Annals of Indian Academy of Neurology
HOW I DO IT
Year
: 2016  |  Volume : 19  |  Issue : 1  |  Page : 29--36

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

Correspondence Address:
Sheffali Gulati
Department of Pediatrics, Division of Child Neurology, All India Institute of Medical Sciences (AIIMS), Ansari Nagar, 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.



How to cite this article:
Gulati S, Kaushik JS. How I treat a first single seizure in a child.Ann Indian Acad Neurol 2016;19:29-36


How to cite this URL:
Gulati S, Kaushik JS. How I treat a first single seizure in a child. Ann Indian Acad Neurol [serial online] 2016 [cited 2019 Aug 21 ];19:29-36
Available from: http://www.annalsofian.org/text.asp?2016/19/1/29/173404


Full Text

 Introduction



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) causes. [5] The present review focuses on practical approach to acute first seizure in children in terms of initial stabilization, detailed history, focused examination, and sensible choice of investigation and management plan [Figure 1].{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. 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.{Table 1}

 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 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 consciousness are more likely to be febrile seizures. Children with history of fever, seizure, and encephalopathy are likely to have meningoencephalitis. History of developmental delay, perinatal asphyxia or other perinatal or postnatal injury, and positive family history of epilepsy or febrile convulsion points towards an unprovoked epileptic seizures.

 Was it True Seizure?



The description of what the child was doing prior to the event gives a lot of hint toward the diagnosis of seizure. Paroxysmal episode that occurs following an exercise (prolonged QT syndrome or cardiogenic syncope), crying (breath holding spells), or trivial head trauma (reflex anoxic seizure) are more likely to nonepileptic. It is essential to know whether these clinical events occur during sleep (nocturnal epilepsy or parasomnias) or wakeful state.

Paroxysmal events that occur following psychological stressor (school maladjustment, peer bullying, parental quarrels, and separation anxiety) could hint toward psychogenic paroxysmal nonepileptic events. The presence of provoking factors such as prolonged standing, crowded place, lack of food, unpleasant circumstances could point to syncope. [10] History of drug ingestion (metoclopramide or prochlorperazine) prior to the episode could point to possibility of dystonic reaction (oculogyric crises). The common seizure mimickers are classified based on type of presentation [Table 2] and age at presentation [Table 3].{Table 2}{Table 3}

Many of the nonepileptic events are benign and are related to normal stages of development. The most common benign developmental movement disorder in infants and toddlers include breath holding spells. [11] These episodes starts with provoking factors such as angry, fussy and crying baby who 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 consciousness, and tonic posturing is classical with breath holding spells. Other benign nonepileptic events on infants are summarized in [Table 4]. Most of these benign movement disorders occur in typically developing infants and toddlers with normal electroencephalogram (EEG) study. {Table 4}

Most common nonepileptic events in older children and adolescents that mimic seizure include syncope, pseudoseizures and parasomnias. Syncope is characterized by precipitating factor (such as crowded place and prolonged standing), presence of prodromal symptoms (tinnitus, dizziness), gradual onset, associated pallor, and sweating that occurs for a brief duration (<30 s) with rapid recovery and no postictal confusion. [10] It is important to understand that tongue bite, urinary incontinence, and convulsive seizures can occur rarely in syncope.

Features that could point to psychogenic nonepileptic seizures (PNESs) in contrast to seizure include presence of psychosocial stressor, paroxysmal events occurring in stressful situation in presence of others, bizarre nonstereotypic motor movement, no resultant injury, presence of resisted eyelid opening, avoidance or guarding behavior, and no effect of antiepileptic drug. [12] PNES refers to discernible changes in behavior or consciousness that resemble epileptic seizure but not accompanied by electrophysiological changes. [13]

 Description of Seizure Semiology



Once the possibility of nonepileptic event is ruled based on clinical history, detailed description of the clinical seizure is of paramount importance. Auras can occur at the beginning of seizure that lasts for seconds to minutes and defined by subjective symptoms such as somatosensory, visual, auditory, olfactory, gustatory, autonomic, abdominal, and psychic phenomena.

It is essential to delineate the seizure semiology and its classification for correct diagnosis, treatment, and prognosis. 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. {Table 5}

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 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.

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 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].{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 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] {Table 7}

Parental counseling

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.

