RATION A L DIAGNOSTICS

Electroencephalography in Pediatric Epilepsy

JAYA SHANKAR KAUSHIK1 AND RAJNI FARMANIA2
From Departments of Pediatrics; 1Pt BD Sharma Post Graduate Institute of Medical Sciences, Rohtak, Haryana, and 2BL Kapur
Superspeciality Hospital, Delhi; India.
Correspondence: Dr Jaya Shankar Kaushik, Associate Professor, Department of Pediatrics, Pt BD Sharma Post Graduate Institute
of Medical Sciences, Rohtak 124 001, Haryana, India. [email protected]

Surface electroencephalography (EEG) is a useful electrophysiological investigation for evaluating a paroxysmal event in children. It
measures the electro potential difference between two points on the scalp. It is a non-invasive tool that analyzes neuronal maturation and
abnormal cortical excitability. EEG helps in differentiating epileptic from non-epileptic clinical event and focal seizures from generalized
seizure. This review is to discuss the rational use of interictal scalp EEG in diagnosis of epilepsy and different types of epilepsy syndromes
in children. It further highlights its role in febrile seizure, first unprovoked seizure, status epilepticus and unexplained coma.
Keywords: Diagnosis, EEG, Epileptic syndromes, Guideline, Review, Seizures.

E
lectroencephalography (EEG) is a non- and the net signal from each amplifier is displayed on a
invasive, readily available and inexpensive monitor to provide a graphic record. EEG signals are
investigation to study the neuronal dysfunction generated by the summation of excitatory and inhibitory
and abnormal cortical excitability in children post-synaptic potentials from large, vertically-oriented
who present with seizures [1]. Traditional analog EEG pyramidal neurons located in layer III, V and VI [6].
machines are being replaced by digital EEG with These EEG signals are synchronized by subcortical
simultaneous video recording. Surface scalp EEG structures like thalamus and brainstem reticular
recording can be conventional short-term recording (30 formation. Sleep spindles are considered a result of these
minutes) or long-term video EEG record (for witnessing thalamocortical phenomena [6]. Large numbers of
and localizing seizure activity). cortical spikes are not recordable on a routine scalp EEG
due to attenuating effect of cerebrospinal fluid, duramater
Sensitivity and specificity of surface scalp EEG to and skull scalp tissue.
localize the epileptogenic focus depends on factors such as
age, type of epilepsy, and nature of EEG recording [2]. TECHNICAL ASPECTS
Ictal EEG (EEG recording during the seizure) helps to The surface EEG electrodes made of gold or silver discs
recognize the type of seizure that may not be evident from (silver chloride) are placed at standard points over scalp
history and for localizing the epileptogenic zone [3]. with a conductive paste. The International 10-20 system
Electrocorticography (ECoG) or intracranial EEG is (10 and 20% gap between electrodes) is used for electrode
useful for invasive recording of cortical electrical activity placement [7]. Pediatric EEG routinely requires the
by use of electrodes directly on the surface of brain placement of 21 electrodes on the scalp with fewer
(subdural grids or strips) or deep inside the brain (depth electrodes (minimum of 12 electrodes) in neonates and
electrodes) [4]. It helps to localize the epileptogenic zone young infants [8]. EEG can be performed in a laboratory or
and to map cortical functional areas in drug-resistant bedside ambulatory EEG could be used. Additional
epilepsy. Detailed discussion of invasive EEG studies and channels of electrocardiogram (EKG) and respiration are
its role in planning epilepsy surgery is beyond the scope of recommended to record physiologic artefacts. EKG
this review. American Clinical Neurophysiology Society during EEG recording helps detect ictal arrhythmia and
(ACNS) has published technical guidelines for recording asystole in children with epilepsy who are prone to sudden
digital EEG [5]. unexpected death (SUDEP) [9]. Surface
PRINCIPLE OF EEG electromyography (EMG) during EEG helps to
distinguish epileptic from non-epileptic movements [10].
EEG measures the electropotential difference that arises Electrodes are named according to the underlying area of
from the ion trafficking between two points on the scalp. brain: FP: frontopolar, F: frontal, P: parietal, T: temporal,
Potential differences between electrodes are amplified and O: occipital. Central electrodes are abbreviated as Z

