Letters to Editor
to psychotropics should not be a ground to rule out neurological pathology as earlier reports suggest that psychotic symptoms and catatonia with identifiable medical or neurological illness also respond to psychotropics.[5] To conclude, medial prefrontal tuberculoma can present with symptoms of psychosis and catatonia. It is advisable that neuro‑radiological investigations should be considered even in long‑standing psychiatric illnesses where the symptoms are mixed or atypical or if there is a sudden change in a clinical picture. Figure 1: Tuberculoma extending into the medial prefrontal lobes bilaterally (magnetic resonance imaging)
This patient presented with stupor, mutism and negativism thus, the diagnosis of catatonia was made.[2] Akinetic mutism, locked in syndrome and apallic state were ruled out due to lack of visual scanning and/or attempt to communicate visually. Acute onset of the stupor and mutism ruled out stiff person syndrome and akinetic parkinsonism. Absence of fever, autonomic fluctuations, and a normal serum CPK ruled out neuroleptic malignant syndrome and serotonin syndrome.
Sourav Das, Ravi Gupta, Mohan Dhyani
Department of Psychiatry and Sleep Clinic, Himalayan Institute of Medical Sciences, Doiwala, Dehradun, Uttarakhand, India. E‑mail: [email protected] REFERENCES 1. 2. 3.
A variety of symptoms including anxiety symptoms, obsessions, compulsions, apathy, negative symptoms and catatonia have been associated with neuronal loss or damage in the medial frontal cortex.[3,4] This explains the mixed clinical picture in this case. Although the anxiety disorders and obsessive‑compulsive disorder can co‑occur with schizophrenia, still, co‑occurrence of symptoms of more than one diagnostic category must alert the clinician to screen for a general medical disorder. The patient developed catatonic symptoms late in the course of illness. A slow growing tumor appears to be a likely explanation of the current case. Tuberculoma also grows slowly, and this could be one reason for late development of catatonia in this case. The response
4.
5.
Clark T, Rickards H. Catatonia 1: History and clinical features. Hosp Med 1999;60:740‑2. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Health Disorders: DSM‑5. 5th ed. Washington, DC: American Psychiatric Publishing; 2013. John G, Eapen V, Shaw GK. Frontal glioma presenting as anxiety and obsessions: A case report. Acta Neurol Scand 1997;96:194‑5. Delamillieure P, Fernandez J, Constans JM, Brazo P, Benali K, Abadie P, et al. Proton magnetic resonance spectroscopy of the medial prefrontal cortex in patients with deficit schizophrenia: Preliminary report. Am J Psychiatry 2000;157:641‑3. Spiegel DR, Klaiber N. A case of catatonia status‑post left middle cerebral artery cerebrovascular accident, treated successfully with olanzapine. Clin Neuropharmacol 2013;36:135‑7. Access this article online Quick Response Code
Website: www.indianjpsychiatry.org
DOI: 10.4103/0019-5545.148544
Catatonic depression precipitated by amiodarone prescribed for atrial fibrillation Sir, I am writing to report what appears to be the first recorded case of catatonic depression induced by amiodarone. Amiodarone is an antiarrhythmic that is the drug of choice for life‑threatening ventricular arrhythmias; it is a second‑line treatment for atrial fibrillation. Mrs. V was a 71‑year‑old housewife, who lived with her Indian Journal of Psychiatry 57(1), Jan-Mar 2015
husband. I saw her for the first time at her home, as an emergency, at the family’s request. According to them, she had been her usual self until about 4 weeks previously. She had then started to complain of reduced appetite, nausea, tiredness, decreased interest or enjoyment in life, lack of motivation, reduced sleep, etc. She was no longer able to do her routine housework as before. She stopped going out of her home, an activity she did almost daily previously. She had a brief admission for 105
Letters to Editor