References

1Fisher RS, van Emde Boas W, Blume W, Elger C, Genton P, Lee P, et al. Epileptic seizures and epilepsy: Definitions proposed by the international league against epilepsy (ILAE) and the international bureau for epilepsy (IBE). Epilepsia 2005;46:470-2.
2Panayiotopoulos CP. Epileptic seizures and their classification. In: Panayiotopoulos CP, editor. A Clinical Guide to Epileptic Syndromes and their Treatment. London: Springer-Verlag; 2010. p. 21-63.
3Sridharan R, Murthy BN. Prevalence and pattern of epilepsy in India. Epilepsia 1999;40:631-6.
4Goel D, Agarwal A, Dhanai JS, Semval VD, Mehrotra V, Saxena V, et al. Comprehensive rural epilepsy surveillance programme in Uttarakhand state of India. Neurol India 2009;57:355-6.
5Wallace SJ, Farrell K. Epilepsy in Children. 2 nd ed. London: CRC Press; 2004. p. 535.
6Tasker RC. Emergency treatment of acute seizures and status epilepticus. Arch Dis Child 1998;79:78-83.
7Gray JT, Gavin CM. 14 Assessment and management of neurological problems. Emerg Med J 2005;22:440-5.
8Sasidaran K, Singhi S, Singhi P. Management of acute seizure and status epilepticus in pediatric emergency. Indian J Pediatr 2012;79:510-7.
9Guidelines for epidemiologic studies on epilepsy. Commission on Epidemiology and Prognosis, International League Against Epilepsy. Epilepsia 1993;34:592-6.
10Panayiotopoulos CP. Imitators of epileptic seizures. In: Panayiotopoulos CP, editor. A Clinical Guide to Epileptic Syndromes and their Treatment. London: Springer; 2010. p. 97-134.
11Fung CW, Wong VC. Paroxysmal non-epileptic movements in childhood. HK J Paediatr (New Series) 2012;17:85-96.
12Wichaidit BT, Østergaard JR, Rask CU. Diagnostic practice of psychogenic nonepileptic seizures (PNES) in the pediatric setting. Epilepsia 2015;56:58-65.
13Reilly C, Menlove L, Fenton V, Das KB. Psychogenic nonepileptic seizures in children: A review. Epilepsia 2013;54:1715-24.
14Fisher RS, Acevedo C, Arzimanoglou A, Bogacz A, Cross JH, Elger CE, et al. ILAE official report: A practical clinical definition of epilepsy. Epilepsia 2014;55:475-82.
15Dash D, Tripathi M. The extratemporal lobe epilepsies in the epilepsy monitoring unit. Ann Indian Acad Neurol 2014;17(Suppl 1):S50-5.
16Paolicchi JM. The spectrum of nonepileptic events in children. Epilepsia 2002;43(Suppl 3):60-4.
17Chapman M, Iddon P, Atkinson K, Brodie C, Mitchell D, Parvin G, et al. The misdiagnosis of epilepsy in people with intellectual disabilities: A systematic review. Seizure 2011;20:101-6.
18Woodhall D, Jones JL, Cantey PT, Wilkins PP, Montgomery SP. Neglected parasitic infections: What every family physician needs to know. Am Fam Physician 2014;89:803-11.
19Finkelstein Y, Hutson JR, Freedman SB, Wax P, Brent J; Toxicology Investigators Consortium (ToxIC) Case Registry. Drug-induced seizures in children and adolescents presenting for emergency care: Current and emerging trends. Clin Toxicol (Phila) 2013;51:761-6.
20Wyllie E, Gupta A, Lachhwani DK. The Treatment of Epilepsy: Principles and Practice. Philadelphia: Lippincott, Williams & Wilkins; 2006. p. 1286.
21Subcommittee on Febrile Seizures; American Academy of Pediatrics. Neurodiagnostic evaluation of the child with a simple febrile seizure. Pediatrics 2011;127:389-94.
22McAbee GN, Wark JE. A practical approach to uncomplicated seizures in children. Am Fam Physician 2000;62:1109-16.
23Rajshekhar V, Joshi DD, Doanh NQ, van De N, Xiaonong Z. Taenia solium taeniasis/cysticercosis in Asia: Epidemiology, impact and issues. Acta Trop 2003;87:53-60.
24Pohlmann-Eden B, Beghi E, Camfield C, Camfield P. The first seizure and its management in adults and children. BMJ 2006;332:339-42.
25Hirtz D, Ashwal S, Berg A, Bettis D, Camfield C, Camfield P, et al. Practice parameter: Evaluating a first nonfebrile seizure in children: Report of the quality standards subcommittee of the American Academy of Neurology, the child neurology society, and the American epilepsy society. Neurology 2000;55:616-23.
26Shinnar S, Kang H, Berg AT, Goldensohn ES, Hauser WA, Moshé SL. EEG abnormalities in children with a first unprovoked seizure. Epilepsia 1994;35:471-6.
27Raj D, Gulati S, Lodha R. Status epilepticus. Indian J Pediatr 2011;78:219-26.
28Pellock JM. Standard approach to antiepileptic drug treatment in the United States. Epilepsia 1994;35(Suppl 4):S11-8.
29Desai P, Padma MV, Jain S, Maheshwari MC. Knowledge, attitudes and practice of epilepsy: Experience at a comprehensive rural health services project. Seizure 1998;7:133-8.
30Arthur TM, deGrauw TJ, Johnson CS, Perkins SM, Kalnin A, Austin JK, et al. Seizure recurrence risk following a first seizure in neurologically normal children. Epilepsia 2008;49:1950-4.
31Caviedes BE, Herranz JL. When and how should the long-term anti-epileptic treatment be stopped. Rev Neurol 1997;25:372-8.
32Chen HY, Albertson TE, Olson KR. Treatment of drug-induced seizures. Br J Clin Pharmacol 2015. [Epub ahead of print].
33Galletti F, Sturniolo MG. Counseling children and parents about epilepsy. Patient Educ Couns 2004;55:422-5.