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Obsessive compulsive disorder (OCD) and chronic tic disorders (CTD) including Tourette Syndrome (TS) are often comorbid conditions. While some patients present with distinct symptoms of CTD and/or OCD, a subset of patients demonstrate a unique overlap of symptoms, known as Tourettic OCD (TOCD), in which tics, compulsions, and their preceding premonitory urges are overlapping and tightly intertwined. The specific behaviors seen in TOCD are typically complex tic-like behaviors although with a compulsive and partially anxious nature reminiscent of OCD. TOCD is not classified within the Diagnostic and Statistical Manual of Mental Disorders fifth edition (DSM-5) as an independent diagnostic entity, but mounting evidence suggests that TOCD is an intermediate neuropsychiatric disorder distinct from either TS or OCD alone and as such represents a unique phenomenology. In this review of TOCD we discuss clinical, genetic, environmental, neurodevelopmental, and neurocircuit-based research to better characterize our current understanding of this disorder. TOCD is characterized by earlier age of onset, male predominance, and specific symptom clusters such as lower tendency toward compulsions related to checking, cleaning, and reassurance seeking and higher tendency toward compulsions such as rubbing, tapping, or touching associated with symmetry concerns or thoughts of exactness. Functional magnetic resonance imaging (fMRI) imaging suggests that TOCD symptoms may arise from involvement of an intermediate neurocircuitry distinct from classic OCD or classic CTD. Small cumulative contributions from multiple genetic loci have been implicated, as have environmental factors such as infection and perinatal trauma. In addition, this review addresses the treatment of TOCD which is especially complex and often treatment resistant and requires pharmacology and behavioral therapy in multiple modalities. Given the distressing impact of TOCD on patients' functioning, the goal of this review is to raise awareness of this distinct entity toward the goal of improving standards of care. [ABSTRACT FROM AUTHOR]

Objectives: To explore the impact of the COVID-19 pandemic on the development of obsessivecompulsive disorder (OCD) symptoms and its correlation with the level of perceived stress among the Saudi population. Methods: In July 2020, a cross-sectional survey of 2909 participants in Saudi Arabia during the outbreak was conducted to collect data related to sociodemographic characteristics and scores on the Brief Obsessive-Compulsive Scale (BOCS) and Perceived Stress Scale (PSS). Results: Most participants were female (73.9%) with a university level of education or higher (81%). The prevalence of new-onset obsessions was 57.8%, compulsions 45.9%, and moderate/high perceived stress 72.4%. New-onset dirt, germs, and virus obsessions were significantly higher among 40-49 age group, employees, housewives, students, quarantine discipliners, and those who spent 20 or more days in quarantine. New-onset hand-washing compulsions were significantly higher among the 30-49 age group. A significantly higher level of perceived stress was reported among those in the 18-29 age group, females, singles, participants with no children, students, nonsmokers, those who were unemployed, living with families, diagnosed with a psychiatric disorder, living in the northern region, quarantine discipliners, and those who spent 60 or more days in quarantine. Conclusion: This study revealed a significantly higher prevalence of high perceived stress in respondents with new-onset OCD contamination symptoms during the COVID-19 pandemic. This implies that a biodisaster is associated with high psychological morbidity. [ABSTRACT FROM AUTHOR]

Background: Although the consequences of the COVID-19 pandemic on emotional health are evident, little is known about its impact on patients with obsessive-compulsive disorder (OCD). Methods: One hundred and twenty-seven patients with OCD who attended a specialist OCD Clinic in Barcelona, Spain, were assessed by phone from April 27 to May 25, 2020, during the early phase of the pandemic, using the Yale-Brown Obsessive-Compulsive Scale (Y-BOCS) and a structured interview that collected clinical and sociodemographic information. Results were compared with those for 237 healthy controls from the same geographic area who completed an online survey. Results: Although 65.3% of the patients with OCD described a worsening of their symptoms, only 31.4% had Y-BOCS scores that increased >25%. The risk of getting infected by SARS-CoV2 was reported as a new obsession by 44.8%, but this only became the main obsessive concern in approximately 10% of the patients. Suicide-related thoughts were more frequent among the OCD cohort than among healthy controls. The presence of prepandemic depression, higher Y-BOCS scores, contamination/washing symptoms, and lower perceived social support all predicted a significantly increased risk of OCD worsening. Conclusions: Most patients with OCD appear to be capable of coping with the emotional stress of the COVID-19 outbreak and its consequences during the initial phase of the pandemic. Nevertheless, the current crisis constitutes a risk factor for a significant worsening of symptoms and suicidal ideation. Action is needed to ensure effective and individualized follow-up care for patients with OCD in the COVID-19 era. [ABSTRACT FROM AUTHOR]

