Autism spectrum disorder (ASD) describes a constellation of neurological and developmental disorders in communication, learning, and behavioral areas that affect how people interact with others.1,2
The most extensive study of comorbidity between epilepsy and autism involved nearly 6,000 patients and showed the presence of epilepsy in 26% of patients over 13 years old.3 Other studies correlate these two conditions at a rate of up to 30%.4
EEG patterns in ASD?
There is no distinctive EEG pattern for ASD due to the heterogeneity in its etiology, phenotype, and outcome; nonetheless, epileptiform discharges seem to be more common than non-epileptiform abnormalities in patients with ASD.5
The neuroanatomical regions more frequently found with EEG abnormalities are temporal regions,5,6 suggesting that right temporal regions are more implicated in social deficits while bilateral temporal areas are more involved in language dysfunction.7
Subclinical electroencephalographic abnormalities (SEA) and therapeutic implications
An association between ASD and subclinical electroencephalographic abnormalities (SEA) has been long established. In a large restrospective study, 889 patients with autism and no previous history of epilepsy underwent 24hr EEG recordings. Just over 60% of subjects exhibited abnormalities, mainly consisting of spikes, sharp-waves and polyspikes. Interestingly, these were detected only during sleep, underscoring the importance of sleep monitoring to detect SEA in ASE.10
Still, there is a lack of evidence about the role of SEA in the complex physiopathogenesis of ASD. As a result, there is a question regarding if it should be considered a good biomarker or target from the therapeutic point of view. Recently, studies indicate an improvement of autism core symptoms in patients with SEAs and ASD after treatment with,11 but double-blinded randomized studies are needed to evaluate the effectiveness.
Further high-quality investigations are needed to provide adequate guidance to clinical practices based on EEG findings.
References:
1. NIMH » Autism Spectrum Disorder.
Accessed April 6, 2022. https://www.nimh.nih.gov/health/topics/autism-spe...
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C, Elsabbagh M, Baird G, Veenstra-Vanderweele J. Autism spectrum disorder. Lancet.
2018;392(10146):508-520. doi:10.1016/S0140-6736(18)31129-2
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EW, Triche EW, Pescosolido MF, et al. Clinical characteristics of children with
autism spectrum disorder and co-occurring epilepsy. PLoS One. 2013;8(7).
doi:10.1371/JOURNAL.PONE.0067797
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ML, Kesler M, Candy SA, Rho JM, Pittman QJ. Comorbid epilepsy in autism
spectrum disorder: Implications of postnatal inflammation for brain
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JK, Carosella C, Corbin E, Horn PS, Caine R, Manning-Courtney P. EEG
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DA. Behavioral correlates of epileptiform abnormalities in autism. Epilepsy
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G, Operto FF, Auricchio G, D’Amico A, Fortunato D, Pascotto A. Temporal lobe
dual pathology in malignant migrating partial seizures in infancy. Epileptic
Disord. 2007;9(2):145-148. doi:10.1684/EPD.2007.0106
8. Nicotera
AG, Hagerman RJ, Catania MV, et al. EEG Abnormalities as a Neurophysiological
Biomarker of Severity in Autism Spectrum Disorder: A Pilot Cohort Study. J
Autism Dev Disord 2019 496. 2019;49(6):2337-2347.
doi:10.1007/S10803-019-03908-2
9. Uhlhaas
PJ, Singer W. Neural Synchrony in Brain Disorders: Relevance for Cognitive
Dysfunctions and Pathophysiology. Neuron. 2006;52(1):155-168.
doi:10.1016/J.NEURON.2006.09.020
10. Chez
MG, Chang M, Krasne V, Coughlan C, Kominsky M, Schwartz A. Frequency of
epileptiform EEG abnormalities in a sequential screening of autistic patients
with no known clinical epilepsy from 1996 to 2005. Epilepsy Behav.
2006;8(1):267-271. doi:10.1016/J.YEBEH.2005.11.001
11. Horvath
AA, Csernus EA, Lality S, Kaminski RM, Kamondi A. Inhibiting Epileptiform
Activity in Cognitive Disorders: Possibilities for a Novel Therapeutic
Approach. Front Neurosci. 2020;14. doi:10.3389/FNINS.2020.557416