDCONFUSED

INAPPROPRIATE WORDSINAPPROPRIATE WORDS

INAPPROPRIATE SOUNDSINAPPROPRIATE SOUNDS

NONENONE

55

44

33

22

11

BEST MOTOR BEST MOTOR RESPONSERESPONSE

OBEYS COMMANDSOBEYS COMMANDS

LOCALIZES PAINLOCALIZES PAIN

WITHDRAWS (PAIN)WITHDRAWS (PAIN)

FLEXION (PAIN)FLEXION (PAIN)

EXTENSION (PAIN)EXTENSION (PAIN)

NONENONE

66

55

44

33

22

11

TOTALTOTAL 1515

24

Gustatory Olfactory Sensation

Pupil Reaction PERLA

Muscle strengthDTRs

Tests for CoordinationRomberg’s testFinger to nose Heel to shinRapid alternating movements

Strength is rated from 0 to 5: 0/5 no motion 1/5 slight muscle motion, but

no movement at joint 2/5 full motion parallel to

ground, but can't move against gravity

3/5 can move against gravity, with no resistance

4/5 full strength against some resistance

5/5 full strength against full resistance - normal.

Biceps reflexBiceps reflex Tests C5-6Place your thumb on biceps tendon

and strike your thumb with the reflex hammer

Brachioradialis reflexBrachioradialis reflex Tests C5-6Strike tendon with flat side of

hammer

Triceps reflexTriceps reflex tests C7-8tap proximal to olecranon.

Quadriceps reflex Quadriceps reflex (knee jerk)(knee jerk) tests L2-L4

Achilles reflex Achilles reflex (ankle jerk)(ankle jerk) tests L5-S2

0: nothing happens 1+: some movement, less than normal

2+: normal 3+: more brisk than normal 4+: brisk, with clonus (several beats/ repeated motion; sometimes motion in the other extremity, too.)  

31

Patient stands with feet together and closes eyes

KNOB Kernig’s sign Nuchal rigidity Opisthotonus Brudzinski’s sign

EEG CT Scan MRI Lumbar Puncture Carotid Angiography

Graphical recording of brain activity Measures electrical activity of the brain Diagnostic in seizures Note: Electrodes are NOT painful

Explain its non invasive Shampoo before and after Withhold drugs stimulants and depressants Breakfast hypoglycemia may alter the result of the procedure

Uses narrow x-ray beam to scan Uses narrow x-ray beam to scan the body parts in successive the body parts in successive layerslayersThe view would be cross-The view would be cross-sectionalsectional

Non invasive Ask for fear with close places (+)/(-) contrast medium Pillow will be placed under the head Lie supine and still movement can cause artifacts in the film

Uses magnetic field to Uses magnetic field to obtain images of different obtain images of different areas of the bodyareas of the body No ionizing radiation No ionizing radiation Useful in diagnosis Useful in diagnosis multiple sclerosis, brain multiple sclerosis, brain and spinal cord lesionsand spinal cord lesions

Non invasive Any metal implants are contraindicated Put ear plugs noisy, buzzing sound

Carried out by Carried out by inserting a inserting a needle into the needle into the lumbar lumbar subarachnoid subarachnoid space to space to withdraw CSFwithdraw CSF

WBC 0-5 cells/mmWBC 0-5 cells/mm Protein = 15-45 mgs/100 mlProtein = 15-45 mgs/100 ml Glucose = 40-80 mgs/100 mlGlucose = 40-80 mgs/100 ml

Normal CSF FindingsNormal CSF Findings

Informed consent Position: knee chest, shrimp, C, fetal Between L3 and L4 Most common complication: spinal headache Mgt: Flat on bed for 6 – 8 hours CI: ↑ICP

Visualization of Visualization of brain’s vascular brain’s vascular system by system by injection contrast injection contrast dye into the dye into the circulation bloodcirculation blood

Invasive procedure Informed consent Assess for allergy Warm sensation

Osmotic diuretic Anticonvulsants Antiparkinson’s Antimyasthenic Steroids CNS Stimulants CNS Depressants

Mannitol Hypertonic solution which will shrink the cell V/S BP precaution I and O Assess LOC / less lethargic FAST DRIP crystallization