Not a few patients with obsessive-compulsive disorder (OCD) have experienced events that affected the onset. The onset of OCD is not limited to the original meaning of trauma; rather, traumatic experiences such as unexpected exposure to contaminants or various stressful life events often cause the onset of OCD. It would be useful to understand the experiences surrounding the onset, including stressful life events and traumatic experiences, for comprehension of the pathophysiology of OCD. In the present study, we investigated the onset conditions of 281 patients with OCD and compared clinical characteristics among groups with or without stressful life events including traumatic experiences. As a result, 172 (61.2%) participants had experienced various stressful life events, and 98 (34%) participants had had traumatic experiences before the onset. Furthermore, the participants who had had stressful life events showed more contamination/fear symptoms compared with those without such life events. Meanwhile, the patients who had had specific traumatic experiences showed a tendency toward hoarding obsessions. To comprehend the pathophysiology of OCD, it is important to understand the stressful life events that precede its onset. [ABSTRACT FROM AUTHOR]

The relationships between sexual trauma, cognitive appraisals, and subtypes of sexual intrusive thoughts have not been adequately examined in the context of obsessive–compulsive concerns. We employed variations of a moderated mediation model to test these relationships, situating sexual trauma as the predictor, sexual intrusive thoughts as the outcome, cognitive appraisals of these thoughts as the mediator, and subtypes of sexual intrusive thoughts as the moderator of the predictor–mediator link. Based on the continuum perspective, 180 individuals (159 females, 21 males) with or without a history of sexual trauma were recruited to complete measures assessing their most distressing sexual intrusion, cognitive appraisals, and severity of sexual intrusive thoughts. The results indicated that individuals with a history of sexual trauma reported more intrusions with sexual harm content, greater distress with sexual intrusions, more dysfunctional appraisals, and more severe sexual intrusions. The trauma–sexual intrusions link was also separately mediated by responsibility and importance/control appraisals (and when combined), with medium-to-large effect sizes, although this model was not moderated by whether intrusions contained sexual harm content or not. These findings shed light on the posttraumatic effects of sexual violence on sexual intrusions, their appraisals, and level of distress and functional impairment associated with sexual intrusive thoughts, with key clinical and research implications. [ABSTRACT FROM AUTHOR]

Obsessive-compulsive disorder (OCD) has a worldwide prevalence of 2%–3%. Characterized by the presence of either one or two core symptoms—obsessions and compulsions—it generally runs a chronic course and may cause serious functional impairment. Though previously thought to be of psychogenic origin, the pathophysiology of OCD is now understood to be more complex. A multitude of environmental factors have been shown to contribute to the development of OCD, including infection, neonatal complications, childhood trauma, occurrence of stressful events, and brain injury. It has also been proposed that genetic vulnerability may play a role in OCD pathology, although candidate genes have yet to be identified. Likewise, although it is widely accepted that stress plays a role in OCD pathophysiology, the mechanisms remain unclear. Observations from the clinics indicate that stress may serve as both a triggering and aggravating factor, meaning it can prompt symptoms to appear while also contributing to their exacerbation. Additionally, dysfunction of the hypothalamic-pituitary-adrenal axis and impaired stress response have been identified in OCD patients. In this review, we analyze the role of stress in the pathophysiology of OCD, complemented by relevant findings from recent animal studies. [ABSTRACT FROM AUTHOR]