INDIAN PEDIATRICS 893 VOLUME 55__OCTOBER 15, 2018

KAUSHIK & FARMANIA EEG IN PEDIATRIC EPILEPSY

[Fz, Cz, Pz] and referential electrodes include post Reactivity of EEG background is observed by asking the
auricular (A1, A2). The odd numbers (Fp1, F3, P3, C3, T3, child to close and open the eyes or by touching his various
T5, T7, O1) depict left side of the hemisphere and even body parts.
numbers (Fp2, F4, C4, P4, T4, T6, O2) for the right side.
EEG REQUISITION
These electrodes are either fixed to scalp using conductive
paste or electrodes fixed onto a head cap are used. An EEG requisition form from clinician must contain
basic demographic profile (name, age, gender, telephone
Patient Preparation
number or email), type of seizure, frequency of seizure,
The scalp should be clean and dry. Patient should be age at onset, indication of EEG, neuroimaging findings,
instructed to consume antiepileptic drugs (AED) as any previous EEG findings, and name of antiepileptic
prescribed. However, AED doses can be reduced or drugs. Neurophysician can decide on the EEG protocol
discontinued to facilitate seizure occurrence during long- based on clinical diagnosis. For example, in a child with
term video EEG monitoring [11]. Children can have their suspected absence epilepsy, one would prefer an awake
routine breakfast on the day of appointment. Routine EEG EEG record with hyperventilation. Sleep deprived sleep
recordings usually lasts for 30 minutes, including EEG record will be considered in a child with suspected
hyperventilation for 3 minute and intermittent photic focal epilepsy.
stimulation at 1-30 Hz [5]. Long-term video EEG
EEG INTERPRETATION
recordings are particularly useful for pre-surgical
evaluation for epilepsy surgery [12]. An ideal EEG should ACNS guidelines have outlined five essential
include both awake and sleep record. However, sleep EEG components of an EEG report (Table I) [22].
is preferred in younger children considering excessive Abnormalities in EEG can be divided into background
movement artefacts during the wakeful state. Moreover, abnormalities and abnormal epileptiform discharges.
sleep EEG provides vital information on maturation of Background gives information about the neurologic state
brain [8]. Sleep deprived EEG protocol requires 4-6 hours of the child. Normal awake record consists of posterior
of sleep deprivation [13]. Children older than 3 years dominant alpha rhythm (8-13 Hz) with reactivity to eye
could be kept awake until midnight and woken up at 5:00 closure. Similarly, sleep background consist of sleep
AM on the morning of the test. Sleep deprivation is markers of non-REM sleep such as sleep spindles, vertex
considered to enhance sensitivity of EEG [14]. Triclofos waves, and K-complexes (Web Fig. 1). Epileptiform
(20 mg/kg/dose), melatonin (2-6 mg/dose) or clonidine discharges have distinct waveforms classified as spikes
(0.05-0.2 mg) can be used for sedation [15]. Intravenous (<70 ms) or sharp wave (70-200 ms). EEG findings in
midazolam should not be used to induce sleep due to its common self-limited epilepsies and epileptic
suppressive effect on epileptiform discharges. In addition encephalopathy in children have been summarized in
to sleep deprivation, yield of EEG can be increased by Table II and Table III, respectively.
repeat recording, prolonging the duration of recording,
PITFALLS OF EEG
increasing the number of channels during procedure,
simultaneous video recording, and recording both awake Surface EEG can be normal in few epileptic conditions in
and sleep state [16]. children, especially those with remote and deep location
of epileptogenic lesion such as interhemispheric area, and
Activation Procedure
mesial and basal cortex [19]. Few genetic types of
Infants, young children and children with suspected focal epilepsy such as benign familial neonatal epilepsy and
epilepsies require sleep EEG record [17-19]. Sleep EEG benign familial infantile epilepsy can have normal
is essential for diagnosis of epileptic encephalopathy and interictal EEG. Epileptiform discharges are found in 0-
continuous spike waves during slow sleep (CSWS) [20]. 5.6% of normal healthy children and 0.5% of adults
EEG in awake state is useful to detect generalized without any event of seizure [23]. EEG can be abnormal
epilepsies. Activation procedure include hyperventilation in approximately 5.7-59% of children with autism
(3 Hz spike wave pattern in absence epilepsies) and spectrum disorder without any clinical seizures [24].
intermittent photic stimulation (4-6 Hz generalized Photic driving response can routinely be found in patients
epileptiform discharges in Juvenile myoclonic epilepsy). with migraine without any epilepsy [25]. EEG is often
Other activation procedures indicated for specific reported by neurologist, pediatric neurologist,
conditions are: fixation of sensitivity (late onset occipital psychiatrist, neurophysiologist and other physicians with
lobe epilepsy), precipitation by trigger (e.g., video interest in EEG. Hence, there is lot of variability and
watching) in reflex epilepsies, and suggestion to subjectivity in reporting pediatric EEG. Exclusive
precipitate paroxysmal non-epileptic events [21]. training and experience to interpret pediatric EEGs is

