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Cobalamin deficiency presenting as obsessive compulsive disorder: case report
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General Hospital Psychiatry 34 (2012) 578.e7 – 578.e8
Case Report
Cobalamin deficiency presenting as obsessive compulsive disorder: case report☆ Vivek Sharma, M.D. a,⁎, Devdutta Biswas, M.D. b a
Department of Psychiatry, Kailash Hospital, Greater Noida, Uttar Pradesh, India b Department of Psychiatry, Hindurao Hospital, New Delhi, India Received 28 August 2011; accepted 15 November 2011
Abstract Cobalamin deficiency commonly presents with a wide range of neuropsychiatric manifestations ranging from myelopathy, neuropathy, optic neuritis and dementia to mood disorders, chronic fatigue and psychosis even without classical hematological abnormalities like anemia and macrocytosis. However, obsessive compulsive disorder (OCD) in relation to vitamin B12 deficiency has not been described so far. We report a case of middle-aged man presenting with OCD, low serum cobalamin and a positive family history of vitamin B12 deficiency who responded well to methylcobalamin replacement. © 2012 Elsevier Inc. All rights reserved. Keywords: Cobalamin deficiency; Vitamin B12; Obsessive–compulsive disorder; Subacute combined degeneration
1. Introduction
2. Case
Research has consistently shown that cobalamin deficiency may present with neuropsychiatric syndromes in absence of anemia or macrocytosis in blood, which, if they occur, appear late in the course [1,2]. Whereas subacute combined degeneration (SACD) of the spinal cord is the classical neurological sequela of cobalamin deficiency, peripheral neuropathy, optic neuritis, organic brain syndromes, dementia and seizures have also been described [3,4]. Among the psychiatric presentations mood disorders (both depression and mania), chronic fatigue syndrome and psychosis are notable [5,6]. The pathogenesis in all these conditions has directly implicated low levels of cobalamin and is potentially reversible with timely intervention of vitamin B12 supplementation. We present a case of an adult male with obsessive compulsive disorder (OCD) and positive family history of cobalamin deficiency who responded favorably to methylcobalamin replacement.
Mr. R., a 39-year-old married accountant, presented to us with a 2-year history of recurrent embarrassing thoughts of touching females inappropriately. He tried to control them by keeping himself occupied in work and avoiding female company, nevertheless his occupational and family life was adversely affected. Detailed assessment further revealed excessive need to arrange things in symmetrical fashion and recurrent doubts of having made serious mistakes in work with checking compulsions. This was his first psychiatric consultation. In the last 5 years he had received numerous orthopedic and neurological consultations for recurrent shooting pains in his calves and painful paraesthesia in his feet, but extensive investigations failed to reveal any abnormality and no lasting benefit was observed with gabapentin (600 mg/d) and pregabalin (150 mg/d) in combination with various analgesics. He was nondiabetic, nonhypertensive and a teetotaler. Family history revealed SACD of spinal cord in Mr. R.'s father, diagnosed at the age of 65 years, which lasted nearly 6 months and remitted completely with methylcobalamin replacement. Mr. R.'s physical examination was normal except for impaired vibration and joint position sense in the lower limbs. Investigations including magnetic resonance imaging of brain and spinal cord, electrocardiogram, doppler study of
☆
Conflict of interest: none. ⁎ Corresponding author. C-26, Manas Apartments, Mayur Vihar Phase-1 Extn, New Delhi-110091. Tel.: +91 9873011498. E-mail address: [email protected] (V. Sharma). 0163-8343/$ – see front matter © 2012 Elsevier Inc. All rights reserved. doi:10.1016/j.genhosppsych.2011.11.006
578.e8
V. Sharma, D. Biswas / General Hospital Psychiatry 34 (2012) 578.e7–578.e8
