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173]

How I do it

How I treat a first single seizure in a child

Sheffali Gulati, Jaya Shankar Kaushik
Department of Pediatrics, Division of Child Neurology, All India Institute of Medical Sciences (AIIMS), Delhi, India

Abstract

An epileptic seizure is defined as transient occurrence of signs and/or symptoms due to abnormal excessive or synchronous neuronal
activity in brain. There are diverse etiologies for acute seizure in infants and children. The present review provides a broad approach to
diagnosis and treatment plan for acute seizure in children. The approach to a child with acute seizure is discussed with special emphasis
on clinical approach based on history and focused examination with judicious choice of investigation and further management plan.
The review also emphasizes on recognizing common nonepileptic events that masquerade as true seizure among infants and children.

Key Words

Children, epilepsy, seizure

For correspondence:
Prof. Sheffali Gulati, Department of Pediatrics, Division of Child Neurology, All India Institute of Medical Sciences (AIIMS),
Ansari Nagar, Delhi, India.
E-mail: sheffaligulati@gmail.com

Ann Indian Acad Neurol 2016;19:29-36

Introduction causes.[5] The present review focuses on practical approach to

A conceptual definition of “seizure” was formulated by a task
force of International League against Epilepsy (ILAE, 2005)
that defined “epileptic seizure” as transient occurrence of signs
and/or symptoms due to abnormal excessive or synchronous
neuronal activity in brain.[1] Epileptic seizure is a transient
phenomenon with the onset and termination, of brief duration,
has clinical manifestations (sensory, motor, autonomic,
cognitive, psychogenic, and/or affect alertness, awareness,
and responsiveness) and an ictogenesis due to abnormal
enhanced synchrony in the brain.[2] The overall prevalence of
epilepsy in India was estimated to 5.33 (4.25-6.41). [3] Treatment
gap to a tune of 71% have been the biggest challenge for the
management of epilepsy in India.[4]
The etiology for acute seizure in infants and children could be
diverse ranging from infective (neurocysticercosis, tuberculoma,
meningoencephalitis, and brain abscess), traumatic (intracranial
bleed due to recent or past head trauma), vascular (hemorrhage,
infarct), metabolic (hypoglycemia, dyselectrolytemia, hypoxic
ischemic, and inborn errors of metabolism), structural cause
(congenital malformation) or toxic (drug or toxin induced)
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acute first seizure in children in terms of initial stabilization,
detailed history, focused examination, and sensible choice of
investigation and management plan [Figure 1].
Initial Stabilization
Initial stabilization, diagnostic measures, and therapeutic
measures all go hand in hand while managing a child with
acute seizure. Measures for initial stabilization include
maintenance of airway, breathing, and circulation. Hypoxia is
detrimental to ongoing convulsion.[6] Airway patency may be
maintained by proper positioning by tilting the head back and
lift the chin to open the airway and turn the patient to one side
and suction the secretions. Other measures include suctioning
any excess secretions to maintain patency, reassessing the need
for oral airway and administration of 100% oxygen by nasal
cannula or nonrebreather mask.[7]
Vital signs including pulse rate, respiratory rate, blood
pressure, and oxygen saturation need to be monitored.
This is an open access article distributed under the terms of the
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License, which allows others to remix, tweak, and build upon the
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DOI: How to cite this article: Gulati S, Kaushik JS. How I treat a first
10.4103/0972-2327.173404 single seizure in a child. Ann Indian Acad Neurol 2016;19:29-36.
Received: 17-08-15, Revised: 15-10-15, Accepted: 21-10-15

