EPILEPSY IN CHILDREN

WHAT IS EPILEPSY?

Epilepsy is a chronic neurological condition

characterized by recurrent, unprovoked
seizures, occurrence of at least 2 unprovoked
seizures 24 hours apart.
Epileptic seizure → clinical manifestation of
abnormal & excessive discharge of a set of neurons
in the brain
CAUSES
Idiopathic (70 – 80%) – cause unknown but presumed
genetic
Secondary
 Cerebral dysgenesis /malformation
 Cerebral vascular occlusion
 Cerebral damage
- Antenatal: Congenital infections, drugs, alcohol
- Natal: HIE, birth trauma
- Postnatal: IVH in prematurity, CNS infections,
kernicterus, trauma, tumour
Cerebral tumours
Neurodegenerative disorders
Neurocutaneous syndrome
OLD CLASSIFICATION
 ILAE 2010 CLASSIFICATION
GENERALISED SEIZURES:-
(Discharge arises from both hemisphere)
Absence seizures
Myoclonic seizure
Tonic
Tonic clonic
Atonic seizures

FOCAL – SEIZURES ARISE FROM ONE OR

PART OF ONE HEMISPHERE

Frontal seizures
Temporal lobe seizures
Occipital seizures
Parietal lobe seizures
GENERALIZED SEIZURES
CLASSIFICATION
TONIC CLONIC SEIZURES
Tonic phase
 The tonic phase begins with flexion of the trunk and
elevation and abduction of the elbows. Subsequent
extension of the back and neck is followed by extension
of arms and legs.

 Piercing cry may be present due to passage of air

through closed vocal cords.
 Autonomic signs are common during this phase and
include increase in pulse rate and blood pressure,
profuse sweating

 This stage lasts for 10-20 seconds.

TONIC CLONIC SEIZURES
Clonic phase
 tremor occurs at a rate of 8 tremors per
second, which may slow down to about 4 tremors
per second. This is because phases of atonia
alternate with repeated violent flexor spasms. Each
spasm is accompanied by pupillary contraction and
dilation. Some patients may have tongue or cheek
bites.

 The atonic period lasts about 30 sec.

The clonic phase lasts for 30 sec. to 1minute.

ABSENCE SEIZURES

Patient stares briefly and stop talking or ceases to

respond.
Most of the patient are completely motionless while
some feel some myoclonic movements in eye
lids,facial muscles,fingers at a rate of 3 per sec..and
this rate corresponds to the abnormality in EEG as
generalized 3 per sec.spike & wave pattern.
Occurs at the age of 4-12 years
Prognosis is good.95% remission in adolescense
 MYOCLONIC SEIZURES

These are brisque,brief muscular contractions

some of them involve only single muscle or a part of the
muscle & some of them are so large that they include
whole body or both the limbs.

Myoclonic jerks are common in the morning involving entire

body both the limbs and sometimes absence seizures are
common.
This is the most common form of idiopathic gen.epilepsy in
childhood.it begins at adolescence (15 yr).

 4 to 6 Hz irregular spikes have been noted in EEG.

PARTIAL SEIZURES ---FOCAL SEIZURES
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PARTIAL SEIZURE - FOCAL SEIZURE

 Begin in a relatively small group of dysfunctional

neurones in one of the cerebral hemispheres.
 Mayb e heralded by an aura which reflects the site
of the origin
 May or may not be associated with change in
consciousness or more generalised motor jerking.
 Frontal seizures Temporal lobe seizure
• Involve the motor • Most common
cortex • Strange warning
• May lead to clonic feeling/ aura with
movements → travel smell , taste
proximally→ abnormalities &
(Jacksonian March) distortion of sound &
• Asymmetrical tonic shape
seizures → bizarre • Automatism → spread
,hyperkinetic & easily to the premotor cortex
dismissed as non – • Deja-vu & Jamais-vu
epileptic events
• Consiousness may be
impaired, length of
event is longer than a
typical absence
 Occipital Parietal

Distortion of vision Causes contralateral dysaesthesias (altered sensati

Distorted body image
SPECIAL EPILEPSY SYNDROME

1.INFANTILE SPASM:-
-Most cases appears in 1st yr of life.
- Single brief recurrent gross flexion movements of
the limb …rarely extension movements
-EEG shows multifocal,multiple small spikes.
-On maturity it disappears(4 to 5yr)
-CT & MRI mostly normal.
-Later progress to LENOX GASTAUT SYND.
HISTORY TAKING
HOPI:-
 Two unprovoked seizures >24 hr apart suggest the presence of
an epileptic disorder
 Any aura?change in the behaviour?
 Types of seizures
-tonic clonic(tensing,then shaking,LOC)
-atonic(drop attack)
-absence(jus staring,not responding,blinking)
-partial(maybe consciouss,only ½ limbs shaking/jerking
 How long did it last?frequency?time of day?precipatating factor?
 Any loss of consciousness?tongue bitting?
 What did you do for the child?(appropriate first aid measures)
 Post ictal:drowsy?sleeping?vomiting?
PERINATAL HISTORY
 Infection during pregnancy?TORCH
Birth history - birth asphyxia , birth trauma
Neonatal jaundice