CNS depressants, muscle relaxants SGPT Sodium Luminal Gabapentin Phenytoin sodium (Dilantin) Tegretol, Topamax

Drug compliance Instruct to wear medic alert bracelet Liquid meds shake well before using Aplastic anemia most common Notify dentist gum hyperplasia (massage) Toxicity >20mg/dL I-report if patient complains of nystagmus Neurotoxic

Dopaminergic Inhibits excitation of neuro impulses

AUTOIMMUNE DISEASE OF THE NEUROMUSCULAR JUNCTION CAUSED BY AUTOANTIBODY ATTACK ON THE ACETYLCHOLINE RECEPTORS IN THE NEUROMUSCULAR JUNCTION

A progressive neuromuscular disease of the lower motor neurons characterized by muscle weakness andfatigue.

MYASTHENIA GRAVIS

MYASTHENIA GRAVISETIOLOGYFAMILIAL 5%THYMOMAHYPERTHYROIDISMDRUG INDUCED

Causes and Incidence The cause of myasthenia gravis (MG) is unknown. More than 80% of individuals with MG also have thymic abnormalities, but the link is unclear. The incidence is 3 to 6 per 100,000 individuals in the United States. The age of onset is either 20 to 30 years (primarily in women) or 50 to 60 years (primarily in men).

Disease Process An antigen attack on the acetylcholine receptor of the postsynaptic neuromuscular junction results in dysfunction of the receptor, which fails to act on the acetylcholine. Because of this, nerve impulses do not pass on to the skeletal muscle at the myoneural junction.

Symptoms The most common manifestations are ptosis, diplopia, and muscle fatigue after exercise. Dysarthria, dysphagia, ocular palsy, head bobbing, and facial and proximal limb weakness are also reported. Symptoms are milder on awakening and become worse as the day progresses. Rest temporarily improves symptoms. Respiratory involvement leads to breathlessness and reduced tidal volume and vital capacity. Manifestations can be remitting, static, or progressive. Factors such as stress, menses, heat, and illness can exacerbate symptoms.

Potential Complications Myasthenic crisis is an acute exacerbation of symptoms; it usually involves respiratory distress and can lead to respiratory failure or aspiration and cardiopulmonary arrest.

DIAGNOSTIC TESTA characteristic pattern of fatigue and weakness on exertion that improves with rest, and a positive Tensilon test, are indicators.

A computed tomography scan may indicate the presence of thymoma;

electromyography may show muscle fiber contraction with progressive decremental response.

Surgery Thymectomy for treatment of thymoma and remission of

adult onset MG Drugs Anticholinesterases and corticosteroids to counteract

muscle weakness and fatigue; immunosuppressants with autoimmune pathogenesis; flu shots to prevent respiratory infection

General Plasmapheresis to treat weakness and fatigue; ventilatory

support in respiratory crisis; physical therapy to prevent disuse problems, occupational therapy to aid in activities of daily living; balance of exercise and rest; instruction about cholinergic crisis caused by excessive anticholinesterase medication; counseling for long-term adaptation to disease; information about the importance of preventing respiratory infection or recognizing and treating symptoms early

MYASTHENIA GRAVIS

MYASTHENIA GRAVIS

Impairment of one or more vessels in the cerebral circulation, caused by thrombosis, embolus, stenosis, or hemorrhage, which interrupts the blood supply and results in ischemia of brain tissues.

Cerebrovascular Accident (Stroke)

Causes and Incidence A cerebrovascular accident (CVA) is caused by occlusion of a cerebral vessel. Most cerebrovascular occlusions occur secondary to atherosclerosis or hypertension, or a combination of the two. Other risk factors are diabetes mellitus, myocardial infarction, bacterial endocarditis, rheumatic heart disease, aneurysms, head trauma, and a history of previous stroke or transient ischemic attacks (TIAs). CVA is the second most common cause of neurologic disability and the third most common cause of death in the Western Hemisphere. The incidence increases with age, with adults 65 years of age or older at greatest risk.

