They are repetitive, unpleasant and distressing to the patient. Patient is aware that these originate from their own mind. Obsessions (unwanted ideas, images or impulses that repeatedly enter a person's mind) and compulsions (repetitive stereotyped behaviours or mental acts driven by rules that must be applied rigidly) share the following features: However, other small studies suggest that OCD in this population responds as well to standard treatments, and effectiveness of prophylactic antibiotics has been inconsistent.īox 1 International Classification of Diseases-10 diagnostic criteria for obsessive-compulsive disorderĮither obsessions or compulsions or both present on most days for a period of 2 weeks. The exact mechanism of sudden onset neuropsychiatric disorder is unknown, but there has been interest in delivering therapies that target immune and infectious causes. 20 These children tend to have more widespread neuropsychiatric difficulties than other children with OCD, including enuresis, deterioration in handwriting and impulsivity. This group of children was originally given the acronym PANDAS (paediatric autoimmune neuropsychiatric disorders associated with streptococcus), 19 but more recently the term PANS (paediatric acute-onset neuropsychiatric syndrome) has been used in preference, as it is felt to capture both the sudden onset and the uncertainty about aetiology. There has been emerging clinical evidence over the past 10–15 years of a subgroup of children who experience sudden onset OCD and/or tics after streptococcal infection. 17 In contrast, a recent retrospective study found no evidence for an association between adverse childhood experiences and OCD, although such experiences were related to certain comorbidities, including depression. For example, one longitudinal study found that social isolation, physical abuse and negative emotionality were specific predictors of an adult OCD diagnosis. Few prospective studies have been conducted, and results have been inconsistent. While genetic factors clearly influence the expression of OCD, environmental factors also play a significant role, but remarkably little is known about these effects. 16 Importantly, treatment studies have demonstrated reduced activation in the orbitofrontal cortex following cognitive behaviour therapy (CBT) for OCD, 15 demonstrating some degree of plasticity. 15 Interestingly, orbitofrontal brain dysfunction has also been found in unaffected relatives of patients with OCD, who are at genetic risk of OCD. There is robust evidence from functional neuroimaging studies of increased activation in the lateral and medial orbitofrontal cortex in both children and adults with OCD. Hyperactivation of the orbitofrontal cortex has been proposed to mediate persistent thoughts about threat and harm (ie, obsessions), which in turn lead to attempts to neutralise the perceived threat (ie, compulsions). Neuropsychological models of OCD propose that OCD arises from alterations to frontostriatal circuitry. In particular, genes within the serotonergic, dopaminergic and glutamatergic system appear to influence OCD. The results of genome-wide association studies 12, 13 and meta-analyses of candidate gene studies 14 suggest that the genetic influence on OCD is polygenic, with many genes involved which individually exert a relatively small effect on the phenotype. 11 Interestingly, the heritability of OCD appears to be greater in paediatric compared with adult cohorts, 10 supporting the notion of early-onset OCD as a putative developmental subtype of the disorder. 9 Twin studies have shown that genetic factors explain 45%–65% of the variance of OCD in children, 10 pointing to a higher heritability in OCD relative to most other anxiety disorders and depression in youth. Data from twin, family and segregation studies strongly support a genetic component. The aetiology of paediatric OCD remains relatively poorly understood, despite considerable research to date.
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