INDIAN PEDIATRICS 894 VOLUME 55__OCTOBER 15, 2018

KAUSHIK & FARMANIA EEG IN PEDIATRIC EPILEPSY

TABLE I ESSENTIAL COMPONENT OF AN EEG REPORT (AS PER ACNS GUIDELINES FOR REPORTING EEG).
Parts of report Description Sample EEG report
History Clinical history, indication, medication, imaging findings 10-year-old boy with multiple episodes of
left focal seizure with normal MRI
Technical details Number of electrodes (21 channel electrodes) 21 channel electrodes were placed using
Electrode placement technique (10-20 system) 10-20 system. Record lasted for 30
use of filters (1.6 Hz-70 Hz) minutes
sensitivity (7-10 uV)
duration of recording (20-30 minutes)
Use of premedication must be documented.
State of the patient: awake, sleep, drowsy or comatose Child was awake and cooperative during
must also be mentioned. the record. HV and PS were performed
EEG description Background electro cerebral activity Background consist of 9-10 Hz, 60-80 uV
Normal awake- as posterior dominant rhythm with posterior dominant reactive rhythm
reactivity to external stimuli
Normal Sleep- presence of sleep markers and preservation
of sleep architecture in sleep record
Abnormality in background described in terms of : There was intermittent delta (2-3 Hz,
-Frequency, voltage 60-90uv) slowing in right temporal region
-Continuous or intermittent
-Location (right or left)
-Topography (frontal, parietal, temporal or occipital)
Epileptiform discharges are described in terms of: There were frequent runs of spike wave
-Morphology (spike, sharp, spike wave, polyspike) discharges (3.5-4.5 Hz, 150-250 uV)
-Frequency (Hz) arising from right temporal region that
-Voltage, location, pattern (run, rhythmic, periodic) lasts for variable duration of 3-5 sec.
-Incidence (rare, intermittent, occasional, frequent, These discharges occupy almost 60% of
continuous) or preferably quantification and duration of EEG epochs. HV and PS did not augment
abnormality the discharges
Impression Normal or abnormal; if abnormal: background Abnormal EEG record suggestive of right
abnormality and epileptiform discharges temporal epileptiform discharges with
background slowing
Clinical correlation Focal slowing could indicate underlying structural lesion Possibility of underlying structural lesion
Lack of organized background could indicate needs to be explored.
encephalopathy
Suggestions for sleep record and comparison with
previous EEG should be mentioned
HV: Hyperventilation, PS: Photic stimulation.

essential to understand the normal age-dependent with suspected rolandic epilepsy, structural focal epilepsy
variations and correct characterization of epileptiform or CSWS. These abnormalities are detected only on sleep
discharges. Some of the common errors in pediatric EEG EEG record. Similarly, among those with suspected
reporting include misinterpreting movement artefacts, childhood absence epilepsy and juvenile myoclonic
high amplitude delta slowing during hyperventilation and epilepsy, hyperventilation and photic stimulation during
normal sleep markers including vertex waves, and K awake EEG record is mandatory.
complexes as epileptiform discharges (Web Fig. 1).
INDICATIONS OF EEG
Other benign epileptiform variants like wicket waves,
benign epileptiform transients of sleep (BETS) and EEG is an adjunct to clinical evaluation and should be
rhythmic midtemporal theta bursts of drowsiness interpreted in clinical context. Indications of using and
(RMTD) can mimic epileptiform discharges to a naïve not using EEG are summarized in (Box 1). Diagnosis of
reader [26]. Awake EEG record can be normal in children epilepsy should not be reached solely on the basis of EEG

INDIAN PEDIATRICS 895 VOLUME 55__OCTOBER 15, 2018

KAUSHIK & FARMANIA EEG IN PEDIATRIC EPILEPSY

TABLE II CLINICAL AND EEG FINDINGS IN SELF-LIMITED EPILEPTIC SEIZURES AND SYNDROMES
Epilepsy Clinical features EEG pattern
Neonatal onset
Benign neonatal seizure (Fifth day fit) Unilateral focal clonic seizure on 4-6th day Normal or discontinuous background
of life in healthy neonate with focal or multifocal abnormalities.
Focal, rhythmic theta activity with sharp
waves (Theta pointu alternans) can be
seen in 60%
Benign familial neonatal seizure Focal clonic seizure with occasional apneic Normal background or theta pointu
spells on day-2 or day-3 of life, persist alternans
longer in otherwise healthy neonate
Infantile onset
Benign myoclonic epilepsy in infancy Myoclonic jerk for 1-3 s in develop- Normal background with generalized
(BMEI) mentally normal child; onset 4 mo to 3 y spike and polyspike discharges
Childhood onset
Childhood absence epilepsy Frequent absence seizures in school going Normal background with 3-4.5 Hz
child; can be precipitated by hyper- generalized spike wave discharge with
ventilation frontal dominance
Benign epilepsy with centrotemporal spikes Seizures during sleep with orofacial motor Normal sleep background, with sharps/
signs, speech arrest, sialorrhea and spike waves in centrotemporal region
unilateral sensory symptoms with a horizontal dipole
Early onset childhood occipital epilepsy It occurs in sleep with ictal vomiting and Normal background with multifocal,
(Panayiotopoulos syndrome) autonomic features occipital spikes
Late onset childhood occipital epilepsy Visual hallucinations, Runs of rhythmic occipital spikes and
(Gastaut syndrome) coloured circular patterns sharp waves seen during eye closure
called ‘fixation off’ sensitivity.
It disappears when eyes are open and
fixating at an object 'fixation on'
Adolescent
Juvenile absence epilepsy* Speech and behavioural arrest without 3-4 Hz spike and wave and polyspike
aura. May have automatisms wave discharges
Juvenile myoclonic epilepsy* Myoclonic jerks in morning, generalized 4-6 Hz bilateral polyspike wave and spike
or absence seizures slow wave discharges; accentuation by
photic stimulation
Nocturnal frontal lobe epilepsy Focal hypermotor seizures during sleep Runs of bilateral frontal spike, sharp
waves
*May require lifelong antiepileptic medications.

