Scalp EEG is an electrophysiological tool that examines the electrical activity of the human brain. EEG is commonly ordered as part of the evaluation of “spells” or suspected seizures in children, and is a useful study that can guide the diagnosis of epilepsy and direct medication management. In patients with known epilepsy, EEG can help understand seizure burden. It also is used in pre-surgical evaluation.
While EEG can be helpful, misinterpretation of an EEG can lead to a misdiagnosis of epilepsy. The results must be interpreted in relationship to the patient’s history. Epileptiform discharges can be found in up to 5 percent of normal healthy children (1). In addition, benign epileptiform variants have a prevalence of about 3.4 to 18 percent. These benign variants can be misinterpreted as abnormal, even though these variants do not increase the risk of epilepsy (3,4). Thus, overemphasis of an EEG can consequently lead to unnecessary treatment and have psychologic and social implications. As a result, it is important to understand the various components, indications and proper uses of an EEG.
What are the indications for an EEG?
The main indication of an EEG is to aide in the diagnosis of epilepsy. History and examination are used primarily to diagnose epilepsy, but an EEG can be a tool to help support the diagnosis of epilepsy. If the patient does have seizures, an EEG can help guide diagnosis of specific syndromes and treatments (5). For instance, 3Hz spike and wave generalized discharges are typically seen in childhood absence epilepsy. Polyspike and wave discharges are seen in juvenile myoclonic epilepsy. Benign rolandic epilepsy is characterized by stereotyped centrotemporal spikes activated in sleep.
Additionally, EEG can help distinguish epileptic events from non-epileptic events, such as syncope or psychogenic non-epileptic events, if the events are captured during EEG recording (5). Non-epileptic paroxysmal events can be seen in infancy and childhood. They are often repetitive or stereotyped movements that can mimic seizures, such as benign sleep myoclonus, shuddering attacks, breath-holding spells, or spasmus nutans. Movement disorders, such as alternating hemiplegia, dystonia, or paroxysmal dyskinesia, also can resemble seizures. Additionally, staring, which is a symptom seen in children with absence seizures, are a common non-epileptic symptom prompting referral to pediatric neurology. A normal EEG during an event in these patients can support that these are seizure mimickers, rather than true epileptic events.
What are the key components of an EEG?
There is an important methodology to EEG reading in pediatric patients. The most important aspect of history is the age of a patient. In infants, gestational age is particularly important, as maturation patterns vary week by week (6).
With known age, the EEG reader interprets the background, or the baseline electrical activity of the patient. There are different components of the background, which includes amplitude (or height of the EEG waves) in microvolts, frequency (or how fast the EEG waves are) in hertz, synchrony and symmetry. These components often comprise specific age-related patterns that change as the child matures into adulthood.
Another aspect of an EEG is to determine what state the patient is in (awake, drowsy, asleep, obtunded or comatose). Drowsiness can produce waveforms or discharges in children that are normal variants and can be misinterpreted as pathologic discharges. There are different sleep stages (N1, N2, N3 and REM), and each stage has different features on the EEG. Pediatric patients have specific sleep patterns that change with age (6).
Additionally, the EEG also can be used to evaluate for interictal epileptiform discharges (IED), which represents a synchronous summation of potentials of electrical activity in a group of neurons and can indicate a potential area of seizure genesis (7). For a discharge to be considered epileptiform, several criteria must be fulfilled to meet a specificity of 95 percent (8). Presence of epileptiform discharges can help confirm the diagnosis of epilepsy or predict seizure reoccurrence in patients. Epileptiform discharges also can guide medication treatment and management in patients with known epilepsy.
What is the diagnostic yield of an EEG?
The first routine EEG study does not always show abnormalities, even in patients with known epilepsy. The yield of epileptiform abnormality in an EEG on a patient with unprovoked seizures or epilepsy ranges from 32-59 percent (9, 10). Diagnostic yield of serial EEGs increased to 60-77 percent in patients with epilepsy who had three studies and > 90 percent in patients with more than six studies (9). Sleep during an EEG may increase yield of epileptiform abnormalities in patients with epilepsy (10). In a population-based study, interictal epileptiform activity was seen in 30 percent of patients with wakefulness versus 67 percent in those with wakefulness and sleep (10).
