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Increased neural error-signals have been observed in obsessive-compulsive disorder (OCD), anxiety disorders, and inconsistently in depression. Reduced neural error-signals have been observed in substance use disorders (SUD). Thus, alterations in error-monitoring are proposed as a transdiagnostic endophenotype. To strengthen this notion, data from unaffected individuals with a family history for the respective disorders are needed. The error-related negativity (ERN) as a neural indicator of error-monitoring was measured during a flanker task from 117 OCD patients, 50 unaffected first-degree relatives of OCD patients, and 130 healthy comparison participants. Family history information indicated, that 76 healthy controls were free of a family history for psychopathology, whereas the remaining had first-degree relatives with depression (n = 28), anxiety (n = 27), and/or SUD (n = 27). Increased ERN amplitudes were found in OCD patients and unaffected first-degree relatives of OCD patients. In addition, unaffected first-degree relatives of individuals with anxiety disorders were also characterized by increased ERN amplitudes, whereas relatives of individuals with SUD showed reduced amplitudes. Alterations in neural error-signals in unaffected first-degree relatives with a family history of OCD, anxiety, or SUD support the utility of the ERN as a transdiagnostic endophenotype. Reduced neural error-signals may indicate vulnerability for under-controlled behavior and risk for substance use, whereas a harm- or error-avoidant response style and vulnerability for OCD and anxiety appears to be associated with increased ERN. This adds to findings suggesting a common neurobiological substrate across psychiatric disorders involving the anterior cingulate cortex and deficits in cognitive control.

Key Points Obsessive–compulsive disorder (OCD) is a phenotypically complex multidimensional neuropsychiatric disorder. Family and twin studies provide definitive evidence that genetic and environmental factors can increase risk of the disorder. Candidate gene and genome-wide association studies provide strong suggestive evidence that genes in the serotonergic, dopaminergic and glutamatergic systems confer risk for the manifestation of OCD. Imaging studies as well as neuropsychological and treatment studies have implicated frontal–subcortical circuits in the pathophysiology of OCD. A cortico–striato–thalamo–cortical circuit is the prevailing model regarding the neural and pathophysiological underpinnings of OCD. The prevailing treatments include both pharmacological agents (selective serotonin-reuptake inhibitors) and cognitive behavioural therapy (CBT), with CBT and/or a combination of pharmacological and CBT being the most efficacious. Animal studies provide strong evidence for the involvement of the glutamatergic system in the expression of OCD-like behaviours. A model incorporating both genetic and epigenetic mechanisms in the manifestation of OCD is suggested as a heuristic for the pathophysiology of OCD. Obsessive–compulsive disorder has been scrutinized in many genetic, neuropsychological and neuroimaging studies. Pauls and colleagues provide an overview of our current understanding of the vulnerability factors, triggers and mechanisms underlying this devastating condition. Obsessive–compulsive disorder (OCD) is characterized by repetitive thoughts and behaviours that are experienced as unwanted. Family and twin studies have demonstrated that OCD is a multifactorial familial condition that involves both polygenic and environmental risk factors. Neuroimaging studies have implicated the cortico–striato–thalamo–cortical circuit in the pathophysiology of the disorder, which is supported by the observation of specific neuropsychological impairments in patients with OCD, mainly in executive functions. Genetic studies indicate that genes affecting the serotonergic, dopaminergic and glutamatergic systems, and the interaction between them, play a crucial part in the functioning of this circuit. Environmental factors such as adverse perinatal events, psychological trauma and neurological trauma may modify the expression of risk genes and, hence, trigger the manifestation of obsessive–compulsive behaviours.

Why do we repeat choices that we know are bad for us? Decision making is characterized by the parallel engagement of two distinct systems, goal-directed and habitual, thought to arise from two computational learning mechanisms, model-based and model-free. The habitual system is a candidate source of pathological fixedness. Using a decision task that measures the contribution to learning of either mechanism, we show a bias towards model-free (habit) acquisition in disorders involving both natural (binge eating) and artificial (methamphetamine) rewards, and obsessive-compulsive disorder. This favoring of model-free learning may underlie the repetitive behaviors that ultimately dominate in these disorders. Further, we show that the habit formation bias is associated with lower gray matter volumes in caudate and medial orbitofrontal cortex. Our findings suggest that the dysfunction in a common neurocomputational mechanism may underlie diverse disorders involving compulsion.