findings [27]. A wrong diagnosis of epilepsy has correlation [27]. Routine surface scalp EEG report
widespread social implications apart from side effects of should ideally comprise five components: history,
antiepileptic drugs and restriction of physical activities. technical description, EEG description, impression and
EEG is often misused in evaluation of a child with clinical correlation [22].
abnormal paroxysm to differentiate epileptic from non-
First Unprovoked Seizure
epileptic event [28]. Over-interpretation of EEG
abnormalities, including focal slowing, generalized and First unprovoked seizure (FUS) is defined as first non-
focal epileptiform discharges has often led to syncope febrile seizure that cannot be explained by an immediate,
being misdiagnosed as epileptic seizures [21]. There is obvious precipitating cause such as head trauma or
limited role of EEG in children with breath holding intracranial infection. In developing countries including
spells. Common reasons for misinterpretation of EEG India, focal lesions such as neurocysticercosis (NCC) and
include poor expertise, lack of good quality recording, tuberculoma are common causes of first unprovoked
inappropriate indication, and absence of clinical seizure in children [29]. Thus, in many centers,

INDIAN PEDIATRICS 896 VOLUME 55__OCTOBER 15, 2018

KAUSHIK & FARMANIA EEG IN PEDIATRIC EPILEPSY

TABLE III CLINICAL AND EEG FEATURES OF EPILEPTIC ENCEPHALOPATHY

Age Clinical phenotype Interictal EEG Features Background abnormality Epileptiform
abnormalities
Neonatal onset
Ohtahara syndrome Tonic spasm BS in wakefulness Bursts of high voltage Intermixed multifocal
and sleep slow waves 2 to 3 s spikes
suppression 3 to 5 s
EME Erratic fragmentary BS in sleep, may dis- Burst 1-3 s Multifocal spikes
myoclonus appear in awake Suppression 2-10 s
Infantile onset
Migratory focal seizures Multifocal clonic Migrating epileptiform Normal to dis- Migrating or multifocal
(previously MPSI) autonomic discharges continuous epileptiform discharges
West syndrome Epileptic spasms in Hypsarrhythmia Chaotic, high amplitude, Multifocal spikes and
clusters, after waking Classical or modified asynchronous slow polyspikes
up from sleep waves
Dravet syndrome Recurrent febrile and May be normal initially Slow diffuse Generalized, focal or
afebrile seizure for 1-2 y multifocal discharges
Myoclonic, atypical
absence and focal
seizures
Childhood onset
MAE Myoclonic- atonic, Doose rhythm Normal or doose rhythm Burst of 2-5 Hz
(Doose syndrome) absences, tonic clonic, photosensitive (rhythmic parietal theta generalized spike and
tonic activity) polyspike waves
LGS Tonic seizures, atypical 2-2.5 spike wave dis- Diffuse slow, absence 2-2.5 spike wave
absences, myoclonic charges, PFA of sleep markers discharges
seizures PFA
CSWS GTCs during sleep, Frontocentral conti- Awake normal 1.5-2.5 Hz spike wave
atypical absence, atonic, nuous spike wave Sleep: diffuse slow discharges; activation
myoclonic wave during sleep; upto 85%
LKS Seizures in 70% Temporo-parietal Awake normal Continuous temporo-
Autistic regression spike wave Sleep: diffuse slow parietal spike wave
wave
BS: Burst suppression, EME: early myoclonic epilepsy, MPSI: migrating partial epilepsy of infancy, MAE: Myoclonic astatic epilepsy; LGS: Lennox
Gastaut syndrpome, PFA: paroxysmal fast activity; CSWS: continuous spike and wave during sleep; GTC: generalized tonic clonic; LKS: Landau-
Kleffner syndrome.

neuroimaging often precedes EEG in evaluation of such hours of seizure shows background and epileptiform
children. EEG is recommended as first tier investigation abnormality more frequently [33]. These background
among children with first unprovoked seizure for diagnosis abnormalities are often transient and warrant repeat EEG
of seizure, epilepsy type and an epileptic syndrome. It may after certain duration to look for persistence of abnormality.
be useful for prediction of long-term outcome or recurrence
Characterization of Type of Seizure and Syndromic
[30]. Children who have focal epileptiform discharges on
Diagnosis
EEG have a higher risk for recurrence when compared to
those with normal EEG [31]. However, in obvious etiology EEG abnormalities are broadly divided into background
like neuro-cysticercosis or tuberculoma, EEG should not abnormalities and abnormal epileptiform waveforms.
be routinely requested at outset. EEG may be helpful before Background abnormalities include diffuse slowing,
withdrawing AED in such patients. Among children with asymmetric slowing, discontinuous background and
new onset seizures, 18-56% display epileptiform electrodecremental response. Group of disorders with
discharges on initial EEG and 15% will never show discontinuous EEG background where epileptiform
abnormal findings [32]. EEG done early within first 24 activities contribute to encephalopathy or non-attainment

