An overview of Indian research in obsessive compulsive disorder

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31 An overview of Indian research in obsessive compulsive disorder Y. C. Janardhan Reddy, Naren P. Rao, Sumant Khanna ABSTRACT Obsessive-compulsive disorder (OCD) was considered a relatively rare disorder
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31 An overview of Indian research in obsessive compulsive disorder Y. C. Janardhan Reddy, Naren P. Rao, Sumant Khanna ABSTRACT Obsessive-compulsive disorder (OCD) was considered a relatively rare disorder until about two decades ago. Since then, considerable advance has been made in understanding the various aspects of OCD that include epidemiology, clinical features, comorbidity, biology and treatment. In the last one decade, there has also been interest in a group of related disorders called obsessive-compulsive spectrum disorders. There is substantial research from India on various aspects of OCD, particularly from the National Institute of Mental Health and Neurosciences (NIMHANS), Bangalore. We attempt to review all the relevant Indian data on OCD. Key words: OCD, Research, India ADULT OBSESSIVE-COMPULSIVE DISORDER Epidemiology There is only one epidemiological study from India.[1] The study found lifetime prevalence of 0.6%. This rate is considerably lower compared to the 2-3% rate reported in the European and North American studies.[2,3] However, similar low rate ranging from % was observed in a study from Taiwan.[4] It is not clear why lifetime prevalence rate of OCD is lower in some countries although the rates are not very low compared to the conservative estimate of 1% rate of OCD.[5] However, further research is needed into the epidemiological aspects of OCD in India since the data available is limited. Phenomenology of obsessive-compulsive disorder in adults Reddy et al.: OCD in India Phenomenology has been an important area of research in the field of OCD Jaisoorya et al. examined gender differences in OCD. [30] Males had an early onset of OCD, and had a higher prevalence of symmetry/religious obsessions, miscellaneous compulsions, and comorbid attention deficit hyperactivity was by Dutta Ray in 1964[6] followed by a series of articles by Akhtar et al. on phenomenology and socio-cultural determinants of symptoms in OCD,[7-9] Chakraborty and Banerji, in a study that compared 200 obsessionals with 200 controls reported a high rate of family history of obsessional illness (26%) and premorbid obsessional personality (26%).[10] Two other studies also reported high rates of obsessive personality.[11,12] Khanna et al. in an exploratory study examined whether a reactiveendogenous dichotomy exists.[13] Acute onset and fluctuating course was significantly commoner in the reactive subgroup. In an attempt to clarify the nosological status of OCD, Gojer et al. compared 53 cases of OCD with an equal number of subjects with depression and anxiety neurosis.[14] There were more similarities in the OCD and anxiety neurosis group than the depressive group. Khanna and Channabasavanna developed a classificatory system for obsessions and compulsions based on form and content.[15,16] Obsessions were categorized into six categories of form and twelve categories of content and compulsions in to four categories of form and eight categories of content. In the same sample of patients, phenomenology was analyzed using cluster analysis.[17] Four reliable clusters were derived using variables present in 10-90% of the subjects: Washing, checking, thoughts of past and embarrassing behavior. Depression occurred as a unique cluster. Subtypes of OCD were also examined in the same sample.[18] The study showed that washers and checkers are valid subtypes of OCD. In another study,[19] 222 consecutive subjects were evaluated using the Yale- Brown Obsessive-Compulsive Scale (Y-BOCS) symptom checklist[20] and the Scale for Assessment of Form and Content (SFC).[21] The data was subjected to factor analysis with varimax rotation. The main factors that emerged were washers, checkers, hoarding and two pure obsession factors. The obsession groups had a preponderance of sexual and religious themes. The findings are largely in concordance with those of studies from other parts of the world suggesting similarity across cultures.[22,23] The study, however, supports separating obsessions from compulsions because two pure obsession factors emerged, which is in keeping with the findings of the two previous studies.[24,25] Three recent studies of OCD in adults have also used the Y- BOCS to measure obsessive-compulsive symptoms.[19,26-28] The phenomenology of OCD in these studies is similar to that described in the western population.[29] There is paucity of data regarding the clinical correlates and treatment response of poor insight in OCD. A significant limitation of most of the studies is that they did not use validated measure of insight. Only one study[33] used the Brown Assessment of Beliefs Scale (BABS) developed specifically to assess insight.