© 2006 - 2016 Annals of Indian Academy of Neurology | Published by Wolters Kluwer - Medknow
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30 Gulati and Kaushik: Treating first seizure in children
Figure 1: Flowchart depicting approach to the diagnosis and management of acute seizure in infants and children
Indications for endotracheal intubation includes those with
persistent desaturation (SPo2 <92%), increased work of
breathing, refractory status epilepticus or presence of clinical
features of raised intracranial pressure. [8] A peripheral venous
access is required to draw the samples for electrolytes, blood
sugar, and serum calcium. Circulation needs to be maintained
with fluid resuscitation and need of inotropes may be decided
based on reassessment so as to stabilize circulating volume
to maintain cerebral perfusion pressure.[8] Management of
hypoglycemia (5 mL/kg of 10% dextrose) and hypocalcemia
(2 mL/kg of calcium gluconate) is essential in all children
presenting with acute seizure. Once the child is stabilized,
the first step is ascertain the most probable etiology of acute
seizure in the child.
History Taking
History is the most essential key to diagnosis of seizure. Parents
may be asked to narrate the entire episode including the
preceding events, events during the episode, and post episode.
Table 1 summarizes brief history that needs to be elicited. In
children, it is essential to differentiate a provoked seizure from
unprovoked seizure.
Provoking Factors
Unprovoked seizure would be considered when the seizure
cannot be explained by an immediate, obvious provoking cause
such as head trauma or intracranial infection.[1] Definition of
“unprovoked seizure” would be a seizure or a cluster of seizures
occurring within 24 h in a person older than 1 month, occurring
Annals of Indian Academy of Neurology, January-March 2016, Vol 19, Issue 1
Table 1: Table summarizing history taking points
in history of presenting complaints
History of presenting complaints
Age at onset and presentation (neonate, infancy, childhood)
Provocation factors (head trauma, fever, and preceding diarrheal
illness)
Frequency of seizure (Is it first episode?)
Preceding events (awake, sleep, playing, exercise, and following cry)
Presence of aura (somatosensory, auditory, visual, and abdominal)
(child >5 years)
Ictal manifestations (motor, sensory, autonomic, cognitive, and
behavioral)
Postictal period (postictal dizziness, loss of consciousness, immediate
return to normal)
Does the semiology suggest a nonepileptic event rather than epileptic
seizure
Birth history and developmental history
Family history of epilepsy and febrile convulsions
in the absence of precipitating factors.[9] The provoking factors
include fever, head trauma, previous central nervous system
(CNS) infection or tumor, hypoglycemia, electrolyte imbalance
(hyponatremia, hypernatremia, hypocalcemia), or history of
toxic or drug ingestion.
Seizure episodes could be provoked by prolonged fasting
(hypoglycemic seizure) or following a diarrheal illness
(dyselectrolytemia). Episodes provoked by fever could be
either due to febrile seizures or CNS infection (meningitis).
Presence of fever (temperature >38°C), generalized seizures,
seizure duration of less than 15 min with no postictal loss of
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Gulati and Kaushik: Treating first seizure in children 31

