A Comparison of Schemas, Schema Modes and Childhood Traumas in Obsessive-Compulsive Disorder, Chronic Pain Disorder and Eating Disorders

BACKGROUND In this study, we investigated early maladaptive schemas (EMS), schema modes and childhood traumas in patients suffering from obsessive-compulsive disorder (OCD) in contrast to patients with other Axis I disorders. Based on cognitive theories on OCD, our main research question was whether schemas belonging to the domain of 'impaired autonomy and performance' are more prevalent in OCD than in both eating disorders (ED) and chronic pain disorder (CPD). SAMPLING AND METHODS EMS, schema modes and traumatic childhood experiences were measured in 60 patients with OCD, 41 with ED, 40 with CPD and 142 healthy controls. To analyze differences between the groups, MANCOVAs were conducted followed by deviation contrasts. Depression level, age and gender were considered as possible covariates. RESULTS OCD patients scored higher on 4 EMS, 2 of which belong to the domain 'impaired autonomy and performance'. ED patients had higher scores in the EMS 'emotional inhibition' and CPD patients on the Childhood Trauma Questionnaire subscale 'physical neglect'. CONCLUSIONS These results suggest that there might be typical schema patterns associated with OCD and ED. We can also conclude that a higher prevalence of traumatic experiences does not necessarily coincide with more EMS and schema modes

Do Children and Adolescents with Anorexia Nervosa Display an Inefficient Cognitive Processing Style?

Objective: This study aimed to examine neuropsychological processing in children and adolescents with Anorexia Nervosa (AN). The relationship of clinical and demographic variables to neuropsychological functioning within the AN group was also explored.  Method: The performance of 41 children and adolescents with a diagnosis of AN were compared to 43 healthy control (HC) participants on a number of neuropsychological measures.  Results: There were no differences in IQ between AN and HC groups. However, children and adolescents with AN displayed significantly more perseverative errors on the Wisconsin Card Sorting Test, and lower Style and Central Coherence scores on the Rey Osterrieth Complex Figure Test relative to HCs.  Conclusion: Inefficient cognitive processing in the AN group was independent of clinical and demographic variables, suggesting it might represent an underlying trait for AN. The implications of these findings are discussed

Brain activation during cognitive planning in twins discordant or concordant for obsessive–compulsive symptoms

Neuroimaging studies have indicated abnormalities in cortico-striatal-thalamo-cortical circuits in patients with obsessive–compulsive disorder compared with controls. However, there are inconsistencies between studies regarding the exact set of brain structures involved and the direction of anatomical and functional changes. These inconsistencies may reflect the differential impact of environmental and genetic risk factors for obsessive–compulsive disorder on different parts of the brain. To distinguish between functional brain changes underlying environmentally and genetically mediated obsessive–compulsive disorder, we compared task performance and brain activation during a Tower of London planning paradigm in monozygotic twins discordant (n = 38) or concordant (n = 100) for obsessive–compulsive symptoms. Twins who score high on obsessive–compulsive symptoms can be considered at high risk for obsessive–compulsive disorder. We found that subjects at high risk for obsessive–compulsive disorder did not differ from the low-risk subjects behaviourally, but we obtained evidence that the high-risk subjects differed from the low-risk subjects in the patterns of brain activation accompanying task execution. These regions can be separated into those that were affected by mainly environmental risk (dorsolateral prefrontal cortex and lingual cortex), genetic risk (frontopolar cortex, inferior frontal cortex, globus pallidus and caudate nucleus) and regions affected by both environmental and genetic risk factors (cingulate cortex, premotor cortex and parts of the parietal cortex). Our results suggest that neurobiological changes related to obsessive–compulsive symptoms induced by environmental factors involve primarily the dorsolateral prefrontal cortex, whereas neurobiological changes induced by genetic factors involve orbitofrontal–basal ganglia structures. Regions showing similar changes in high-risk twins from discordant and concordant pairs may be part of compensatory networks that keep planning performance intact, in spite of cortico-striatal-thalamo-cortical deficits

Are obsessive–compulsive symptoms impulsive, compulsive or both?

This is the author accepted manuscript. The final version is available from Elsevier via http://dx.doi.org/10.1016/j.comppsych.2016.04.010Background:\ud \ud The relationships between obsessive?compulsive symptoms and distinct forms of impulsivity and compulsivity are unclear. Such examination would be relevant in terms of how best to classify psychiatric disorders and in understanding candidate ?traits? that extend across a continuum between normalcy and clinical disorders.\ud \ud Method:\ud \ud 515 young adults (aged 18?29 years) completed the Padua Inventory and undertook detailed clinical and neurocognitive assessments. Relationships between obsessive?compulsive symptoms and distinct types of impulsivity and compulsivity were evaluated using linear regression modeling.\ud \ud Results:\ud \ud Obsessive?Compulsive symptoms were significantly predicted by female gender, lower quality of life, psychiatric disorders in general (but not impulse control disorders), and worse extra-dimensional set-shifting. Obsessive?Compulsive symptoms were not significantly predicted by alcohol/nicotine consumption, stop-signal reaction times, or decision-making abilities.\ud \ud Conclusion:\ud \ud These data indicate that obsessive?compulsive symptoms are more related to certain forms of compulsivity than to impulsivity. These findings have important implications for diagnostic conceptualizations and neurobiological models.This research was supported by a grant from the National Center for Responsible Gaming to Dr. Grant. Dr. Chamberlain?s involvement in this work was funded by a grant from the Academy of Medical Sciences, UK. Dr. Grant has received research grants from NIMH, National Center for Responsible Gaming, and Forest and Roche Pharmaceuticals Dr. Grant receives yearly compensation from Springer Publishing for acting as Editor-in-Chief of the Journal of Gambling Studies and has received royalties from Oxford University Press, American Psychiatric Publishing, Inc., Norton Press, and McGraw Hill. Dr. Chamberlain consults for Cambridge Cognition. The other authors have no disclosures

Projection-specific deficits in synaptic transmission in adult Sapap3-knockout mice

Obsessive-compulsive disorder (OCD) is a circuit disorder involving corticostriatal projections, which play a role in motor control. The Sapap3-knockout (KO) mouse is a mouse model to study OCD and recapitulates OCD-like compulsion through excessive grooming behavior, with skin lesions appearing at advanced age. Deficits in corticostriatal control provide a link to the pathophysiology of OCD. However, there remain significant gaps in the characterization of the Sapap3-KO mouse, with respect to age, specificity of synaptic dysfunction, and locomotor phenotype. We therefore investigated the corticostriatal synaptic phenotype of Sapap3-KO mice using patch-clamp slice electrophysiology, in adult mice and with projection specificity. We also analyzed grooming across age and locomotor phenotype with a novel, unsupervised machine learning technique (MoSeq). Increased grooming in Sapap3-KO mice without skin lesions was age independent. Synaptic deficits persisted in adulthood and involved the projections from the motor cortices and cingulate cortex to the dorsolateral and dorsomedial striatum. Decreased synaptic strength was evident at the input from the primary motor cortex by reduction in AMPA receptor function. Hypolocomotion, i.e., slowness of movement, was consistently observed in Sapap3-KO mice. Our findings emphasize the utility of young adult Sapap3-KO mice to investigate corticostriatal synaptic dysfunction in motor control