A Case of Schizophrenia with Diagnostic Challenges Between Non-convulsive Status Epilepticus and Malignant Catatonia: Therapeutic Implications based on the GABA-A Dysfunction Hypothesis.

Abstract

Catatonia is a psychomotor syndrome that occurs in various psychiatric, neurological, and medical conditions. Differentiating malignant catatonia from neuroleptic malignant syndrome (NMS) and non-convulsive status epilepticus (NCSE) is particularly challenging in complex cases involving multiple contributing factors. Both catatonia and NCSE have been associated with dysfunction of the gamma-aminobutyric acid (GABA)-A receptor system, which may underlie overlapping clinical features. We report the case of a 43-year-old man with a long-standing history of schizophrenia who developed malignant catatonia following a suicide attempt that resulted in multiple traumatic injuries. Postoperatively, he exhibited autonomic instability, decreased consciousness, muscle rigidity, and catatonic signs. An electroencephalogram revealed generalized spike-and-wave activity consistent with NCSE, and levetiracetam was initiated. Despite the resolution of the epileptiform discharges, the catatonic symptoms persisted. A transient positive response to lorazepam supported the diagnosis of malignant catatonia. Modified electroconvulsive therapy (m-ECT) was introduced on day 40 of hospitalization. After four sessions, the patient showed marked improvement in both motor and autonomic symptoms. Thirteen sessions were completed, and the patient was discharged on day 81. He remained relapse-free for over five years. This case highlights the importance of considering malignant catatonia in patients with schizophrenia who present with persistent catatonic symptoms despite adequate treatment of NCSE. Although antiepileptic therapy suppressed epileptiform activity, resolution of catatonia required m-ECT, suggesting that seizure control alone may be insufficient. Clinicians should recognize that catatonia and NCSE may coexist and overlap in GABA-A-related pathophysiology, and that early GABA-A-targeted interventions, including m-ECT, may be critical for recovery.