consciousness are more likely to be febrile seizures. Children Many of the nonepileptic events are benign and are related
with history of fever, seizure, and encephalopathy are likely to normal stages of development. The most common benign
to have meningoencephalitis. History of developmental delay, developmental movement disorder in infants and toddlers
perinatal asphyxia or other perinatal or postnatal injury, and include breath holding spells.[11] These episodes starts with
positive family history of epilepsy or febrile convulsion points provoking factors such as angry, fussy and crying baby who
towards an unprovoked epileptic seizures. suddenly becomes apneic, gets cyanosed, lose consciousness
and may have urinary incontinence and become stiff. This
sequence of crying followed by apnea, cyanosis, loss of
Was it True Seizure? consciousness, and tonic posturing is classical with breath
holding spells. Other benign nonepileptic events on infants
The description of what the child was doing prior to the event are summarized in Table 4. Most of these benign movement
gives a lot of hint toward the diagnosis of seizure. Paroxysmal disorders occur in typically developing infants and toddlers
episode that occurs following an exercise (prolonged QT with normal electroencephalogram (EEG) study.
syndrome or cardiogenic syncope), crying (breath holding
spells), or trivial head trauma (reflex anoxic seizure) are more Most common nonepileptic events in older children and
likely to nonepileptic. It is essential to know whether these adolescents that mimic seizure include syncope, pseudoseizures
clinical events occur during sleep (nocturnal epilepsy or and parasomnias. Syncope is characterized by precipitating
parasomnias) or wakeful state. factor (such as crowded place and prolonged standing),
presence of prodromal symptoms (tinnitus, dizziness),
Paroxysmal events that occur following psychological stressor gradual onset, associated pallor, and sweating that occurs for
(school maladjustment, peer bullying, parental quarrels, and a brief duration (<30 s) with rapid recovery and no postictal
separation anxiety) could hint toward psychogenic paroxysmal confusion.[10] It is important to understand that tongue bite,
urinary incontinence, and convulsive seizures can occur rarely
nonepileptic events. The presence of provoking factors such as
in syncope.
prolonged standing, crowded place, lack of food, unpleasant
circumstances could point to syncope.[10] History of drug
Features that could point to psychogenic nonepileptic
ingestion (metoclopramide or prochlorperazine) prior to the
seizures (PNESs) in contrast to seizure include presence of
episode could point to possibility of dystonic reaction (oculogyric
psychosocial stressor, paroxysmal events occurring in stressful
crises). The common seizure mimickers are classified based on situation in presence of others, bizarre nonstereotypic motor
type of presentation [Table 2] and age at presentation [Table 3]. movement, no resultant injury, presence of resisted eyelid
opening, avoidance or guarding behavior, and no effect of
Table 2: Types of seizure mimic based on type antiepileptic drug.[12] PNES refers to discernible changes in
of presentation behavior or consciousness that resemble epileptic seizure but
Seizure like Hyperkinetic Transient and Sleep related not accompanied by electrophysiological changes.[13]
movement developmental disorder
disorder movement disorder Description of Seizure Semiology
Syncope Tremors Jitteriness Parasomnias
Psychogenic Stereotypies Shuddering Restless leg Once the possibility of nonepileptic event is ruled based on
nonepileptic Hyperekplexia Benign paroxysmal syndrome clinical history, detailed description of the clinical seizure is
seizures torticollis of infancy
Paroxysmal of paramount importance. Auras can occur at the beginning
dyskinesia Gratification of seizure that lasts for seconds to minutes and defined by
Tics Benign paroxysmal subjective symptoms such as somatosensory, visual, auditory,
Episodic ataxia tonic upward gaze olfactory, gustatory, autonomic, abdominal, and psychic
Sandifer syndrome phenomena.
Breath-holding
attacks
It is essential to delineate the seizure semiology and its
Spasmus nutans classification for correct diagnosis, treatment, and prognosis.

Table 3: Table lists Non epileptic event (age wise)

Newborn Infant Children Adolescent
Benign neonatal sleep myoclonus Cyanotic or pallid breath-holding spell Breath-holding spells Syncope
Jitteriness Shuddering Syncope Migraine variants
Hyperekplexia Paroxysmal torticollis Benign paroxysmal vertigo Tremor/tics
Sandifer syndrome Paroxysmal dyskinesia Paroxysmal dyskinesia
Stereotypies Dystonic drug reaction Sleep disorders
Spasmus nutans Day dreaming
Gratification Stereotypies
Benign paroxysmal vertigo Pseudoseizure
Rhythmic movement disorders of sleep

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32 Gulati and Kaushik: Treating first seizure in children

Table 4: Table summarizes when to suspect nonepileptic events in infants

Clinical situation What does it mimic Benign nonepileptic event
Abnormal tonic posturing of neck, trunk, and limb (opisthotonus) occurring within Tonic seizure Sandifer syndrome
minutes of feeding and regurgitation of feeds
Baby aged 3-15 months with cluster of tonic or myoclonic jerks involving head and trunk Epileptic spasms Benign myoclonus of infancy
with remission within 3 months of onset
Baby aged 3-6 months with paroxysms of behavioral arrest associated with shivering-like Epileptic spasms Shuddering attacks
movement of head and shoulder as if cold water was poured on the baby’s back
Baby aged 2-8 months with paroxysmal attacks of torticollis associated with pallor, Focal or versive seizures Benign paroxysmal torticollis
irritability, with remission by 3-5 years of age
Episodes of dystonic posturing, rocking, grunting, facial flushing and diaphoresis with Tonic seizure Gratification
pressure on perineum that may cease with distraction
Periods of sustained upward tonic conjugate upward deviation with or without ataxia Versive seizure Paroxysmal tonic upward
gaze
Paroxysms of torticollis, nystagmus, and head nodding Versive seizure Spasmus nutans
Excessive startle response to unexpected noise or touch resulting in generalized stiffness Tonic seizure Hyperekplexia
of body

