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| CASE REPORT |
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| Year : 2019 | Volume
: 6
| Issue : 2 | Page : 101-103 |
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An interesting presentation of psychotic catatonia in an elderly patient with alcohol dependence
Migita Michael Dcruz, Jayant Mahadevan, Prabhat Kumar Chand, Pratima Murthy
Department of Psychiatry, National Institute of Mental Health and Neurosciences, Bengaluru, Karnataka, India, Indiaa
| Date of Submission | 10-Sep-2019 |
| Date of Decision | 14-Sep-2019 |
| Date of Acceptance | 18-Oct-2019 |
| Date of Web Publication | 20-Feb-2020 |
Correspondence Address:
Dr. Jayant Mahadevan
Department of Psychiatry, National Institute of Mental Health and Neurosciences, Bengaluru - 560 029, Karnataka
Indiaa
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/jgmh.jgmh_33_19
Catatonia is a neuropsychiatric syndrome with multifactorial etiopathogenesis. It can be seen in patients with alcohol dependence in the context of withdrawal in the presence of comorbid psychiatric disorders (substance induced or independent) or as a consequence of medications used to treat dependence. This is a case of an elderly patient with alcohol dependence, and a prior episode of psychosis, who developed acute psychosis with catatonia following the concurrent use of disulfiram and baclofen.
Keywords: Baclofen, catatonia, disulfiram, psychosis
How to cite this article:
Dcruz MM, Mahadevan J, Chand PK, Murthy P. An interesting presentation of psychotic catatonia in an elderly patient with alcohol dependence. J Geriatr Ment Health 2019;6:101-3 |
How to cite this URL:
Dcruz MM, Mahadevan J, Chand PK, Murthy P. An interesting presentation of psychotic catatonia in an elderly patient with alcohol dependence. J Geriatr Ment Health [serial online] 2019 [cited 2023 Jun 7];6:101-3. Available from: https://www.jgmh.org/text.asp?2019/6/2/101/278744 |
| Introduction | |  |
Catatonia is a neuropsychiatric syndrome with both functional and organic causes, including general medical conditions.[1] Dysregulation of dopaminergic, gamma-aminobutyric acid (GABA)-ergic, and N-methyl-D-aspartate glutamatergic neurotransmission has been implicated in the pathophysiology of catatonia.[2] Catatonia in patients with alcohol dependence has been described in the context of withdrawal, in the presence of comorbid psychiatric disorders or as a consequence of medication used to treat dependence.[3]
We present a case of alcohol dependence syndrome with a history of psychosis, who presented with acute and transient psychotic disorder with catatonia, when on a combination of baclofen and disulfiram.
| Case Report | | |
A 63-year-old male presented with a history of alcohol use from the age of 22 years, which by the age of 30 years fulfilled DSM 5 criteria for dependence, with an average use of 18–24 units of spirits per day.
He sought treatment for the first time at the age of 45 years on developing two episodes of generalized tonic–clonic seizures followed by delirium after abrupt cessation of alcohol. He underwent detoxification with diazepam and was later started on disulfiram 250 mg. He remained abstinent from alcohol on disulfiram for the next 10 years, without any adverse events, and functioned well.
At the age of 55 years, he stopped disulfiram, as he felt he no longer required it and soon relapsed, due to craving and removal of the deterrent. He then consumed 24 units/day until the age of 63 years, at his current presentation.
The patient also had nicotine dependence, smoking 10–15 cigarettes per day from 22 years of age. He was on treatment for diabetes mellitus and dyslipidemia, detected at 48 years of age, with oral hypoglycemics and hypolipidemics, which were well controlled.
He had a prior episode of psychosis with catatonic symptoms subsequent to an interpersonal stressor at 36 years of age, which lasted for a week and resolved spontaneously. During this episode, the patient reported he was abstinent from alcohol due to catatonia. He had not had catatonia in the context of withdrawal or when on medication in the past.
The patient presented currently with features of uncomplicated withdrawal, was detoxified with diazepam, and later prescribed 60 mg baclofen as an anticraving agent. Disulfiram 250 mg was added at the family's request, after consent from the patient, due to a history of good response (in terms of alcohol abstinence). His investigative workup including biochemistry and hemogram was normal.
Following discharge, the patient remained abstinent from alcohol. Three weeks after discharge, when on medication, he developed 2 days of aphonia which resolved spontaneously. There were no other associated symptoms or signs. He was evaluated for a cerebrovascular event, and computed tomography brain was found to be normal. One week later, following an interpersonal stressor, the patient had abrupt onset of catatonic symptoms and signs including mutism, rigidity, posturing, staring, and waxy flexibility.
