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Objective: Although attention-deficit/hyperactivity disorder (ADHD) is frequently comorbid with Tourette's disorder (TD), it is unclear whether they have a common genetic etiology. Familial relationships between DSM-IV ADHD and TD are studied in TD+ADHD, TD-only (TD-ADHD), ADHD-only (ADHD-TD), and control groups.Method: Case-control, direct-interview family study of 692 relatives of 75 TD+ADHD, 74 TD-only, 41 ADHD-only, and 49 control probands collected between 1999 and 2004. Age-corrected prevalence rates, odds ratios, and predictors of TD, ADHD, and OCD among relatives are estimated from blinded best-estimate diagnoses using survival Kaplan-Meier and generalized estimating equation regression analyses.Results: In relatives of the TD-only group, although ADHD exceeded control rates (p=.03), ADHD-TD (p=.51) rates were not increased. In the ADHD-only group, TD was increased (p=.004) but TD-ADHD rates were not increased (p=.18). Comorbid ADHD+TD diagnoses in relatives were elevated in all case groups (pConclusions: TD and ADHD are not alternate phenotypes of a single underlying genetic cause. There is an increased risk of comorbid ADHD and TD in affected families, possibly reflecting some overlapping neurobiology or pathophysiology. [ABSTRACT FROM AUTHOR]

Childhood adversity is associated with the development or expression of many neuropsychiatric disorders, including those with strong genetic underpinnings. Despite reported associations between perceived stress and tic severity, the relationship between potentially traumatic events in childhood and Tourette Syndrome (TS), a highly heritable neuropsychiatric disorder, is unknown. This study aimed to assess whether exposure to eight categories of adverse childhood experiences (ACEs) is associated with TS severity and impairment, and whether TS genetic risk modifies this association. Online survey data were collected from 351 adult males with TS who previously participated in genetic studies. Participants completed the ACE questionnaire and a lifetime version of the Yale Global Tic Severity Scale (YGTSS). Demographic and relevant health data were assessed; polygenic risk scores (PRS) measuring aggregated TS genetic risk were derived using genome-wide association data. Univariable and multivariable linear regressions examined the relationships between childhood adversity and retrospectively recalled worst-ever tic severity and impairment, adjusting for covariates. Potential gene-by-environment (GxE) interactions between ACE and PRS were estimated. After covariate adjustment, there was a significant graded dose-response relationship between ACE Scores and increases in lifetime worst-ever tic severity and impairment. There was some evidence that TS genetic risk moderated the relationship between ACE Score and tic impairment, but not tic severity, particularly for individuals with higher TS polygenic risk. We provide evidence that childhood adversity is associated with higher lifetime TS severity and impairment, although future longitudinal studies with genetically-sensitive designs are needed to determine whether these relationships are causal and/or directional. • Tourette syndrome has genetic and environmental influences on severity/impairment. • Adverse childhood experiences associated with higher tic severity and impairment. • Complex gene-by-environment relationship between TS genetic risk and adversity. [ABSTRACT FROM AUTHOR]

Objective: Obsessive-compulsive disorder (OCD) and Tourette syndrome (TS) are heritable neurodevelopmental disorders with a partially shared genetic etiology. This study represents the first genome-wide investigation of large (>500 kb), rare (<1%) copy number variants (CNVs) in OCD and the largest genome-wide CNV analysis in TS to date. Method: The primary analyses used a cross-disorder design for 2,699 case patients (1,613 ascertained for OCD, 1,086 ascertained for TS) and 1,789 controls. Parental data facilitated a de novo analysis in 348 OCD trios. Results: Although no global CNV burden was detected in the cross-disorder analysis or in secondary, disease-specific analyses, there was a 3.3-fold increased burden of large deletions previously associated with other neurodevelopmental disorders (p = .09). Half of these neurodevelopmental deletions were located in a single locus, 16p13.11 (5 case patient deletions: 0 control deletions, p = .08 in the current study, p = .025 compared to published controls). Three 16p13.11 deletions were confirmed de novo, providing further support for the etiological significance of this region. The overall OCD de novo rate was 1.4%, which is intermediate between published rates in controls (0.7%) and in individuals with autism or schizophrenia (2-4%). Conclusion: Several converging lines of evidence implicate 16p13.11 deletions in OCD, with weaker evidence for a role in TS. The trend toward increased overall neurodevelopmental CNV burden in TS and OCD suggests that deletions previously associated with other neurodevelopmental disorders may also contribute to these phenotypes. [ABSTRACT FROM AUTHOR]

The article presents a study focusing on the validity of the four-factor model of obsessive-compulsive disorder (OCD) symptom structure in children, adolescents and adult groups. It states that OCD is characterized by the presence of repetitive thoughts, images, impulses, behaviors, or mental acts that are performed to relieve anxiety or distress. It cites that the study has significant clinical and research implications and have several limitations that must be recognized which include the reliance on the symptom checklists of the Y-BOCS and CYBOCS and the categories that was used.

Objective: Tourette's disorder (TD) and autism spectrum disorder (ASD) share clinical features and possibly an overlapping etiology. The aims of this study were to examine ASD symptom rates in participants with TD, and to characterize the relationships between ASD symptom patterns and TD, obsessive-compulsive disorder (OCD), and attention-deficit/hyperactivity disorder (ADHD).Method: Participants with TD (n = 535) and their family members (n =234) recruited for genetic studies reported TD, OCD, and ADHD symptoms and completed the Social Responsiveness Scale Second Edition (SRS), which was used to characterize ASD symptoms.Results: SRS scores in participants with TD were similar to those observed in other clinical samples but lower than in ASD samples (mean SRS total raw score = 51; SD = 32.4). More children with TD met cut-off criteria for ASD (22.8%) than adults with TD (8.7%). The elevated rate in children was primarily due to high scores on the SRS Repetitive and Restricted Behaviors (RRB) subscale. Total SRS scores were correlated with TD (r = 0.27), OCD (r = 0.37), and ADHD (r = 0.44) and were higher among individuals with OCD symptom-based phenotypes than for those with tics alone.Conclusion: Higher observed rates of ASD among children affected by TD may in part be due to difficulty in discriminating complex tics and OCD symptoms from ASD symptoms. Careful examination of ASD-specific symptom patterns (social communication vs. repetitive behaviors) is essential. Independent of ASD, the SRS may be a useful tool for identifying patients with TD with impairments in social communication that potentially place them at risk for bullying and other negative sequelae. [ABSTRACT FROM AUTHOR]