Letters to Editor
The proposed mental health care bill in India is likely supersede the present legal provisions by decriminalizing suicide.[4] Previous literature suggests that decriminalization of suicide attempts may increase the absolute number of attempts,[5] but such an increase is less likely when coupled with intensive suicide prevention measures.[6] Further research on suicides in India is both desirable and necessary. In this regards, this pilot study furthers the evidence of stakeholder perspectives on legalities of suicide attempts, at the same time emphasizing the need for further comprehensive research. ACKNOWLEDGMENT
REFERENCES 1. 2. 3. 4. 5. 6.
National Crime Records Bureau, Ministry of Home Affairs. Accidental Deaths and Suicides in India, 2012; 2013. Available from: http://www.ncrb. nic.in/ADSI2010/ADSI2010‑full‑report.pdf. [Last cited on 2014 Apr 24]. Radhakrishnan R, Andrade C. Suicide: An Indian perspective. Indian J Psychiatry 2012;54:304‑19. Grover S, Sarkar S. Suicidal behaviour in adolescents: What can be done? Andhra Pradesh J Psychol Med 2013;14:13‑6. Bhaumik S. Mental health bill is set to decriminalise suicide in India. BMJ 2013;347:f5349. Latha KS, Geetha N. Criminalizing suicide attempts: Can it be a deterrent? Med Sci Law 2004;44:343‑7. Gunnell D, Fernando R, Hewagama M, Priyangika WD, Konradsen F, Eddleston M. The impact of pesticide regulations on suicide in Sri Lanka. Int J Epidemiol 2007;36:1235‑42.
The authors would like to thank the participants.
Access this article online Quick Response Code
Shivanand Kattimani, Siddharth Sarkar, Aniruddha Mukherjee, Kaliaperumal Mathan
Department of Psychiatry, Jawaharlal Institute of Postgraduate Medical Education and Research, Puducherry, India. E‑mail: [email protected]
Website: www.indianjpsychiatry.org
DOI: 10.4103/0019-5545.148543
Calloso‑frontal tuberculoma presenting with symptoms of psychosis and catatonia Sir,
A 26‑year‑old male presented with a history of incontinence, not responding to verbal commands and not communicating with family members and appearing perplexed for 2 days.
During last 4 months, he started acting slowly, lost interest in his daily activities, quit the job and reduced the communication with family members. Sleep and appetite were also decreased. 2 days before presenting to us, he became nonresponsive, incontinent and mute. On examination, he appeared apathetic, stuporous and mute. He kept his eyes mostly closed and when opened, a vacant stare was noticed. Motor examination gave findings of negativism and gagenhalten. He was not following verbal commands, but was able to locate deep painful stimuli. Further neurological or mental status examination was not possible. His vitals were stable. A diagnosis of catatonia was made and routine investigations including creatine phosphokinase (CPK) and computed tomography (CT)‑scan: Brain without contrast was ordered.
7 years ago, a gradual and progressive change in his behavior became conspicuous over 3–4 months. He preferred isolation, was nervous, restless and anorexic with poor self‑care. He was fearful and saw some white ghost‑like figures that nobody else could see. He started compulsive hand washing and was sad with weeping spells. He used to stand alone in the sunshine without changing his posture for hours. There was no reported history of substance abuse, seizures, neurological symptoms or head trauma in the past. He was diagnosed with schizophrenia and started on risperidone and trihexyphenidyl. He showed partial improvement and treatment was continued on and off till 1‑year back.
All investigations were within normal limits except the CT scan that showed mild hydrocephalus and hypodense areas in both frontal lobes (not shown here). Magnetic resonance imaging of brain with contrast enhancement was then done, which showed isodense to hypodense lesion arising from genu region of the corpus callosum and extending into the medial prefrontal cortex of both sides symmetrically with some perilesional edema [Figure 1]. He was immediately referred to the Neurosurgery Department for further management. Debulking of the tumor was done, and tuberculosis was found on histopathological examination. Antitubercular therapy was started.
Schizophrenia is diagnosed in most of the cases of catatonia despite the fact that nearly one third of cases with catatonia have an identifiable medical condition associated with it.[1] Here we present a case of young male with psychosis lasting 7 years who had tuberculoma in anterior callosal and frontal area and developed catatonia recently. To the best of our knowledge, this is the first case of anterior callosal tuberculoma with catatonia.
104
Indian Journal of Psychiatry 57(1), Jan-Mar 2015
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
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.