INDIAN PEDIATRICS 897 VOLUME 55__OCTOBER 15, 2018

KAUSHIK & FARMANIA EEG IN PEDIATRIC EPILEPSY

BOX 1 INDICATIONS OF ELECTROENCEPHALOGRAPHY IN PEDIATRIC EPILEPSY

When to use
• EEG helps in differentiating epileptic from non-epileptic clinical event. Video EEG with capture of ictal event
is useful adjunct to support clinical possibility of epileptic event.
• To classify the type of epilepsy into focal or generalized epilepsy and diagnosis of various electro-clinical epilepsy
syndrome.
• Video EEG monitoring with spell capture is vital to localize the epileptic focus in case of focal epilepsy.
• To characterize the type of epileptic syndrome based on cluster of clinical seizure semiology, age at onset and
EEG findings.
• It helps clinician decide on tapering antiepileptic drugs after a seizure free interval and to predict possible relapse
after tapering antiepileptic drug.
• To guide about the etiology in a case of meningo-encephalitis (e.g., periodic lateralized epileptiform discharges
in case of herpes simplex encephalitis).
• To diagnose NCSE in case of prolonged coma after status epilepticus or encephalopathy of unknown etiology.
• In children with cognitive or language regression even without seizures, it is indispensable to rule out epileptic
encephalopathy like CSWS and LKS.
• To prognosticate an epileptic disorder e.g., Periodic complexes, triphasic waves in a sick patient in ICU is
suggestive of poor prognosis. Also, presence of epileptiform discharges predicts seizure recurrence in epilepsy.
• Ancillary test for documentation of brain death.
When not to use
• To exclude a diagnosis of epilepsy; since epilepsy is largely a clinical diagnosis.
• To monitor the progress of epilepsy with EEG.
(Note: In a children with epilepsy, new onset clinical features like cognitive decline or behavioural issue warrants
fresh EEG to rule out NCSE).
• To monitor the efficacy of antiepileptic drugs (AED) in epilepsy except in infantile spasm, LKS, CSWS or absence
epilepsy where there could be no change with AED.
(Note: Valproate and benzodiazepines can decrease the spike burden).
• Intracranial space occupying lesions including stroke without any history of seizures or raised intracranial pressure
to form the basis of starting prophylactic AED.
• Clinical history that clearly suggests paroxysmal non epileptic event like shuddering spells, gratification, and
syncopal attacks.
CSWS: Continuous spike wave in sleep, LKS: Landau Kleffner syndrome, NCSE: Non convulsive status epilepticus, AED:
antiepileptic drug, EEG: Electroencephalography.

of milestones is called epileptic encephalopathy. This are a group of self-limited epilepsies with focal stereotyped
includes Early myoclonic encephalopathy, Ohtahara spikes wherein the focal spikes can be seen with normal
syndrome, West syndrome (Web Fig. 2), Lennox Gestaut interictal EEG background. This includes Rolandic
syndrome, and Landau Kleffner syndrome. There are epilepsy (Web Fig. 4), Panayiotopoulos syndrome and
signature EEG features to diagnose epileptic benign occipital epilepsies. Children with structural lesion
encephalopathies as these conditions have urgent treatment like Neurocysticercosis, glioma or vascular lesion can also
implications (Table III). Interictal EEG can be categorized have focal epileptiform discharges (Web Fig. 5). Children
into focal or generalized based on the morphology of with subacute sclerosing panencephalitis can have periodic
epileptiform discharges and organization of background epileptiform discharges (Web Fig. 6).
activity. Generalized spike and spike-wave discharges with
Status Epilepticus
normal interictal background activity is observed in
childhood/juvenile absence epilepsy (CAE/JAE), epilepsy EEG is required to rule out nonconvulsive status
with myoclonic astatic seizures (Doose syndrome), epilepticus among those with no improvement of altered
juvenile myoclonic epilepsy (JME) (Web Fig. 3), and sensorium following convulsive seizures [34]. EEG is
epilepsy with eyelid myoclonia (Jeavon syndrome). There also useful adjunct to monitor seizure activity among

INDIAN PEDIATRICS 898 VOLUME 55__OCTOBER 15, 2018

KAUSHIK & FARMANIA EEG IN PEDIATRIC EPILEPSY

KEY MESSAGES
• A normal EEG does not exclude the diagnosis of epilepsy.
• EEG helps in differentiating epileptic from non-epileptic clinical event, determine seizure type and specific epilepsy
syndrome.
• An ideal EEG record must include both awake and sleep state as far as possible.
• Single routine surface EEG can miss majority of focal epilepsies. Surface EEG can be normal in children with
remote and deep location of epileptogenic focus.
• EEG report must always be interpreted in clinical context to avoid erroneous clinical diagnosis and management.