Moreover, the type of seizure determines the choice of
antiepileptic drug (AED) and need for surgical interventions.
Description of the event should be elicited from the person who
witnessed the event rather than hearing it as a second-hand
information. The information would become more meaningful
if parents were able to capture the event as video. The
description must include presence or absence of motor, sensory,
autonomic, cognitive, behavioral and psychic symptoms along
with the description of postictal phase.
How to Classify the Seizure?
The ILAE task force has classified seizures as generalized
onset and focal onset seizures.[14] Generalized seizure refers to
those arising within and rapidly engaging bilateral distributed
networks. Generalized seizures include seizures with tonic,
clonic, tonic–clonic, absences (typical, atypical, myoclonic
absence, eyelid myoclonia), myoclonic seizures (myoclonic,
myoclonic atonic, myoclonic tonic), epileptic spasms, and
atonic seizures. Focal onset seizures refer to those that originate
within networks limited to one hemisphere characterized by
one or more of aura, motor, autonomic, altered awareness
(dyscognitive) that may evolve to bilateral convulsive seizure.
Earlier terminologies of simple partial seizures (without
impairment of consciousness) and complex partial seizures
(with impairment of consciousness) have been abandoned by
newer ILAE classification.[14] Localizing and lateralizing value
of seizure semiology has been well delineated in a previous
review.[15]
Developmental History
History of developmental delay, intellectual disability, autism,
and other pervasive developmental disorders becomes essential
among children presenting with first seizure. Paroxysmal
movements such as self-stimulation, hyperventilation,
stereotypies, Sandifer syndrome, and dystonic posturing may
mimic a seizure.[16] It is often difficult to differentiate a seizure
from nonepileptic events in children with intellectual disability
owing to limited ability to communicate and higher risk of
seizure among these children.[17]
Family and Personal History
Family history of epilepsy and febrile convulsion is essential
among those suspected with benign neonatal familial
convulsion, juvenile myoclonic epilepsy, and generalized
epilepsy with febrile seizure (GEFS) plus. In addition, history
of drug rash and personal allergies would be useful. Contact
history of tuberculosis is essential among those presenting
with first episode of seizure. Poor socioeconomic condition,
poor hygiene of food, consumption of raw uncooked
food, and street foods are risk factors for developing
neurocysticercosis.[18]
Drug History
Exposures to medications and recreational drugs (such as
cocaine) have been implicated among adolescents and adults
presenting with seizure. Adolescents presenting with new
onset of seizure should be enquired for consumption of
antidepressants or antipsychotic medications. Family history
of depression and psychosis with their drug treatment history
will be useful in this context. Drugs that provoke seizure
among children and adolescents include antidepressants, such
as bupropion, that are consumed intentionally and tricyclic
antidepressants or unintentional pharmacological overdosage
of drugs such as anticholinergics (such as diphenhydramine),
antihistamines, antipsychotics, theophylline, and isoniazid.[19]
Examination
Rapid assessment of airway, breathing, and circulation are the
first priority in examination. Presence of altered sensorium
in a child with acute seizure could indicate evidence of
encephalopathy. General physical examination must focus to
look for any evidence of neurocutaneous stigmata [Table 5].[20]
Similarly presence of injury marks on forehead could indicate
drop attacks or myoclonic jerks.
Higher mental function must focus on cognition, learning,
behavior, communication, social interaction, sleep, and
memory. Pupillary size and reaction could hint toward
presence of toxidrome (organophosphorus and opioid

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Gulati and Kaushik: Treating first seizure in children 33

