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32,579 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The dopaminergic system, and in particular the dopamine D2 receptor, has been implicated in reward mechanisms. The net effect of neurotransmitter interaction at the mesolimbic brain region induces "reward" when dopamine (DA) is released from the neuron at the nucleus accumbens and interacts with a dopamine D2 receptor. "The reward cascade" involves the release of serotonin, which in turn at the hypothalmus stimulates enkephalin, which in turn inhibits GABA at the substania nigra, which in turn fine tunes the amount of DA released at the nucleus accumbens or "reward site." It is well known that under normal conditions in the reward site DA works to maintain our normal drives. In fact, DA has become to be known as the "pleasure molecule" and/or the "antistress molecule." When DA is released into the synapse, it stimulates a number a DA receptors (D1-D5) which results in increased feelings of well-being and stress reduction. A consensus of the literature suggests that when there is a dysfunction in the brain reward cascade, which could be caused by certain genetic variants (polygenic), especially in the DA system causing a hypodopaminergic trait, the brain of that person requires a DA fix to feel good. This trait leads to multiple drug-seeking behavior. This is so because alcohol, cocaine, heroin, marijuana, nicotine, and glucose all cause activation and neuronal release of brain DA, which could heal the abnormal cravings. Certainly after ten years of study we could say with confidence that carriers of the DAD2 receptor A1 allele have compromised D2 receptors. Therefore lack of D2 receptors causes individuals to have a high risk for multiple addictive, impulsive and compulsive behavioral propensities, such as severe alcoholism, cocaine, heroin, marijuana and nicotine use, glucose bingeing, pathological gambling, sex addiction, ADHD, Tourette's Syndrome, autism, chronic violence, posttraumatic stress disorder, schizoid/avoidant cluster, conduct disorder and antisocial behavior. In order to explain the breakdown of the reward cascade due to both multiple genes and environmental stimuli (pleiotropism) and resultant aberrant behaviors, Blum united this hypodopaminergic trait under the rubric of a reward deficiency syndrome.
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PMID:Reward deficiency syndrome: a biogenetic model for the diagnosis and treatment of impulsive, addictive, and compulsive behaviors. 1128 Sep 26

Obsessive-compulsive disorder (OCD) is classified as an anxiety disorder in the DSM-IV-TR [American Psychiatric Association, 2000. Diagnostic and statistical manual of mental disorders, Fourth ed., rev. Washington, DC: Author]; however, the notion of a spectrum of obsessive-compulsive (OC) related disorders that is comprised of such disparate disorders as OCD, body dysmorphic disorder, certain eating disorders, pathological gambling, and autism, is gaining acceptance. The fact that these disorders share obsessive-compulsive features and evidence similarities in patient characteristics, course, comorbidity, neurobiology, and treatment response raises the question of whether OCD is best conceptualized as an anxiety or an OC spectrum disorder. This article reviews evidence from comorbidity and family studies, as well as biological evidence related to neurocircuitry, neurotransmitter function, and pharmacologic treatment response that bear on this question. The implications of removing OCD from the anxiety disorders category and moving it to an OC spectrum disorders category, as is being proposed for the DSM-V, is discussed.
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PMID:Is obsessive-compulsive disorder an anxiety disorder? 1645 75

The Stop Signal Task (SST) is a measure that has been used widely to assess response inhibition. We conducted a meta-analysis of studies that examined SST performance in patients with various psychiatric disorders to determine the magnitude and generality of deficient inhibition. A five-item instrument was used to assess the methodological quality of studies. We found medium deficits in stop signal reaction time (SSRT), reflecting the speed of the inhibitory process, for attention-deficit hyperactivity disorder (ADHD) (g = 0.62), obsessive compulsive disorder (OCD) (g = 0.77) and schizophrenia (SCZ) (g = 0.69). SSRT was less impaired or normal for anxiety disorder (ANX), autism, major depressive disorder (MDD), oppositional defiant disorder/conduct disorder (ODD/CD), pathological gambling, reading disability (RD), substance dependence, and Tourette syndrome. We observed a large SSRT deficit for comorbid ADHD + RD (g = 0.82). SSRT was less than moderately impaired for ADHD + ANX and ADHD + ODD/CD. Study quality did not significantly affect SSRT across ADHD studies. This confirms an inhibition deficit in ADHD, and suggests that comorbid ADHD has different effects on inhibition in patients with ANX, ODD/CD, and RD. Further studies are needed to firmly establish an inhibition deficit in OCD and SCZ.
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PMID:Inhibitory control and psychopathology: a meta-analysis of studies using the stop signal task. 2071 43