Childhood-onset Obsessive–Compulsive Disorder (OCD) shows distinct comorbidity patterns and developmental pathways, as well as an increased risk of psychosis with respect to adult-onset forms. Nevertheless, little is known about the prodromal symptoms of psychosis in children and adolescents with a primary diagnosis of OCD. The present study was aimed at evaluating the occurrence of Cognitive–Perceptual basic symptoms (COPER) and high- risk criterion Cognitive Disturbances (COGDIS) in pediatric and adults OCD patients, verifying if they might vary according to the age of onset of OCD. The study included 90 outpatients with a primary diagnosis of obsessive–compulsive disorder. The study sample was collapsed into three groups according to the age at onset: 1) very early onset group (< 10 years); 2) early onset group (11–18 years); 3) adult-onset group (> 18 years). All patients were administered the Yale-Brown Obsessive- Compulsive Scale (Y-BOCS) and its Child version (CY-BOCS), the Schizophrenia Proneness Instrument-Adult (SPIA) and its Child and Adolescent version (SPI-CY) and the Social and Occupational Functioning Assessment Scale (SOFAS). COPER and COGDIS symptoms were positively associated with OCD severity and detectable, respectively, in 28.9 and 26.7% of our study sample. The very early onset group significantly had higher COPER and COGDIS symptoms than the adult-onset group. Our data suggest that COPER and COGDIS symptoms are frequent in obsessive patients, in particular in those with earlier onset; therefore, their detection in childhood-onset OCD may represent an early and specific indicator of psychotic vulnerability.

Experts have proposed removing obsessive-compulsive disorder (OCD) from the anxiety disorders section and grouping it with putatively related conditions in DSM-5. The current study uses co-morbidity and familiality data to inform these issues. Case family data from the OCD Collaborative Genetics Study (382 OCD-affected probands and 974 of their first-degree relatives) were compared with control family data from the Johns Hopkins OCD Family Study (73 non-OCD-affected probands and 233 of their first-degree relatives). Anxiety disorders (especially agoraphobia and generalized anxiety disorder), cluster C personality disorders (especially obsessive-compulsive and avoidant), tic disorders, somatoform disorders (hypochondriasis and body dysmorphic disorder), grooming disorders (especially trichotillomania and pathological skin picking) and mood disorders (especially unipolar depressive disorders) were more common in case than control probands; however, the prevalences of eating disorders (anorexia and bulimia nervosa), other impulse-control disorders (pathological gambling, pyromania, kleptomania) and substance dependence (alcohol or drug) did not differ between the groups. The same general pattern was evident in relatives of case versus control probands. Results in relatives did not differ markedly when adjusted for demographic variables and proband diagnosis of the same disorder, though the strength of associations was lower when adjusted for OCD in relatives. Nevertheless, several anxiety, depressive and putative OCD-related conditions remained significantly more common in case than control relatives when adjusting for all of these variables simultaneously. On the basis of co-morbidity and familiality, OCD appears related both to anxiety disorders and to some conditions currently classified in other sections of DSM-IV.

Substantial empirical evidence has indicated impairment in the cognitive functioning of patients with obsessive-compulsive disorder (OCD) despite inconsistencies. Although several confounding factors have been investigated to explain the conflicting results, the findings remain mixed. This study aimed to investigate cognitive dysfunction in patients with OCD using a meta-analytic approach. The PubMed database was searched between 1980 and October 2012, and reference lists of review papers were examined. A total of 221 studies were identified, of which 88 studies met inclusion criteria. Neuropsychological performance and demographic and clinical variables were extracted from each study. Patients with OCD were significantly impaired in tasks that measured visuospatial memory, executive function, verbal memory and verbal fluency, whereas auditory attention was preserved in these individuals. The largest effect size was found in the ability to recall complex visual stimuli. Overall effect estimates were in the small to medium ranges for executive function, verbal memory and verbal fluency. The effects of potentially confounding factors including educational level, symptom severity, medication status and co-morbid disorders were not significant. Patients with OCD appear to have wide-ranging cognitive deficits, although their impairment is not so large in general. The different test forms and methods of testing may have influenced the performance of patients with OCD, indicating the need to select carefully the test forms and methods of testing used in future research. The effects of various confounding variables on cognitive functioning need to be investigated further and to be controlled before a definite conclusion can be made.

