SEIZURE

DISORDERS
 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.
Definition of epilepsy

It is a chronic disorder of abnormal,recurrent

excessive and self termianting discharge from
neurons.
 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 COMPLEX PARTIAL

• a. Motor seizures • . Impairment of

• d. Sensory seizures consciousness
• e. Autonomic seizures • b. Associated with
• f. Psychic seizures 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
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
• Sudden,Seizure
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
• Characterized by sudden bilateral
seizures
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 los s of con scious
ness;
• b. Mo tor seiz ur e s :
• c. Sensory seizures:
• d. Auton omic seizures:
• e. Psychic seizure s :
 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
• A (AED)
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 AEDs
Classical Newer
• Phenytoin • Lamotrigine
• • Felbamate
Phenobarbital
• Topiramate
• Primidone • Gabapentin/Prega
• Carbamazepine balin
• • Tiagabine
Ethosuximide
• Vigabatrin
• Valproate (valproic • Oxycarbazepine
acid) • Levetiracetam
• Trimethadione (not • Fosphenytoin
currently in use)
 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
 AEDs:
Mechanisms of
Action
Voltage-gated sodium channel
Open Inactivated
Na + Na +

I I
Carbamazepin Lamotrigin
Na + e Phenytoin e
Valproate
 AEDs:
Mechanisms of Action
• Calcium channel blockade
 AEDs:
Mechanisms of Action
• GAB
A
 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
 GABA
Barbiturate
Benzodiazepines,
s
Gabapentin
Levetiracetam,Topiramate
Valproate,Vigabatrin

Na+ Ca2+

Carbamazepine, Ethosuximide
Oxcarbazepine,
Phenytoin Topiramate, Levetiraceta
Valproate m Pregabalin
Valproate
 GENERALIZED PARTIAL ABSENCE MYOCLONIC STATUS
TONIC- SEIZURES & ATYPICAL EPILEPTICUS
CLONIC SEIZURES SYNDROMES
SEIZURES

Drugs of Valproic Acid Carbamazepine Ethosuximide Valproic Acid Diazepam

Choice Carbamazepine Lamotrigine Valproic Clonazepam Lorazepam
Phenytoin Phenytoin

Alternative Phenobarbital Felbamate Clonazepam Levetiracetam Phenytoin

Agents Phenobarbital Topiramate Phenobarbital
Topiramate Zonisamide
Valproic Acid

Adjunctive Lamotrigine Gabapentin Lamotrigine Lamotrigine

Drugs Topiramate Pregabalin Levetiracetam Felbamate
Zonisamide
 Other Clinical Uses
 Valproic acid –mania
 Carbamazepine, Lamotrigine –
bipolar disorder
 Carbamazepine –trigeminal
neuralgia
 Gabapentin –pain of neuropathic
origin
 Topiramate –migraine
 Pregabalin –neuropathic pain
M A I N I N D I C AT I O N S O F A N T I E P I L E P T I C D R U G S
 T OX I C IT Y
• Teratogenicity
• Overdosage Toxicity
• Life-Threatening Toxicity
 Teratogenicity
 Valproic acid –neural tube defects
Carbamazepine –craniofacial
anomalies, spina bifida
 Phenytoin –fetal hydantoin
syndrome
 Overdosage Toxicity
• Respiratory depression

 Management: supportive
 Airway management
 Mechanical ventilation
 Life-Threatening Toxicity
 Valproic acid –fatal hepatoxicity
Lamotrigine –Stevens-Johnson
syndrome
 Zonisamide –severe skin
reactions
Felbamate –aplastic anemia, acute
hepatic failure
KETOGENIC / LOW CARBOHYDATE
DIET

 VAGAL NERVE STIMULATION (VNS)

SURGICAL MANAGEMENT
• Temporal lobe resection
• Lesionectomy
• Functional Hemispherectomy
• Corpus Callosotomy
• Extratemporal Cortical Resection
DO WITH PRECAUTION------

•DRIVING

•ASCENDING HEIGHTS

•WORKING WITH FIRE OR COOKING

•USING POWER TOOLS

•DANGEROUS ITEMS

•TAKING UNSUPERVISED BATHS

ASSESSMENT:

•HISTORY, INCLUDING PRENATAL,

BIRTH, AND DEVELOPMENTAL
HISTORY, 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 DIAGNOSIS
1. Risk for trauma related to seizure activities
2. Risk for suffocation related to seizure activities
3. Risk for Ineffective Airway Clearance
4. Risk for Ineffective Breathing Pattern
5.Low Self-Esteem related to Stigma
associated with condition perception of being
out of control evidence by social isolation
6.Knowledge Deficit related to lack of exposure, unfamiliarity
with resources Information misinterpretation lack of recall;
cognitive limitationevidence by asking questions
Complications
• Ventilator insufficiency
• Hypoxemia
• Cardiac dysarryhtmia
• Hyperthermia
• Systemic acidosis
• Severe injury
• Death
• Fracture of bone.
• Impair intelligence.
• Unable to get job, driver’s license, life insurance.
• Socially stigmated.
• Reduced quality of life.
Health education

• Drug must be taken as prescribed

• Use relaxation therapy,Bio-feedback training •
Avoilance of excessive alchol intake,Fatigue, Loss of
sleep