those with neuromuscular blockade (which might mask febrile seizure [41]. Hence, there is limited utility of EEG
convulsive activity) and high dose suppressive therapy among children with febrile seizures with lack of clinical
for refractory status epilepticus. Among those with significance of an abnormal EEG in predicting recurrence
refractory status epilepticus, suppression of epileptiform or subsequent development of epilepsy.
discharges to achieve burst suppression on EEG is often
Discontinuation of AED
considered end point for titrating the dose of antiepileptic
and anesthetic agents [35]. Majority of children who are seizure-free for a duration
of at least 2 years or more have minimal risk for seizure
Comatose Child
recurrence [42]. However, the risk of recurrence
Continuous EEG monitoring in intensive care unit (ICU) following withdrawal will depend on type of epilepsy,
setting is ideal during management of a child with polytherapy, abnormality on neuroimaging and EEG
refractory status epilepticus, heavy sedation, those on [43]. Patients with intellectual disability, abnormal
neuromuscular blocker, or those being treated with neurological examination, older age at onset of seizure,
barbiturate for raised intracranial pressure [36]. A focal seizures and epileptiform abnormalities on EEG
comatose child with past history of seizure or seizure like have a higher risk of relapse [42]. Abnormal EEG at the
activity requires an EEG to rule out non convulsive status time of AED withdrawal has been shown to be associated
epilepticus. The most common EEG finding in a child with a relative risk of recurrence of 1.45 (95% CI 1.18-
with coma is diffuse slowing with reduction in amplitude 1.79) [44]. There is an emerging interest on serial EEG
of waveform. Triphasic waves on EEG could point to monitoring during AED withdrawal to predict risk of
ward underlying metabolic disorder. Similarly, periodic recurrence. In a study on 84 children who had seizure
lateralized epileptiform discharges (PLED) suggest a recurrence despite normal EEG at the time of drug
focus of irritable cortex seen in space occupying lesion or withdrawal, 24 had abnormal EEG during AED
herpes encephalitis. Serial EEG can help with withdrawal [45].
prognostication. In children with post anoxic coma, burst
CONCLUSION
suppression or isoelectric pattern on EEG is a poor
prognostic marker for recovery [37]. EEG monitoring in A normal interictal EEG does not exclude the diagnosis
ICU setting has limited role because of environmental of epilepsy. EEG is useful to establish the diagnosis of
noise and use of sedative drugs. epilepsy, classify the type of epilepsy and to rule out
Febrile Seizure nonconvulsive status epilepticus among children with
unexplained coma. EEG is often misused to justify the
There is no role of EEG in children with simple febrile need for AED among children with clear history of
seizures [38]. However, EEG is more likely to be abnormal paroxysmal non-epileptic events, headache, simple
among those with complex febrile seizures, including febrile seizures and head trauma. An abnormal EEG
febrile status epilepticus and focal febrile seizures. Focal report should always be interpreted in clinical context.
epileptiform abnormalities were significantly more
Acknowledgments: Dr Suvasini Sharma and Dr Rachana Dubey
frequent among children with complex febrile seizure who
Gupta for their suggestions in improving the manuscript; and
subsequently developed epilepsy [39]. However, Prof Kiran Bala and Prof Surekha Dabla, Department of
epileptiform EEG has poor positive predictive value for Neurology, PGIMS, Rohtak for their guidance in the manuscript
subsequent development of epilepsy [40], and there is no and for providing images of EEG tracings.
evidence to support or refute the use of EEG after complex Contributors: Both authors contributed to review and synthesis