Obsessive–compulsive disorder (OCD) is a heterogeneous mental illness characterized by a variety of clinical manifestations and underlying neurobiological mechanisms. Modern research highlights the importance of identifying subtypes of OCD—separate categories that are characterized by specific phenotypic manifestations. This review provides a systematic integration of multi-level biomarker data (genetic, neuroimaging, neuropsychological) specifically aligned with the most consistently replicated, symptom-based subtypes of OCD. Our findings demonstrate that distinct OCD subtypes are underpinned by divergent neurobiological pathways, involving dysregulation across glutamatergic, serotonergic, dopaminergic, and neurotrophic systems, as well as distinct patterns of brain region engagement. The most extensive body of evidence currently exists for the contamination/cleaning and symmetry/ordering OCD subtypes. In contrast, other subtypes require more rigorous investigation. The findings from this study can provide theoretical prerequisites for future experimental studies involving larger cohorts of OCD patients, who can then be classified based on their detected biomarkers and tested accordingly.

Despite significant advances in the study of obsessive-compulsive disorder (OCD), important questions remain about the disorder's public health significance, appropriate diagnostic classification, and clinical heterogeneity. These issues were explored using data from the National Comorbidity Survey Replication, a nationally representative survey of US adults. A subsample of 2073 respondents was assessed for lifetime Diagnostic and Statistical Manual of Mental Disorders , 4th edn (DSM-IV) OCD. More than one quarter of respondents reported experiencing obsessions or compulsions at some time in their lives. While conditional probability of OCD was strongly associated with the number of obsessions and compulsions reported, only small proportions of respondents met full DSM-IV criteria for lifetime (2.3%) or 12-month (1.2%) OCD. OCD is associated with substantial comorbidity, not only with anxiety and mood disorders but also with impulse-control and substance use disorders. Severity of OCD, assessed by an adapted version of the Yale–Brown Obsessive Compulsive Scale, is associated with poor insight, high comorbidity, high role impairment, and high probability of seeking treatment. The high prevalence of subthreshold OCD symptoms may help explain past inconsistencies in prevalence estimates across surveys and suggests that the public health burden of OCD may be greater than its low prevalence implies. Evidence of a preponderance of early onset cases in men, high comorbidity with a wide range of disorders, and reliable associations between disorder severity and key outcomes may have implications for how OCD is classified in DSM-V.

A consensus has yet to emerge whether deep brain stimulation (DBS) for treatment-refractory obsessive-compulsive disorder (OCD) can be considered an established therapy. In 2014, the World Society for Stereotactic and Functional Neurosurgery (WSSFN) published consensus guidelines stating that a therapy becomes established when “at least two blinded randomized controlled clinical trials from two different groups of researchers are published, both reporting an acceptable risk-benefit ratio, at least comparable with other existing therapies. The clinical trials should be on the same brain area for the same psychiatric indication.” The authors have now compiled the available evidence to make a clear statement on whether DBS for OCD is established therapy. Two blinded randomized controlled trials have been published, one with level I evidence (Yale-Brown Obsessive Compulsive Scale (Y-BOCS) score improved 37% during stimulation on), the other with level II evidence (25% improvement). A clinical cohort study (N = 70) showed 40% Y-BOCS score improvement during DBS, and a prospective international multi-center study 42% improvement (N = 30). The WSSFN states that electrical stimulation for otherwise treatment refractory OCD using a multipolar electrode implanted in the ventral anterior capsule region (including bed nucleus of stria terminalis and nucleus accumbens) remains investigational. It represents an emerging, but not yet established therapy. A multidisciplinary team involving psychiatrists and neurosurgeons is a prerequisite for such therapy, and the future of surgical treatment of psychiatric patients remains in the realm of the psychiatrist.

Purpose of Review This review highlights recent research regarding gender differences in OCD, with a focus on prevalence, course of illness, symptom presentation, comorbidity, and treatment response. Recent Findings Overall, findings remain mixed. OCD may be more common among males in childhood, but is more common among females in adolescence and adulthood. Males tend to report an earlier age of onset and present with symptoms related to blasphemous thoughts. Females often describe symptom onset as occurring during or after puberty or pregnancy and present with symptoms related to contamination and/or aggressive obsessions. Females also tend to report significantly higher depression and anxiety. There are no reported gender differences in treatment outcome. Summary Gender may play a role in the onset, presentation, and impact of OCD symptoms. However, more work is needed to account for differences across studies, with one promising future direction being the study of reproductive hormones.