Compulsive sexual behavior disorder (CSBD) will be included in ICD-11 as an impulse-control disorder. CSBD also shares clinical features with obsessive-compulsive spectrum disorders (OCSDs) and behavioral addictions. There has been relatively little systematic investigation of CSBD in obsessive-compulsive disorder (OCD), the paradigmatic compulsive disorder. We aimed to determine prevalence of CSBD in OCD, and its associated sociodemographic and clinical features, including associated comorbidity, to learn more about the nature of CSBD.

Recently, much attention has been devoted to the possible alterations of the immune system in obsessive-compulsive disorder (OCD). Therefore, the aim of this paper was to review the current literature on the relationships between OCD and immune system.

Patients suffering from obsessive-compulsive disorder (OCD) are characterized by dysregulated neuronal processing of disorder-specific and also unspecific affective stimuli. In the present study, we investigated whether generic fear-inducing, disgust-inducing, and neutral stimuli can be decoded from brain patterns of single fMRI time samples of individual OCD patients and healthy controls. Furthermore, we tested whether differences in the underlying encoding provide information to classify subjects into groups (OCD patients or healthy controls). Two pattern classification analyses were conducted. In analysis 1, we used a classifier to decode the category of a currently viewed picture from extended fMRI patterns of single time samples (TR=3s) in individual subjects for several pairs of categories. In analysis 2, we used a searchlight approach to predict subjects' diagnostic status based on local brain patterns. In analysis 1, we obtained significant accuracies for the separation of fear-eliciting from neutral pictures in OCD patients and healthy controls. Separation of disgust-inducing from neutral pictures was significant in healthy controls. In analysis 2, we identified diagnostic information for the presence of OCD in the orbitofrontal cortex, and in the caudate nucleus. Accuracy obtained in these regions was 100% (p<10(-6)). To summarize our findings, by using multivariate pattern classification techniques we were able to identify neurobiological markers providing reliable diagnostic information about OCD. The classifier-based fMRI paradigms proposed here might be integrated in future diagnostic procedures and treatment concepts.

Obsessive Compulsive Disorder (OCD) and Obsessive Compulsive Symptoms (OCS) are known to be highly comorbid with bipolar disorder and schizophrenia. Comorbid OCD/OCS influences the course of schizophrenia and bipolar disorder. There is also some evidence to suggest that a diagnosis of OCD may be associated with elevated risk for later development of psychosis and bipolar disorder. Comorbid OCD/OCS is associated with a greater severity of schizophrenia phenotype and poorer prognosis. In addition, certain atypical antipsychotics, clozapine in particular are known to induce or worsen OCS in schizophrenia. OCD when comorbid with bipolar disorder mostly runs an episodic course with worsening and improvement of OCD/OCS in depressive and in manic/hypomanic phases respectively. There is limited systematic data on the treatment of OCD in schizophrenia and bipolar disorder. When OCD presents in the context of schizophrenia, management may include treatment with atypical antipsychotics with limited serotonergic properties, changing the antipsychotic, reduction in the dose of the antipsychotic, addition of cognitive-behavior therapy (CBT), or a specific serotonin reuptake inhibitor (SSRI). When OCD is comorbid with bipolar disorder, mood stabilization is the priority. CBT may be preferred over SSRIs to treat OCD/OCS that persist in between the mood episodes because SSRIs may induce a switch or worsen the course of bipolar disorder. SSRIs when indicated have to be used judiciously under the cover of adequate mood stabilization.