INDIAN PEDIATRICS 899 VOLUME 55__OCTOBER 15, 2018

KAUSHIK & FARMANIA EEG IN PEDIATRIC EPILEPSY

of literature, manuscript writing, and final approval of the Efficacy and safety of oral triclofos as sedative for children
version to be published. undergoing sleep electroencephalogram: An observational
Funding: None; Competing Interest: None stated. study. J Pediatr Neurosci. 2016;11:105-8.
16. Panayiotopoulos CP. EEG and Brain imaging. In:
REFERENCES
Panayiotopoulos CP, editors. A clincal guide to epileptic
1. Clancy RR, Bergvist AGC, Dlugos DJ, Nordli DR. Normal syndromes and their treatment. 2nd ed. London: Springer
pediatric EEG: neonate and children. In: Ebersole JS, publication; 2010. p. 147-71.
editors. Current Practice of Clinical Electro- 17. Pillai J, Sperling MR. Interictal EEG and the diagnosis of
encephalography. 4th ed. Philadelphia: Lippincott epilepsy. Epilepsia. 2006;47:14-22.
Williams & Wilkins; 2014. p. 125-212. 18. Noachtar S, Rémi J. The role of EEG in epilepsy: A critical
2. Noachtar S, Peters AS. Semiology of epileptic seizures: A review. Epilepsy Behav. 2009;15:22-33.
critical review. Epilepsy Behav. 2009;15:2-9. 19. Fowle AJ, Binnie CD. Uses and abuses of the EEG in
3. Yoshinaga H, Hattori J, Ohta H, Asano T, Ogino T, epilepsy. Epilepsia. 2000;41:S10-18.
Kobayashi K, et al. Utility of the scalp-recorded ictal EEG 20. Gencpinar P, Dundar NO, Tekgul H. Electrical status
in childhood epilepsy. Epilepsia. 2001;42:772-7. epilepticus in sleep (ESES)/continuous spikes and waves
4. Fernández IS, Loddenkemper T. Electrocorticography for during slow sleep (CSWS) syndrome in children: An
seizure foci mapping in epilepsy surgery. J Clin electroclinical evaluation according to the EEG patterns.
Neurophysiol. 2013;30:554-70. Epilepsy Behav. 2016;61:107-11.
5. Halford JJ, Sabau D, Drislane FW, Tsuchida TN, Sinha SR. 21. Fattouch J, Casciato S, Lapenta L, Morano A, Fanella M,
American Clinical Neurophysiology Society Guideline 4: Lombardi L, et al. The spectrum of epileptic syndromes
Recording Clinical EEG on Digital Media. J Clin with fixation off sensitivity persisting in adult life.
Neurophysiol. 2016;33:317-9. Epilepsia. 2013;54:59-65.
6. Olejniczak P. Neurophysiologic basis of EEG. J Clin 22. Tatum WO, Olga S, Ochoa JG, Munger Clary H, Cheek J,
Neurophysiol. 2006;23:186-9. Drislane F, et al. American Clinical Neurophysiology
7. Maus D, Epstein CM, Herman ST. Digital EEG. In: Society Guideline 7: Guidelines for EEG Reporting. J Clin
Schomer DL, Lopes Da Silva FH, (editors). Niedermeyer's Neurophysiol. 2016;33:328-32.
Electroencephalography: Basic Principles, Clinical 23. So EL. Interictal epileptiform discharges in persons
Applications, and Related Fields. 5th ed. Philadelphia: without a history of seizures: What do they mean? J Clin
Lippincott Williams & Wilkins;. 2005. p. 127-38. Neurophysiol. 2010;27:229-38.
8. Kaminska A, Cheliout-Heraut F, Eisermann M, Touzery de 24. Spence SJ, Schneider MT. The role of epilepsy and
Villepin A, Lamblin MD. EEG in children, in the epileptiform EEGs in autism spectrum disorders. Pediatr
laboratory or at the patient's bedside. Neurophysiol Clin Res. 2009;65:599-606.
Clin Neurophysiol. 2015;45:65-74. 25. Fogang Y, Gérard P, De Pasqua V, Pepin JL, Ndiaye M,
9. Bartlam R, Mohanraj R. Ictal bradyarrhythmias and Magis D, et al. Analysis and clinical correlates of 20 Hz
asystole requiring pacemaker implantation: Combined photic driving on routine EEG in migraine. Acta Neurol
EEG-ECG analysis of 5 cases. Epilepsy Behav. Belg. 2015;115:39-45.
2016;64:212-5. 26. Hernandez-Frau PE, Benbadis SR. Pearls and oysters:
10. Hill AT, Briggs BA, Seneviratne U. Simultaneous errors in EEG interpretations: What is misinterpreted
recording of EEG and electromyographic polygraphy besides temporal sharp transients? Neurology. 2011;76:
increases the diagnostic yield of video-EEG monitoring. J 57-9.
Clin Neurophysiol. 2014;31:203-7. 27. Benbadis SR. The tragedy of over-read EEGs and wrong
11. Rizvi SAA, Hernandez-Ronquillo L, Wu A, Téllez Zenteno diagnoses of epilepsy. Expert Rev Neurother. 2010;10:343.
JF. Is rapid withdrawal of anti-epileptic drug therapy 28. Laffan A, Langan Y. Understanding EEG indications and
during video EEG monitoring safe and efficacious? reports: A survey of NCHDs. Ir Med J. 2013;106:59-60.
Epilepsy Res. 2014;108:755-64. 29. Sahu PS, Seepana J, Padela S, Sahu AK, Subbarayudu S,
12. Kobulashvili T, Höfler J, Dobesberger J, Ernst F, Ryvlin P, Barua A. Neurocysticercosis in children presenting with
Cross JH, et al. Current practices in long-term video-EEG afebrile seizure: clinical profile, imaging and
monitoring services: A survey among partners of the serodiagnosis. Rev Inst Med Trop São Paulo. 2014;56:
epilepsy pilot network of reference for refractory epilepsy 253-8.
and epilepsy surgery. Seizure. 2016;38:38-45. 30. Pohlmann-Eden B, Newton M. First seizure: EEG and
13. DeRoos ST, Chillag KL, Keeler M, Gilbert DL. Effects of neuroimaging following an epileptic seizure. Epilepsia.
sleep deprivation on the pediatric electroencephalogram. 2008;49(Suppl.1):19-25.
Pediatrics. 2009;123:703-8. 31. Mizorogi S, Kanemura H, Sano F, Sugita K, Aihara M.
14. Giorgi FS, Guida M, Caciagli L, Maestri M, Carnicelli L, Risk factors for seizure recurrence in children after first
Bonanni E, et al. What is the role for EEG after sleep unprovoked seizure. Pediatr Int. 2015;57:665-9.
deprivation in the diagnosis of epilepsy? Issues, 32. Wirrell EC. Prognostic significance of interictal
controversies, and future directions. Neurosci Biobehav epileptiform discharges in newly diagnosed seizure
Rev. 2014;47:533-48. disorders. J Clin Neurophysiol. 2010;27:239-48.
15. Jain P, Sharma S, Sharma A, Goel S, Jose A, Aneja S. 33. King MA, Newton MR, Jackson GD, Fitt GJ, Mitchell LA,

