SEIZURE

DISORDERSBY- SAMPURNA DAS

WHAT IS SEIZURES

Seizures are discrete, time-limited alterations in brain function - including changes in motor activity, autonomic function, consciousness, or sensation -that result from an abnormal and excessive electrical discharge of a group of neurons within the brain.

CAUSES• Genetic influence• Head trauma• Brain conditions• Infectious diseases• Prenatal injury• Developmental disorders

RISK FACTORS• Age• Family history• Stroke• Other vascular diseases• Dementia• Seizures in childhood.

PATHOPHYSIOLOGY Seizure producing stimuli(trauma,high

fever,brain injury)

 

a small group of abnormal neurons undergo prolonged depolarizations associated with the rapid firing of repeated action potentials.

These abnormally discharging epileptic neurons recruit adjacent neurons or neurons with which they are connected into the process

 

PATHOPHYSIOLOGY (CONT.)

the electrical discharges of a large number of cells become abnormally linked together

 

creating a storm of electrical activity in the brain

Seizures may spread to involve adjacent areas of the brain or through established anatomic pathways to other distant areas

GENERALIZED SEIZURES

• 1. Generalized Tonic-Clonic

(Grand Mal)• 2. Absence (Petit Mal)• 3 Atypical Absence• 4. Atonic seizures• 5. Myoclonic Seizure• 6. Tonic seizures

PARTIAL SEIZURES

SIMPLE PARTIAL

• a. Motor seizures  • d. Sensory seizures • e. Autonomic seizures • f. Psychic seizures

COMPLEX PARTIAL

• . Impairment of consciousness

• b. Associated with initial aura 

• c. Simple to complex automatisms

OTHERS• Partial Seizures Secondarily Generalized •  Selected Epileptic Syndromes

A. Infantile Spasms

B. Febrile Seizure

C. Lennox-Gastaut Syndrome

D. Benign Rolandic epilepsy

E. Juvenile myoclonic epilepsy

PHASES OF CONVULSION (1)PRODROMAL PHASE WITH SIGNS OR ACTIVITY WHICH PRECEDE A SEIZURE;

(2)AURAL PHASE, WITH A SENSORY WARNING;

(3)ICTAL PHASE WITH FULL SEIZURE;

(4) POSTICTAL PHASE WHICH IS THE PERIOD OF RECOVERY AFTER THE SEIZURE.

GENERALIZED TONIC-CLONIC SEIZURE• Loss of consciousness is quickly followed by a

sudden fall to ground. • In the tonic phase, muscles become rigid and

the simultaneous contractions of diaphragm and chest muscles may produce the characteristic "epileptic cry".

• The patient's eyes roll up or turn to the side and the tongue may be bitten.

• The rigidity is replaced shortly by series of synchronous clonic movements of head, face, legs and arms.

GENERALIZED TONIC-CLONIC SEIZURE

• Autonomic changes also observed included: increased blood pressure,increased heart rate, and bladder pressure; pupillary mydriasis; hypersecretion of skin and salivary glands; cyanosis of skin.

• Average duration 2 to 5 minutes.• Postictally, patients lethargic/sleepy lasting

several minutes to hours.• Incontinence seen in early postictal phase

ABSENCE SEIZURE• Onset between 4 and 14 years and

often resolve by age 18.• Brief episodes of staring with

impairment of awareness and responsive that begin without warning and end suddenly, leaving patient alert and attentive.

• In simple absence seizures, patient only stares.

Atypical Absence:• Onset between 1 to 7 years of age• similar to typical absence except that loss of

responsiveness during seizure is often less complete and more gradual in onset and cessation; Also clonic, tonic and atonic components (i.e., increase or decreases in muscle tone) are more pronounced than in typical absence

• EEG findings: slow spike and wave (< 2.5 Hz) discharge and/or incompletely generalized spike-waves

ATONIC SEIZURE

• In the more common complex absence seizures, staring is accompanied by simple automatic movements such as blinking of eyes, drooping of head, or chewing.

• Duration - short (10-45 secs), patients usually unaware of occurrence.

• Abrupt recovery without after effects

Myoclonic Seizure• Sudden, brief shock-like jerk of a

muscle or group of muscles, often occurs in healthy people as they fall asleep.

• Epileptic myoclonus usually causes synchronous and bilateral jerks of the neck, shoulders, upper arms, body, and upper legs.

Tonic seizures• Characterized by sudden bilateral

stiffening of the body, arms, or legs. Tonic seizures usually last less than 20 seconds and are more common during sleep.

• Primarily seen in younger children; commonly associated with metabolic disorder or underlying neurological deficit

• Duration 10-60 seconds; brief, if any, postictal symptoms

SIMPLE PARTIAL SEIZURES

• a. No loss of consciousness;• b. Motor seizures :• c. Sensory seizures:• d.  Autonomic seizures:• e. Psychic seizures:

Complex partial seizures (temporal lobe, psychomotor epilepsy)

• A. IMPAIRMENT OF CONSCIOUSNESS OBSERVED:

• Patients may appear to be conscious, closer examination shows that they are unaware of their environment

• fail to respond or respond inappropriately to questions

• are unable to remember the seizure episode.

