Abstract

Recent advances in electroencephalography (EEG) have uncovered significant associations between subclinical epileptiform activity and autism spectrum disorder (ASD), even in the absence of epileptic seizures (Spence and Schneider, 2009). There is significant clinical data demonstrating the potential of EEG to help guide medication selection in the treatment of complex and treatment-resistant psychiatric patients (Swatzyna et al., 2024). The reluctance of psychiatry to recognize the growing evidence for EEG biomarkers and utilize this relatively simple, inexpensive, and noninvasive technology as a precision medicine tool may be resulting in missed opportunities for improving patient outcomes.
ASD is associated with a high incidence of subclinical epileptiform activity. Twenty to 60% of patients with ASD demonstrate EEG abnormalities, including isolated epileptiform discharges (IEDs), which may represent readily identifiable biomarkers of CNS neuroelectric dysfunction. A research team used valproic acid to treat 176 nonepileptic ASD patients with epileptiform discharges, with nearly half of follow-up EEGs having normalized (Chez et al., 2006).
Subclinical EEG abnormalities, though common in ASD, are not yet widely acknowledged as clinically relevant in psychiatric practice. Many neurologists interpret IEDs as “subtle” or “incidental” findings. However, this position has been challenged by an evolving evidence base showing that pharmacologic treatment with antiseizure medication of individuals demonstrating these EEG abnormalities—especially when associated with behavioral regression or treatment resistance—can lead to notable improvements in attention, executive function, sleep, and affect regulation (Swatzyna et al., 2024).
We believe the time has come for psychiatry to critically reevaluate the role of routine EEG in ASD, particularly for those with ASD, developmental regression, catatonia, or medication resistance. EEGs are widely available and relatively inexpensive, thus making their use in evaluations practical and cost efficient. Experts in diagnostic neurophysiology are of the opinion that psychiatrists should be trained to read and interpret routine EEGs themselves to ensure that so-called subtle EEG findings are identified (Swatzyna et al., 2024).
EEG can improve our understanding of autism-related differences in neurophysiology. Seizures and ASD have shared underlying neuraltransmitter mechanisms, such as abnormalities in GABA receptor functioning. Recent advances in quantitative EEG data analysis in patients with epilepsy and ASD demonstrate the role of aberrant GABAergic transmission, with impacts on neuronal organization and connectivity, particularly evident in the frontal cortex (Milovanovic and Grujicic, 2021).
Despite ongoing controversy about the clinical utility of abnormal epileptiform activity in the evaluation and management of complex neuropsychiatric disorders, we suggest that EEG biomarkers deserve further consideration within the broader precision medicine framework, and thus urge the field to reconsider existing practice guidelines that fail to recognize the relevance of EEG in psychiatric practice, particularly for those with neurodevelopmental disabilities. Future studies in ASD should incorporate biomarkers and demonstrate target engagement in pilot samples and subsequently develop these measures into larger clinical trials (Thom et al., 2025).
Footnotes
Disclosures
Neither Dr. M.Y. nor Dr. A.C.G. have no personal interests to disclose.