INDIAN PEDIATRICS 900 VOLUME 55__OCTOBER 15, 2018

KAUSHIK & FARMANIA EEG IN PEDIATRIC EPILEPSY

Silvapulle MJ, et al. Epileptology of the first-seizure Clinical and EEG risk factors for subsequent epilepsy in
presentation: A clinical, electroencephalographic, and patients with complex febrile seizures. Epilepsy Res.
magnetic resonance imaging study of 300 consecutive 2013;105:158-63.
patients. Lancet. 1998;352:1007-11. 40. Harini C, Nagarajan E, Kimia AA, de Carvalho RM, An S,
34. Trinka E, Leitinger M. Which EEG patterns in coma are Bergin AM, et al. Utility of initial EEG in first complex
nonconvulsive status epilepticus? Epilepsy Behav. febrile seizure. Epilepsy Behav. 2015;52:200-4.
2015;49:203-22. 41. Shah PB, James S, Elayaraja S. EEG for children with
35. Bergey GK. Refractory Status Epilepticus: Is EEG burst complex febrile seizures. Cochrane Database Syst Rev.
suppression an appropriate treatment target during drug- 2015;CD009196.
induced coma? What is the holy grail? Epilepsy Curr. 42. Beghi E, Giussani G, Grosso S, Iudice A, La Neve A, Pisani
2006;6:119-20. F, et al. Withdrawal of antiepileptic drugs: guidelines of the
36. Seshia SS, Bingham WT, Kirkham FJ, Sadanand V. Italian League Against Epilepsy. Epilepsia. 2013 ;54:2-12.
Nontraumatic coma in children and adolescents: Diagnosis 43. Afshari D, Moradian N. Evaluating the rate of recurrence
and management. Neurol Clin. 2011;29:1007-43. of epilepsy after therapy discontinuation in 2-year seizure-
37. Zandbergen EG, de Haan RJ, Stoutenbeek CP, Koelman free epileptic patients. Int J Neurosci. 2012;122:598-601.
JH, Hijdra A. Systematic review of early prediction of poor 44. Berg AT, Shinnar S. Relapse following discontinuation of
outcome in anoxic-ischaemic coma. Lancet. 1998; antiepileptic drugs: A meta-analysis. Neurology.
352:1808-12. 1994;44:601-8.
38. Subcommittee on Febrile Seizures, American Academy of 45. Verrotti A, Matricardi S, Di Giacomo DL, Rapino D,
Pediatrics. Neurodiagnostic evaluation of the child with a Chiarelli F, Coppola G. Neuropsychological impairment in
simple febrile seizure. Pediatrics. 2011;127:389-94. children with Rolandic epilepsy and in their siblings.
39. Kim H, Byun SH, Kim JS, Lim BC, Chae J-H, Choi J, et al. Epilepsy Behav. 2013;28:108-12.

INDIAN PEDIATRICS 901 VOLUME 55__OCTOBER 15, 2018

KAUSHIK & FARMANIA EEG IN PEDIATRIC EPILEPSY

WEB FIG. 1 EEG (Electroencephalography) showing runs of vertex waves (arrow) observed in normal stage II NREM sleep.

WEB FIG. 2 EEG (Electroencephalography) showing Classical hysarryhythmia with chaotic background with high voltage
epileptiform discharges (arrow).

INDIAN PEDIATRICS 903 VOLUME 55__OCTOBER 15, 2018

KAUSHIK & FARMANIA EEG IN PEDIATRIC EPILEPSY

WEB FIG. 3 EEG (Electroencephalography) showing generalized interictal epileptiform discharges (arrow) (4-4.5 Hz) on photic
stimulation in a child with Juvenile myoclonic epilepsy.

WEB FIG. 4 EEG (Electroencephalography) showing Rolandic centrotemporal spikes with tangential dipole (arrow).

INDIAN PEDIATRICS 904 VOLUME 55__OCTOBER 15, 2018

KAUSHIK & FARMANIA EEG IN PEDIATRIC EPILEPSY

WEB FIG. 5 EEG (Electroencephalography) showing left temporal interictal epileptiform discharges (arrow) in a child with left mesial
temporal sclerosis.

WEB FIG.6 EEG (Electroencephalography) showing generalized epileptiform discharges (arrow) in periodic interval in subacute
sclerosing panencephalitis.

INDIAN PEDIATRICS 905 VOLUME 55__OCTOBER 15, 2018