Dopamine Supersensitivity Psychosis Resolved With Electroconvulsive Therapy (ECT) in a Patient With Treatment-Resistant Schizophrenia: A Case Report

TL;DR

A patient with treatment-resistant schizophrenia and dopamine supersensitivity psychosis showed significant improvement after electroconvulsive therapy, reducing her antipsychotic medication needs.

Contribution

This case report suggests electroconvulsive therapy may reverse dopamine supersensitivity in schizophrenia, restoring antipsychotic effectiveness.

Findings

The patient achieved over 2 years of remission with a 35% reduction in antipsychotic dose after ECT.

ECT may lead to dopamine D2 receptor downregulation, resolving dopamine supersensitivity psychosis.

The case demonstrates ECT's potential to restore antipsychotic responsiveness in treatment-resistant schizophrenia.

Abstract

In individuals with schizophrenia, high-dose antipsychotic medication can induce an upregulation of the brain's dopamine D2 receptors (D2Rs), leading to dopamine supersensitivity (DS) or dopamine supersensitivity psychosis (DSP). For patients with established DSP, a reduction in the increased D2R density is sought, which in theory will restore the patients' therapeutic responsiveness to antipsychotics. We describe the case of a 50-year-old Japanese woman with schizophrenia who fulfilled the criteria for DSP and recovered from DSP after undergoing electroconvulsive therapy (ECT). Before the ECT, she had exhibited serious psychotic symptoms requiring admission and was treated with the chlorpromazine (CPZ) equivalent dose of 1,250 mg. After the ECT, she achieved a >2-year period of remission with a 35% reduction in the dose of the antipsychotic. Considering that ECT leads to D2R downregulation, the reduction in this patient's maintained antipsychotic dose may reflect the normalization of increased D2R density, resulting in the resolution of the DS state by ECT. This patient's case indicates that for individuals with schizophrenia and DPS, the application of ECT may effectively restore the therapeutic response to antipsychotics.

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