Disulfiram-Induced Catatonia Following a Disulfiram–Alcohol Reaction: A Case Report

INTRODUCTION

Catatonia is a neuropsychiatric syndrome characterized by abnormalities in motor behavior, speech, and responsiveness, including mutism, posturing, negativism, and reduced interaction with the environment. Although historically associated with schizophrenia, it is now recognized across a broad spectrum of psychiatric, medical, and substance-induced conditions.^[1] Early identification is important, as catatonia is often reversible with appropriate treatment.

The pathophysiology of catatonia is thought to involve dysregulation of neurotransmitter systems, particularly gamma-aminobutyric acid (GABA), dopamine, and glutamate pathways.^[1,2] The effectiveness of benzodiazepines in treating catatonia supports the role of impaired inhibitory neurotransmission.

Disulfiram is an aversive agent used in alcohol dependence that inhibits aldehyde dehydrogenase, leading to the accumulation of acetaldehyde when alcohol is consumed, producing unpleasant effects known as the disulfiram–alcohol reaction.^[3] In addition to this action, disulfiram interferes with dopamine metabolism by inhibiting dopamine β-hydroxylase, leading to increased dopamine levels, which may contribute to neuropsychiatric adverse effects.^[2,4]

Although uncommon, catatonia has been reported following disulfiram use, particularly in the context of a disulfiram– alcohol reaction.^[2-5] We report a similar case highlighting this association. Such cases, though previously reported, remain infrequently encountered in routine clinical practice, particularly in settings like Chhattisgarh where unsupervised disulfiram use and limited awareness regarding strict alcohol abstinence are not uncommon.

CASE REPORT

A 32-year-old male, educated up to class 10th, belonging to a low socioeconomic status, with no prior history of any medical or psychiatric illness, including psychotic illness or prior psychotic episodes, presented with a history of alcohol dependence since 6 years, characterized by craving, tolerance, impaired control over use, and withdrawal symptoms. His alcohol use had led to significant impairment in the social domain, including strained family relationships, reduced participation in social activities, and a decline in occupational functioning.

In view of ongoing alcohol use and associated difficulties, his wife, out of desperation, initiated disulfiram 500 mg daily without any medical consultation. Following this, the patient initially abstained from alcohol; however, he was not adequately informed about the strict need for complete avoidance of alcohol while on disulfiram.

While continuing disulfiram therapy, the patient consumed approximately 30 ml of alcohol on 19 March 2026, following which he developed fever and 1–2 episodes of vomiting suggestive of a disulfiram–alcohol reaction, which subsided spontaneously. Within a few hours, family members noticed behavioral changes in the patient.

Following this, the patient developed reduced speech progressing to mutism, decreased responsiveness, and prolonged staring. He also exhibited posturing and negativism, with resistance to examination and reduced interaction with others. There was a marked reduction in spontaneous activity, and he refused food and fluids, consistent with a catatonic syndrome. Due to worsening symptoms, he was admitted to the hospital on the morning of 20 March 2026.

On mental status examination, the patient was poorly interactive, with mutism, decreased psychomotor activity, and minimal response to external stimuli. Affect could not be adequately assessed. Thought content and perceptual abnormalities could not be elicited due to reduced verbal output. Insight and judgment were impaired.

On neurological examination, there were no focal neurological deficits and no signs of meningeal irritation, with the absence of neck rigidity, negative Kernig’s sign, and negative Brudzinski’s sign. The patient was afebrile. Routine blood investigations, liver function tests, serum electrolytes, and other metabolic parameters were within normal limits, and a non-contrast computed tomography (NCCT) of the head was normal. Differential diagnoses considered included hepatic encephalopathy, encephalitis, metabolic abnormalities, and primary psychotic disorder with catatonia. These were ruled out based on clinical examination, absence of delirium or autonomic instability, normal investigations, normal NCCT findings, and absence of meningeal signs. The patient also did not exhibit altered sensorium, flapping tremors, or other features suggestive of hepatic encephalopathy.

On admission, the Bush–Francis Catatonia Rating Scale (BFCRS) score was 15, indicating significant catatonia.^[6] The temporal association between disulfiram–alcohol exposure and onset of symptoms suggested a drug-induced etiology.

After around 5–6 days, the catatonic symptoms resolved; however, the patient subsequently developed auditory hallucinations, complaining of hearing voices of multiple males, while his orientation remained intact.

Disulfiram was discontinued. The patient was treated with intravenous lorazepam and intravenous fluids. In view of the emergence of psychotic symptoms, olanzapine was started, following which the patient showed further improvement.

DISCUSSION

Catatonia is a syndrome with diverse etiologies, including psychiatric disorders, medical conditions, and drug-induced states.^[1] Disulfiram-induced catatonia is rare but has been documented in the literature.^[3,7,8]

One of the proposed mechanisms involves inhibition of dopamine β-hydroxylase by disulfiram, leading to increased dopamine levels and disruption of neurotransmitter balance, which may contribute to catatonic symptoms.^[2,4]

An important observation in reported cases is that catatonia may occur following a disulfiram–alcohol reaction, suggesting a possible triggering role.^[2] A similar temporal sequence was observed in the present case.

Certain risk factors have been described, including higher doses of disulfiram, underlying psychiatric illness, and organic brain pathology. However, such factors may not always be present.^[2]

In this case, contributing factors included:

• Unsupervised use of disulfiram

• Lack of patient education

Management involves discontinuation of the offending agent and symptomatic treatment. Benzodiazepines are considered first-line therapy and are often associated with rapid improvement.^[2,3] The favourable response observed in this case is consistent with previous reports. ^[7,8]

CONCLUSION

Disulfiram-induced catatonia following a disulfiram–alcohol reaction is a rare but clinically important adverse effect. Awareness of this association is essential for early recognition and management. Proper supervision and patient education during disulfiram therapy can help prevent such complications.