2 days to a local private hospital where she underwent a range of investigations including blood tests (slightly raised thyroid stimulating hormone [TSH], but normal T3, T4). She was discharged from hospital without any psychiatric assessment with the family being reassured by the physician that, as there was no major physical illness, she would soon start improving. A day after discharge, her mental state deteriorated precipitously. Apart from a few sips of water, she refused to take anything orally. Her speech was restricted to occasional words. She remained in her bed the whole day. When I saw her at home in the evening, she was sitting on the bed, a posture she had maintained for most of the day. There was obvious psychomotor retardation. She spoke only a few words during the whole assessment. Most of the time, she was staring into space. On physical examination, there was no fever or obvious rigidity. Further examination, to try to elicit specific catatonic signs, was not possible, as the patient was not cooperative. Mrs. V had no past personal or family history of mental illness. She had suffered a myocardial infarction about 15 years previously, which was treated conservatively. Since then, she had periodic cardiology reviews. She was on metoprolol, losartan, hydrochlorothiazide, aspirin, atorvastatin and amiodarone. While she had been taking all the first 5 drugs for at least a few years, amiodarone had been started only about 5 weeks previously. At that time, an electrocardiogram (ECG) during a routine cardiology review had shown atrial fibrillation. The family confirmed that deterioration in her mental state started about a week after commencing amiodarone. Her history and presentation were consistent with a diagnosis of a depressive episode (F32 in the International Classification of Diseases‑10 classification).[1] Although she was not in full‑blown stupor, she was clearly exhibiting some catatonic signs (same sitting posture, almost mute, staring, etc.), which had persisted for almost a day. Hence, her presentation could be classified as a severe depressive episode (with catatonic features). Considering the temporal relationship between starting amiodarone and emergence of depressive symptoms, I felt that this was an amiodarone‑induced depressive episode, and it was stopped. The main differential diagnosis was a functional, late‑onset, first depressive episode. I prescribed oral zolpidem 5 mg at night and oral clonazepam 0.25 mg 3 times daily. With a lot of encouragement from the family, the patient took both zolpidem and clonazepam. This was followed by a remarkable improvement – she slept well, made her own coffee in the morning, had breakfast, etc. Over the next few days, there was continuing improvement in her mental state. Both clonazepam and zolpidem were 106
discontinued after a week. She was back to her normal self within the next 3 weeks. I requested a repeat ECG which showed persisting atrial fibrillation. A cardiology review was arranged, and she was commenced on digoxin. Although depression and other psychiatric problems are mentioned as possible side‑effects of amiodarone, their exact incidence is not known. A search of the medical literature identified only a few case reports, all of them in those aged 65 or over.[2‑5] The exact mechanism by which amiodarone causes psychiatric side‑effects is unclear. Amiodarone‑induced hypothyroidism and amiodarone‑induced thyrotoxicosis may play a role in depression and delirium respectively. However, in the patient presented here, the TSH was only marginally elevated and is unlikely to satisfactorily explain the severe depressive symptoms seen. Taking a full history, including medical history, helped in identifying the underlying cause. Benzodiazepines have previously also been shown to result in rapid and complete remission of catatonia, particularly in mood disorders.[6] By delaying antidepressant prescription, it was established that full improvement from depression occurred just by withdrawing amiodarone, thus avoiding unnecessary maintenance antidepressant treatment.
Sundararajan Rajagopal
Consultant Psychiatrist, Psychiatry Outpatients Clinic, Girishwari Hospital, Chennai, Tamil Nadu, India. E‑mail: [email protected] REFERENCES 1. 2. 3. 4. 5. 6.
World Health Organization. The ICD‑10 Classification of Mental and Behavioural Disorders: Clinical Descriptions and Diagnostic Guidelines. Geneva: WHO; 1992. Trohman RG, Castellanos D, Castellanos A, Kessler KM. Amiodarone‑induced delirium. Ann Intern Med 1988;108:68‑9. Ambrose A, Salib E. Amiodarone‑induced depression. Br J Psychiatry 1999;174:366‑7. Cheesman N, Taylor D. Psychosis and depression associated with alteration to amiodarone therapy. J Psychopharmacol 2010;24:131‑3. Foley KT, Bugg KS. Separate episodes of delirium associated with levetiracetam and amiodarone treatment in an elderly woman. Am J Geriatr Pharmacother 2010;8:170‑4. Huang YC, Lin CC, Hung YY, Huang TL. Rapid relief of catatonia in mood disorder by lorazepam and diazepam. Biomed J 2013;36:35‑9.