• B. ASSOCIATED WITH INITIAL AURA (I.E., SIMPLE PARTIAL SEIZURE) IN >50% OF PATIENTS

• The aura is a simple partial seizure which may then progress to a complex partial (and/or generalized tonic-clonic) seizure. Most common forms of aura: fear, rising epigastric sensation, unilateral "funny feeling" or "numbness", or visual disturbances; focal twitching of face or fingers.

C. SIMPLE TO COMPLEX AUTOMATISMS (REPETITIVE MOTOR ACTIVITY THAT IS PURPOSELESS, UNDIRECTED, AND INAPPROPRIATE)

• They are frequently observed during complex partial seizures. Examples include repetitive chewing or swallowing, lip smacking, fumbling movements of fingers or hands, picking at clothing, mumbling, moving about aimlessly, purposeless behavior, and clumsy perseverance of a preceding motor act.

• Average duration 1 to 3 minutes• Postictal phase - confusion, lethargy,

altered behaviour, amnesic for event

3. PARTIAL SEIZURES SECONDARILY GENERALIZED –

• partial seizure may progress through several stages reflecting spread of discharge to different brain areas. For example, seizure may begin as simple partial (i.e., aura), progress to complex partial and subsequently become secondarily generalized (tonic-clonic).

4. Selected Epileptic Syndromes-

A. Infantile Spasms• Consist of sudden flexion of the head

with abduction and extension of arms, accompanied by flexion of knees and often a little grunt or cry. Spasms may also be extension rather than flexion..

• Onset -between 4 to 7 months of age

• Characterized by spasms, developmental retardation.

• Spasms may be flexor (jackknife), extensor or mixed flexor-extensor.

• spasms usually disappear by age 3 or 4, but child left profoundly handicapped, retarded, and often with Lennox-Gaustaut syndrome

• B. Febrile Seizures

• Convulsions that occur with fever (> 38oC) in children between 6 months and 6 years of age, not secondary to an infection of brain or meninges.

• Prevalence: 2 to 5% of all children will have a febrile seizure before 6 y/o; Peak incidence at 2 years of age.

• Intellectual dysfunction and neurologic sequelae may occur following febrile status epilepticus.

• C. Lennox-Gastaut Syndrome: • This syndrome is characterized by the triad

of intractable seizures, mental and developmental retardation, and slow spike and wave pattern on the EEG.

• begin between ages 1 and 6 years • respond poorly to antiepileptic drugs. • Behavioral problems are common • Probably result from the underlying

neurologic injury, effects of frequent seizures and head injuries, and high-dose combinations of antiepileptic drugs.

• D. Benign Rolandic epilepsy:

• This syndrome frequently begins in children with a family history of epilepsy.

• Characteristic sign is a partial motor or somatosensory seizure involving the face.

• Tonic-clonic seizures may also occur, especially during sleep.

• The seizures are infrequent (some patients require no medications), are easily controlled with antiepileptic drug therapy, and stop spontaneously by age 15.

• E. Juvenile myoclonic epilepsy:

• These myoclonic seizures, with or without tonic-clonic or absence seizures, usually begin shortly before or after puberty but may first occur in early adulthood.

• Mental developemnt is normal.

COMPLICATION:

• Physical Injuries from Epilepsy• Status Epilepticus• Sudden Unexplained Death in Epilepsy• Eclampsia• Social Challenges• Anxiety

WHAT IS STATUS EPILEPTICUS?

Status epilepticus (acute prolonged seizure activity) is a series of generalised that occur without full recovery of consciousness between attack.The term has been broadened to include clinical or electrical seizure lasting at least 30 minutes,even without impairment of consciousness.

TREATMENT

• DIAZEPAM

• PHENYTOIN

• PHENOBARBITOL

• GENERAL ANAESTHESIA

FIRST AID

DIAGNOSTIC STUDIES

• 1. HISTORY

• 2. PHYSICAL EXAMINATION

• 3. NEUROLOGICAL EXAMINATION• 4.BLOOD TESTS

• 5.ELECTROENCEPHALOGRAM

6.CT SCAN

7.MAGNETIC RESONANCE IMAGING

8.FUNCTIONAL MRI (FMRI)

9.POSITRON EMISSION TOMOGRAPHY

10.SINGLE-PHOTON EMISSION COMPUTERIZED TOMOGRAPHY

11.NEUROPSYCHOLOGICAL TESTS

MEDICAL MANAGEMENT

ANTI-EPILEPTIC DRUG (AED)• A drug which decreases the frequency

and/or severity of seizures in people with epilepsy

• Treats the symptom of seizures, not the underlying epileptic condition

• Goal: maximize quality of life by minimizing seizures and adverse drug effects

• Currently no “anti-epileptogenic” drugs available

Choosing the right AED

Seizure type

Epilepsy syndrome

Pharmacokinetic profile

Interactions/other medical conditions

Efficacy

Expected adverse effects

Cost

Classification of AEDsClassical

• Phenytoin• Phenobarbital• Primidone• Carbamazepine• Ethosuximide• Valproate

(valproic acid)• Trimethadione

(not currently in use)

Newer• Lamotrigine• Felbamate• Topiramate• Gabapentin/

Pregabalin• Tiagabine• Vigabatrin• Oxycarbazepine• Levetiracetam• Fosphenytoin

Targets for AEDs

• Increase inhibitory neurotransmitter system—GABA

• Decrease excitatory neurotransmitter system—glutamate

• Block voltage-gated inward positive currents—Na+ or Ca++

• Increase outward positive current—K+

• Many AEDs pleiotropic—act via multiple mechanisms

A = activation gateI = inactivation gate

McNamara JO. Goodman & Gilman’s. 9th ed. 1996:461-486.

