# Heterogeneous Changes in Mismatch Negativity Peak Latency Following Electroconvulsive Therapy: A Case Series of Three Cases

## TL;DR

This study shows how ECT affects brain responses in different psychiatric patients, with mismatch negativity (MMN) changes not always matching cognitive decline.

## Contribution

The study reveals heterogeneous MMN responses to ECT across different psychiatric conditions and treatment stages.

## Key findings

- MMN latency in atypical psychosis patients prolonged after ECT and returned to baseline with transient cognitive decline.
- Schizophrenia patients showed no MMN latency changes, suggesting reduced cortical reactivity.
- MDD patients had prolonged MMN latency with preserved cognition, indicating possible cumulative neural effects.

## Abstract

Mismatch negativity (MMN), a pre-attentive auditory event-related potential, is a sensitive neurophysiological marker of cortical dysfunction. Electroconvulsive therapy (ECT), which is effective for various psychiatric disorders, may transiently affect cognitive and neurophysiological processes.This case series examined MMN peak latency and cognitive outcomes following ECT in three patients with distinct psychiatric diagnoses: atypical psychosis, treatment-resistant schizophrenia, and major depressive disorder (MDD). In patients with atypical psychosis, MMN peak latency was markedly prolonged immediately after two ECT sessions and returned to baseline by 40 days, in parallel with transient cognitive decline and mild delirium. Conversely, the patient with schizophrenia demonstrated no MMN latency changes and stable cognitive scores, suggesting diminished cortical reactivity, possibly due to chronic illness or medication effects. The patient with MDD, assessed after the final two sessions of a 10-session course, exhibited sustained MMN latency prolongation with preserved cognitive function, indicating potential cumulative subclinical neural effects. These findings highlight the diagnostic and temporal heterogeneity of MMN responses to ECT, with MMN alterations not always correlating with cognitive decline. MMN may serve as a sensitive but nonspecific biomarker of neural instability during ECT, offering clinical value for the early detection of cortical vulnerability. Our results suggest that MMN monitoring, especially when interpreted alongside the diagnosis and treatment stages, may complement standard cognitive assessments and inform individualized ECT management.