CONVULSIONS IN CHILDREN

Seizure/convulsion- paroxysmal, timerelated change in motor activity and/ or behaviour that results from abnormal electrical activity in the brain

Epilepsy- considered to be present when 2/

more unprovoked seizures occur at an interval greater than 24hrs apart

Febrile seizures
Most common
Excellent prognosis 9m 5yrs
Simple, benign
Atypical, complex

Differentiation from Infections of central nervous system eg: meningitis/encephalitis important as it is cause of convulsions wirh fever

Simple, benign :
within 24hrs of fever onset

<10min usually single/ febrile episode generalised convulsions no post-ictal neurological deficit family history may be seen

Treatment prompt reduction of temperature with antipyretics/ hydrotherapy Supportive therapy, semi- prone position , adequate airway, oxygen, IV line Inj. Diazepam 0.2- 0.3 mg/ kg/ dose (slow push iv for control Phenobarbitone- sustained action and slower acting

Prophylaxis

Intermittent desirble, for 1st 3 days of fever Oral diazepam, midazolam, clobazam BZD- attain desired levels quickly
Continuous when failure of above sodium valproate/ phenobarbitone

Classification of epilepsy
Generalized
Tonic clonic (grand mal) Tonic Clonic

Absence (petit mal)

Atonic, akinetic (minor, motor)

 Idiopathic Childhood absence

Juvenile abscence

Cryptogenic West syndrome Lennox gastaut syndrome

Localised
Simple partial Complex partial

Syndromes Idiopathic
Benign childhood focal epilepsy with

centrotemporal spikes

Symptomatic
c/c progressive epilepsy

Undetermined syndromes
Neonatal seizures Severe myoclonic eplepsy of infancy

Tonic- clonic seizures

Most frequent form of chldhood epilepsy
Classic form- 4 phases
Aura Tonic Clonic Postictal phase

 Aura
vague unpleasant feelings, epigastric discomfort or

tear Sensory, visceral, motor or autonomic

Tonic
Sustained spasm of skeletal muscles, shrill cry Around 30 seconds

Most marked: antigravity muscles

Unconscious, falls on ground, pale face, dilated pupils,

eyes rolled, frothing, involuntary stool/ urine passage

 Clonic
rythmic alternating contractions

Few minutes

Postictal
Headache, confusion, automatism EEG: gen. burst of spikes & irregular 4-6 hz spike

wave complex

Absence attacks

peak: 6-8 yrs < 30 s EEG: 3/ s spike & slow wave pattern Brief lapse of consciousness, sudden discontinuity of activity, staring spell, eye fluttering, rythmic movements No aura Nl. Devt. Postictal phase & neurological manifestatons absent

Partial seizures
60% of childhood seizures

Cause: infl. Granuloma, atrophic lesions, vascular

insults, b irth asphyxia, head trauma

Classification
Simple partial Elementary symptoms, no impairment of consciousness Motor, sensory, autonomic or mixed symptoms
Complex partial (impaired consciousness) SP but with LOC With automatism Partial with secondary generalisation

Psychomotor epilepsy
CP seizures originating from temporal lobe
Brief visceral, olfactory or visual aura

followed by peculiar posture, tonic jerks etc. Inappropriate repititive movements eg: chewing Complex automatisms/ acts No memory of events

Benign childhood epilepsy with centrotemporal spikes

2- 13 yrs No neurological/ intellectual deficit

Usually during sleep, SP with motor signs

Interictal EEG: spike focus over

centrotemporal/ rolandic area Self limiting with spontaneous remission around adolescence Rx: carbamazepine/ valproate

Neonatal seizures
Signal underlying neurological disease, severe

asphyxia or metabolic cause

Can present as Subtle(eyelid blinking, fluttering,

buccal lingual movement), Focal clonic, Multifocal clonic, Gen. tonic, myoclonic
Hypoxic ischemic encephalopathy(50%) Metabolic(hypo-glycemia, calcemia, magnesemia) (25%)

Cause

LP for meningitis diagnosis

Myoclonic epilepsies
West syndrome( infantile spasms) 3-8 m Combination of salaam spells (sudden dropping of head & flexion of arms), mental retardation & hypsarrythmia on EEG(diffuse high voltage slow spike & chaotic actvity) Cause: HIE, hge, injury Rx: ACTH & corticosteroids

Lennox -gustaut syndrome

Late infancy/ childhood Mixed seizures Intellectual regression Cause: head injury, anoxia Rx: valproic acid, benzodiazepine, ACTH EEG: very slow background & slow gen. spike wave discharges(2/ sec)

mechanism
To initiate seizure- there must be a group of

neurons, capable of generating a significant burst discharge & inhibition of GABA-ergic inhibitory system Excitatory amino acid neurotransmitters (glutamate, aspartate) may have role Neuronal death- devt. Of novel hyperexcitable synapses Brain injury
Inhibitory neurons selectively damaged aberrant excitatory circuits formed

treatment
1st afebrile seizure with nl. phy. Examination & EEG no need to start therapy
Goal
Use only 1 drug with lowest possible S/E
Drug increased slowly until seizure ctrl.

Accomplished or undesirable S/E develop

Complete seizure ctrl. min. 2 seizure free yrs

Abrupt withdrawal can cause status

epilepticus

Drugs phenytoin- GTCS & status epilepticus Carbamazepine-GTCS, SPS Valproic acid
Broad spectrum Myoclonic & atonic seizures GTCS, SPS, CPS

BZD-diazepam, clonazepam Barbiturates- phenobarbitone

Surgery Unresponsive to anticonvulsants

Counselling the parents

Status epilepticus
Continuous convulsions lasting for more than 30 min. or occurrence of serial convulsions between which

there is no return of consciousness Classification

Convulsive (tonic-clonic, clonic, tonic or myoclonic)- ass.

With sign. Mortality & morbidity Non- convulsive( absence, non- convulsive speech sensorial alteration)

Cause: sudden AED withdrawal, sleep deprivation,

intercurrent infection, hippocampal sclerosis, encepalitis, meningitis Blockage of N-methyl-d-aspartate channels by Mg2+ impt. In pathogenesis of neuronal damage here

Treatment A,B,C Diazepam 0.1-0.3 mg/kg iv & 0.2-0.5 mg/kg rectally Phenytoin- loading dose: 15 mg/ kg iv Phenobarbital- LD: 15-20 mg/kg iv Unresponsive: constant infusion of midazolam/ propofol (1-2 mg/kg) Valproic acid
Prognosis-potentially life threatening