Objective: To evaluate the lifetime prevalence of infectious, inflammatory, and autoimmune disorders in a multisite study of probands with childhood-onset obsessive compulsive disorder (OCD) and their first-degree relatives. Methods: Medical questionnaires were completed by 1401 probands and 1045 first-degree relatives in the OCD Collaborative Genetics Association Study. Lifetime prevalence of immune-related diseases was compared with the highest available population estimate and reported as a point estimate with 95% adjusted Wald interval. Worst-episode OCD severity and symptom dimensions were assessed with the Yale-Brown Obsessive Compulsive Scale (YBOCS) and Symptom Checklist (YBOCS-CL). Results: Probands reported higher-than-expected prevalence of scarlet fever (4.0 [3.1-5.2]% vs. 1.0%-2.0%, z = 1.491, p < 0.001, n = 1389), encephalitis or meningitis (1.4 [0.9-2.1]% vs. 0.1%-0.4%, z = 5.913, p < 0.001, n = 1393), rheumatoid arthritis (1.1 [0.6-2.0]% vs. 0.2%-0.4%, z = 3.416, p < 0.001, n = 949) and rheumatic fever (0.6 [0.3-1.2]% vs. 0.1%-0.2%, z = 3.338, p < 0.001, n = 1390), but not systemic lupus erythematosus, diabetes, asthma, multiple sclerosis, psoriasis, or inflammatory bowel disease. First-degree relatives reported similarly elevated rates of scarlet fever, rheumatic fever, and encephalitis or meningitis independent of OCD status. There was no association between worst-episode severity and immune-related comorbidities, although probands reporting frequent ear or throat infections had increased severity of cleaning-/contamination-related symptoms (mean factor score 2.5 ± 0.9 vs. 2.3 ± 1.0, t = 3.183, p = 0.002, n = 822). Conclusion: These data suggest high rates of streptococcal-related and other immune-mediated diseases in patients with childhood-onset OCD and are consistent with epidemiological studies in adults noting familial clustering. Limitations include potential reporting bias and absence of a control group, underscoring the need for further prospective studies characterizing medical and psychiatric disease clusters and their interactions in children. Such studies may ultimately improve our understanding of OCD pathogenesis and aid in the development of adjunctive immune-modulating therapeutic strategies.

The Yale-Brown Obsessive Compulsive Scale (Y-BOCS) is widely used in the assessment of obsessive-compulsive disorder (OCD), but the psychometric properties of the instrument have not been examined in African Americans with OCD. Therefore, the purpose of this study is to explore the properties of the Y-BOCS severity scale in this population. Participants were 75 African American adults with a lifetime diagnosis of OCD. They completed the Y-BOCS, the Beck Anxiety Inventory (BAI), the Beck Depression Inventory-II (BDI-II), and the Multigroup Ethnic Identity Measure (MEIM). Evaluators rated OCD severity using the Clinical Global Impression Scale (CGI) and their global assessment of functioning (GAF). The Y-BOCS was significantly correlated with both the CGI and GAF, indicating convergent validity. It also demonstrated good internal consistency (α=0.83) and divergent validity when compared to the BAI and BDI-II. Confirmatory factor analyses tested five previously reported models and supported a three-factor solution, although no model exhibited excellent fit. An exploratory factor analysis was conducted, supporting a three-factor solution. A linear regression was conducted, predicting CGI from the three factors of the Y-BOCS and the MEIM, and the model was significant. The Y-BOCS appears to be a valid measure for African American populations.

This review provides an overview of obsessive-compulsive disorder (OCD) symptoms, including the four partially distinct subtypes of the disorder, current diagnostic criteria, and common comorbidities. Critically, it focuses on the etiology of OCD, including its underlying neuropathology, and examines cognitive dysfunction in OCD.

Obsessive-compulsive disorder (OCD) has been linked to reward dysfunctions, highlighting a possible role of anhedonia in OCD. Surprisingly, anhedonia in OCD has never been evaluated. Moreover, although nicotine typically has anti-anhedonic effects, anecdotal reports suggest low prevalence rates of smoking in OCD. To address these two phenomena, 113 individuals with OCD completed a battery of questionnaires assessing symptom severity, anhedonia, and smoking. 28.3% of the sample met criteria for clinically significant anhedonia, which correlated with Y-BOCS scores (r=0.44), even when controlling for depressive symptoms. 13.3% of the sample endorsed current smoking, a lower rate than seen in psychiatric disorders (40-90%) and the general adult population (19%). Results highlight high rates of anhedonia and yet reduced prevalence of smoking in OCD. In contrast to the known positive association between anhedonia and smoking, a negative association emerged. Future research is needed to address the unique interface between anhedonia and reward responsiveness in OCD. Potential clinical implications are discussed.

Impaired decision-making is well documented in obsessive-compulsive disorder (OCD) and a range of electrophysiological and functional neuroimaging measures have begun to reveal the pathological mechanisms that underlie the decision-making process. Obsessive-compulsive personality disorder (OCPD) has core symptoms that often overlap with OCD, but similarities between these disorders at the behavioral and neurological levels are often unclear, including whether OCPD exhibits similar decision-making deficits and shared neurological dysfunction. To address these issues, we examined 24 cases of OCD, 19 cases of OCPD, and 26 matched normal control (NC) subjects during the revised Iowa Gambling Task (IGT) using event-related potentials (ERPs). The net IGT scores were lower for OCD subjects than for OCPD or NC subjects, thus indicating that OCD subjects chose more disadvantageous options and were "short-sighted" with regards to information. The feedback-related negativity (FRN) waveform (lose-win) was larger in both OCD and OCPD subjects, which suggested that obstacles exist in the feedback process. Consequently, these subjects might share similar neural mechanisms under ambiguous decision-making circumstances. Furthermore, IGT net scores were significantly and negatively correlated with Hamilton Anxiety Rating Scale (HAMA) and Hamilton Depression Rating Scale (HAMD) scales. This implies that more severe obsessive-compulsive symptoms inspired more negative emotions that led to worse decision-making ability. Therefore, although similar neural mechanisms might exist, this led to different behaviors in which OCPD is associated with better behavioral performance compared to OCD patients.