AEDs: Mechanisms of Action

Na+ Na+

CarbamazepinePhenytoin

LamotrigineValproateNa+ Na+

I I

Voltage-gated sodium channel

Open Inactivated

X

AEDs: Mechanisms of Action

• Calcium channel blockade

AEDs: Mechanisms of Action

• GABA

Side effect issues

• Sedation - especially with barbiturates• Cosmetic - phenytoin• Weight gain – valproic acid, gabapentin• Weight loss - topiramate• Reproductive function – valproic acid• Cognitive - topiramate• Behavioral – felbamate, leviteracetam• Allergic - many

Carbamazepine,Oxcarbazepine, PhenytoinTopiramate, Valproate

EthosuximideLevetiracetamPregabalinValproate

BarbituratesBenzodiazepines, GabapentinLevetiracetam,TopiramateValproate,Vigabatrin

Na+ Na+ Ca2+ Ca2+

GABA GABA

GENERALIZED TONIC-CLONIC SEIZURES

PARTIAL SEIZURES

ABSENCE SEIZURES

MYOCLONIC & ATYPICAL SYNDROMES

STATUS EPILEPTICUS

Drugs of Choice

Valproic AcidCarbamazepinePhenytoin

CarbamazepineLamotriginePhenytoin

EthosuximideValproic

Valproic AcidClonazepam

DiazepamLorazepam

Alternative Agents

Phenobarbital FelbamatePhenobarbitalTopiramateValproic Acid

Clonazepam LevetiracetamTopiramateZonisamide

PhenytoinPhenobarbital

Adjunctive Drugs

LamotrigineTopiramate

GabapentinPregabalin

LamotrigineLevetiracetamZonisamide

LamotrigineFelbamate

Other Clinical Uses

Valproic acid –maniaCarbamazepine, Lamotrigine –

bipolar disorderCarbamazepine –trigeminal

neuralgiaGabapentin –pain of neuropathic

originTopiramate –migrainePregabalin –neuropathic pain

MAIN INDICATIONS OF ANTIEPILEPTIC DRUGS

TOXICITY

• Teratogenicity• Overdosage Toxicity• Life-Threatening Toxicity

Teratogenicity

Valproic acid –neural tube defectsCarbamazepine –craniofacial

anomalies, spina bifidaPhenytoin –fetal hydantoin syndrome

Overdosage Toxicity

• Respiratory depression

Management: supportive Airway management Mechanical ventilation

Life-Threatening Toxicity

Valproic acid –fatal hepatoxicityLamotrigine –Stevens-Johnson

syndromeZonisamide –severe skin reactionsFelbamate –aplastic anemia, acute

hepatic failure

NON PHARMACOLOGICALMANAGEMENT

KETOGENIC / LOW CARBOHYDATE DIET

VAGAL NERVE STIMULATION (VNS)

SURGICAL MANAGEMENT

• Temporal lobe resection• Lesionectomy• Functional Hemispherectomy• Corpus Callosotomy• Extratemporal Cortical Resection

ACTIVITY MODIFICATION AND

RESTRICTIONS

DO WITH PRECAUTION------

•DRIVING

•ASCENDING HEIGHTS

•WORKING WITH FIRE OR COOKING

•USING POWER TOOLS

•DANGEROUS ITEMS

•TAKING UNSUPERVISED BATHS

•SWIMMING

NURSING MANAGEMENT

ASSESSMENT:

• HISTORY, INCLUDING PRENATAL, BIRTH, AND DEVELOPMENTALHISTORY, FAMILY HISTORY, AGE AT SEIZURE ONSET, HISTORY OF ALL ILLNESS AND TRAUMAS.

•DETERMINE WHETHER THE PATIENT HAS AN AURA BEFORE AN EPILEPTIC SEIZURE, WHICH MAY INDICATE THE ORIGIN OF SEIZURE.

•OBSERVE AND ASSESS NEUROLOGICAL CONDITION.

•ASSESS VITALS AND NEUROLOGICAL SIGNS CONTINUOUSLY.

•ASSESS EFFECT OF EPILEPSY ON LIFESTYLE.

NURSING DIAGNOSIS1. Risk for trauma2. Risk for suffocation3. Risk for Ineffective Airway

Clearance4. Risk for Ineffective Breathing

Pattern5. Low Self-Esteem related to Stigmaassociated with condition perception

of beingout of control6. Knowledge Deficit related to lack

of exposure, unfamiliaritywith resources Information

misinterpretation lack of recall;cognitive limitation

NURSING MANAGEMENT