Disease Process The general pathophysiology of a CVA involves occlusion of a cerebral vessel, which leads to ischemia of the brain tissue supplied by that vessel. If the obstruction is not removed, the affected tissue infarcts and dies, causing permanent neurologic deficit or death. The severity of the CVA depends on the location and extent of the obstruction, the degree of collateral circulation, and the promptness of diagnosis and treatment.

Symptoms The signs and symptoms of a stroke depend on the site and size of the obstruction. They typically include altered mental status, hemiparesis or hemiplegia, receptive or expressive aphasia, dysarthria, dysphagia, apraxia, hemianopsia, urinary incontinence, and emotional lability. Headache, seizures, stupor, and marked hypertension may also be present.

Potential Complications Coma and death are the most severe consequences of CVA. Permanent neurologic deficits (e.g., paralysis, impaired intellectual capability, speech defects, loss of short-term memory, impaired judgment and problem-solving abilities, reduced impulse control) are common residual complications.

Diagnostic Tests Clinical evaluation

>Any of the above manifestations, particularly in individuals with identifiable risk factors

Computed tomography/ magnetic resonance imaging

>To identify area of infarct or bleeding

Ultrasonography >To identify diminished blood flow in

vessels Angiography

>To detect occlusion of large vessels

Treatments Surgery Evacuation of hematoma or clot;

placement of intracranial pressure monitor; endarterectomy to remove atherosclerotic plaques

Drugs Anticoagulants during stroke

evolution; antihypertensives to control blood pressure; diuretics to reduce edema in the brain; anticonvulsants to control seizures; long-term aspirin therapy to prevent future stroke

General Monitoring and support of vital

functions; prevention of decubitus ulcers, thrombosis, and pneumonia; rehabilitation: occupational therapy for adapting activities of daily living, physical therapy to increase strength and endurance; gait training to improve ambulation; cognitive therapy to improve memory and problem solving; speech therapy to improve communication; counseling for poststroke depression and altered sexual functioning; vocational retraining

A slowly progressive, degenerative neurologic disorder characterized by slow, impoverished movement; muscle rigidity; resting tremor; and postural instability.

A CHRONIC PROGRESSIVE NEUROLOGIC DISORDER THAT RESULTS FROM THE LOST OF NEUROTRANSMITTER DOPAMINE IN A GROUP OF BRAIN STRUCTURES THAT CONTROL MOVEMENT

PARKINSON’S DISEASE

Causes and Incidence Primary parkinsonism is idiopathic, whereas secondary forms of the disease can be caused by drugs (neuroleptics, reserpine, metoclopramide, tetrabenazine, N-MPTP [a byproduct of heroin synthesis]); toxins (carbon monoxide, carbon disulfide, manganese); structural lesions of the midbrain or basal ganglia; vascular lesions of the striatum from repeated head trauma; and in rare cases encephalitis. Parkinsonism is the fourth most common neurodegenerative disease of the elderly. Men and women are equally affected; the mean age of onset is 57 years, and peak onset is in the seventh decade.

Disease Process Some agent or event triggers a degeneration and loss of pigmented neurons in the substantia nigra, locus ceruleus, and other brainstem dopaminergic cell groups. The loss of these neurons leads to a depletion in neurotransmitter dopamine and interferes with the motor production of the basal ganglia. Interneuronal inclusion bodies (Lewy bodies) are left in surviving pigmented neurons and serve as biologic markers of the disease. Clinical manifestations emerge only after 75% to 80% of the dopamine innervation has been destroyed.

Symptoms Early Infrequent blinking; lack of facial expression;

deliberateness of speech; impaired postural reflexes, particularly in the arm; resting pill-rolling tremor of one hand that is absent during sleep.

Midcourse Progressive rigidity, slowness and poverty of

movement, difficulty initiating movement; muscle aches and fatigue; masklike, openmouthed facial expression; stooped posture; gait begins slow and shuffling and quickens to a run with a forward lean; hypophonic speech with stuttering dysarthria; drooling; dysphagia; forgetfulness; resting tremors of lips, jaw, tongue, and limbs; depression

Late Severe postural instability; urinary retention;

orthostatic hypotension; paranoia with visual hallucinations; delirium; dementia

Potential Complications Injury from falls is a common threat. Other complications include aspiration pneumonia, drug reactions, and disuse syndrome.