In addition, activation procedures of photic stimulation and hyperventilation are performed and can increase diagnostic yield. Photic stimulation involves an intermittent flash stimulus at a range of 1-30 Hz. A photoparoxysmal response is when there is an abnormal EEG response during photic stimulation and can be seen in patients with generalized and focal epilepsies (11). However, photoparoxysmal responses can be seen in 2 percent of patients without epilepsy, and patients who do not have epilepsy and have photoparoxysmal response rarely develop epilepsy (12).
Hyperventilation most commonly activates absence seizures or produces epileptiform discharges in generalized or focal epilepsies, as well as localized slowing in focal epilepsies (12). Epileptiform discharges are more likely to be provoked in patients with generalized epilepsy, with 50-80 percent of patients with generalized epilepsies having epileptiform abnormalities compared to 6.6 percent in patients with focal epilepsy (12). Hyperventilation is contraindicated in patients with recent history of stroke, Moya-Moya disease, pulmonary disease, sickle cell disease, severe cardiac disease and subarachnoid hemorrhage.
When is an EEG not helpful?
Simple febrile seizures are the most commonly occurring seizures in the first two years of life. In healthy children with simple febrile seizures with a normal neurologic examination, observational studies and anecdotal data suggest that an EEG should not be performed. An EEG in these situations do not alter outcome, predict epilepsy or recurrence of febrile seizures within the next two years (13).
Syncope is defined as a sudden or transient loss of consciousness and brief loss of tone, most often due to inadequate cerebral blood flow due to decreased blood pressure. Syncope can sometimes be accompanied by convulsive movements, which can be mistaken for seizure activity. Patients with syncope often have return to spontaneous activity and baseline mentation within several seconds, which distinguishes it from seizure. While an EEG during a syncopal event can help clarify if the event is epileptic versus non-epileptic, baseline routine EEGs have low diagnostic yield in patients with syncope. The prevalence of epileptiform discharges in patients with syncope was reported to have 1.46-1.79 percent, which is similar to the incidence of epileptiform discharges in healthy individuals (14). Thus, abnormal results should be interpreted with caution based on history and clinical suspicion.
Headaches are a common neurologic disorder in children and adolescents. An EEG may be performed as part of the diagnostic workup for recurrent headaches or migraines. However, previous studies have demonstrated that children with migraines and recurrent headaches have a normal EEG or nonspecific or paroxysmal abnormalities. However, even with an abnormal EEG, this does not provide any diagnostic clarity or confirm the etiology being seizure. Further, studies have shown that patients with migraines who have paroxysmal EEG abnormalities did not go on to develop seizures (15).
When should an urgent EEG be considered?
Infantile spasms are a specific type of seizure seen in infancy, characterized by clusters of flexor or extensor movements (16). West syndrome is characterized by a clinical triad of infantile spasms, developmental regression and a high-amplitude chaotic background on an EEG called hypsarrhythmia. Infants with infantile spasms may develop other seizure types and have alterations in cognitive development and outcome. Prompt diagnosis and early treatment could alter prognosis, with earlier treatment portending a more favorable outcome in infants with cryptogenic infantile spasms (17,18). Thus, if there is clinical suspicion of infantile spasms, urgent referral for an EEG is warranted, because early institution of treatment could profoundly impact developmental outcome.
Electrical status epilepticus in sleep (ESES) are sleep-activated epileptiform abnormalities that can cause language regression and epileptic aphasia. Landau-Kleffner syndrome (LKS) is a rare syndrome characterized by language regression, auditory agnosia (often mistaken for acquired deafness) and behavioral changes. These patients exhibit ESES on EEG. Children with LKS can be mistaken for autism due to their language regression, but these children exhibit normal language development prior to age 3 years. They develop language regression between 3 and 8 years of age, in contrast to children with autism (19). These children also have subacute difficulty understanding spoken language. Early diagnosis and treatment achieve better long-term prognosis and language improvement. Negative factors of outcome included age of onset before 4 years and length of ESES, with those who have ESES for longer than 36 months had no recovery of language (20, 21, 22). Thus, patients with normal language development with subacute auditory agnosia (difficulty understanding speech) should be referred for a neurological evaluation and EEG, since earlier treatment can provide a more favorable prognosis.