lower limb vasculature, serum electrolytes, blood glucose, renal and liver functions, thyroid profile, serum folate and hematological parameters were in normal range, while serum B12 was low at 177 pg/ml (normal range: 200–900 pg/ml). He scored 24 on the Yale Brown Obsessive Compulsive Severity Scale (Y-BOCS), corresponding to severe impairment [7]. His illness was diagnosed as OCD-mixed obsessions and compulsions (International Classification of Diseases, 10th Revision) based on his psychiatric evaluation with cobalamin deficiency, as evidenced by his low B12 levels. Discussions regarding treatment options revealed his reluctance to take psychotropic medications, however, he consented to be placed on cognitive behavior therapy wait-list and receive vitamin B12 replacement in the meantime; vitamin B12 replacement was considered in view of his low serum cobalamin levels, history of SACD in his father and favorable response of the latter to cobalamin replacement. He was started on intramuscular methylcobalamin 1000 µg thrice weekly for 2 weeks followed by weekly administration, as per recommendations [8]. Within 2 weeks Mr. R. reported significant improvement in his well-being and requested continuation of methylcobalamin monotherapy. By the fourth week, he reported a significant reduction in obsessions, associated compulsions and distress while his painful paresthesia subsided completely. His Y-BOCS score came down to 13. At 10 weeks his Y-BOCS score was 5 while his psychiatric and neurological examinations were both unremarkable. At the time of writing this report, he has remained well for 7 months on vitamin B12 alone. There is emerging consensus in recent literature that cobalamin deficiency should be suspected in persons presenting with unexplained neuropsychiatric symptoms especially when there is family history of cobalamin deficiency states [5]. This view is supported by a significant body of research which ascribes a variety of psychiatric illnesses to cobalamin deficiency ranging from mild depression to paranoid psychosis and dementia [5]; however, OCD has not been described so far. Although, Hermesh et al. did report a significantly higher prevalence of low serum cobalamin levels in OCD patients (20%) compared to healthy and schizophrenic controls (4%) [9], they did not imply any etiological relationship between the two. To our
knowledge, this is the first clear-cut case of cobalamin deficiency presenting as OCD. Recent research has shown that vitamin B12 along with folate influences the rate of serotonin synthesis [6], a key neurotransmitter in the etiopathogenesis of OCD. The fact that Mr. R. responded dramatically and completely to methylcobalamin replacement alone suggests a possible etiological role of vitamin B12 in his psychiatric illness. Though one might argue that the observed clinical benefit with B12 replacement was in fact a placebo response or due to spontaneous resolution, it is noteworthy that OCD consistently demonstrates very low placebo response rates and lesser propensity for spontaneous remission compared to other anxiety disorders [10]. Spontaneous remission is all the more unlikely in the present case as Mr. R. was suffering from unabated illness for the last 2 years. References [1] Lindenbaum J, Healton EB, Savage DG, et al. Neuropsychiatric disorders caused by cobalamin deficiency in the absence of anemia or macrocytosis. N Engl J Med 1988;318:1720–8. [2] Carmel R. Pernicious anemia. The expected findings of very low serum cobalamin levels, anemia and macrocytosis are often lacking. Arch Intern Med 1988;148:1712–4. [3] Healton EB, Savage DG, Brust JC, Garrett TJ, Lindenbaum J. Neurologic aspects of cobalamin deficiency. Medicine (Baltimore) 1991;70:229–45. [4] Aaron S, Kumar S, Vijayan J, et al. Clinical and laboratory features and response to treatment in patients presenting with vitamin B12 deficiency-related neurological symptoms. Neurol India 2005;53: 55–9. [5] Dommisse J. Subtle vitamin B12 deficiency and psychiatry: a largely unnoticed but devastating relationship? Med Hypotheses 1991;34:131–40. [6] Hutto BR. Folate and cobalamin in psychiatric illness. Compr Psychiatry 1997;38:305–14. [7] Goodman WK, Price LH, Rasmussen SA. The Yale–Brown Obsessive Compulsive Scale: part I. development, use, and reliability. Arch Gen Psychiatry 1989;46:1006–11. [8] Oh RC, Brown DL. Vitamin B12 Deficiency. Am Fam Physician 2003;67:979–86. [9] Hermesh H, Weizman A, Shahar A, Munitz H. Vitamin B12 and folic acid serum levels in obsessive compulsive disorder. Acta Psychiatr Scand 1988;78:8–10. [10] Huppert JD, Shultz LT, Foa EB, et al. Differential response to placebo among patients with panic disorder, social phobia, and obsessive compulsive disorder. Am J Psychiatry 2004;161:1485–7.