The obsessive-compulsive spectrum is an important concept referring to a number of disorders drawn from several diagnostic categories that share core obsessive-compulsive features. These disorders can be grouped by the focus of their symptoms: bodily preoccupation, impulse control, or neurological disorders. Although the disorders are clearly distinct from one another, they have intriguing similarities in phenomenology, etiology, pathophysiology, patient characteristics, and treatment response. In combination with the knowledge gained through many years of research on obsessive-compulsive disorder (OCD), the concept of a spectrum has generated much fruitful research on the spectrum disorders. It has become apparent that these disorders can also be viewed as being on a continuum of compulsivity to impulsivity, characterized by harm avoidance at the compulsive end and risk seeking at the impulsive end. The compulsive and impulsive disorders differ in systematic ways that are just beginning to be understood. Here, we review these concepts and several representative obsessive-compulsive spectrum disorders including both compulsive and impulsive disorders, as well as the three different symptom clusters: OCD, body dysmorphic disorder, pathological gambling, sexual compulsivity, and autism spectrum disorders.
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PMID:Obsessive-compulsive spectrum disorders. 2203 47

An obsessive-compulsive disorder (OCD) spectrum has been proposed, which includes a group of disorders that share certain features with OCD including clinical symptoms (repetitive behaviours and thoughts), neurobiology (e.g. neurotransmitters) and preferential response to anti-obsessional treatments, such as the selective serotonin reuptake inhibitors (SSRIs). Three distinct clusters have been identified within the OCD spectrum, i.e. disorders concerning preoccupations with bodily sensations or appearance, impulsive disorders, and neurologically based disorders, and these share phenotypic features. Using one example from each of these clusters, body dysmorphic disorder (BDD), pathological gambling (PG) and autism, respectively, the phenomenology, neurobiology and pharmacotherapy indicates that specific biological factors are shared by OCD and by these disorders and correlate with the severity of repetitive behaviours. Thus, in common with OCDs, in BDD there is increased activity in the limbic regions; in PG there is evidence of deficiencies in 5-HT function and receptors; and in autism there are restricted interests and repetitive behaviours which may be influenced by serotonergic mechanisms. Our findings support the notion that targeted treatments, for example using SSRIs, for the behaviours associated with these disorders are effective. Our review considers one SSRI treatment in particular, fluvoxamine, and conclusions should be drawn in light of this. Further testing of our hypothesis would be prudent to confirm its validity.
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PMID:Obsessive-compulsive disorder and spectrum across the life span. 2493 Jul 87

Objective. To systematically assess previous findings on the orbitofrontal sulcogyral pattern in psychiatric disorders and to address the utility of this pattern as a transdiagnostic trait marker of early neurodevelopment in the social brain. Methods. An online literature search was conducted using the PubMed database from inception to August 2019. Studies included in this review were based on the Chiavaras's original classification method of this H-shaped sulcus (type I, II, and III), intermediate orbital sulcus (IOS), and posterior orbital sulcus (POS). Results. Twenty-six studies were included in the review. Sixteen studies (62%) focused on schizophrenia spectrum (Sz) disorders, and the remaining studies focused on autism spectrum disorder (ASD), attention-deficit/hyperactivity disorder (ADHD), history of extremely preterm and extremely low birth weight, bipolar disorder (BD), panic disorder, obsessive-compulsive disorder, cannabis users, and pathological gambling. In Sz, compared with healthy controls, the orbitofrontal sulcogyral pattern was decreased in type I, increased in type II and III, and there were fewer numbers of IOS and POS reported, although specificity in sex and hemispheric dominance was not consistent. BD and neurodevelopmental disorders in ASD and ADHD showed a similar pattern of alteration to that observed in the Sz. Conclusions. The present review of the orbitofrontal sulcogyral pattern indicated that type I expression might reflect a neurodevelopmental protective marker, and type II and III expressions, as well as fewer numbers of IOS and POS, might reflect neurodevelopmental risk markers. These trait markers may be transdiagnostic among socially disabling diseases.
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PMID:Orbitofrontal Sulcogyral Pattern as a Transdiagnostic Trait Marker of Early Neurodevelopment in the Social Brain. 3202 99