ArticleBiomedicines2026
From Signal to Symptom: EEG Paroxysms and Background Slowing as Potential Biomarkers and Compensatory Failures in Treatment-Resistant Schizophrenia.
Article in Biomedicines, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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4 authors.
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Abstract
backgroundSchizophrenia is a heterogeneous disorder, and treatment-resistant schizophrenia (TRS) affects 20-30% of patients, yet objective biomarkers for its identification remain limited. Routine electroencephalography (EEG) offers a non-invasive window into cortical network dynamics, with previous studies reporting paroxysmal epileptiform activity and background slowing in a subset of patients. However, the biological significance of these findings-whether purely pathological or potentially compensatory-remains unclear. This study aimed to compare EEG abnormalities between TRS patients and those in clinical remission and to propose an integrative neurobiological interpretation.
methodsIn a cross-sectional design, 89 patients with schizophrenia (39 TRS, 50 in remission) underwent routine EEG recordings using the international 10-20 system. TRS was defined according to TRRIP consensus criteria, requiring <20% symptom reduction after adequate antipsychotic trials. EEG analysis focused on the prevalence of interictal epileptiform discharges (IEDs) and the severity of background slowing, assessed on a 4-point ordinal scale.
resultsIEDs were more than twice as prevalent in TRS patients compared to those in remission. Background slowing was significantly more severe in the TRS group, with the majority showing moderate-to-severe abnormalities versus predominantly normal-to-mild patterns in remission patients. Focal EEG abnormalities also followed this pattern. Multivariate analysis confirmed that both IEDs and background severity were independent predictors of TRS.
conclusionsEEG abnormalities, particularly IEDs and background slowing, are potential neurophysiological signatures associated with treatment resistance. We propose an integrative hypothesis suggesting that IEDs may originate as a failed compensatory mechanism-the brain's attempt to restore network homeostasis. In chronic TRS these discharges become maladaptive, contributing to excitotoxicity and network dysfunction. This framework opens avenues for EEG-based stratification and novel therapeutic strategies targeting cortical excitability.
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