Objective Family accommodation refers to ways in which family members assist the proband in the performance of rituals, avoidance of anxiety provoking situations, or modification of daily routines to assist a relative with obsessive-compulsive disorder. The purpose of this review was to analyze and integrate the available data on the role of family accommodation in pediatric obsessive compulsive disorder including its prevalence and its relationship the course of the disorder. Method A search of available peer reviewed English language papers was conducted through PubMed and PsycINFO cross-referencing the keyword OCD, with accommodation, family relations, and parents. Resulting papers were individually evaluated for relevance to the scope of the review. Results Accommodation is common in pediatric OCD and is strongly associated with symptom severity. Levels of accommodation have been also associated with treatment outcomes for both cognitive behavioral and pharmacological treatment. Significant improvement with treatment in OCD is often associated with reductions in family accommodation.. Conclusion Family accommodation represents important clinical data that is worth measuring, monitoring and tracking in clinical care. Therapies targeting family accommodation may be successful in improving treatment outcomes in pediatric OCD.

Even though the symptoms of HD are fairly well characterized, their progression, especially in the early and middle stages, remains uncertain. Clarification of the disease progression is vital to improved understanding of the pathogenesis of HD and to the evaluation of therapeutic agents that are designed to slow the progression of disease. The results of this study assist in clarifying HD progression from early involuntary movements and emotional changes to more overt motor symptoms and difficulty with activities of daily living.

Heritability, the proportion of phenotypic variance explained by genetic factors, can be estimated from pedigree data 1 , but such estimates are uninformative with respect to the underlying genetic architecture. Analyses of data from genome-wide association studies (GWAS) on unrelated individuals have shown that for human traits and disease, approximately one-third to two-thirds of heritability is captured by common SNPs 2-5 . It is not known whether the remaining heritability is due to the imperfect tagging of causal variants by common SNPs, in particular if the causal variants are rare, or other reasons such as overestimation of heritability from pedigree data. Here we show that pedigree heritability for height and body mass index (BMI) appears to be fully recovered from whole-genome sequence (WGS) data on 21,620 unrelated individuals of European ancestry. We assigned 47.1 million genetic variants to groups based upon their minor allele frequencies (MAF) and linkage disequilibrium (LD) with variants nearby, and estimated and partitioned variation accordingly. The estimated heritability was 0.79 (SE 0.09) for height and 0.40 (SE 0.09) for BMI, consistent with pedigree estimates. Low-MAF variants in low LD with neighbouring variants were enriched for heritability, to a greater extent for protein altering variants, consistent with negative selection thereon. Cumulatively variants in the MAF range of 0.0001 to 0.1 explained 0.54 (SE 0.05) and 0.51 (SE 0.11) of heritability for height and BMI, respectively. Our results imply that the still missing heritability of complex traits and disease is accounted for by rare variants, in particular those in regions of low LD.