Evidence suggests that a hyperactive frontal-striatal-thalamic-frontal circuit is associated with the symptoms of obsessive-compulsive disorder (OCD), but there is little agreement about the function of the exaggerated activity. We report electrophysiological evidence suggesting that part of this system monitors events and generates error signals when the events conflict with an individual's internal standards or goals. Nine individuals with OCD and 9 age-, sex-, and education-matched control participants performed a speeded reaction time task. The error-related negativity, an event-related brain potential component that reflects action-monitoring processes, was enhanced in the individuals with OCD. The magnitude of this enhancement correlated with symptom severity. Dipole modeling suggested that the locus of the enhancement corresponded to medial frontal regions, possibly the anterior cingulate cortex.
Background Patients with diabetes and depression often have self-management needs that require between-visit support. This study evaluated the impact of telephone-delivered cognitive behavioral therapy (CBT) targeting patients’ management of depressive symptoms, physical activity levels, and diabetes-related outcomes. Methods 291 patients with type 2 diabetes and significant depressive symptoms (Beck Depression Inventory scores ≥14)were recruited from a community-university-and VA healthcare system. A manualized telephone CBT program was delivered by nurses weekly for 12weeks, followed by nine monthly booster sessions. Sessions initially focused exclusively on patients’ depression management and then added a pedometer-based walking program. The primary outcome was hemoglobin A1cmeasured at 12-months. Blood pressure was a secondary outcome; levels of physical activity were determined by pedometer readings; depression, coping, and health related quality of life (HRQL) were measured using standardized scales. Results Baseline A1c levels were relatively good and there was no difference in A1c at follow-up. Intervention patients experienced a4.26 mmHg decrease in systolic blood pressure relative to controls (p=.05). Intervention patients had significantly greater increases in step-counts (mean difference 1,131 steps/day; p=.0002) and greater reductions in depressive symptoms (58%remitted at12 months versus 39%; p=.002). Intervention patients also experienced relative improvements in coping and HRQL. Conclusions This program of telephone delivered CBT combined with a pedometer-based walking program did not improve A1c values but significantly decreased patients’ blood pressure, increased physical activity, and decreased depressive symptoms. The intervention also improved patients’ functioning and quality of life.
The central aim of this study is to estimate prevalence, ages of onset, severity, and associated disability of anxiety disorders among African Americans, Caribbean Blacks, and non-Hispanic whites in the U.S. Results indicated that whites were at elevated risk for generalized anxiety disorder, panic disorder, and social anxiety compared to Caribbean Blacks and African Americans. Black respondents were more likely to meet criteria for PTSD. When African American and Caribbean Black respondents met criteria for an anxiety disorder, they experienced higher levels of overall mental illness severity and functional impairment compared to whites. White respondents were at greater risk to develop generalized anxiety, social anxiety, and panic disorders late in life. Risk of developing PTSD endured throughout the life course for blacks whereas whites rarely developed PTSD after young adulthood. These results can be used to inform targeted interventions to prevent or remediate anxiety disorders among these diverse groups.
The 3' region of SLC1A1 may contain a susceptibility allele for early-onset OCD, with differential effects in males and females. The results also provide further support for the involvement of a glutamatergic dysfunction in the pathogenesis of early-onset OCD.
The goal of this study was to identify chromosomal regions likely to contain susceptibility alleles for early-onset obsessive-compulsive disorder (OCD). A genome scan was done in 56 individuals from seven families ascertained through pediatric OCD probands; 27 of the 56 subjects had a lifetime diagnosis of definite OCD. Denser mapping of regions on chromosomes 2, 9, and 16 was subsequently done with those subjects and ten additional subjects from the largest family in the study. Direct interviews were completed with 65 of the 66 genotyped individuals. Relatives were interviewed blind to proband status. Of the 65 interviewed individuals, 32 had a lifetime diagnosis of definite OCD. Three of the seven probands had a history of Tourette disorder. Two of the 25 relatives with OCD had a tic history, whereas none of the 33 relatives without OCD had tics. The genome scan consisted of 349 microsatellite markers with an average between-marker distance of 11.3 centiMorgan (cM). Fine mapping was done with 24 additional markers at an average spacing of 1.6 cM. Parametric and nonparametric linkage analyses were conducted using GENEHUNTER(+). The maximum multipoint LOD score with a dominant model was 2.25 on 9p. However, with fine mapping and additional subjects, that LOD score decreased to 1.97. The maximum multipoint nonparametric LOD* score was 1.73 on 19q. The maximum multipoint LOD score with a recessive model was 1.40 on 6p. The results provide suggestive evidence for linkage on 9p and identify regions requiring further study with much larger samples.
Making an error elicits activity from brain regions that monitor performance, especially the medial frontal cortex (MFC). However, uncertainty exists about whether the posterior or anterior/rostral MFC processes errors and to what degree affective responses to errors are mediated in the MFC, specifically the rostral anterior cingulate cortex (rACC). To test the hypothesis that rACC mediates a type of affective response, we conceptualized affect in response to an error as a reaction to loss and amplified this response with a monetary penalty. While subjects performed a cognitive interference task during functional magnetic resonance imaging, hemodynamic activity in the rACC was significantly greater when subjects lost money as a result of an error compared with errors that did not lead to monetary loss. A significant interaction between the incentive conditions and error events demonstrated that the effect was not merely attributable to working harder to win (or not lose) money, although an effect of motivation was noted in the mid-MFC. Activation foci also occurred in similar regions of the posterior MFC for error and interference processing, which were not modulated by the incentive conditions. However, at the level of the individual subject, substantial functional variability occurred along the MFC during error processing, including foci in the rostral/anterior extent of the MFC not appearing in the group analysis. The findings support the hypothesis that the rostral extent of the MFC (rACC) processes loss-related responses to errors, and individual differences may account for some of the reported variation of error-related foci in the MFC.
Obsessive-compulsive disorder (OCD) is a heterogeneous disorder of unknown etiology. We examined the lifetime history of obsessions, compulsions, and OCD in the first- and second-degree relatives of 35 pediatric probands with OCD and 17 controls with no psychiatric diagnosis. All available first-degree relatives were directly interviewed blind to proband status with two semi-structured interviews. Parents were also interviewed to systematically assess the family psychiatric history of first- and second-degree relatives. Best-estimate lifetime diagnoses were made using all available sources of information. Data were analyzed with logistic regression by the generalized estimating equation method and with robust Cox regression models. The lifetime prevalence of definite OCD was significantly higher in case than control first-degree relatives (22.5% vs. 2.6%, P < 0.05). Compared to controls, case first-degree relatives also had significantly higher lifetime rates of obsessions and compulsions (both P < 0.05). There was no significant difference between case and control second-degree relatives in lifetime rates of OCD. First-degree relatives of case probands with ordering compulsions had a significantly higher lifetime rate of definite and subthreshold OCD than relatives of case probands without ordering compulsions (45.4% vs. 18.8%, P < 0.05). The lifetime prevalence of definite OCD was significantly higher in case first-degree relatives with a history of tics than in case first-degree relatives without a tic history (57.1% vs. 20.9%, P < 0.01). The results provide further evidence that early-onset OCD is highly familial and suggest that two clinical variables are associated with its familial aggregation.
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