Epilepsy is a chronic neurological condition characterized by recurrent, unprovoked seizures. It can be classified as generalized seizures originating from both hemispheres of the brain or focal seizures arising from one hemisphere. The majority of childhood epilepsy cases are idiopathic, while secondary causes include brain malformations, infections, tumors or trauma. Diagnosis involves clinical history and examination along with an EEG. Treatment primarily consists of antiepileptic drug monotherapy tailored to the seizure type, with the goal of seizure control and prevention of recurrence. Status epilepticus is a medical emergency defined by prolonged or repeated seizures, and requires rapid treatment to prevent neurological injury.

1. EPILEPSY IN CHILDREN

2. 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

3. 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

4. OLD CLASSIFICATION

5. 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
ILAE 2010 CLASSIFICATION

6. GENERALIZED SEIZURES

7. CLASSIFICATION

8. 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.

9. 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.
TONIC CLONIC SEIZURES

10. 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

11. 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.

12. PARTIAL SEIZURES ---FOCAL SEIZURES

14. 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.

15. Frontal seizures
• Involve the motor
cortex
• May lead to clonic
movements → travel
proximally→
(Jacksonian March)
• Asymmetrical tonic
seizures → bizarre
,hyperkinetic & easily
dismissed as non –
epileptic events
Temporal lobe seizure
• Most common
• Strange warning
feeling/ aura with
smell , taste
abnormalities &
distortion of sound &
shape
• Automatism → spread
to the premotor cortex
• Deja-vu & Jamais-vu
• Consiousness may be
impaired, length of
event is longer than a
typical absence

16. Occipital
• Distortion of vision
Parietal
• Causes contralateral
dysaesthesias (altered
sensation )
• Distorted body image

17. 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.

18. 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?

19.  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)

20. 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

21.  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?

22.  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?

23. 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

25. MANAGEMENT AND TREATMENT

26. 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

27. FOCAL DISCHARGES

28. GENERALIZED DISCHARGES

29. 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

30. 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.

31.  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

32. 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

33. 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

34. 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.

35. PARTIAL SEIZURES
Simple partial
Complex partial
Sec.generalised
FIRST LINE
carbamazepine
valproate
SECOND LINE
lamotrigine
topiramate
levetiracetam
phenytoin
Phenobarbitame
clonazepam
GENERALISED
SEIZURES
tonic clonic
Clonic
Absence
Atpical absence
Atonic,clonic
Myoclonic
Infantile spasms
valproate
valproate
valproate
Valproate,clonazepam
ACTH,prednisolone
lamotrigine
topiramate
levetiracetam
phenytoin
Phenobarbitame
Clonazepam
Lamotrigine
Topiramate,clonazepam
Topiramate,phenobarbitone,
piracetam,levetiracetam,lam
otrigine.
Nitrazepam,valproate

36. 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)

37.  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

38. STATUS EPILECTUS
 Any seizures lasting > 30 minutes OR
 Intermittent seizures longer than 30 minutes from which the
patient does not regain consciousness

39. CURRENT DEFINITION
 IMPENDING STATUS EPILEPTICUS
0 to 5-10 mins
 ESTABLISHED STATUS EPILEPTICUS
>30 mins
 REFRACTORY STATUS EPILEPTICUS
>60 mins

40. •Highest incidence in very young children
• 70% of children with epilepsy experience
at least one episode of SE
Mortality rate 8 to 32%

41. 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

42. 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

43. CAUSES OF SE(CONTINUED)
 Acute head trauma
 Brain tumor
 Neurodegenerative disorders
 Hepatic or renal encephalopathy
 Storage diseases.

44. 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

45. 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)

47. 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.

48. REFERENCES
 PAEDIATRIC PROTOCOL
2ND EDITION
 ILLUSTRATED TEXTBOOK OF PAEDIATRICS
3RD EDITION BY TOM LISSAUER,GRAHAM
CLAYDEN
 NELSON TEXTBOOK OF PEADITRICS
19TH EDITION

49. THANK YOU