The proposed mental health care bill in India is likely supersede the present legal provisions by decriminalizing suicide.[4] Previous literature suggests that decriminalization of suicide attempts may increase the absolute number of attempts,[5] but such an increase is less likely when coupled with intensive suicide prevention measures.[6] Further research on suicides in India is both desirable and necessary. In this regards, this pilot study furthers the evidence of stakeholder perspectives on legalities of suicide attempts, at the same time emphasizing the need for further comprehensive research. ACKNOWLEDGMENT
REFERENCES 1. 2. 3. 4. 5. 6.
National Crime Records Bureau, Ministry of Home Affairs. Accidental Deaths and Suicides in India, 2012; 2013. Available from: http://www.ncrb. nic.in/ADSI2010/ADSI2010‑full‑report.pdf. [Last cited on 2014 Apr 24]. Radhakrishnan R, Andrade C. Suicide: An Indian perspective. Indian J Psychiatry 2012;54:304‑19. Grover S, Sarkar S. Suicidal behaviour in adolescents: What can be done? Andhra Pradesh J Psychol Med 2013;14:13‑6. Bhaumik S. Mental health bill is set to decriminalise suicide in India. BMJ 2013;347:f5349. Latha KS, Geetha N. Criminalizing suicide attempts: Can it be a deterrent? Med Sci Law 2004;44:343‑7. Gunnell D, Fernando R, Hewagama M, Priyangika WD, Konradsen F, Eddleston M. The impact of pesticide regulations on suicide in Sri Lanka. Int J Epidemiol 2007;36:1235‑42.
The authors would like to thank the participants.
Access this article online Quick Response Code
Shivanand Kattimani, Siddharth Sarkar, Aniruddha Mukherjee, Kaliaperumal Mathan
Department of Psychiatry, Jawaharlal Institute of Postgraduate Medical Education and Research, Puducherry, India. E‑mail: [email protected]
Website: www.indianjpsychiatry.org
DOI: 10.4103/0019-5545.148543
Calloso‑frontal tuberculoma presenting with symptoms of psychosis and catatonia Sir,
A 26‑year‑old male presented with a history of incontinence, not responding to verbal commands and not communicating with family members and appearing perplexed for 2 days.
During last 4 months, he started acting slowly, lost interest in his daily activities, quit the job and reduced the communication with family members. Sleep and appetite were also decreased. 2 days before presenting to us, he became nonresponsive, incontinent and mute. On examination, he appeared apathetic, stuporous and mute. He kept his eyes mostly closed and when opened, a vacant stare was noticed. Motor examination gave findings of negativism and gagenhalten. He was not following verbal commands, but was able to locate deep painful stimuli. Further neurological or mental status examination was not possible. His vitals were stable. A diagnosis of catatonia was made and routine investigations including creatine phosphokinase (CPK) and computed tomography (CT)‑scan: Brain without contrast was ordered.
7 years ago, a gradual and progressive change in his behavior became conspicuous over 3–4 months. He preferred isolation, was nervous, restless and anorexic with poor self‑care. He was fearful and saw some white ghost‑like figures that nobody else could see. He started compulsive hand washing and was sad with weeping spells. He used to stand alone in the sunshine without changing his posture for hours. There was no reported history of substance abuse, seizures, neurological symptoms or head trauma in the past. He was diagnosed with schizophrenia and started on risperidone and trihexyphenidyl. He showed partial improvement and treatment was continued on and off till 1‑year back.
All investigations were within normal limits except the CT scan that showed mild hydrocephalus and hypodense areas in both frontal lobes (not shown here). Magnetic resonance imaging of brain with contrast enhancement was then done, which showed isodense to hypodense lesion arising from genu region of the corpus callosum and extending into the medial prefrontal cortex of both sides symmetrically with some perilesional edema [Figure 1]. He was immediately referred to the Neurosurgery Department for further management. Debulking of the tumor was done, and tuberculosis was found on histopathological examination. Antitubercular therapy was started.
Schizophrenia is diagnosed in most of the cases of catatonia despite the fact that nearly one third of cases with catatonia have an identifiable medical condition associated with it.[1] Here we present a case of young male with psychosis lasting 7 years who had tuberculoma in anterior callosal and frontal area and developed catatonia recently. To the best of our knowledge, this is the first case of anterior callosal tuberculoma with catatonia.
104
Indian Journal of Psychiatry 57(1), Jan-Mar 2015
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
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.