Previous research showed that dysfunctions of fronto-striatal neural networks are implicated in the pathophysiology of obsessive-compulsive disorder (OCD). Accordingly, patients with OCD showed altered performances during decision-making tasks. As P300, evoked by oddball paradigms, is suggested to be related to attentional and cognitive processes and generated in the medial temporal lobe and orbitofrontal and cingulate cortices, it is of special interest in OCD research. Therefore, this study aimed to investigate P300 in OCD and its associations with brain activity during decision-making: P300, evoked by an auditory oddball paradigm, was analysed in 19 OCD patients and 19 healthy controls regarding peak latency, amplitude and source density power in parietal cortex areas by sLORETA. Afterwards, using a fMRI paradigm, Blood-oxygen-level-dependent (BOLD) contrast imaging was conducted during a delay-discounting paradigm. We hypothesised differences between groups regarding P300 characteristics and associations with frontal activity during delay-discounting. The P300 did not differ between groups, however, the P300 latency over the P4 electrode correlated negatively with the NEO-FFI score openness to experience in patients with OCD. In healthy controls, P300 source density power correlated with activity in frontal regions when processing rewards, a finding which was absent in OCD patients. To conclude, associations of P300 with frontal brain activation during delay-discounting were found, suggesting a contribution of attentional or context updating processes. Since this association was absent in patients with OCD, the findings could be interpreted as being indeed related to dysfunctions of fronto-striatal neural networks in patients with OCD.

Astrocytes and neurons extensively interact in the brain. Identifying astrocyte and neuron proteomes is essential for elucidating the protein networks that dictate their respective contributions to physiology and disease. Here we used cell-specific and subcompartment-specific proximity-dependent biotinylation1 to study the proteomes of striatal astrocytes and neurons in vivo. We evaluated cytosolic and plasma membrane compartments for astrocytes and neurons to discover how these cells differ at the protein level in their signalling machinery. We also assessed subcellular compartments of astrocytes, including end feet and fine processes, to reveal their subproteomes and the molecular basis of essential astrocyte signalling and homeostatic functions. Notably, SAPAP3 (encoded by Dlgap3), which is associated with obsessive-compulsive disorder (OCD) and repetitive behaviours2-8, was detected at high levels in striatal astrocytes and was enriched within specific astrocyte subcompartments where it regulated actin cytoskeleton organization. Furthermore, genetic rescue experiments combined with behavioural analyses and molecular assessments in a mouse model of OCD4 lacking SAPAP3 revealed distinct contributions of astrocytic and neuronal SAPAP3 to repetitive and anxiety-related OCD-like phenotypes. Our data define how astrocytes and neurons differ at the protein level and in their major signalling pathways. Moreover, they reveal how astrocyte subproteomes vary between physiological subcompartments and how both astrocyte and neuronal SAPAP3 mechanisms contribute to OCD phenotypes in mice. Our data indicate that therapeutic strategies that target both astrocytes and neurons may be useful to explore in OCD and potentially other brain disorders.

We investigated whether obsessive-compulsive (OC) symptoms from a population-based sample could be analyzed to detect genetic variants influencing obsessive-compulsive disorder (OCD). We performed a genome-wide association studies (GWAS) on the obsession (rumination and impulsions) and compulsion (checking, washing, and ordering/precision) subscales of an abbreviated version of the Padua Inventory (N = 8,267 with genome-wide genotyping and phenotyping). The compulsion subscale showed a substantial and significant positive genetic correlation with an OCD case-control GWAS (r G = 0.61, p = .017) previously published by the Psychiatric Genomics Consortium (PGC-OCD). The obsession subscale and the total Padua score showed no significant genetic correlations (r G = -0.02 and r G = 0.42, respectively). A meta-analysis of the compulsive symptoms GWAS with the PGC-OCD revealed no genome-wide significant Single-Nucleotide Polymorphisms (SNPs combined N = 17,992, indicating that the power is still low for individual SNP effects). A gene-based association analysis, however, yielded two novel genes (WDR7 and ADCK1). The top 250 genes in the gene-based test also showed a significant increase in enrichment for psychiatric and brain-expressed genes. S-Predixcan testing showed that for genes expressed in hippocampus, amygdala, and caudate nucleus significance increased in the meta-analysis with compulsive symptoms compared to the original PGC-OCD GWAS. Thus, the inclusion of dimensional symptom data in genome-wide association on clinical case-control GWAS of OCD may be useful to find genes for OCD if the data are based on quantitative indices of compulsive behavior. SNP-level power increases were limited, but aggregate, gene-level analyses showed increased enrichment for brain-expressed genes related to psychiatric disorders, and increased association with gene expression in brain tissues with known emotional, reward processing, memory, and fear-formation functions.

