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| GUEST EDITORIAL |
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| Year : 2008 | Volume
: 54
| Issue : 2 | Page : 81-82 |
Neurobiological underpinnings of obsessive compulsive disorder and schizophrenia: Explanations for disability and severity
J Sareen
Psychiatry and Community Health Sciences, University of Manitoba, Canada
Correspondence Address:
J Sareen
Psychiatry and Community Health Sciences, University of Manitoba
Canada
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/0022-3859.40768
How to cite this article:
Sareen J. Neurobiological underpinnings of obsessive compulsive disorder and schizophrenia: Explanations for disability and severity. J Postgrad Med 2008;54:81-2 |
How to cite this URL:
Sareen J. Neurobiological underpinnings of obsessive compulsive disorder and schizophrenia: Explanations for disability and severity. J Postgrad Med [serial online] 2008 [cited 2023 Mar 30];54:81-2. Available from: https://www.jpgmonline.com/text.asp?2008/54/2/81/40768 |
In the present issue of this journal a paper examines the family burden, quality of life and disability in obsessive compulsive disorder (OCD). [1] Gururaj et al., demonstrate in a study of inpatients with OCD similar rates of disability and family burden in comparison to those with schizophrenia. The authors are commended for detailed examination of the impact of OCD on the family that has not been done extensively in the past.
Although the study is limited by the fact that the sample includes only inpatients, [1] this paper is still important because it shows that in severe cases of OCD, the level of dysfunction is significant. Previous work by Kessler et al. , [2] has shown that in the US general population OCD has a high level of impairment and this seems to be higher than other anxiety disorders. Further study of the impact of OCD on family burden and disability is required utilizing random samples to reduce the selection bias of treatment-seeking samples.
One possible explanation for these findings might involve looking at the neurobiological correlates of OCD and schizophrenia. Although there has been a significant interest in the amygdala and the prefrontal cortex in the anxiety disorders, [3] there is substantial evidence of dysfunction in the cortical striatal-thalamic network among patients with OCD [4] and schizophrenia. [5] This dysfunctional network overlap may account for some of the obsessions, for example that in severe form be associated with lack of insight. At times, the obsessive thoughts are so strong that they are at a delusional level of severity. Even in the DSM criteria there is a subtype of OCD called "OCD with poor insight" and this severe form of OCD is often associated with significant and severe dysfunction.
Neuroimaging studies in OCD have shown that response to pharmacotherapy and behavior therapy involves changes in blood flow to orbital frontal cortex and striatal structures. [4] While neuroimaging studies in other anxiety disorders, specifically social phobia, have shown that response to treatment is associated with reduction in blood flow to the amygdala. [3] A large body of literature suggests that blockade dopamine in striatal structures is important in the treatment of schizophrenia. [5] The neuroimaging literature is limited by sample sizes and lack of direct comparison between different anxiety disorders.
From a treatment perspective, there has been a significant amount of literature that has shown the utility of adjunct antipsychotics in treating OCD. [6] We believe that this may also be related to the fact that OCD shares a lot of the underpinnings with schizophrenia. Future studies are required to directly compare patients with schizophrenia and obsessive compulsive disorder using neuroimaging and biological studies.
| :: References | |  |
| 1. | Gururaj GP, Bada Math S, Reddy JY, Chandrashekar CR. Family burden, quality of life and disability in obsessive compulsive disorder: An Indian perspective. J Postgrad Med 2008;54: 91-7.  |
| 2. | Kessler RC, Chiu WT, Demler O, Merikangas KR, Walters EE. Prevalence, severity and comorbidity of 12-month DSM-IV disorders in the National Comorbidity Survey Replication. Arch Gen Psychiatry 2005;62:617-27. [PUBMED] [FULLTEXT] |
| 3. | Furmark T, Tillfors M, Garpenstrand H, Marteinstdottir I, Langstrom B, Oreland L, et al. Common changes in cerebral blood flow in patients with social phobia treated with citalopram or cognitive-behavioral therapy. Arch Gen Psychiatry 2002;59:425-33. |
| 4. | Saxena S. Neuroimaging and frontal-subcortical circuitry in obsessive-compulsive disorder. Br J Psychiatry Suppl 1998;35:26-37. |
| 5. | Toda M, Abi-Dargham. Dopamine hypothesis of schizophrenia: Making sense of it all. Curr Psychiatry Rep 2007;9:329-36. |
| 6. | Sareen J, Kirshner A, Lander M, Kjernisted KD, Eleff MK, ReissJP. Do atypical antipsychotics ameliorate or exacerbate obsessive compulsive disorder symptoms: A systematic review. J Affect Disord 2004;82:167-74. |
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