[38] In a recent Indian study, demographic and clinical correlates of poor insight OCD, and the association between response to specific serotonin reuptake inhibitors (SSRIs) and baseline insight was examined in a sample of 100 DSM-IV OCD subjects by using the BABS as a measure of insight.[27] The sample had 25 subjects with poor insight and the remaining 75 had good insight. Those with poor insight had earlier age-at-onset, more severe illness, higher comorbidity rate particularly major depression, over representation of miscellaneous obsessions and hoarding and poorer treatment response. The study suggests that OCD with poor insight could be a distinct subtype. That a significant proportion of OCD patients have poor insight has important treatment implications. Patients with poor insight could easily get misdiagnosed as psychotic and treated accordingly. The study suggests that drug treatment response is poor in those with poor insight. The finding is in sharp contrast to the findings of a previous study that reported that degree of insight at baseline did not predict response to sertraline. [33] It disorder (ADHD). Females had higher prevalence of cleaning compulsions and comorbid trichotillomania. Kamath et al. examined suicidal behavior in 100 consecutive DSM-IV OCD patients;[28] 59% had 'worst ever' (lifetime) suicidal ideation and 28% had current suicidal ideation. History of suicidal attempt was reported in 27% of the subjects. Major depression, unmarried status and hopelessness were the major risk factors for suicidal behavior. Gururaj et al. assessed the family burden, quality of life and disability in OCD patients and compared them with patients with schizophrenia of comparable severity.[31] Patients with schizophrenia had higher family burden but were comparable to OCD patients with respect to quality of life and disability. The study showed that OCD patients were associated with significant disability, poor quality of life and high family burden comparable to schizophrenia. Insight into obsessive-compulsive disorder Traditionally, OCD is described as a condition in which patients have good insight into their symptoms. The DSM- IV field trial demonstrated a broad range of insight with 30% having poor insight.[32] Subsequent studies have also reported poor insight in 15-36% of patients with OCD. [33-36] The DSM- IV has added a new OCD specifier: With poor insight which involves a lack of recognition that the symptoms are unreasonable or excessive.[37] In a chart review of comorbidity in 218 OCD subjects, 17% had major depression, 6% dysthymia, and 7% any anxiety disorder.[45] Comorbidity rates were low and there were not many differences between those with and is clinically pertinent to examine if poor insight patients do better with addition of neuroleptics. There is, however, no evidence as yet to suggest that those with poor insight respond better to augmentation with antipsychotics. On the other hand, a few studies have shown that insight improves after treatment with SSRIs.[35,36] Comorbidity Studies of comorbidity are varied and have examined a broad range of topics including spectrum disorders, comorbidity with schizophrenia and bipolar disorder and even prevalence of OCD in Parkinson's disease. Obsessive-compulsive (OC) spectrum disorders have over the past few years emerged as a unique and fascinating category of related conditions.[39] Jaisoorya et al. examined the prevalence of putative OC spectrum disorders in a large sample of OCD subjects (n 5 231) in comparison with relatives of neurologically ill patients (n 5 200).[26] Prevalence of tic disorders (39% vs. 12%), hypochondriasis (13% vs. 0), BDD (3% vs. 0) and trichotillomania (3% vs. 0) were significantly greater in OCD subjects compared to controls. However, the prevalence of sexual compulsions, pathological gambling, eating disorders, and depersonalization disorder was not greater in the OCD subjects compared to controls. The findings of this study suggest that tic disorders, hypochondriasis, BDD, and trichotillomania are perhaps part of the OC spectrum disorders. The evidence for exclusion of other disorders from the hypothesized OC spectrum is not conclusive because of the rarity of the occurrence of some of these disorders in the study sample. The findings are somewhat similar to those of a study that reported high rates of BDD, hypochondriasis and low rate of eating disorders and most impulse control disorders other than pathological skin picking.[40] Only one patient in the sample had an eating disorder. The finding is in sharp contrast to a previous study that reported high rates of eating disorders among OCD patients.[41] This divergence should be viewed in the light of the rare reporting of eating disorders in Asian countries[42,43] but could well be a correlate of cultural beliefs and attitudes that have been identified as significant contributing factors in the development of eating disorders.[43] Jaisoorya et al. examined the differences between tic related and non tic related OCD with respect to sociodemographics, symptom profile, and comorbidity.