Diagnostic Tests The diagnosis is based primarily on the pattern of clinical manifestations and must be distinguished from individuals with essential tremor in which the tremor is action related and without facial or gait involvemenT.

Treatments Surgery Stereotactic thalamotomy to alleviate

tremors and rigidity in drug-resistant individual

Drugs Antiparkinsonian agents such as levodopa,

Sinemet, Artane, Cogentin, Parsidol, and Parlodel to reduce tremor and rigidity; antihistamines and anticholinergics to extend the effects of levodopa; antidepressants for depression; anticholinergics with neuroleptics to prevent parkinsonism

General TREATMENTS: Long-term physical therapy to maintain muscle tone,

function, and range of motion, gait training, and transfer training; occupational therapy to maintain activities of daily living and teach safety skills; speech therapy to evaluate and improve swallowing abilities, reduce dysarthria, and strengthen facial muscles; warm baths and massage to relax muscles; consistent exercise program; assistive devices (canes, walkers, wheelchairs, electric lift chairs, grab bars, raised toilet seats, bath seats, eating and hygiene devices); counseling for depression and long-term adaptation; measures to prevent skin breakdown, urinary tract infections, falls, and corneal abrasions; deep breathing to maintain vital capacity; balanced, low-protein diet; bowel and bladder programs; treatment of underlying cause in secondary parkinsonism

PARKINSON’S DISEASE

PARKINSON’S DISEASE

Dementia – a progressive organic mental disorder characterized by chronic personality disintegration---changes in memory, judgment, language, mathematic calculation, abstract reasoning, problem solving ability, impulsive behavior, stupor, confusion, and disorientation.

--- most common type is AD, with an unknown cause

--- no cure or specific tx.

ALZHEIMER’S DISEASEPROGRESSIVE DECLINE IN TWO OR MORE AREAS OF COGNITION CAUSING DEMENTIA

--A chronic, progressive, neurologic disorder characterized by degeneration of the neurons in the cerebral cortex and subcortical structures, resulting in irreversible impairment of intellect and memory.

Causes and Incidence The cause is unknown, although theories involving genetic links, neurotransmitter deficiencies, viruses, aluminum poisoning, autoimmune diseases have been advanced

. Approximately 3% of individuals over 65 years of age show signs of the disease; the proportion climbs to 20% in those over 80 years of age. The incidence is higher in women.

Disease Process Selective neuronal cells, primarily those involved in the transmission and reception of acetylcholine, degenerate in the cerebral cortex and basal forebrain, resulting in cerebral atrophy of the frontal and temporal lobes, with wide sulci and dilated ventricles. Senile plaques and neurofibrillary tangles are present. The basic pathophysiologic processes accompanying the brain damage are unknown.

Symptoms Early Short-term memory loss, impaired insight/judgment,

momentary disorientation, emotional lability, anxiety, depression, decline in ability to perform activities of daily living (ADLS)

Midcourse Apraxia, ataxia, alexia, astereognosis, auditory agnosia,

agraphia, prolonged disorientation, progressive memory loss (longand shortterm), aphasia, lack of comprehension, decline in care abilities, insomnia, loss of appetite, repetitive behavior, socially unacceptable behavior, hallucinations, delusions, paranoia

Late Total dependence in ADLs, bowel and bladder

incontinence, loss of speech, loss of individuation, myoclonic jerking, seizure activity, loss of consciousness

Potential Complications The end stage of Alzheimer's disease invites complications commonly associated with comatose conditions (e.g., skin breakdown, joint contractures, fractures, emaciation, aspiration pneumonia, infections).

Diagnostic Tests Definitive diagnosis can be made only through autopsy.