Non-convulsive status epilepticus (NCSE) is defined as seizure activity lasting at least 10 minutes with no clear motor symptoms. Patients can present with altered mentation, disturbance in consciousness, or acute confusion without signs of convulsive activity. Patients also can be ambulatory during non-convulsive status epilepticus. NCSE can occur in patients with both generalized and focal epilepsies and also can be caused by autoimmune or infectious etiologies. Absence status is a form of non-convulsive status epilepticus that occurs in children and adults. In patients with clinical suspicion of NCSE, EEG can particularly be useful for confirmation diagnosis and treatment guidance, as it can help clarify if status epilepticus is ongoing or responding to treatment (23).
Comprehensive Epilepsy Program
Cook Children’s Neurosciences team
Great outcomes begin with great input. Having a medical system where every department, doctor, and care team member works together means that your child can have quick access to testing, diagnosis and treatment, and that means better outcomes now and in the future.
Contact the Jane and John Justin Neuroscience Center at Cook Children’s with your questions at 682-885-2500.
- Zivin L, Marsan CA. Incidence and prognostic significance of “epileptiform” activity in the eeg of non-epileptic subjects. Brain. 1968;91(4):751-78. doi: 10.1093/brain/91.4.751. PMID: 5704833.
- Amin U, Benbadis SR. The Role of EEG in the Erroneous Diagnosis of Epilepsy. J Clin Neurophysiol. 2019 Jul;36(4):294-297. doi: 10.1097/WNP.0000000000000572. PMID: 31274692.
- Santoshkumar B, Chong JJ, Blume WT, McLachlan RS, Young GB, Diosy DC, Burneo JG, Mirsattari SM. Prevalence of benign epileptiform variants. Clin Neurophysiol. 2009 May;120(5):856-61. doi: 10.1016/j.clinph.2009.03.005. Epub 2009 Apr 10. PMID: 19362516.
- Rathore C, Prakash S, Rana K, Makwana P. Prevalence of benign epileptiform variants from an EEG laboratory in India and frequency of their misinterpretation. Epilepsy Res. 2021 Feb;170:106539. doi: 10.1016/j.eplepsyres.2020.106539. Epub 2021 Jan 5. PMID: 33461042.
- Valente KD, Freitas A, Fiore LA, Gronich G, Negrão N. The diagnostic role of short duration outpatient V-EEG monitoring in children. Pediatr Neurol. 2003 Apr;28(4):285-91. doi: 10.1016/s0887-8994(03)00002-x. PMID: 12849882.
- Sheth RD. Patterns Specific to Pediatric EEG. J Clin Neurophysiol. 2019 Jul;36(4):289-293. doi: 10.1097/WNP.0000000000000600. PMID: 31274691.
- Chvojka J, Kudlacek J, Chang WC, Novak O, Tomaska F, Otahal J, Jefferys JGR, Jiruska P. The role of interictal discharges in ictogenesis – A dynamical perspective. Epilepsy Behav. 2021 Aug;121(Pt B):106591. doi: 10.1016/j.yebeh.2019.106591. Epub 2019 Dec 2. PMID: 31806490.
- Kural MA, Duez L, Sejer Hansen V, Larsson PG, Rampp S, Schulz R, Tankisi H, Wennberg R, Bibby BM, Scherg M, Beniczky S. Criteria for defining interictal epileptiform discharges in EEG: A clinical validation study. Neurology. 2020 May 19;94(20):e2139-e2147. doi: 10.1212/WNL.0000000000009439. Epub 2020 Apr 22. PMID: 32321764; PMCID: PMC7526669.
- Baldin E, Hauser WA, Buchhalter JR, Hesdorffer DC, Ottman R. Yield of epileptiform electroencephalogram abnormalities in incident unprovoked seizures: a population-based study. Epilepsia. 2014 Sep;55(9):1389-98. doi: 10.1111/epi.12720. Epub 2014 Jul 9. PMID: 25041095; PMCID: PMC4167205.
- Carpay JA, de Weerd AW, Schimsheimer RJ, Stroink H, Brouwer OF, Peters AC, van Donselaar CA, Geerts AT, Arts WF. The diagnostic yield of a second EEG after partial sleep deprivation: a prospective study in children with newly diagnosed seizures. Epilepsia. 1997 May;38(5):595-9. doi: 10.1111/j.1528-1157.1997.tb01145.x. PMID: 9184606.