Copyright of Anatolian Journal of Psychiatry / Anadolu Psikiyatri Dergisi is the property of Anatolian Journal of Psychiatry and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Rationale: Obsessive-compulsive disorder (OCD) is characterized by repetitive behaviors exacerbated by stress. Many OCD patients do not respond to available pharmacotherapies, but neurosurgical ablation of the anterior cingulate cortex (ACC) can provide symptomatic relief. Although the ACC receives noradrenergic innervation and expresses adrenergic receptors (ARs), the involvement of norepinephrine (NE) in OCD has not been investigated. Objective: To determine the effects of genetic or pharmacological disruption of NE neurotransmission on marble burying (MB) and nestlet shredding (NS), two animal models of OCD. Methods: We assessed NE-deficient (Dbh −/−) mice and NE-competent (Dbh +/−) controls in MB and NS tasks. We also measured the effects of anti-adrenergic drugs on NS and MB in control mice and the effects of pharmacological restoration of central NE in Dbh −/− mice. Finally, we compared c-fos induction in the locus coeruleus (LC) and ACC of Dbh −/− and control mice following both tasks. Results: Dbh −/− mice virtually lacked MB and NS behaviors seen in control mice but did not differ in the elevated zero maze (EZM) model of general anxiety-like behavior. Pharmacological restoration of central NE synthesis in Dbh −/− mice completely rescued NS behavior, while NS and MB were suppressed in control mice by anti-adrenergic drugs. Expression of c-fos in the ACC was attenuated in Dbh −/− mice after MB and NS. Conclusion: These findings support a role for NE transmission to the ACC in the expression of stress-induced compulsive behaviors and suggest further evaluation of anti-adrenergic drugs for OCD is warranted. [ABSTRACT FROM AUTHOR]

Objective: Cognitive models of Obsessive-Compulsive Disorder (OCD) identified four types of beliefs, which would develop during childhood and play a role in the aetiology and maintenance of OCD: Inflated Responsibility, Threat Overestimation, Importance/Control of Thoughts, Perfectionism/Intolerance of Uncertainty. Whereas research produced consistent evidence in adults that these beliefs constitute vulnerability factors for OCD, no study examined whether the obsessive beliefs prospectively predict OCD symptoms over time in youth. The current study investigated the role of the obsessive beliefs as predictors of OCD symptoms after one year in a large cohort sample of community children and early adolescents prospectively followed-up. Method: Seven hundred and fifty-four children and early adolescents recruited from the community (mean age= 10.87 years, 51.46% females) completed the Obsessive Belief Questionnaire-Child Version (OBQ-CV) as a measure of obsessive beliefs, the Obsessive-Compulsive Inventory-Child Version (OCI-CV) as a measure of OCD symptoms, the Children's Depression Inventory for depression (CDI) at baseline (t0) and at one-year follow-up (t1). A multiple linear regression analysis was run entering the scores on the OBQ-CV and the CDI as predictors and the scores on the OCI-CV at t1 as dimensional outcome. Results: More intense Perfectionism/Intolerance of Uncertainty at t0 (ß= 0.17, t= 4.33, p<0.001) and to a lesser extent more intense Threat Overestimation at t0 (ß= 0.08, t= 1.97, p<0.05) predicted more severe OCD symptoms at t1 controlling for the effects of depression at t0 (ß= 0.19, t= 5.53, p<0.001). Evidence of the predictive effects of the other cognitions at t0 on OCD symptoms at t1 was not found. Conclusions: Perfectionism/Intolerance for Uncertainty and to a lesser Threat Overestimation may be early predictors of OCD symptoms in youth. Early detection and prevention of OCD in children and adolescents could focus on these cognitive vulnerability factors. The current findings appear to raise some doubts about the role of Inflated Responsibility and Importance/Control of Thoughts as cognitive vulnerability factors specific to OCD among youth. Future studies should use clinical interviews to assess the presence of an OCD diagnosis. [ABSTRACT FROM AUTHOR]

Background/Aims: Recent findings suggest an involvement of insulin-like growth factor-1 (IGF-1) in the pathogenesis of many psychiatric disorders; however, there is a lack of data regarding IGF-1 in patients with obsessive-compulsive disorder (OCD). The aims of the present study were (1) to analyze putative alterations of IGF-1 serum content in patients with OCD compared to patients with major depressive disorder (MDD) and healthy controls, and (2) to analyze putative changes of IGF-1 levels during drug treatment in subjects with OCD compared to patients with MDD. Methods: We recruited 40 OCD patients, 37 MDD patients, and 43 healthy controls. All participants were adults. Serum IGF-1 levels were measured by the ELISA method on venous blood samples collected at baseline and after 10 ± 1 weeks of drug treatment. Results: IGF-1 levels were increased in OCD patients compared to controls (149.9 ± 60.2 vs. 121.2 ± 51.6 ng/ ml; p = 0.040). No correlations were observed between base-line IGF-1 levels, clinical features, and response to treatment at follow-up in OCD or MDD patients. No changes in serum IGF-1 were observed after drug treatment. Conclusion: Our results show for the first time that serum IGF-1 levels are altered in patients with OCD. Further research on the role of IGF-1 in OCD is warranted. [ABSTRACT FROM AUTHOR]