Clinical evaluation Any of the above manifestations after

depression, delirium, and other dementia disorders (e.g., head injury, brain tumor, alcoholism, drug toxicity, arteriosclerosis) have been ruled out; family history

Mental status examination Decreased orientation, impaired

memory, impaired insight/ judgment, loss of abstraction/ calculation abilities, altered mood

Computed tomography/magnetic resonance imaging

Brain atrophy; symmetric, bilateral, ventricular enlargement

ElectroencephalogramSlowed brain wave activity, reduced voltage

Treatments SurgeryNone Drugs Medications for treating specific symptoms or

behavioral manifestations (i.e., antidepressants, stimulants, antipsychotics, sedatives); experimental drugs include cholinergic, dopamine, and serotonin precursors; neuropeptides; and transcerebral dilators

General Structured, supportive, familiar environment;

orientation and cueing program for daily tasks; safety program; family support and counseling; ; institutionalization when home care is no longer possible

3 STAGES1. FIRST STAGE 2. SECOND STAGE

OR CONFUSIONAL

STAGE3. TERMINAL STAGE

ALZHEIMER’S DISEASEINTERVENTIONS1. DECREASING ENVIRONMENTAL STIMULI2. APPROACHING THE CLIENT CALMLY WITH REASSURANCE3. TAKING CARE NOT TO PLACE ANY DEMANDS ON CLIENT

MULTIPLE SCLEROSISA CHRONIC DEMYELINATING DISEASE THAT AFFECTS THE MYELIN SHEATH OF THE NEURONS IN THE CENTRAL NERVOUS SYSTEM

ETIOLOGYHEREDITARY/GENETICVIRAL INFECTION

(EPSTEIN-BARR)

MULTIPLE SCLEROSISPATHOPHYSIOLOGYPLAQUES FORM ALONG THE MYELIN SHEATH CAUSING INFLAMMATION, EDEMA AND EVENTUALLY SCARRING AND DESTRUCTION

MULTIPLE SCLEROSIS DISEASE CATEGORY1. RELAPSING REMITTING – EPISODES

OF ACUTE WORSENING WITH RECOVERY AND A STABLE COURSE BETWEEN RELAPSES

2. SECONDARY PROGRESSIVE – GRADUAL NEUROLOGIC DETERIORATION WITH OR WITHOUT SUPERIMPOSED RELAPSES IN A CLIENT WHO IS PREVIOUSLY HAD RELAPSING REMITTING MS

MULTIPLE SCLEROSIS3. PRIMARY PROGRESSIVE – GRADUAL NEARLY CONTINUOUS NEUROLOGIC DETERIORATION FROM THE ONSET OF MANIFESTATIONS

4. PROGRESSIVE RELAPSING – GRADUAL NEUROLOGIC DETERIOTATION FROM THE ONSET OF MANIFESTATIONS BUT WITH SUBSEQUENT SUPERIMPOSED RELAPSES

MULTIPLE SCLEROSIS CLINICAL MANIFESTATIONS1. WEAKNESS OR TINGLING

SENSATION2. VISION LOSS FROM OPTIC

NEURITIS3. INCOORDINATION THAT IS DUE TO

CEREBELLAR INVOLVEMENT4. BOWEL AND BLADDER

DYSFUNCTION AS A RESULT OF SPINAL CORD INVOLVEMENT

MULTIPLE SCLEROSISMANAGEMENT1. TREAT ACUTE RELAPSES – IV

OR ORAL STEROIDS2. TREAT EXACERBATIONS –

INTERFERONS3. SYMPTOMATIC TREATMENT

LIKE BLADDER/BOWEL DYSFUNCTION, TREMOR, COGNITIVE & PERCEPTUAL DISTURBANCES

MULTIPLE SCLEROSIS

MANAGEMENT Surgery

Rhizotomy for unresponsive spasms; contracture releases

Drugs Muscle relaxants for spasticity; corticosteroids for acute attacks; immunosuppresive use is in clinical trials

MULTIPLE SCLEROSISMANAGEMENT General Balance of rest and activity; long-term

rehabilitation (occupational, physical, and speech therapy) to maintain activities of daily living, adapt to progressive loss of function, prevent disuse syndrome, and promote bowel and bladder control; assistive devices (canes, walkers, bracing, casting, wheelchairs); counseling and psychologic support of individual and family; ventilatory assistance and communication devices in end-stage disease; care in feeding if dysphagia is present; evaluation for cognitive dysfunction; plasmapheresis and total lymphoid irradiation are under investigation

GUILLAIN-BARRE SYNDROME

AN INFLAMMATORY DISEASE OF UNKNOWN ORIGIN THAT INVOLVES DEGENERATION OF MYELIN SHEATH IN THE PERIPHERAL NERVES

ETIOLOGYCMV, EBV,

CAMPYLOBACTER JEJUNI

Disease Process Mononuclear cells infiltrate the peripheral

nervous system and set up an inflammatory response in the blood vessels of the cranial and spinal nerves.

