Sir: Catatonia is a clinical syndrome characterized by alterations in motor behavior and changes in thought, mood, and vigilance1 and occurs in a variety of medical and neuropsychiatric conditions.2 Catatonia has been documented as occurring in alcohol withdrawal in rodents,3 but not in humans. We report the case of a patient in whom alcohol withdrawal presented as catatonia.
Case report
Mr. A, aged 35 years, presented in January 2006 with a history of alcohol use over the last 10 years. He fulfilled the DSM-IV criteria for alcohol dependence for the last 5 years.
He presented with tremors, irritability, anorexia, and insomnia within 24 hours of abrupt cessation of alcohol intake. Seventy-two hours after cessation of alcohol intake, he developed signs of negativism, mutism, and psychomotor agitation lasting 2 days, followed by psychomotor retardation, stereotypies, and stupor over the next 2 days, fulfilling DSM-IV criteria for catatonia. There were no psychotic or mood symptoms, clouding of consciousness, disorientation, or any general medical condition that could explain these symptoms.
He had experienced a similar episode 2 years previous, following 3 days of abstinence from alcohol, that remitted upon treatment with lorazepam. Family history was positive for alcohol dependence in first- and second-degree relatives but was negative for psychotic or mood disorders. The findings of laboratory investigations were within normal limits.
As the patient's condition could not be described adequately by DSM-IV criteria for alcohol withdrawal or catatonia, the diagnosis of alcohol-induced psychotic disorder was made, with onset during alcohol withdrawal and presenting with catatonia. Mr. A was treated with loraze-pam 16 mg per day and with vitamin supplements. His symptoms remitted completely within 72 hours.
Catatonia has been documented in alcohol dependence in relation to drug interactions involving disulfiram4 and in delirium.1 The temporal correlation between alcohol abstinence and the appearance of catatonia in the absence of these other causes suggests that the catatonia in this case was due to alcohol withdrawal. Perturbations in γ-aminobutyric acid (GABA)-ergic and glutamatergic transmission have been implicated in the pathophysiology of both catatonia2 and alcohol withdrawal.5,6 Furthermore, the GABAA modulator lorazepam is effective in both conditions.1,7 To our knowledge, this case is the first such case reported in the literature.
Acknowledgments
The authors report no financial or other affiliations that can be considered a conflict of interest relevant to the subject of this letter.
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