- van Win OA, Barnes JG, Ferrier CF, Booth F, Prasad AN, Kasteleijn-Nolst Trenite DGA. A study of the significance of photoparoxysmal responses and spontaneous epileptiform discharges in the EEG in childhood epilepsy. Epilepsy Behav. 2020 Jun;107:107046. doi: 10.1016/j.yebeh.2020.107046. Epub 2020 Apr 15. PMID: 32304987.
- Mendez OE, Brenner RP. Increasing the yield of EEG. J Clin Neurophysiol. 2006 Aug;23(4):282-93. doi: 10.1097/01.wnp.0000228514.40227.12. PMID: 16885703.
- Subcommittee on Febrile Seizures; American Academy of Pediatrics. Neurodiagnostic evaluation of the child with a simple febrile seizure. Pediatrics. 2011 Feb;127(2):389-94. doi: 10.1542/peds.2010-3318. PMID: 21285335.
- Dantas FG, Cavalcanti AP, Rodrigues Maciel BD, Ribeiro CD, Napy Charara GC, Lopes JM, Martins Filho PF, Júnior LA. The role of EEG in patients with syncope. J Clin Neurophysiol. 2012 Feb;29(1):55-7. doi: 10.1097/WNP.0b013e318246b589. PMID: 22353986.
- Lewis DW, Ashwal S, Dahl G, Dorbad D, Hirtz D, Prensky A, Jarjour I; Quality Standards Subcommittee of the American Academy of Neurology; Practice Committee of the Child Neurology Society. Practice parameter: evaluation of children and adolescents with recurrent headaches: report of the Quality Standards Subcommittee of the American Academy of Neurology and the Practice Committee of the Child Neurology Society. Neurology. 2002 Aug 27;59(4):490-8. doi: 10.1212/wnl.59.4.490. PMID: 12196640.
- Wilmshurst JM, Gaillard WD, Vinayan KP, Tsuchida TN, Plouin P, Van Bogaert P, Carrizosa J, Elia M, Craiu D, Jovic NJ, Nordli D, Hirtz D, Wong V, Glauser T, Mizrahi EM, Cross JH. Summary of recommendations for the management of infantile seizures: Task Force Report for the ILAE Commission of Pediatrics. Epilepsia. 2015 Aug;56(8):1185-97. doi: 10.1111/epi.13057. Epub 2015 Jun 30. PMID: 26122601.
- Kivity S, Lerman P, Ariel R, Danziger Y, Mimouni M, Shinnar S. Long-term cognitive outcomes of a cohort of children with cryptogenic infantile spasms treated with high-dose adrenocorticotropic hormone. Epilepsia. 2004 Mar;45(3):255-62. doi: 10.1111/j.0013-9580.2004.30503.x. PMID: 15009227.
- Pellock JM, Hrachovy R, Shinnar S, Baram TZ, Bettis D, Dlugos DJ, Gaillard WD, Gibson PA, Holmes GL, Nordl DR, O’Dell C, Shields WD, Trevathan E, Wheless JW. Infantile spasms: a U.S. consensus report. Epilepsia. 2010 Oct;51(10):2175-89. doi: 10.1111/j.1528-1167.2010.02657.x. PMID: 20608959.
- Trevathan E. Seizures and epilepsy among children with language regression and autistic spectrum disorders. J Child Neurol. 2004 Aug;19 Suppl 1:S49-57. doi: 10.1177/088307380401900106. PMID: 15526970.
- Mikati MA, Shamseddine AN. Management of Landau-Kleffner syndrome. Paediatr Drugs. 2005;7(6):377-89. doi: 10.2165/00148581-200507060-00006. PMID: 16356025.
- Robinson RO, Baird G, Robinson G, Simonoff E. Landau-Kleffner syndrome: course and correlates with outcome. Dev Med Child Neurol. 2001 Apr;43(4):243-7. doi: 10.1017/s0012162201000469. PMID: 11305401.
- Rossi PG, Parmeggiani A, Posar A, Scaduto MC, Chiodo S, Vatti G. Landau-Kleffner syndrome (LKS): long-term follow-up and links with electrical status epilepticus during sleep (ESES). Brain Dev. 1999 Mar;21(2):90-8. doi: 10.1016/s0387-7604(98)00071-0. PMID: 10206525.
- Brenner RP. Is it status? Epilepsia. 2002;43 Suppl 3:103-13. doi: 10.1046/j.1528-1157.43.s.3.9.x. PMID: 12060012.