General Hospital Psychiatry 34 (2012) 578.e7 – 578.e8
Case Report
Cobalamin deficiency presenting as obsessive compulsive disorder: case report☆ Vivek Sharma, M.D. a,⁎, Devdutta Biswas, M.D. b a
Department of Psychiatry, Kailash Hospital, Greater Noida, Uttar Pradesh, India b Department of Psychiatry, Hindurao Hospital, New Delhi, India Received 28 August 2011; accepted 15 November 2011
Abstract Cobalamin deficiency commonly presents with a wide range of neuropsychiatric manifestations ranging from myelopathy, neuropathy, optic neuritis and dementia to mood disorders, chronic fatigue and psychosis even without classical hematological abnormalities like anemia and macrocytosis. However, obsessive compulsive disorder (OCD) in relation to vitamin B12 deficiency has not been described so far. We report a case of middle-aged man presenting with OCD, low serum cobalamin and a positive family history of vitamin B12 deficiency who responded well to methylcobalamin replacement. © 2012 Elsevier Inc. All rights reserved. Keywords: Cobalamin deficiency; Vitamin B12; Obsessive–compulsive disorder; Subacute combined degeneration
1. Introduction
2. Case
Research has consistently shown that cobalamin deficiency may present with neuropsychiatric syndromes in absence of anemia or macrocytosis in blood, which, if they occur, appear late in the course [1,2]. Whereas subacute combined degeneration (SACD) of the spinal cord is the classical neurological sequela of cobalamin deficiency, peripheral neuropathy, optic neuritis, organic brain syndromes, dementia and seizures have also been described [3,4]. Among the psychiatric presentations mood disorders (both depression and mania), chronic fatigue syndrome and psychosis are notable [5,6]. The pathogenesis in all these conditions has directly implicated low levels of cobalamin and is potentially reversible with timely intervention of vitamin B12 supplementation. We present a case of an adult male with obsessive compulsive disorder (OCD) and positive family history of cobalamin deficiency who responded favorably to methylcobalamin replacement.
Mr. R., a 39-year-old married accountant, presented to us with a 2-year history of recurrent embarrassing thoughts of touching females inappropriately. He tried to control them by keeping himself occupied in work and avoiding female company, nevertheless his occupational and family life was adversely affected. Detailed assessment further revealed excessive need to arrange things in symmetrical fashion and recurrent doubts of having made serious mistakes in work with checking compulsions. This was his first psychiatric consultation. In the last 5 years he had received numerous orthopedic and neurological consultations for recurrent shooting pains in his calves and painful paraesthesia in his feet, but extensive investigations failed to reveal any abnormality and no lasting benefit was observed with gabapentin (600 mg/d) and pregabalin (150 mg/d) in combination with various analgesics. He was nondiabetic, nonhypertensive and a teetotaler. Family history revealed SACD of spinal cord in Mr. R.'s father, diagnosed at the age of 65 years, which lasted nearly 6 months and remitted completely with methylcobalamin replacement. Mr. R.'s physical examination was normal except for impaired vibration and joint position sense in the lower limbs. Investigations including magnetic resonance imaging of brain and spinal cord, electrocardiogram, doppler study of
☆
Conflict of interest: none. ⁎ Corresponding author. C-26, Manas Apartments, Mayur Vihar Phase-1 Extn, New Delhi-110091. Tel.: +91 9873011498. E-mail address: [email protected] (V. Sharma). 0163-8343/$ – see front matter © 2012 Elsevier Inc. All rights reserved. doi:10.1016/j.genhosppsych.2011.11.006
578.e8
V. Sharma, D. Biswas / General Hospital Psychiatry 34 (2012) 578.e7–578.e8