poisoning). Fundus examination must be done to rule out
intraocular cysticercus and any evidence of papilledema.
Presence of focal neurological deficit such as facial nerve
palsy, hemiparesis point to cerebrovascular cause. Similarly,
features of raised intracranial pressure (bradycardia,
hypertension, irregular breathing, hypertonia, hyperreflexia,
fundus showing papilledema) must be looked. Presence of
meningeal sign could indicate meningitis or subarachnoid
bleeding.
Laboratory Investigation
Routine investigations
Choice of investigation will depend upon differential diagnosis
generated based on the history and examination. All children
who present to the pediatric casualty department with a history
of acute seizure must be subjected to tests of blood glucose level,
serum electrolytes, and blood calcium.[8] In febrile children with
acute seizure, complete blood counts and serum C reactive
proteins may be estimated. In children with suspected toxic
or drug-induced etiology, blood levels of suspected drug must
be ordered.
Lumbar puncture
Any child with meningeal signs is an indication of lumbar
puncture. In children who present with fever and seizure,
indications of lumbar puncture include those with meningeal
signs or where the history and examination suggests an
intracranial infection.[21] Lumbar puncture is optional among
children aged 6-12 months who are unimmunized or have
undergone incomplete immunization with hemophilus
influenzae type b (Hib) and pneumococcal vaccine and those
who were pretreated with antibiotics.[21] Lumbar puncture is
warranted once features of raised intracranial pressure have
been ruled out both clinically and radiologically [contrast
enhanced computed tomography (CECT) brain].
Neuroimaging
CECT brain would be a preferred modality of investigation
in all the cases where immediate causes of seizures, such as
hypoglycemia and dyselectrolytemia, have been ruled out.
Neuroimaging is indicated among those with convulsive
seizures, focal seizures, cluster of seizures, or focal neurological
deficit. CECT is helpful in identifying etiologies such as
neurocysticercosis, tuberculoma, meningitis (meningeal
enhancement), ventricular size, vascular infarct. Among those
with a history of head trauma or where intracranial bleed is
suspected, noncontrast CT (NCCT) will be indicated. Magnetic
resonance imaging (MRI) brain (contrast) would be indicated
in nonemergent and nontraumatic cases with developmental
delay, intellectual disability to rule out structural malformation,
and hypoxic or perinatal injury sequelae. In children with
refractory seizures, suspected temporal lobe epilepsy or in
cases where equivocal lesions are evident on CT scan, MRI
brain would be a useful adjunct.[22]
Electroencephalogram (EEG)
EEG must be considered among those with unprovoked seizure
where neuroimaging is normal. Precedence of neuroimaging
prior to EEG is owing to large incidence of focal structural
lesions such as neurocysticercosis among Indian children
presenting with unprovoked seizure.[23] This is in contrast
to American and European guidelines of preferring EEG
as the first-line investigation among those presenting with
unprovoked seizure.[24]
EEG is useful in diagnosis of the event, identification of
a specific syndrome, prediction of long-term outcome/
recurrence, and suggesting the presence of focal lesions (focal
slowing) among those with normal neuroimaging.[24] EEG
abnormalities are considered the best predictors of recurrence
in children who were neurologically normal.[25] It is estimated
that recurrence risk was significantly less among those with
normal EEG (25% of 165 children) when compared to those
with abnormal EEG (54% of 103 children).[26]
Management
General measures
The goals in the management of acute seizure in the pediatric
casualty department are initial stabilization, treatment of
dyselectrolytemia and hypoglycemia, drugs to abort the
ongoing seizure activity, determining the etiology, and deciding
on need of long-term anticonvulsants.

Table 5: Table outlining the neurocutaneous stigmata
to look for in the examination
Skin lesions
Ash leaf macule, shagreen patch,
subungual fibroma, and adenoma
sebaceum
Unilateral cutaneous hemangioma
(port-wine stain) in face and presence
of glaucoma
Raised verrucous skin lesions in ovoid
or linear plaques
Café au lait macules,
neurofibromatosis
Evolution of erythematous skin
lesions to crusted, pigmented then
hypopigmented lesions
Multiple hairy pigmented nevi
Neurocutaneous syndrome
presenting with epilepsy
Tuberous sclerosis
Sturge–Weber syndrome
Epidermal nevus syndrome
Neurofibromatosis
Incontinentia pigmenti
Neurocutaneous melanosis
Drugs to abort the ongoing seizure
Correction of primary electrolyte disturbance remains
the mainstay of therapy among those with hypoglycemia
(5 mL/kg of 10% dextrose), hypocalcemia (2 mL/kg of 10%
calcium gluconate), hyponatremia (if serum sodium <120 meq/L,
administer 3% NaCl 4-6 mL/kg) or hypernatremia. Drugs that
can be used to abort the ongoing seizure in hospital setting
include intravenous (IV) lorazepam (0.1 mg/kg), IV diazepam
(0.3-0.5 mg/kg), or IV midazolam (0.1-0.2 mg/kg). The drugs that
may be used as an abortive measure in an out-of-hospital setting
include intranasal midazolam (0.2 mg/kg; 0.5 mg/puff) or per
rectal diazepam (0.5 mg/kg).[27] In addition, among those with
raised intracranial pressure, measures to decrease the raised
intracranial pressure (3% saline or mannitol) must be initiated.
Decision whether to load with AED
Short acting benzodiazepines are often used as acute abortive
measures. Among those with epileptic seizures, loading doses