The current study examined the association of OCD symptoms and OCD belief domains, for individuals engaged in Technology Supported Mindfulness training (TSM) using an EEG-based biofeedback device (called "Muse") that permits individuals to engage in home based mindfulness meditation practices. In this randomized controlled study, treatment-seeking participants with a principal DSM-5 diagnosis of OCD (N = 71) were randomly assigned to eight weeks of: 1) a meditation program involving daily use of the "Muse" device, or 2) wait list control. At weeks 1, 4, and 8, participants completed self-report measures of OCD symptoms (YBOCS: Yale-Brown Obsessive Compulsive Scale) and OCD beliefs (OBQ; OCCWG, 2005). Latent Difference Score (LDS) models indicated that there was no significant longitudinal relationship between OBQ "Responsibility/Threat" (OBQ R/T) scores and OCD symptoms. The analysis of OBQ "Perfectionism/Certainty" (OBQ P/C) and OCD symptoms demonstrated a significant reciprocal relationship between these two variables, in which OCD symptoms predicted subsequent increases in OBQ P/C and vice versa. The analysis of OBQ "Importance/Control of Thoughts" (OBQ I/C) and OCD symptoms demonstrated a significant reciprocal relationship between these two variables, in which OCD symptoms predicted subsequent increases in OBQ I/C and vice versa. The analysis of OBQ domains and EEG derived attentional changes demonstrated a significant association between OBQ P/C and Alpha band frequencies. These results clarify the association of OBQ belief domains, OCD symptom change and EEG derived indicators of attention during TSM.

Obsessive compulsive disorder (OCD) is a syndrome characterized by recurrent and intrusive thoughts and ritualistic behaviors or mental acts that a person feels compelled to perform. Twin studies, family studies, and segregation analyses provide compelling evidence that OCD has a strong genetic component. The SLITRK1 gene encodes a developmentally regulated stimulator of neurite outgrowth and previous studies have implicated rare variants in this gene in disorders in the OC spectrum, specifically Tourette syndrome (TS) and trichotillomania (TTM). The objective of the current study was to evaluate rare genetic variation in SLITRK1 in risk for OCD and to functionally characterize associated coding variants. We sequenced SLITRK1 coding exons in 381 individuals with OCD as well as in 356 control samples and identified three novel variants in seven individuals. We found that the combined mutation load in OCD relative to controls was significant (p = 0.036). We identified a missense N400I change in an individual with OCD, which was not found in more than 1000 control samples (P<0.05). In addition, we showed the the N400I variant failed to enhance neurite outgrowth in primary neuronal cultures, in contrast to wildtype SLITRK1, which enhanced neurite outgrowth in this assay. These important functional differences in the N400I variant, as compared to the wildtype SLITRK1 sequence, may contribute to OCD and OC spectrum symptoms. A synonymous L63L change identified in an individual with OCD and an additional missense change, T418S, was found in four individuals with OCD and in one individual without an OCD spectrum disorder. Examination of additional samples will help assess the role of rare SLITRK1 variation in OCD and in related psychiatric illness.

Obsessive-compulsive personality disorder (OCPD) traits and obsessive-compulsive disorder (OCD) are commonly associated with patients with Anorexia Nervosa (AN). The aim of this review was to systematically search the literature to examine whether OCPD and OCD are positively associated with excessive exercise in patients with AN.

In this position statement, developed by The International College of Obsessive-Compulsive Spectrum Disorders, a group of international experts responds to recent developments in the evidence-based management of obsessive-compulsive disorder (OCD). The article presents those selected therapeutic advances judged to be of utmost relevance to the treatment of OCD, based on new and emerging evidence from clinical and translational science. Areas covered include refinement in the methods of clinical assessment, the importance of early intervention based on new staging models and the need to provide sustained well-being involving effective relapse prevention. The relative benefits of psychological, pharmacological and somatic treatments are reviewed and novel treatment strategies for difficult to treat OCD, including neurostimulation, as well as new areas for research such as problematic internet use, novel digital interventions, immunological therapies, pharmacogenetics and novel forms of psychotherapy are discussed.