Demyelination of the peripheral nerves results, causing muscle weakness that begins in the lower extremities and ascends through the body in a symmetric fashion.

Respiratory paralysis and facial weakness occur in 30% to 40% of cases. In some cases axonal destruction can cause atrophy in distal muscles and permanent neurologic impairment.

GUILLAIN-BARRE SYNDROMECLINICAL MANIFESTATIONS1. ASCENDING WEAKNESS2. LOSS OF DTR3. PARESTHESIAS4. AUTONOMIC NEUROPATHY5. RESPIRATORY MUSCLE

WEAKNESS

Symptoms The first sign is symmetric muscle weakness in the distal extremities accompanied by paresthesia. This weakness spreads upward to the arms and trunk and then to the face. This ascension usually peaks about 2 weeks after onset. Deep tendon reflexes are absent. Difficulty chewing, swallowing, and speaking may occur, and respiratory paralysis may develop. Bladder atony, postural hypotension, tachycardia, and heart block may be seen. Deep, aching muscle pain is also common.

Diagnostic Tests The diagnosis is based on the clinical presentation and cerebrospinal fluid samples, which show an increase in protein without an increase in lymphocyte count.

Electromyography produces abnormal nerve conduction results.

Treatments Surgery Tracheostomy to provide ventilation in the event of respiratory failure

Drugs Immunoglobulin given IV to counteract neurologic defect; narcotic analgesics for pain; prophylactic antiinfectives

Corticosteroids are contraindicated because they worsen the ultimate outcome

Treatments General Plasma exchange to speed recovery of neurologic deficit;

respiratory monitoring and mechanical ventilation for respiratory paralysis;

cardiac monitoring for sinus tachycardia, bradyarrhythmia;

communication systems if ventilator is used or with facial paralysis;

Treatments General passive range-of-motion exercises; turning to prevent contracture and skin breakdown; rehabilitation to aid neurologic recovery; counseling and support of individual and family for long-term adaptation

Seizures (Convulsions, Epilepsy)

Paroxysmal episodes of sudden, involuntary muscle contractions and alterations in consciousness, behavior, sensation, and autonomic functioning.

The episodes may be partial (simple, complex) or generalized (absence,myoclonic, tonic, clonic, tonic-clonic) and are labeled epilepsy if they are recurrent.

Causes and IncidenceThe etiology of seizures may be idiopathic or

symptomatic.Identified causes include pathologic processes

in the brain (e.g., vascular anomalies or lesions, space-occupying lesions, trauma, acute cerebral edema, infection, degeneration, and neuronal injury);

endogenous or exogenous toxic substances (e.g., uremia, lead ingestion, alcohol intoxication, or phenothiazides);

metabolic disturbances; febrile states; developmental abnormalities; or birth defects.

Disease Process Seizures result from a generalized disturbance

in cerebral function. An internal or external stimulus causes abnormal hypersynchronous discharges in a focal area in the cerebrum that spread throughout the cerebrum.

During the seizure, neuropeptides and neurotransmitters are released and blood flow is increased.

Extracellular concentrations of potassium are increased, and concentrations of calcium are decreased.

Changes occur in pH and utilization of glucose increases.

Disease Process It is hypothesized that the seizure ceases when the neuronal cell membrane hyperpolarizes and causes the neuronal cells to cease firing, suppressing the surface potentials of the cerebrum.

Partial seizures begin locally with a specific aberration of sensory, motor, or psychic origin, reflecting the cerebellar origin of the seizure.

A complex partial seizure progresses to impairment of consciousness.