lower limb vasculature, serum electrolytes, blood glucose, renal and liver functions, thyroid profile, serum folate and hematological parameters were in normal range, while serum B12 was low at 177 pg/ml (normal range: 200–900 pg/ml). He scored 24 on the Yale Brown Obsessive Compulsive Severity Scale (Y-BOCS), corresponding to severe impairment [7]. His illness was diagnosed as OCD-mixed obsessions and compulsions (International Classification of Diseases, 10th Revision) based on his psychiatric evaluation with cobalamin deficiency, as evidenced by his low B12 levels. Discussions regarding treatment options revealed his reluctance to take psychotropic medications, however, he consented to be placed on cognitive behavior therapy wait-list and receive vitamin B12 replacement in the meantime; vitamin B12 replacement was considered in view of his low serum cobalamin levels, history of SACD in his father and favorable response of the latter to cobalamin replacement. He was started on intramuscular methylcobalamin 1000 µg thrice weekly for 2 weeks followed by weekly administration, as per recommendations [8]. Within 2 weeks Mr. R. reported significant improvement in his well-being and requested continuation of methylcobalamin monotherapy. By the fourth week, he reported a significant reduction in obsessions, associated compulsions and distress while his painful paresthesia subsided completely. His Y-BOCS score came down to 13. At 10 weeks his Y-BOCS score was 5 while his psychiatric and neurological examinations were both unremarkable. At the time of writing this report, he has remained well for 7 months on vitamin B12 alone. There is emerging consensus in recent literature that cobalamin deficiency should be suspected in persons presenting with unexplained neuropsychiatric symptoms especially when there is family history of cobalamin deficiency states [5]. This view is supported by a significant body of research which ascribes a variety of psychiatric illnesses to cobalamin deficiency ranging from mild depression to paranoid psychosis and dementia [5]; however, OCD has not been described so far. Although, Hermesh et al. did report a significantly higher prevalence of low serum cobalamin levels in OCD patients (20%) compared to healthy and schizophrenic controls (4%) [9], they did not imply any etiological relationship between the two. To our
knowledge, this is the first clear-cut case of cobalamin deficiency presenting as OCD. Recent research has shown that vitamin B12 along with folate influences the rate of serotonin synthesis [6], a key neurotransmitter in the etiopathogenesis of OCD. The fact that Mr. R. responded dramatically and completely to methylcobalamin replacement alone suggests a possible etiological role of vitamin B12 in his psychiatric illness. Though one might argue that the observed clinical benefit with B12 replacement was in fact a placebo response or due to spontaneous resolution, it is noteworthy that OCD consistently demonstrates very low placebo response rates and lesser propensity for spontaneous remission compared to other anxiety disorders [10]. Spontaneous remission is all the more unlikely in the present case as Mr. R. was suffering from unabated illness for the last 2 years. References [1] Lindenbaum J, Healton EB, Savage DG, et al. Neuropsychiatric disorders caused by cobalamin deficiency in the absence of anemia or macrocytosis. N Engl J Med 1988;318:1720–8. [2] Carmel R. Pernicious anemia. The expected findings of very low serum cobalamin levels, anemia and macrocytosis are often lacking. Arch Intern Med 1988;148:1712–4. [3] Healton EB, Savage DG, Brust JC, Garrett TJ, Lindenbaum J. Neurologic aspects of cobalamin deficiency. Medicine (Baltimore) 1991;70:229–45. [4] Aaron S, Kumar S, Vijayan J, et al. Clinical and laboratory features and response to treatment in patients presenting with vitamin B12 deficiency-related neurological symptoms. Neurol India 2005;53: 55–9. [5] Dommisse J. Subtle vitamin B12 deficiency and psychiatry: a largely unnoticed but devastating relationship? Med Hypotheses 1991;34:131–40. [6] Hutto BR. Folate and cobalamin in psychiatric illness. Compr Psychiatry 1997;38:305–14. [7] Goodman WK, Price LH, Rasmussen SA. The Yale–Brown Obsessive Compulsive Scale: part I. development, use, and reliability. Arch Gen Psychiatry 1989;46:1006–11. [8] Oh RC, Brown DL. Vitamin B12 Deficiency. Am Fam Physician 2003;67:979–86. [9] Hermesh H, Weizman A, Shahar A, Munitz H. Vitamin B12 and folic acid serum levels in obsessive compulsive disorder. Acta Psychiatr Scand 1988;78:8–10. [10] Huppert JD, Shultz LT, Foa EB, et al. Differential response to placebo among patients with panic disorder, social phobia, and obsessive compulsive disorder. Am J Psychiatry 2004;161:1485–7.