At the time of presentation, his Bush–Francis Catatonia Rating Scale score was 21. A detailed workup including 3-day repeat serum ammonia and serum lactate, serum calcium, serum magnesium, autoantibody panel, paraneoplastic panel, autoimmune encephalitis panel, antinuclear antibody, antineutrophil cytoplasmic antibody, rheumatoid arthritis, and C-reactive protein was done. All of the above were nonreactive or within normal limits. In addition, lumbar puncture with cerebrospinal fluid biochemistry; cytology; and staining and culture for bacteria, acid-fast bacilli, and fungus were also nonreactive. Magnetic resonance imaging brain showed diffuse age disproportionate cerebral and cerebellar atrophy. There were no infarcts or hemorrhages visualized.
He received 2 mg lorazepam following which catatonic symptoms resolved completely. Disulfiram was stopped as it was considered the most proximal agent, while baclofen was continued. Lorazepam was tapered and stopped, while the patient continued to receive baclofen. However, catatonia recurred the day after lorazepam was stopped. Hence, lorazepam was reintroduced, and baclofen was stopped. Lorazepam was then tapered and stopped over the next week in the absence of any anticraving or deterrent medication. A provisional diagnosis of catatonia secondary to medications was made, with a differential of recurrent acute psychoses. He was started on acamprosate 1332 mg as an anticraving agent. On the application of Naranjo's algorithm to our case report, we obtained a total score of 6, which indicates the reaction is considered probable.
Around 1 week later, the patient presented with delusions of persecution, reference, and a suicidal attempt. The diagnosis was revised to recurrent acute psychoses, and the patient was initiated on risperidone 3 mg, while acamprosate was continued. The patient remained abstinent from alcohol and free of psychotic symptoms for 1 year following which risperidone had been stopped without reemergence of psychotic symptoms.
| Discussion | | |
Acute and transient psychotic disorders are well known to present with symptoms of catatonia.[4] Catatonia continues to be reported in up to 9%–17% of patients hospitalized with acute psychiatric illnesses across the world.[5]
Literature on drug-induced catatonia is limited to case reports and systematic reviews, with no published data available on the prevalence of drug-induced catatonia.
Neuroleptics, dopaminergic agents, mood stabilizers, antiepileptics, acetyl cholinesterase inhibitors, cannabinoids, amphetamines, opioids, phenyl alkyl amines, antibiotics, antivirals, antiemetics, and steroids have variously been associated with reports of substance-induced psychosis.[6]
Neuroleptics, dopaminergic agents, alcohol, and benzodiazepines have been associated with reports of substance withdrawal psychosis.[6]
Alcohol and benzodiazepines act as positive allosteric modulators of the GABA-A receptor and regulate motor activity through top-down regulation of the cortico-striato-thalamo-cortical circuit. Withdrawal from alcohol has been associated with reports of catatonia.[3],[7] Similarly, withdrawal from benzodiazepines has also been associated with reports of catatonia.[8],[9],[10] Elderly patients have been reported to be at higher risk of such withdrawal-associated catatonia.[9],[10]
Disulfiram is an inhibitor of the aldehyde dehydrogenase and dopamine beta-hydroxylase and is a deterrent agent in the treatment of alcohol dependence.[11] It inhibits the metabolism of dopamine and elevates the level of dopamine in the prefrontal cortex, causing bottom-up modulation of motor activity through the nigrostriatal pathway. It has been known to precipitate psychosis in susceptible patients for whom it is considered a relative contraindication. It has also been associated with reports of catatonia in overdose and rarely at therapeutic doses as well.[12],[13],[14] Baclofen is a GABA-B agonist which is used in the long-term management of alcohol dependence.[11] It has been associated with psychosis in therapeutic doses and may contribute to catatonic presentations.[15],[16] It has been known to induce catatonia in animal models, through selective increase of potassium conductance, and reciprocal modulation of serotonergic neurotransmission.[17] The combination of agents for the treatment of alcohol dependence is a fairly common practice.[18]
Our patient seems to have had a preexisting vulnerability, as evident from his history of psychosis. However, he had tolerated withdrawal from both alcohol and benzodiazepines in the past without developing catatonia. Similarly, he had tolerated disulfiram for 10 years without developing psychosis or catatonia. It is possible that the combination of disulfiram and baclofen in this person may have unmasked a vulnerability to develop acute psychosis and catatonia. The aphonia preceding catatonia may have been a transient ischemic attack, though the absence of focal neurological signs and unremarkable neuroimaging do not support this speculation.
| Conclusion | | |
This case highlights the role of multiple interacting factors in the precipitation of acute psychosis and catatonia. It informs us on the caution we must exercise in the use of medications such as baclofen and disulfiram in conjunction, particularly in patients with preexisting risk factors or vulnerability for psychosis.
Declaration of patient consent
The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.
Acknowledgment
We would like to acknowledge our patients.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
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