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Joshua Perez Professor Green Biology 1900 4 November 2013 Obsessive Compulsive Disorder An informative paper by Joshua Perez This paper is on Obsessive Compulsive Disorder in which I will outline the fallowing questions what causes the condition / what organ systems are compromised. What is happening physiogicaly with the body/ disease process? What are the current treatment options? How do these options affect/correct the physiological compromise that caused the disease in the first place? How does the fallowing fit in to the disorder? Genetics, environment, physiological, anatomic, metabolic ,and/ or neurologic factors that may be associated with the condition. To open this paper I would like to direct your attention to an article by Tracey L. Waters and Paula M. Barrett entitled The Role of the Family in Childhood ObsessiveCompulsive Disorder in which she states that Although the research is inconsistent, there is increasing evidence that OCD has a strong genetic component. She later states that Higher than average prevalence rates for OCD in immediate relatives have led some authors to speculate that the modeling of avoidance, caution, and fearfulness may predispose a vulnerable child to develop obsessive compulsive symptoms. So what the Arthur is getting is that there are a number of things that influence when and how and to what level of severity a person may develop O.C.D But once you got it; the big question is what does it do to you or rather how does it affect you? In a academic journal entitled Abnormal Spontaneous Neural Activity in ObsessiveCompulsive Disorder: A Resting-State we learn that Although the pathophysiology of OCD remains unclear, neuroimaging studies have reported abnormalities in brain structure and function [2,3]. Most abnormalities have been reported in orbitofronto-striato-thalamic circuitry, including the orbitofrontal cortex (OFC), anterior cingulate cortex (ACC), caudate, and thalamus [2,4,5,6,7,8]. In contrast, a recent neuroimaging study suggested that the pathophysiology of OCD may involve more widely distributed large-scale brain systems, including the parietal and occipital lobes and the cerebellum, rather than the conventional orbitofronto-striatal model this article is stating that although O.C.D is flexible in the way one can contract it; it affects us all in the same way through the brain. One of the treatments for O.C.D is taken from the Journal of Child Psychology & Psychiatry, they had this to say CBT was protocol-driven, and broadly based on a published treatment manual (March & Mulle, 1998). It involved the following key components: psychoeducation about OCD and anxiety, and development of a hierarchy of compulsions (Sessions 1 and 2); graded exposure with response prevention (ERP; Session 3 onwards); and relapse prevention (final session). The treatment was carefully tailored to the developmental

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level of the young person, for example, by modifying the language and worksheets used. The extent of parental involvement varied depending both on the developmental level of the young person and the extent to which parents were involved in, or accommodating, compulsive behaviors and avoidance. Sessions usually lasted 1 hr, and were conducted on a weekly basis whenever possible. In most cases, 812 sessions were offered. For most patients, CBT was delivered in an individual, face-to-face format, although some received group CBT (n = 4) or telephone-based CBT (n = 2). A proportion of young people (n = 77) also received SSRI medication in combination with CBT; in most cases, medication was started and had reached a stable dose before CBT commenced. So what the doctors used was a combination of drugs and psychology in the hopes of controlling the disorder. However the same article then goes on to state how effective the treatment actually was Effectiveness of CBT Of the total sample, 109 (40 very early onset, 69 later onset) were treated with CBT at the clinic and had available CY-BOCS scores before and after the treatment. Analysis of this subgroup with respect to demographic and clinical characteristics yielded similar findings to the total sample. Patients in the very early onset were significantly younger (M = 12.7 vs. M = 14.8 years, p < .001) and had a longer duration of illness (M = 5.3 vs. M = 2.4 years, p < .001). There were no significant differences in terms of gender distribution in the very early and later onset groups (boys: 60.5% and 55.1%; v2 = .251, df = 1, p = .69). Of the 109 treated patients, 75 received CBT concomitant with SSRI medication. The proportion of patients receiving combined treatment was equivalent in the very early and later onset groups (77.5% vs. 63.8%; v2 = 2.22, df = 1, p = .20). Mean CY-BOCS scores pre- and post-treatment are shown in Table 3. The mean percentage reduction in total CY-BOCS score from the baseline to posttreatment was 58.4% for very early onset group and 51.5% for the later onset group. A mixedmodel ANOVA with the within-subjects factor of time (pre- vs. post-treatment) And the between-subjects factor of onset group (very early vs. later onset) was conducted and revealed a main effect of time [F(1, 108) = 332.46, p < .001], as indicated by a significant reduction in CY-BOCS score over the course of the treatment [M = 23.40, SD = 5.60 vs. M = 10.76, SD = 6.92; t(108) = 18.51, p < .001]. As you can see the treatment was very effective for penchants with O.C.D Scientist have discovered that OC symptoms and OC personality traits were related because they were both etiologically influenced by a nonspecific genetic factor; that is, the factor associated with negative emotionality. Therefore we find that O.C.D is genetically influenced and that it actually programs someone to think negatively! So to sum up 1. O.C.D has no known trigger but it is believed that it is a Genetic disorder 2. O.C.D really messes with your brain

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3. Even though there is little known about this increasingly prevalent disorder we still have some very effective treatment and means, and ways about how to help the people who suffer from this disease. Therefore In closing the research going in to understanding this disorder is an ever expanding field that will continue to grow until we fully understand it and can find a more effective treatment.

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References Authors: Waters, Tracey L.1 Barrett, Paula M. Source: Clinical Child & Family Psychology Review. Sep2000, Vol. 3 Issue 3, p173-184. 12p. Document Type: Article Subject Terms: *OBSESSIVE-compulsive disorder in children *OBSESSIVE-compulsive disorder in adolescence *OBSESSIVE-compulsive disorder *NEUROSES in children *NEUROSES in adolescence *NEUROSES *FAMILIES Author-Supplied Keywords: children family-relations obsessivecompulsive disorder treatment Author Affiliations: Griffith University, Gold Coast ISSN:1096-4037 Accession Number: 11307661 2.Citation:Ping L, Su-Fang L, Hai-Ying H, Zhang-Ye D, Jia L, et al. (2013) Abnormal Spontaneous Neural Activity in Obsessive-Compulsive Disorder: A Resting-State Functional Magnetic Resonance Imaging Study. PLoS ONE 8(6): e67262. doi:10.1371/journal.pone.0067262 Editor:Krish Sathian, Emory University, United States of America ReceivedJanuary 21, 2013;AcceptedMay 15, 2013;PublishedJune 27, 2013

3. Source: Journal of Child Psychology & Psychiatry Date: December 1, 2011 Authors:

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Taylor, Steven1 Asmundson, Gordon J.G.2 Jang, Kerry L.1 Source: Depression & Anxiety (1091-4269). Oct2011, Vol. 28 Issue 10, p863-869. 7p. Document Type: Article

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