POST NATAL HISTORY

Central nervous system (CNS) infection e.g.

meningitis, encephalitis etc.
Head injury
Lead contact (lead fumes from burning batteries, pica)
 PAST HISTORY

 Age at 1st seizure?describe seizure?

h/o febrile seizures
When and how diagnosed?any event preceding seizure?

DRUG HISTORY
1. Anticonvulsant medications
2. How many?
3. Any increase in dosage?types?
4. Compliance,how often dose missed?what to do if missed?
5. Side effect?
6. Responding current medication or not
Outpatient review
1. Frequency
2. Test done
3. Other investigations(eg.EEG to date)

 Hospitalization
1. How many?reasons?

 Any identified medical problems associated with seizures?

1. Any history of trauma,meningitis?encephalitis?
2. How are this problem managed?
 FAMILY HISTORY
1. Of convulsion?inborn error metabolism?
SOCIAL HISTORY:-
Impact on child:
1. Schooling
2. Athletic participation?
3. Self esteem
4. Does teacher know about the condition?
5. On family:financial burden

 CONTINGENCY PLAN:
1. What to do in the event of a seizure?
 PHYSICAL EXAMINATION

•Consciouss level
•Posture
•Deformity
•movement
•Dysmorphism,head size and shape
•Cranial nerves
•Gait
•Spine

•Neurocutaneous signs
1. café-au-lait spots
2. Neurofibromata
3. adenoma sebaceum
MANAGEMENT AND TREATMENT
DIAGNOSIS
The clinical diagnosis is more important then any
tool… (H/O, Eye witnesses, substantiated by video
if available)
# EEG:-
EEG is most sensitive tool for diagnosis which
shows electrical activity changes in the brain but it
also require clinical correlation
Many children with epilepsy may have normal EEG
and many children who will never have epilepsy
have EEG abnormalities
Done for dx, classification, selection of anti-
epileptic drugs and prognosis
FOCAL DISCHARGES
GENERALIZED DISCHARGES
 MRI and CT
 -not required routinely for childhood generalized epilepsy.

 To identify a tumour,vascular lesion or area of sclerosis.

 PET and SPECT.

 To detect areas of hypometabolism in epileptogenic
lesions
 OTHER INVESTIGATIONS

 Blood test and metabolic investigations(seizures related to

feed and fasting).
 Genetic studies

 Lumbar puncture
PRINCIPLES OF ANTICONVULSANT THERAPY
 Treatment recommended if ≥ 2 episodes→ recurrence
risk 80%
 Attempt to classify the seizure type & epileptic syndrome

 Monotherapy as far as possible → most appropriate drug

→ increase dose gradually till epilepsy controlled,
maximum dose reached / side effects occur

 Alternative monotherapy (Add on the 2nd drug if 1st

drug failed. Optimise 2nd drug, then try to withdraw 1st
drug.

 Rational combination therapy (usually 2 or maximum 3 drugs

)
 Combines drugs with different mechanism of action &
consider their spectrum of efficacy, drug interactions
& adverse affects.
 Monitor drug levels
(carbamazepine, phenytoin, phenobarbitone) to check
compliance → if seizures not well controlled/in situations
of polypharmacy where drug interaction is suspected.

 When withdrawal of medication is planned → seizure

free for 2 years, consideration should be given to
epilepsy syndrome, likely prognosis & individual
circumstances before attempting slow withdrawal of
medication over 3-6 months (longer if clonazepam/
phenobarbitone)

 If seizures recur → last dose reduction is reversed &

medical advice sought
INTRACTABLE EPILEPSY?
 Re- evaluate the following possibilities
 Is it a seizure /non epileptic event
 Anticonvulsant dose not optimized
 Poor compliance to anticonvulsant
 Wrong classification of epilepsy syndrome →
wrong anticonvulsant
 Anticonvulsant aggravating seizures
 Lesional epilepsy, hence a potential epilepsy
surgery candidate
 Progressive epilepsy or neurodegenerative disorder
REFERRAL TO PAEDIATRIC NEUROLOGIST
 Poor seizure control despite monotherapy with 2
different anticonvulsants
 Difficult to control seizures beginning in the 1st year
of life
 Seizures & developmental regression

 Structural lesion on neuroimaging

ADVICE FOR PATIENTS
 Educate and counsel on epilepsy.
 Emphasize compliance if on anticonvulsant.