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34 Gulati and Kaushik: Treating first seizure in children
of long acting AEDs are required. Children with the presence of
global developmental delay, static or progressive brain insult,
head trauma, focal seizures, family history of epilepsy are
more likely to have epileptic seizures. This obviously excludes
provoked causes such as febrile seizure, seizure secondary to
dyselectrolytemia that does not require AED loading.
What is a right choice of AED?
The correct choice of antiepileptic drug for loading will be
determined by a number of factors such as age of patient,
development, established diagnosis, was the child already on AEDs,
and availability of drug in IV preparation and center.[28] In addition,
in developing countries cost of drug becomes one of the most
limiting factors. For example, if a child presents with first episode
of focal seizure both phenytoin and levetiracetam are good choice.
However, phenytoin being a cheaper drug, this may be preferred
to ensure long-term compliance. It has been observed that large
number of patients of epilepsy rely on free drug supply and might
stop the medicines once the drug is not available or affordable.[29]
Among children with multiple types of seizures, especially
myoclonic and absence seizure, broad spectrum AEDs, such
as valproate and levetiracetam, may be preferred. However,
in infants with suspected neurometabolic disorders including
mitochondrial disorders, valproate may be avoided. The choice
of drug will also be determined by the type of seizure: Focal
seizures (phenytoin or levetiracetam) and for generalized
seizures (phenytoin or valproate) [Table 6].
Drug therapy for ongoing seizure
Drug therapy to terminate acute convulsion include benzodiazepines
[IV lorazepam (0.1 mg/kg) or IV midazolam (0.1-0.2 mg/kg) or IV
diazepam (0.3-0.5 mg/kg)] followed by administering a loading
dose of IV phenytoin (15-20 mg/kg loading dose @1 mg/kg/min)
or in neonates (<1 month) IV phenobarbitone (20 mg/kg loading
@ 1.5 mg/kg/min). If seizures continue to persist, valproate,
phenobarbitone, or levetiracetam is indicated.[27] Management
protocols for status epilepticus have been reviewed extensively.[27]
Plan for long-term AEDs
Long-term AEDs are discouraged for the first episode of
unprovoked seizure with normal neuroimaging and EEG
Table 6: Decision for antiepileptic drug for children presenting with acute seizure
Clinical condition
Febrile seizure, dyselectrolytemia, paroxysmal non epileptic
events
Seizure following head trauma
First episode of unprovoked seizure (focal or generalized)
Seizure in child with developmental delay with coexistent other
seizure types such as myoclonic seizure, infantile spasms
If child was on antiepileptic drug and had poor compliance
and presented with breakthrough seizure
If the child was on antiepileptic drug at submaximal dose
with good compliance
If the child was on antiepileptic drug at maximal dosage
with good compliance
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findings once parents have been explained about the risk
of recurrence of up to 50-60%.[30] Among these children
with normal investigations, AEDs are started with second
episode of unprovoked epileptic seizure. Long-term AEDs are
initiated following the first unprovoked seizure among those
with parenchymal structural lesions such as tuberculoma,
neurocysticercosis, or infarct. Children with developmental
delay, family history of epilepsy, presence of neurocutaneous
markers, and congenital brain malformation also require broad
spectrum AEDs such as valproate and levetiracetam.
Duration of AED therapy
Duration of AED therapy will depend on the etiology.
Among children with acute symptomatic seizure AEDs
can be withdrawn after 7 days (head trauma) or 3 months
(meningoencephalitis with brain parenchymal lesion). Among
those patients with neurocysticercosis, AEDs are continued
till the disappearance of lesion on neuroimaging or seizure
freedom for 2 years following calcification of the lesion
(author’s experience). Children with epileptic syndromic
diagnosis including juvenile myoclonic seizure might require
life-long AEDs. Recurrence risk of 25% following AED
stopping needs to be emphasized to parents.[31] Documenting
a normal sleep deprived EEG prior to stopping the AED is
recommended. [31]
Specific treatment
Treatment of underlying etiology includes administration of
intravenous antibiotics (meningitis), febrile prophylaxis with
oral clobazam (febrile seizure), and anticoagulant (aspirin
or low molecular weight heparin) for arterial or venous
stroke. Other specific treatment options include withdrawal
of offending drug if any, treatment of active lesions of
neurocysticercosis with albendazole under the cover of oral
steroids, antitubercular drugs for tuberculoma, and surgical
intervention for brain abscess and posttraumatic extradural
and intracranial bleeds [Table 7]. Most of the drug-induced
seizures are self-limited. Treatment for drug-induced seizures
will include benzodiazepine, barbiturates, and propofol.
Phenytoin should preferably be avoided in such conditions.
Isoniazid [or, isonicotinylhydrazide (INH)]-induced seizures
are reversible with pyridoxine.[32]
AED of choice for IV loading
No antiepileptic drugs
Phenytoin
Phenytoin
Valproate
Same antiepileptic drug loading followed by same preexisting dosage
Load with same antiepileptic drug and hike the dosage by 5-10 mg/kg till
maximum permissible dosage is reached. One can opt for a short course
(7-10 days) of add on benzodiazepines (clobazam 0.1 mg/kg or clonazepam
0.02-0.05 mg/kg) to achieve better control
Load with next best choice of antiepileptic drug depending on the seizure
type and etiology. One can opt for a short course (7-10 days) of add on
benzodiazepines (clobazam 0.1 mg/kg or clonazepam 0.02-0.05 mg/kg)
to achieve better control
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Gulati and Kaushik: Treating first seizure in children 35