ObjectivesThere is growing evidence supporting a role for stressful life events (SLEs) at obsessive–compulsive disorder (OCD) onset, but neurobiological correlates of such effect are not known. We evaluated regional grey matter (GM) changes associated with the presence/absence of SLEs at OCD onset.MethodsOne hundred and twenty-four OCD patients and 112 healthy controls were recruited. Patients were split into two groups according to the presence (n = 56) or absence (n = 68) of SLEs at disorder’s onset. A structural magnetic resonance image was acquired for each participant and pre-processed with Statistical Parametric Mapping software (SPM8) to obtain a volume-modulated GM map. Between-group differences in sociodemographic, clinical and whole-brain regional GM volumes were assessed.ResultsSLEs were associated with female sex, later age at disorder’s onset, more contamination/cleaning and less hoarding symptoms. In comparison with controls, patients without SLEs showed GM volume increases in bilateral dorsal putamen and the central tegmental tract of the brainstem. By contrast, patients with SLEs showed specific GM volume increases in the right anterior cerebellum.ConclusionsOur findings support the idea that neuroanatomical alterations of OCD patients partially depend on the presence of SLEs at disorder’s onset. [ABSTRACT FROM PUBLISHER]

Anticompulsive activity of a novel compound GIZh-72 (4,6-dimethyl-2-(4-chlorphenyl)-2,3-dihydro-1H-pyrazolo[4,3-C]Pyridine-3-on, chloral hydrate) in a dose of 20 mg/kg (single, subchronic, and chronic administration) in comparison with fluvoxamine (25 mg/kg) was studied in the marble burying test in the model of unpredictable chronic mild stress on BALB/c mice. GIZh-72 produced an anticompulsive effect that increased with increasing treatment duration under stress conditions in contrast to fluvoxamine that induced inversion of this effect after long-term administration. Neuroleptic activity of GIZh-72 in doses of 20 and 40 mg/kg was studied on the model of apomorphine-induced climbing in C57Bl/6 mice. In contrast to haloperidol (0.5 mg/kg), GIZh-72 exhibited no neuroleptic properties. Our results indicate that GIZh-72 holds much promise for pharmacotherapy of obsessive-compulsive disorder. [ABSTRACT FROM AUTHOR]

The gut microbiome has become a topic of major interest as of late, with a new focus specifically on psychiatric disorders. Recent studies have revealed that variations in the composition of the gut microbiota may influence anxiety and mood and vice versa. Keeping the concept of this bidirectional "microbiota-gut-brain" axis in mind, this review aims to shed light on how these findings may also be implicated in obsessive-compulsive disorder (OCD); potentially outlining a novel etiological pathway of interest for future research in the field. [ABSTRACT FROM AUTHOR]

Copyright of Revista de la Asociación Española de Neuropsiquiatría is the property of Asociacion Espanola de Neuropsiquiatria and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Individuals with obsessive-compulsive disorder often identify psychosocial stress as a factor that exacerbates their symptoms, and many trace the onset of symptoms to a stressful period of life or a discrete traumatic incident. However, the pathophysiological relationship between stress and obsessive-compulsive disorder remains poorly characterized: it is unclear whether trauma or stress is an independent cause of obsessive-compulsive disorder symptoms, a triggering factor that interacts with a preexisting diathesis, or simply a nonspecific factor that can exacerbate obsessive-compulsive disorder along with other aspects of psychiatric symptomatology. Nonetheless, preclinical research has demonstrated that stress has conspicuous effects on corticostriatal and limbic circuitry. Specifically, stress can lead to neuronal atrophy in frontal cortices (particularly the medial prefrontal cortex), the dorsomedial striatum (caudate), and the hippocampus. Stress can also result in neuronal hypertrophy in the dorsolateral striatum (putamen) and amygdala. These neurobiological effects mirror reported neural abnormalities in obsessive-compulsive disorder and may contribute to an imbalance between goal-directed and habitual behavior, an imbalance that is implicated in the pathogenesis and expression of obsessive-compulsive disorder symptomatology. The modulation of corticostriatal and limbic circuits by stress and the resultant imbalance between habit and goal-directed learning and behavior offers a framework for investigating how stress may exacerbate or trigger obsessive-compulsive disorder symptomatology. [ABSTRACT FROM AUTHOR]