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Epilepsy
Epilepsy
Prepared by
Dr : Ahlam Abdulmalik
Learning Objectives
Simple partial
partial
Complex partial
Seizures
Absence
Generalized
Tonic colonic
Myoclonic
Atonic
Partial seizures
1. Simple partial seizures :
Not associated with impairment in consciousness
Brief motor seizures ( tonic, clonic, atonic) occur in the
face and can extends to the arm and leg
2. Complex partial seizures :
Associated with impairment in consciousness
Usually last 1-2 minutes
Preceded by Aura ( periectal phase) occur as visual
hallucinations, sense of fear, deja vu
Partial seizures
2. Complex partial seizures :
Ictal phase: decrease response with staring look
May be associated with automatims that are automatic
semipurposeful movements of the mouth (lip smaking ,
chewing) or extremities( rubbing of fingers, shuffling of
feet)
Postictal phase: sleepiness, may be Todd paralysis or
aphasia
3. Partial with secondary generalized : also called
Jacksonian , start as partial then spread to all become
generalized
Generalized seizures
1. Absence seizures :
Usually start at 5-8 years of age, often overlooked by
parents for many months
Occur as brief loss of environmental awareness for few
seconds may be with upward eye rolling
Accompanied by automatism as eye blinking, mouth
movements
No Aura or postictal period
Periceptated by hyperventilation
EEG shows 3 Hz spike and slow wave discharge
The drug of choice is Ethosuximide
Generalized seizures
Atypical absence seizures have associated myoclonic
component and change in the tone of the head ( head
drop), it is difficult to treat
The drug of choice is sodium valporate
Prognosis of absence seizures is good most cases
resolved by puberty
2. Generalized motor seizures :
Most commonly generalized tonic clonic
Start with loss of consciousness , sudden cry upward
rolling of the eyes . Then followed by generalized tonic
clonic or only tonic contraction with falling , apnea and
cyanosis
Generalized seizures
2. Generalized motor seizures :
Take 1-2 minutes
Associated with incontinence and followed by postictal
period that may takes 30 minutes to several hours
Treatment is by sodium valporate or levetiracetam
3. Atonic seizures :
It is a brief loss of muscle tone lasting 1-2 seconds , with
high risk of injuries
Epilepsy syndromes
1. Bengin childhood epilepsy with centrotemporal
spike : also called Rolandic epilepsy
Starts in childhood at 3-10 years and outgrow in
adolescence
Typically occur at night during sleep as simple partial ,
tonic clonic contraction in one side of the face with
drooling and preserved consciousness , complex partial
can also occur
EEG shows centrotemporal spikes , MRI is normal
Treatment is not always necessary, if need by using
carbamazepine with good response
Epilepsy syndromes
2. Juvenile Myoclonic epilepsy ( Janz syndrome)
The most common generalized epilepsy in young adult
account for 5% of all eplipsies
Start in early adolescence as Myoclonic jerks in morning
often cause the patient to drop things, can be associated
with generalized tonic clonic
EEG shows generalized 4-5 Hz polyspikes and slow wave
discharge
Good response to valporate or levetiracetam, need
treatment for life
Epilepsy syndromes
3. Severe Myoclonic Epilepsy of infancy :
It is also called Dravet syndrome, start as focal febrile
seizure and later manifest myoclonic, poor response to
treatment
4. Infantile spasm: also called West syndrome
Start between the age of 2-12 months
May be secondary to CNS malformation, acquired brain
injury, Tuberous sclerosis, inborn error of metabolism ,
also may be cryptogenic
Epilepsy syndromes
4. Infantile spasm:
Triad of 1. infantile epileptic spasms that usually occur in
clusters 2. developmental regression 3. typical EEG
picture called hypsarrythmia
First line treatment options include :
ACTH( adrenocorticotropic hormone) , high dose oral
Corticosteroids, Vigabatrin
Epilepsy syndromes
5. Lennox Gastaut syndrome
Start between 2-10 years
Triad of developmental delay , multiple seizures types
( atypical absence , myoclonic, tonic) and EEG findings 1-
2 Hz spike and slow wave
Often intractable and difficult to control, most left with long
term cognitive impairment
Treatment by anticonvulsants and ketogenic diet, need
treatment for life
Diagnosis
1. Clinical :
full history with complete description for the event
including pre and postictal periods, having the parents
imitate the seizure can be helpful also vedio record for
the events , precipitating factors, frequency , duration ,
time of occurrence, also detailed natal history and
developmental history.
Also complete physical examination
2. Complete laboratory evaluation : Electrolytes
Diagnosis
Na , k , Ca , Po4, BUN , Creatinine, RBS also CBC and
toxic screening
3. EEG : The most useful neurodiagnostic test , used to
distinguish seizure from nonepileptic paroxysmal disorders
and to classify seizure types
4. Brain imaging : MRI is superior to CT scan in showing
most brain pathology , but in emergency cases CT is used (
post Trauma ) and often shows intracranial hemorrhage
EEG
Normal EEG EEG with polyspikes
Differential diagnosis
DD includes other non epileptic paroxysmal events as :
• Psychogenic non epileptic seizures
• Breath holding spells
• Sycopal attacks ( cardiac and non cardiac)
• Bengin paroxysmal vertigo
• Motor tics
• Night terrors
• Sandifer syndrome
• Bengin myoclonus of early infancy ( shuddering attacks)
Treatment
The goal of treatment is to maintain an optimal functional
state
Medication toxicity should be weight against the risk of
seizure recurrence, single agent limit the toxicity
The duration of treatment varies according to seizure type
and epilepsy syndrome, for most children medications can
be weaned off after 2 years without seizures
Treatment
Focal seizures: Generalized seizures:
• Carbamazepine • Clobazam
• Oxcarbazepine
• Flebamate
• Phenytion
• Levetiracetam
• Lamotrigen
• Valporic acid • Levetiracetam
• Topramite • Valporic acid
• Phenobarbital • Topramite
• Lamotrigen
• Phenobarbital
• Epilepsy surgery
• Ketogenic diet
• Ketogenic diet
Treatment
The most important side effects:
1. Steven – Johonson- syndrome
2. Rickets and hypocalcemia
3. Hepatotoxicity