Table 7: Table summarizing the management plan for common pediatric causes of first seizure in children
Condition Treatment
Meningoencephalitis Intravenous antibiotic therapy (IV ceftriaxone 100 mg/kg, IV vancomycin 60 mg/kg, IV acyclovir 20 mg/kg/dose 8 hourly)
for 10-14 days (21 days in neonates)
Febrile seizure Intermittent prophylaxis (clobazam 0.75-1 mg/kg BD for 3 days); continuous prophylaxis with oral valproate
(10-20 mg/kg/day) for febrile status epilepticus, complex febrile seizure or recurrent febrile seizure (>4/year in spite
of intermittent prophylaxis)
Neurocysticercosis Cysticidal treatment (albendazole 15 mg/kg/day) for duration of 7-28 days is recommended for live cyst and transitional
granuloma. Oral dexamethasone (0.6 mg/kg/day in 4 divided doses) is started 3 days prior to 2 days after starting
albendazole. Albendazole is contraindicated among those with ocular cysticerci (prior ophthalmic evaluation essential),
multiple cysticerci (>5 lesions), spinal lesions. AED are continued till the disappearance of lesion on neuroimaging or
seizure freedom for 2 years following calcification of the lesion
Tuberculoma Antitubercular drugs (2HRZE10 HR) along with steroids (oral dexamethasone 0.15 mg/kg/dose 6 hourly)

Parental counseling 8. Sasidaran K, Singhi S, Singhi P. Management of acute seizure

Parental counseling sessions must be an essential part of
the management of first seizure in children in order to
allay parental fears, negative reactions, and apprehensions
of stigma or social taboo.[33] The main focus of discussion
with parents may include the chances of its recurrence,
home management of seizure, need for AEDs, possible
adverse effects of AED, duration of AED therapy, role of
investigations techniques such as MRI brain and EEG, and
based on the etiology explanation of overall outcome of
seizure. Domiciliary management of seizure must focus on
emphasis of recovery position during active seizure and use of
rescue medication such as intranasal midazolam (0.2 mg/kg;
maximum: 10 mg) in case of prolonged seizure (>3-5 min).
In addition, parents must be counseled to maintain strict
compliance with medications, need to administer medications
by correct measurement (using syringe for mL) and to report
to treating physician in case of any adverse event or seizure
recurrence. In this regard, it will be useful to give these
instructions as a patient information sheet.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
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Annals of Indian Academy of Neurology, January-March 2016, Vol 19, Issue 1