[44] Tic related OCD had an early age at onset, over representation of males, aggressive obsessions, cleaning compulsions and comorbid trichotillomania. Harbishettar et al.[51] systematically assessed OC symptoms and OCD in 69 Parkinson's disease patients and matched medically ill controls. There was no difference between the groups with respect to OC symptoms, OCD both clinical and subclinical and tics. Also, there was no relationship between severity of Parkinson's disease and OC symptoms. Authors speculated that different circuitry may be involved in the pathophysiology of OCD and Parkinson's disease although basal ganglia involvement may be common to both the disorders. without comorbidity except that female subjects were more likely to have depression. Kalra et al. compared OCD with and without comorbid Axis I disorders in a sample of 54 subjects and found that those with comorbidity had higher scores on depression and OCD severity scales.[46] The study findings were in tune with earlier literature from rest of the world. Gupta et al. examined level of comorbid depression in patients with OCD, psychotic depression and chronic medical illness.[47] All three groups had moderate to high levels of depression, with OCD group intermediary between psychotic depression and physical illness. However, the OCD group had more life events than depression or physical illness. Rajkumar et al.[48] studied the clinical profile of schizophrenic patients with and without comorbid OCD (50 in each group). Schizo-obsessive patients had higher rates of paranoid symptoms and first-rank symptoms of schizophrenia. They had lower anergia, higher depression scores, more comorbid personality disorders, and disability. Significant correlations were observed between OCD severity scores and schizophrenia symptom dimension scores. Authors concluded that schizo-obsessive schizophrenia may be a distinct subtype with unique clinical characteristics. A retrospective chart analysis of 15 cases OCD with psychosis found that obsessive doubts, washing and checking compulsions were the most common OC symptoms.[49] Twelve cases had a diagnosis of schizophrenia, while three had atypical psychosis. About half the patients had First Rank symptoms of schizophrenia. Nearly three-fourth of the sample showed significant improvement on treatment with a combination of antipsychotic and antiobsessional drugs. Zutshi et al.[50] examined differences between bipolar OCD and non-bipolar OCD. Bipolar OCD was associated with episodic course, a higher family loading for mood disorders, and higher rates of comorbid depression, social phobia and generalized anxiety disorder. In majority of the patients, OCD predated bipolar disorder and OCD worsened during depression and improved during mania. Authors concluded that OCD in those with bipolar disorder may be pathophysiologically related to bipolar disorder. A serotonergic hypothesis of OCD was suggested originally by the observed differential efficacy of SRIs in alleviating OCD symptoms.[55] Since then, numerous studies of peripheral receptor binding in the blood or concentrations of serotonin metabolites in cerebrospinal fluid have been performed but have yielded inconsistent results.[56] Pharmacological challenge studies provide another indirect approach. By administering serotonergic agents and measuring endocrine and behavioral responses, investigators have attempted to study the central serotonergic functioning in Course and outcome There is limited literature on the long-term course and outcome of OCD. In an year follow-up study of 75 subjects with OCD, Reddy et al.[52] reported a favorable outcome in majority of the subjects: 43% had no OCD, 33% had subclinical OCD and only 24% had clinical OCD. Median time to reach 'no OCD' and 'subclinical' status was 42 months and 84 months respectively. Interestingly, 37% were in true remission ('no OCD' and not on any treatment) for a median period of 132 months. Those who had 'mixed' OCD and Axis I comorbidity had poorer outcome. Age of onset and duration of illness had no effect on outcome. Optimistic outcome reported in this study is somewhat different from the findings of studies from other parts of the world which have reported lower rates of remission. Previous studies included samples that were severe and chronically ill with high rates of comorbidity. The subjects in the study by Reddy et al. were largely self-referred, moderately ill, and did not have history of treatment resistance. The findings of this study, therefore, could be generalized for patients routinely seen in the outpatient consultation at clinics and secondary-care hospitals in India. Math et al.[53] in another follow-up study explored if the long term outcome of 'predominantly obsessive' subjects differs from that of 'mixed' OCD. They studied the five to six-year course and outcome of 54 patients with 'predominantly obsessions' and 54 with 'mixed' subtype of OCD. The course of the illness was similar in both and a majority (72%) did not have clinical OCD at follow up. In another study, Shetti et al.