Access this article online Quick Response Code Website: www.indianjpsychiatry.org
DOI: 10.4103/0019-5545.148545
Indian Journal of Psychiatry 57(1), Jan-Mar 2015
Copyright of Indian Journal of Psychiatry is the property of Medknow Publications & Media Pvt. Ltd. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use.
to psychotropics should not be a ground to rule out neurological pathology as earlier reports suggest that psychotic symptoms and catatonia with identifiable medical or neurological illness also respond to psychotropics.[5] To conclude, medial prefrontal tuberculoma can present with symptoms of psychosis and catatonia. It is advisable that neuro‑radiological investigations should be considered even in long‑standing psychiatric illnesses where the symptoms are mixed or atypical or if there is a sudden change in a clinical picture. Figure 1: Tuberculoma extending into the medial prefrontal lobes bilaterally (magnetic resonance imaging)
This patient presented with stupor, mutism and negativism thus, the diagnosis of catatonia was made.[2] Akinetic mutism, locked in syndrome and apallic state were ruled out due to lack of visual scanning and/or attempt to communicate visually. Acute onset of the stupor and mutism ruled out stiff person syndrome and akinetic parkinsonism. Absence of fever, autonomic fluctuations, and a normal serum CPK ruled out neuroleptic malignant syndrome and serotonin syndrome.
Sourav Das, Ravi Gupta, Mohan Dhyani
Department of Psychiatry and Sleep Clinic, Himalayan Institute of Medical Sciences, Doiwala, Dehradun, Uttarakhand, India. E‑mail: [email protected] REFERENCES 1. 2. 3.
A variety of symptoms including anxiety symptoms, obsessions, compulsions, apathy, negative symptoms and catatonia have been associated with neuronal loss or damage in the medial frontal cortex.[3,4] This explains the mixed clinical picture in this case. Although the anxiety disorders and obsessive‑compulsive disorder can co‑occur with schizophrenia, still, co‑occurrence of symptoms of more than one diagnostic category must alert the clinician to screen for a general medical disorder. The patient developed catatonic symptoms late in the course of illness. A slow growing tumor appears to be a likely explanation of the current case. Tuberculoma also grows slowly, and this could be one reason for late development of catatonia in this case. The response
4.
5.
Clark T, Rickards H. Catatonia 1: History and clinical features. Hosp Med 1999;60:740‑2. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Health Disorders: DSM‑5. 5th ed. Washington, DC: American Psychiatric Publishing; 2013. John G, Eapen V, Shaw GK. Frontal glioma presenting as anxiety and obsessions: A case report. Acta Neurol Scand 1997;96:194‑5. Delamillieure P, Fernandez J, Constans JM, Brazo P, Benali K, Abadie P, et al. Proton magnetic resonance spectroscopy of the medial prefrontal cortex in patients with deficit schizophrenia: Preliminary report. Am J Psychiatry 2000;157:641‑3. Spiegel DR, Klaiber N. A case of catatonia status‑post left middle cerebral artery cerebrovascular accident, treated successfully with olanzapine. Clin Neuropharmacol 2013;36:135‑7. Access this article online Quick Response Code
Website: www.indianjpsychiatry.org
DOI: 10.4103/0019-5545.148544
Catatonic depression precipitated by amiodarone prescribed for atrial fibrillation Sir, I am writing to report what appears to be the first recorded case of catatonic depression induced by amiodarone. Amiodarone is an antiarrhythmic that is the drug of choice for life‑threatening ventricular arrhythmias; it is a second‑line treatment for atrial fibrillation. Mrs. V was a 71‑year‑old housewife, who lived with her Indian Journal of Psychiatry 57(1), Jan-Mar 2015
husband. I saw her for the first time at her home, as an emergency, at the family’s request. According to them, she had been her usual self until about 4 weeks previously. She had then started to complain of reduced appetite, nausea, tiredness, decreased interest or enjoyment in life, lack of motivation, reduced sleep, etc. She was no longer able to do her routine housework as before. She stopped going out of her home, an activity she did almost daily previously. She had a brief admission for 105
Letters to Editor
