The aim of this naturalistic survey was to measure the prevalence of metabolic syndrome by collating data on routine physical investigation in an acute psychiatric inpatient population. The size of this study is small, but the results offer some interesting and useful preliminary findings, pertinent to the provision of good physical health care to psychiatric inpatients and from which further research could develop.Metabolic syndrome was found in more than a third (38%) of the population studied and was equally prevalent across a variety of psychiatric disorders. A higher trend was found in females than in males, but this figure did not reach statistical significance. Although small, the naturalistic setting of this survey demonstrates the ease with which metabolic syndrome can be opportunely excluded or identified in this vulnerable population, where physical healthcare is often problematic. With the increasing involvement of non-medically qualified practitioners in psychiatric care, simple techniques such as this hold a valuable place in holistic patient management.
Background Schizophrenia endophenotypes may help elucidate functional effects of genetic risk variants in multiply affected consanguineous families that segregate recessive risk alleles of large effect size. We studied the association between a schizophrenia risk locus involving a 6.1Mb homozygous region on chromosome 13q22–31 in a consanguineous multiplex family and cognitive functioning, haemodynamic response and white matter integrity using neuroimaging. Methods We performed CANTAB neuropsychological testing on four affected family members (all homozygous for the risk locus), ten unaffected family members (seven homozygous and three heterozygous) and ten healthy volunteers, and tested neuronal responses on fMRI during an n-back working memory task, and white matter integrity on diffusion tensor imaging (DTI) on four affected and six unaffected family members (four homozygous and two heterozygous) and three healthy volunteers. For cognitive comparisons we used a linear mixed model (Kruskal–Wallis) test, followed by posthoc Dunn's pairwise tests with a Bonferroni adjustment. For fMRI analysis, we counted voxels exceeding the p < 0.05 corrected threshold. DTI analysis was observational. Results Family members with schizophrenia and unaffected family members homozygous for the risk haplotype showed attention (p < 0.01) and working memory deficits (p < 0.01) compared with healthy controls; a neural activation laterality bias towards the right prefrontal cortex (voxels reaching p < 0.05, corrected) and observed lower fractional anisotropy in the anterior cingulate cortex and left dorsolateral prefrontal cortex. Conclusions In this family, homozygosity at the 13q risk locus was associated with impaired cognition, white matter integrity, and altered laterality of neural activation.
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