[54] examined the differences between SSRI responders and non responders. They assessed 67 SRI responders and 55 non responders. Base line severity of illness, comorbid major depression, sexual obsessions, washing and miscellaneous compulsions, early age at onset, 'mixed' OCD and poor insight were associated with poor response to SRIs. NEUROBIOLOGY Neurotransmitters in obsessive-compulsive disorder In a study by Khanna et al. there was a blunted growth hormone, cortisol and ACTH response to clonidine in OCD. [64] On qualitative analysis three possible responses of growth hormone were obtained: Accentuation (.10 ng/ OCD. It is observed that OCD patients become significantly more anxious and dysphoric after administration of meta- chlorphenyl-piperazine (mcpp), a 5- HT receptor agonist.[55] In addition, obsessive-compulsive symptoms worsen. However, there appears to be blunted cortisol and prolactin response in response to mcpp. In an attempt to replicate these findings, mcpp was administered orally in a randomized double-blind design to 34 OCD patients who were either drug-naïve or drug-free for a minimum of four weeks.[57] The cortisol and prolactin responses were contrasted with those of 18 drug-free healthy subjects. The OCD patients showed significantly blunted cortisol and prolactin responses to mcpp challenge as compared to normal subjects. However, mcpp did not produce any significant exacerbation of obsessive-compulsive symptoms in the patients. These findings are suggestive of a serotonin (5- HT) receptor hyporesponsivity in the HPA axis. Even though previous studies indicate a hyperresponsivity of the 5- HT receptor system as shown by significant symptom worsening following serotonergic challenge,[58,59] the Indian study failed to replicate those results.[58] It was postulated that the 5-HT receptor hyporesponsivity in the HPA axis may be a biological trait marker of OCD, and may not be directly involved in the mediation of symptomatology of the disorder. It could also be inferred that the discrepancy among studies regarding the behavioural responses to mcpp challenge may in part be due to differences in the basic environmental conditions across various studies.[60] In a previous study by the same group, an endocrinological blunting in the absence of a behavioural increase in obsessive-compulsive symptoms was documented after oral administration of mcpp; however, when exposure was incorporated into the paradigm, with oral mcpp, exacerbation of obsessive-compulsive symptoms was noted.[61] A normal endocrinological response after treatment with clomipramine was also independently documented. [62] It is a matter of conjecture whether stimulation of noradrenergic system by the alpha2 adrenergic antagonistic action of mcpp, or behavioral exposure conditions during the challenge procedure are also partly responsible for the symptom exacerbation as noted in previous studies.[57] In summary, pharmacological challenge studies and other studies that have explored serotonergic hypothesis in OCD, have very limited evidence to support a primary serotonergic dysfunction in OCD.[63] However, a modulation of serotonergic system clearly plays a role in effective pharmacotherapy of at least a significant proportion of OCD patients. In a study of resting middle latency auditory and visual evoked potentials in 50 OCD subjects and 40 normal controls, there were no significant differences between the two groups for amplitude and latency or left-right ratios. [68] The study did not support any laterality deficit in OCD and was inconsistent with the hypothesis of left frontal lobe dysfunction in OCD.[69] A more prolonged post imperative negativity and a higher amplitude of the late component of the Contingent Negative Variation (CNV) has been repeatedly recorded.[66] OCD patients exhibited higher amplitude of the 'late' ml), normal (5-10 ng/ml) and attenuation (,10 ng/ml). Most patients with an accentuated response were patients with compulsions, pure obsessions were significantly more likely to have blunted responses. The study findings suggest noradrenergic dysfunction in OCD and also imply noradrenergic heterogeneity in the observation that pure obsessions tend to have a more down regulated noradrenergic system as compared to the compulsives. Based on their work, Khanna et al. concluded that serotonergic hypothesis may not explain all the abnormalities seen in OCD and that complex interactions between various neurotransmitters as well as the environmental conditions may be necessary to cause OCD.[57] Soft neurological signs Thirty-seven drug free non-depressed OCD subjects and 20 normal healthy volunteers were screened for SNS.[65] The OCD subjects had significantly more total SNS as compared to normals. These findings were most marked in the frontal lobe functions. There was a trend towards significance in temporal lobe functions, while other test findings were not impaired. If individual items were studied the problems were predominantly in complex motor tasks. There wa
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