Inheritance in OCD in Moslems

Subjects and Methods: This study was designed in the Institute of psychiatry, Ain Shams University Hospitals. After signing an informed consent form, all the subjects 23 patients and 19 relatives were diagnosed according to DSM-IV and Structured Clinical Interview for DSM-IV (SCID I) and General Health Questionaire for psychiatric morbidity. Severity of OCD symptoms was assessed using Yale-Brown Obsessive Compulsive Scale (Y-BOCS) Symptom analysis was done on four symptom factor levels and presenting symptoms.


Introduction
Obsessive-Compulsive Disorder (OCD) is characterized by the presence of either obsessions or compulsions that cause Significant Distress to Afflicted individuals.
Estimates of prevalence vary slightly across countries and symptom presentation depends on cultural and religious factors. Genetic factors account for 45-65% of OCD symptoms in patients diagnosed with the disorder. Environmental factors also Play Arolein How These Anxiety Symptoms Are expressed [1].
Researchers found that relatives with the disorder possessed a difference in a gene called, SLC1A1, which is the glutamate transporter gene. They found that the discrepancy in the gene caused the flow of glutamine, in relation to brain cells, to happen much quicker for people with the disorder [2][3][4]. The researchers at Yale and the National Institute of Mental Health (NIMH) have found a mutation in the gene coding of the human serotonin transporter (sSERT). Serotonin is a neurotransmitter that helps transmit signals across nerve cells to help process information. Serotonin usually travels back after the signal transports but some people do not receive enough serotonin back. This lack of serotonin reuptake can increase the risk of someone having OCD [2][3][4].
Early-onset OCD appears to be a subtype that exhibits distinct clinical features and that is associated with greater familial loading and clinical data revealed an association between early age of onset and an increased frequency of tics, Tourette's disorder, and trichotillomania (TTM). The genetic studies yielded statistically significant results when the allelic distributions of genetic variants in the dopamine receptor type 4 gene (DRD4) were analyzed. These data support a role for the dopaminergic system, which were (1) symmetry factor, which contained symmetry obsessions and ordering, repeating, and counting compulsions; (2) forbidden thoughts factor, which contained aggression and sexual and religious obsessions; (3) cleaning factor, which contained contamination obsessions and cleaning compulsions; and (4) hoarding factor, which contained hoarding obsessions and compulsions [7]. Most common symptoms of obsessive-compulsive disorder.  [8].

Obsessions
Psychiatric comorbidity was examined in both patients and relatives.
Results were analysed as percentages means and standard deviations. Quantitative values were compared using T.

Discussion
In this study we found 15 (65.22%) out of 23 OCD patients had positive family history for psychiatric disorder. 11(47.83%) relatives had OCD which points to high genetic loading and severity of symptoms according to Y-BOCS 16 (69.57%).6 (31.58%) of affected relatives showed psychotic symptoms according to SCID I (delusions of reference and persecution while 3 (15.79%) showed major depression.
These data goes with research studies that support a role for the dopaminergic and serotonergic systems, which may be relevant to the development of early-onset OCD [5,6]. Imaging studies show dopaminergic hyperfunction in the prefrontal cortex and serotonergic hypofunction in the basal ganglia which can help explanation of comorbid psychosis and depression in relatives of OCD patients.
Patients with a diagnosis of obsessive-compulsive disorder were examined in a longitudinal study with mean length of follow-up from onset to 47 years.
Results showed improvement in 83%, including recovery in 48% (complete recovery, 20%; recovery with subclinical symptoms, 28%). Forty-eight percent had obsessive-compulsive disorder for more than 30 years. Early age of onset, having both obsessive and compulsive symptoms, low social functioning at baseline, and a chronic course were correlated with a worse outcome. Magical obsessions and compulsive rituals were correlated with a worse course. Qualitative symptom changes within the obsessive-compulsive disorder occurred in 58% of the patients [9].
The medial frontal cortex (MFC), including the dorsal anterior cingulate and the supplementary motor area, is critical for adaptive and inhibitory control of behavior. Abnormally high MFC activity has been a consistent finding in functional neuroimaging studies of obsessivecompulsive disorder. Compared with controls, OCD patients had greater relative activation of the supplementary motor area and deactivation of the rostral anterior cingulate.
Patients with OCD also showed reduced levels of neuronal N-acetylaspartate in the dorsal anterior cingulate region, which was negatively correlated with their blood oxygen level-dependent activation of the region. This relationship may partly explain the nature of inhibitory control deficits that are frequently seen in this group of patients [10].
N-acetylaspartate is a metabolite produced in neuronal mitochondria and is thought to reflect neuronal density and functional viability. It remains unclear whether reduced levels reflect neuronal loss or a state of (potentially reversible) neuronal dysfunction [11]. After its release from neurons, NAA is taken up and hydrolyzed by oligodendrocytes to act as a source of acetyl groups in a variety of metabolic processes, including myelin synthesis, lipid repair/fatty acid synthesis, osmotic regulation, and anti-inflammatory action. Reduced dAC NAA levels may, thus, reflect a variety of underlying metabolic and biochemical changes that, when considered in the context of the present findings, suggest that OCD patients have fewer healthy neurons in the region, necessitating the recruitment of adjacent and other task-related brain regions (e.g., the SMA, the lateral premotor, and the superior parietal) to perform at levels comparable with controls [12][13][14][15][16][17].
Planning is the ability to achieve a goal through a series of intermediate steps, such as plan generation, working memory, and internal evaluation and reward.
During planning, decreased frontal-striatal responsiveness was found in OCD patients, mainly in dorsolateral prefrontal cortex and caudate nucleus. In addition, OCD patients showed increased, presumably compensatory, involvement of brain areas known to play a role in performance monitoring and short-term memory processing, such as anterior cingulate, ventrolateral prefrontal, and parahippocampal cortices [31].
Recent neuropsychological studies have shown cognitive impairments in OCD, particularly with regard to visuospatial processing, executive functioning, and motor speed [32,33].
In this study we found the most prevalent symptom with high familial loading is washing related to religious issues (before praying and after menstruation for moslem OCD patients. A recent meta-analysis of 21 factor-analysis studies involving > 5000 subjects demonstrated a fairly robust 4-factor structure for OCD that was remarkably consistent across the lifespan (7). The 4 OCD factors were (1) symmetry factor, which contained symmetry obsessions and ordering, repeating, and counting compulsions; (2) forbidden thoughts factor, which contained aggression and sexual and religious obsessions; (3) cleaning factor, which contained contamination obsessions and cleaning compulsions; and (4) hoarding factor, which contained hoarding obsessions and compulsions. These OCD symptom dimensions have been associated with distinct patterns of comorbid psychiatric conditions, different patterns of heritability, and specific genetic polymorphisms, as well as distinct symptom-associated patterns of neural activity, as measured with functional MRI [34][35][36][37]. Symptom dimensions have been associated with different responses to pharmacologic and non-pharmacologic treatments [38,39].
Different obsessive-compulsive symptom dimensions are mediated by relatively distinct components of frontostriatothalamic circuits. OCD Patients demonstrated significantly greater activation than controls in bilateral ventromedial prefrontal regions and right caudate nucleus (washing); putamen/globus pallidus, thalamus, and dorsal cortical areas (checking); left precentral gyrus and right orbitofrontal cortex (hoarding) [34].