Is psychiatric emergency service (PES) use increasing over time?

<p>Abstract</p> <p>Background</p> <p>Several recent studies have reported a significant increase in medical emergency department (ED) use for reasons of mental health. The diagnostic profile of these patients however differs from that usually described for patients visiting the psychiatric emergency service (PES). Few studies have specifically focused upon long-term PES utilization rates. Those that do typically present data from the early 80s, suggesting that deinstitutionalization may be an important contributing factor to the increases found. The aim of this study was to assess PES use using a more recent time frame and, the effects of non-specific factors, such as population growth, on this use.</p> <p>Methods</p> <p>Visits per year at several different types of PESs were obtained; (a) for an 11-year period at a general hospital PES while the surrounding population remained stable, (b) at that same PES while the catchment area population doubled over a period of a few years, (c) for an 11-year period at two PESs without catchment areas while the surrounding population increased and (d-) for a 12-year period at a PES in a mental health facility while the surrounding population increased. Moderately conservative criteria were used to define either a trend or, a significant increase in utilization rates.</p> <p>Results</p> <p>Each site had an inherent, 7 to 15% yearly variability in the number of PES visits. Over time however, only those where the surrounding population increased (either by an increase in the catchment area size or a regional increase in the population census) showed a trend or, a significant increase in utilization rates. These increases however were modest and of the order of 12 to 19%.</p> <p>Conclusion</p> <p>Long observation periods are required in order to detect stable changes in PES utilization rates over time. As such, population growth may be but one of several factors underlying these increases. Organizational changes in mental health care delivery in the vicinity of the services that showed an increase could also have contributed. These latter would simply have redistributed (to the PES) the pre existing pool of mental health care patients, resulting in an increase that is more apparent than real.</p

The imprinted brain: how genes set the balance between autism and psychosis

The imprinted brain theory proposes that autism spectrum disorder (ASD) represents a paternal bias in the expression of imprinted genes. This is reflected in a preference for mechanistic cognition and in the corresponding mentalistic deficits symptomatic of ASD. Psychotic spectrum disorder (PSD) would correspondingly result from an imbalance in favor of maternal and/or X-chromosome gene expression. If differences in gene expression were reflected locally in the human brain as mouse models and other evidence suggests they are, ASD would represent not so much an extreme male brain as an extreme paternal one, with PSD correspondingly representing an extreme maternal brain. To the extent that copy number variation resembles imprinting and aneuploidy in nullifying or multiplying the expression of particular genes, it has been found to conform to the diametric model of mental illness peculiar to the imprinted brain theory. The fact that nongenetic factors such as nutrition in pregnancy can mimic and/or interact with imprinted gene expression suggests that the theory might even be able to explain the notable effect of maternal starvation on the risk of PSD -not to mention the autism epidemic of modern affluent societies. Finally, the theory suggests that normality represents balanced cognition, and that genius is an extraordinary extension of cognitive configuration in both mentalistic and mechanistic directions. Were it to be proven correct, the imprinted brain theory would represent one of the biggest single advances in our understanding of the mind and of mental illness that has ever taken place, and would revolutionize psychiatric diagnosis, prevention and treatment - not to mention our understanding of epigenomics