2 days to a local private hospital where she underwent a range of investigations including blood tests (slightly raised thyroid stimulating hormone [TSH], but normal T3, T4). She was discharged from hospital without any psychiatric assessment with the family being reassured by the physician that, as there was no major physical illness, she would soon start improving. A day after discharge, her mental state deteriorated precipitously. Apart from a few sips of water, she refused to take anything orally. Her speech was restricted to occasional words. She remained in her bed the whole day. When I saw her at home in the evening, she was sitting on the bed, a posture she had maintained for most of the day. There was obvious psychomotor retardation. She spoke only a few words during the whole assessment. Most of the time, she was staring into space. On physical examination, there was no fever or obvious rigidity. Further examination, to try to elicit specific catatonic signs, was not possible, as the patient was not cooperative. Mrs. V had no past personal or family history of mental illness. She had suffered a myocardial infarction about 15 years previously, which was treated conservatively. Since then, she had periodic cardiology reviews. She was on metoprolol, losartan, hydrochlorothiazide, aspirin, atorvastatin and amiodarone. While she had been taking all the first 5 drugs for at least a few years, amiodarone had been started only about 5 weeks previously. At that time, an electrocardiogram (ECG) during a routine cardiology review had shown atrial fibrillation. The family confirmed that deterioration in her mental state started about a week after commencing amiodarone. Her history and presentation were consistent with a diagnosis of a depressive episode (F32 in the International Classification of Diseases‑10 classification).[1] Although she was not in full‑blown stupor, she was clearly exhibiting some catatonic signs (same sitting posture, almost mute, staring, etc.), which had persisted for almost a day. Hence, her presentation could be classified as a severe depressive episode (with catatonic features). Considering the temporal relationship between starting amiodarone and emergence of depressive symptoms, I felt that this was an amiodarone‑induced depressive episode, and it was stopped. The main differential diagnosis was a functional, late‑onset, first depressive episode. I prescribed oral zolpidem 5 mg at night and oral clonazepam 0.25 mg 3 times daily. With a lot of encouragement from the family, the patient took both zolpidem and clonazepam. This was followed by a remarkable improvement – she slept well, made her own coffee in the morning, had breakfast, etc. Over the next few days, there was continuing improvement in her mental state. Both clonazepam and zolpidem were 106
discontinued after a week. She was back to her normal self within the next 3 weeks. I requested a repeat ECG which showed persisting atrial fibrillation. A cardiology review was arranged, and she was commenced on digoxin. Although depression and other psychiatric problems are mentioned as possible side‑effects of amiodarone, their exact incidence is not known. A search of the medical literature identified only a few case reports, all of them in those aged 65 or over.[2‑5] The exact mechanism by which amiodarone causes psychiatric side‑effects is unclear. Amiodarone‑induced hypothyroidism and amiodarone‑induced thyrotoxicosis may play a role in depression and delirium respectively. However, in the patient presented here, the TSH was only marginally elevated and is unlikely to satisfactorily explain the severe depressive symptoms seen. Taking a full history, including medical history, helped in identifying the underlying cause. Benzodiazepines have previously also been shown to result in rapid and complete remission of catatonia, particularly in mood disorders.[6] By delaying antidepressant prescription, it was established that full improvement from depression occurred just by withdrawing amiodarone, thus avoiding unnecessary maintenance antidepressant treatment.
Sundararajan Rajagopal
Consultant Psychiatrist, Psychiatry Outpatients Clinic, Girishwari Hospital, Chennai, Tamil Nadu, India. E‑mail: [email protected] REFERENCES 1. 2. 3. 4. 5. 6.
World Health Organization. The ICD‑10 Classification of Mental and Behavioural Disorders: Clinical Descriptions and Diagnostic Guidelines. Geneva: WHO; 1992. Trohman RG, Castellanos D, Castellanos A, Kessler KM. Amiodarone‑induced delirium. Ann Intern Med 1988;108:68‑9. Ambrose A, Salib E. Amiodarone‑induced depression. Br J Psychiatry 1999;174:366‑7. Cheesman N, Taylor D. Psychosis and depression associated with alteration to amiodarone therapy. J Psychopharmacol 2010;24:131‑3. Foley KT, Bugg KS. Separate episodes of delirium associated with levetiracetam and amiodarone treatment in an elderly woman. Am J Geriatr Pharmacother 2010;8:170‑4. Huang YC, Lin CC, Hung YY, Huang TL. Rapid relief of catatonia in mood disorder by lorazepam and diazepam. Biomed J 2013;36:35‑9.
Access this article online Quick Response Code Website: www.indianjpsychiatry.org
DOI: 10.4103/0019-5545.148545
Indian Journal of Psychiatry 57(1), Jan-Mar 2015
Copyright of Indian Journal of Psychiatry is the property of Medknow Publications & Media Pvt. Ltd. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use.