Rapid eye movement sleep behavior disorder (RBD) is a common prodromic non-motor symptom of Parkinson's disease (PD). Only few studies have evaluated the personality of RBD patients with conflicting results. Aim of the study was to evaluate the frequency of Personality Disorders (PeDs)in RBD. RBD patients, PD patients and healthy controls (HC) were enrolled. All the enrolled subjects underwent a full neurological examination. Motor symptoms were evaluated with the UPDRS-Motor Examination. PeDs were assessed with the Structured Clinical Interview for DSM-IV Personality Disorders (SCID-II). Twenty-nine RBD patients [14 men (48.3%); mean age 55.6 ± 11.1], 30 PD patients [17 men (56.7%); mean age 65.7 ± 10.7] and 30 HC [12 men (40%); mean age 65.7 ± 5.4] were enrolled in the study. PD patients had a disease duration of 4.5 ± 4.6 and presented a mean UPDRS-ME score of 26.7 ± 9.4. The most frequent PeDs was the Obsessive-Compulsive one (OCPeD); OCPeD was significantly more frequent in RBD (55.2%) patients than HC (13.3%; p-value < 0.001). No significant differences were found comparing the frequency of OCPeD in RBD patients to that in PD. In the present study, the prevalence of OCPeD in RBD patients was close to that reported in PD patients. Our data could suggest the existence of a common disease-specific RBD-PD personality profile.

Treatment-resistance is a frequent condition for obsessive-compulsive disorder (OCD). Over the past decades, a lot of effort has been made to address this issue, and several augmentation strategies of serotonergic drugs have been investigated. Antidopaminergic drugs are considered the first choice as augmentation strategy for treatment-resistant OCD patients, but they seem to work only for a subset of patients, and none of them have been officially approved for OCD. Recently, the role of glutamate and inflammation in OCD pathophysiology clearly emerged, and this has led to several investigations on glutamatergic and anti-inflammatory agents. Results seem promising but still inconclusive. Probiotic interventions (considered to modulate the immune systems and the brain activity) are gaining attention in several psychiatric fields but are still at their early stages in the OCD field. Research on new treatment approaches for OCD is moving forward, and more than one hundred interventional trials are ongoing around the world. While the vast majority of these trials involve neuromodulation and psychotherapeutic approaches, only a small proportion (around 20%) involve the investigation of new pharmacological approaches (tolcapone, nabilone, psilocybin, troriluzole, nitrous oxide, rituximab, naproxen, and immunoglobulins). Here, we provide a comprehensive review of investigational and experimental drugs to treat OCD.

Obsessive-compulsive disorder (OCD) is a debilitating and disabling neuropsychiatric disorder, whose neurobiological basis remains unclear. Although traditional static resting-state magnetic resonance imaging (rfMRI) studies have found aberrant functional connectivity (FC) in OCD, alterations in whole-brain FC and topological properties in the context of brain dynamics remain relatively unexplored. The rfMRI data of 29 patients with OCD and 40 healthy controls were analyzed using group independent component analysis to obtain independent components (ICs) and a sliding-window approach to generate dynamic functional connectivity (dFC) matrices. dFC patterns were clustered into three reoccurring states, and state transition metrics were obtained. Then, graph-theory methods were applied to dFC matrices to calculate the variability of network topological organization. The occurrence of a state (State 1) with the highest modularity index and lowest mean FC between networks was increased significantly in OCD, and the fractional time in brain State 1 was positively correlated with anxiety level in patients. State 1 was characterized by having positive connections within default mode (DMN) and salience networks (SAN), and negative coupling between the two networks. Additionally, ICs belonging to DMN and SAN showed lower temporal variability of nodal degree centrality and efficiency in patients, which was related to longer illness duration and higher current obsession ratings. Our results provide evidence of clinically relevant aberrant dynamic brain activity in OCD. Increased functional segregation among networks and impaired functional flexibility in connections among brain regions in DMN and SAN may play important roles in the neuropathology of OCD.

Patients with obsessive-compulsive disorder (OCD) often have limited exposure to a diverse environment and perform repetitive compulsions such as excessive cleaning and washing, which could lead to altered gut microbiome. Therefore, longitudinal studies that investigate changes in gut microbiome before and after cognitive behavioral therapy based on exposure and response prevention (ERP) are warranted.