To the Editor: Catatonia is a psychomotor syndrome in which motor, behavioral, and emotional changes may occur due to various causes.¹ Affective psychoses and schizophrenia happen to be common causes of catatonia. In most cases, catatonia is treated either with benzodiazepines or electroconvulsive therapy (ECT).²

A PubMed search supplemented with manual search revealed only five case reports^3,4 in which catatonia appeared after ECT administration. We report a case in which catatonia emerged after ECT and improved transiently as ECT was continued, but worsened thereafter.

“Mr. A,” a 31-year-old single man diagnosed with paranoid schizophrenia, presented with 8 years of continuous illness characterized by reduced social interaction, irritability, suspiciousness, and unprovoked outbursts of anger. He was admitted to Central Institute of Psychiatry, a tertiary psychiatric referral center at Ranchi, India, for further evaluation and management. He had made a suicide attempt of high lethality 4 years earlier. He had received treatment with typical antipsychotics previously without much benefit. His grandfather had bipolar affective disorder. He had schizoid traits premorbidly, characterized by preference for solitary activities, had few friends, and low emotional reactivity, which were apparent during adolescence. There were no features suggestive of autistic spectrum disorder. Mental status revealed psychomotor retardation, persecutory delusion, and prominent auditory hallucination with commanding and derogatory voices, depressed affect, and death wishes. Detailed physical and neurological examination did not reveal any abnormality. Baseline investigations were normal. After giving written informed consent, he was put on direct ECT 3 times weekly for suicidal ideas associated with command hallucinations. Also, he received injection haloperidol 10 mg bid and injection promethazine 50 mg bid intramuscularly to control agitation. ECT was administered using a brief pulse device with bitemporal electrode placement. Dosing was calculated empirically. After 3 days, regular injectables were stopped, and he was put on oral olanzapine 15 mg daily along with ECT. After the fourth ECT treatment, catatonic signs appeared in the form of posturing and mutism. There were no features suggestive of drug-induced parkinsonism. After the sixth ECT treatment, mutism improved, although posturing persisted. As ECT was continued, catatonia worsened further as the patient developed automatic obedience and staring in addition to mutism and posturing. The Bush-Francis catatonia rating scale⁵ score was 8, which remained constant until the 13th ECT session. Finally, ECT was discontinued, and, in view of the minimal clinical improvement, olanzapine was cross-tapered with clozapine. Within 2 weeks of ECT discontinuation, the catatonic symptoms resolved gradually. On 300 mg per day of clozapine, there was improvement in psychopathology without recurrence of catatonic signs.

ECT has been recognized as one of the most effective and time-tested modalities of therapy in catatonia. The response to ECT in catatonia approaches 80%.⁶ ECT improves catatonia refractory or only partially responsive to lorazepam^7–9 and nonresponsive to other benzodiazepines^8,10 Furthermore, ECT is often effective in emergency treatment of lethal catatonia¹¹ and neuroleptic malignant syndrome,¹² both of which are potentially life-threatening. Our patient, who did not have previous history of catatonia, showed emergence of catatonic signs during ECT treatment in a case of paranoid schizophrenia. This appears antithetical in light of the current evidence, which overwhelmingly favors the use ECT in catatonia. Previous cases reporting emergence of catatonia during ECT^3,4 were also associated with concomitant benzodiazepine withdrawal, which is known to precipitate catatonia.^13–15 Such an underlying mechanism of catatonia is discounted in our case, as there was no exposure to benzodiazepines.

Various medications, such as disulfiram, corticosteroids, and antipsychotics have been reported to cause catatonia.⁶ Such drug-induced cases present as retarded catatonia, with mutism, staring, posturing, and withdrawal being the most common manifestations. Our case, as well as previously reported cases of catatonia emerging during ECT, also presented with retarded catatonia with similar symptoms, which suggests that ECT-induced catatonia can be regarded as a variant of drug-induced catatonia.

ECT in catatonia causes changes in perfusion in several areas of brain, which differs according to causes of catatonia. For example, Escobar et al.¹⁶ reported an improvement in brain perfusion using single photon-emission computed tomography (SPECT) imaging in those treated with ECT for catatonia in the parietal, temporal, and occipital areas in patients with mood disorder, whereas no change was seen in those with schizophrenia. On the contrary, Galynker et al.¹⁷ reported increased perfusion during SPECT imaging in the left parietal and motor cortices in a patient with schizoaffective disorder and catatonia after ECT treatment. Such variations in brain perfusion can cause unpredictable changes, leading to emergence of catatonic symptoms during ECT. Also, pre-medications such as atropine could contribute to the emergence of catatonic features associated with ECT.¹⁸ Future studies using functional neuroimaging techniques will shed further light on this uncommon phenomenon.