 Don’t stop the medication by themselves.this may

precipitate breakthrough seizures.
 In photosensitive seizures-watch tv in brightly lit
room.avoid sleep deprivation.
 Use a shower with bathroom door unlocked

 No cycling in traffic,climbing sports or

swimming alone.
 Know emergency treatment for seizure

 Inform teachers and school abt the condition.

 FIRST LINE SECOND LINE

PARTIAL SEIZURES lamotrigine

topiramate
Simple partial carbamazepine levetiracetam
Complex partial valproate phenytoin
Sec.generalised Phenobarbitame
clonazepam

GENERALISED lamotrigine
SEIZURES topiramate
tonic clonic valproate levetiracetam
Clonic phenytoin
Phenobarbitame
Clonazepam

Absence valproate Lamotrigine

Atpical absence valproate Topiramate,clonazepam
Atonic,clonic Topiramate,phenobarbitone,
Myoclonic Valproate,clonazepam piracetam,levetiracetam,lam
otrigine.
Infantile spasms ACTH,prednisolone Nitrazepam,valproate
SIDE EFFECTS AND SERIOUS
TOXICITIES OF ANTICONVULSANT
 CARBAMAZEPINE—drowsiness,dizziness,ataxia,diplopia,rash
(serious toxicity—agranulocytosis
Steven Johnson syndrome)

 CLONAZEPAM----
hypotonia,salivary and bronchiol hypersecretion,paradoxical
hyperactivity,aggresiveness

 PHENYTOIN---
ataxia,diplopia,rash,gum hypertrophy,hirsutism
(serious toxicity—megaloblastic anemia)
 PHENOBARBITONE----
cognitive dysfunction,ataxia,rash,behavioural
disturbance
serious toxicity—liver toxicity,steven johnson
syndrome

 VALPROATE----
epigastric pain,tremor,alopecia,weight gain,hair
loss,thrombocytopenia
serious toxicity—hepatic toxicity(<2 yrs age)
hepatitis,pancreatitis,
encephalopathy
STATUS EPILECTUS

Any seizures lasting > 30 minutes OR

Intermittent seizures longer than 30 minutes from which the

patient does not regain consciousness
CURRENT DEFINITION

 IMPENDING STATUS EPILEPTICUS

0 to 5-10 mins

 ESTABLISHED STATUS EPILEPTICUS

>30 mins

 REFRACTORY STATUS EPILEPTICUS

>60 mins
 •Highest incidence in very young children

• 70% of children with epilepsy experience

at least one episode of SE
Mortality rate 8 to 32%
CAUSES OF SE
1)Prolonged febrile seizures

Lasting for >30mins

Particularly in child younger than 3 years old
Associated with severe damage to the
hippocampus in children(Hippocampus sclerosis)
Most common cause of SE
May be the initial manifestation of encephalitis, and
epilepsy may be a long term complication of
meningitis
CAUSES OF SE
2)Idiopathic status epilepticus

Includes epilepticus patients in whom SE followed

sudden withdrawal of anticonvulsants(esp.
benzodiazepines and barbiturates)
Given anticonvulsants on an irregular basis or who
are noncompliant are more likely to develop SE
CAUSES OF SE(CONTINUED)
Acute head trauma
Brain tumor
Neurodegenerative disorders
Hepatic or renal encephalopathy
Storage diseases.
MECHANISM OF SE

Inreased cerebral metabolic rate

Increased in cerebral flow

(half an hour)
Inadequate oxygen tension and togetther with
other factors lead to

Neuronal injury

STATUS EPILEPTICUS
MANAGEMENT OF STATUS EPILEPTICUS

Securing airway ,breathing and circulation

(with continuous monitoring of vital signs ,ECG)

Determination and management of the underlying

etiology(eg.hypoglycemia)
Laboratory studies(glucose,sodium,Ca)
Blood and spinal culture,toxic screens
test for inborn error of metabolism
Antiepilectic drugs level
EEG(ruling out pseudostatus epilepticus)
SUMMARY

 affects 1 in 200 children

Is classified as generalised or focal(partial) or an
epilepsy syndrome of childhood
If suspected EEG is indicated
Most but not all requires antiepileptic drug
therapy,which should be appropriate for the
seizure,compromise as few drugs and with the least
potential for unwanted effects as possible
Requires liaison with the school about the
management of seizures and avoiding situations
ehich could lead to injury.
REFERENCES
PAEDIATRIC PROTOCOL
2ND EDITION

ILLUSTRATED TEXTBOOK OF PAEDIATRICS

3RD EDITION BY TOM LISSAUER,GRAHAM
CLAYDEN

NELSON TEXTBOOK OF PEADITRICS

19TH EDITION
THANK YOU