Disease Process A generalized seizure affects both consciousness

and motor function from the onset. Absence seizures last 10 to 30 seconds and involve

twitching and loss of contact. Myo-clonic seizures involve intermittent

contraction of muscles without loss of consciousness. Tonic seizures are marked by prolonged

involuntary muscle contraction with a 30- to 60-second loss of consciousness.

Clonic seizures involve intermittent muscle contractions and loss of consciousness for several minutes.

Tonic-clonic seizures involve loss of consciousness with sustained muscle contractions, followed by intermittent muscle contractions and then a limp body state.

Symptoms Simple partial Motor: recurrent involuntary muscle

contractions of one body part (e.g., face, finger, hand, or arm) that may spread to other, same-side body parts Sensory: auditory or visual hallucinations, paresthesias, vertigo Psychic: sensation of deja vu, complex hallucinations or illusions, unwarranted anger or fear, pupillary dilation, sweating

Complex partial Onset: may have aura before onset Motor:

automatisms (patting body parts, smacking lips, aimless walking, picking at clothes), unintelligible muttering, staggering gait Sensory: 1 to 2 minutes of loss of contact with surroundings, hallucinations

Symptoms Generalized Absence: transient loss of consciousness,

flickering of eyelids or intermittent jerking of hands Myoclonic: rapid, jerky movements in extremities or over entire body, which may cause a fall Tonic: sudden abnormal dystonic posture, deviation of eyes and head to one side Clonic: symmetric jerking of extremities for several minutes with loss of consciousness Tonicclonic: aura of epigastric discomfort, outcry, loss of consciousness, cyanosis, fall; tonic then clonic contractions, then limpness, sleep, headache, muscle soreness, confusion, and lethargy; loss of bowel and bladder control

Potential Complications Complications may occur as a result of the

onset of seizure activity and can include injury from a fall or from jerking, as well as airway occlusion and aspiration.

A condition known as status epilepticus, in which motor sensory or psychic seizures follow one another with no intervening periods of consciousness, is a medical emergency.

Failure to get immediate treatment can lead to hypoxia, hyperthermia, hypoglycemia, acidosis, and death.

Diagnostic Tests The presence of seizures is diagnosed by clinical history and examination. The diagnostic priority is to distinguish idiopathic seizure activity from symptomatic activity.

Computed tomography/ magnetic resonance imaging/positron emission tomography Structural changes

Skull x-ray Evidence of fractures; shift in calcified

pineal gland; bony erosion; separated sutures

Cerebral angiography Vascular abnormalities; subdural hematoma

Diagnostic Tests Cerebral angiography

Vascular abnormalities; subdural hematoma Echoencephalography

Midline shifts in brain structures Urine

To detect medication toxicity Serum

Hypoglycemia; electrolyte imbalance; increased blood urea nitrogen; increased blood alcohol levels

Electroencephalography Tonicclonic: high, fast voltage spiked in all leads

Absence: 3/s, rounded, spiked wave complexes in all leads Complex partial: squaretopped, 4-6/s spike wave complexes over involved lobe Inherited pattern: 2.5 to 3/s spike and wave pattern; presence of delta waves indicates destroyed brain tissue

Treatments Surgery

Resection of epileptic focus or stereotactic lesions in the brain

Drugs Anticonvulsants to prevent or control seizure

activity General

During seizure: safety precautions to prevent injury (i.e., loosen restrictive clothing, roll on side to prevent aspiration, place a small pillow under the head, ease from a standing or sitting position to the floor)

Do not place a finger or other object into the person's mouth to protect or straighten the tongue--it is unnecessary and dangerous; do not try to hold the person still because you may injure the individual or yourself

Treatments Maintain a patent airway; note frequency, type, time, involved body parts,

and length of seizure; monitor vital signs and neurologic status; reorient individual as seizure ceases Other: eliminate causative or precipitating

factors; encourage normal lifestyle, moderate exercise, and participation in sports with proper safeguards; a driver's license is permitted in most states if the person is seizure free for 1 year; alcohol is contraindicated; medical and laboratory monitoring of anticonvulsant blood levels and possible side effects; information about the importance of taking medications as directed and not deleting doses; individual and family support to adapt to seizure disorder; wearing a Medic-Alert tag