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Patients with a first episode of psychosis (FEP) display clinical, cognitive, and structural brain abnormalities at illness onset. Ventricular enlargement has been identified in schizophrenia since the initial development of neuroimaging techniques. Obstetric abnormalities have been associated with an increased risk of developing psychosis but also with cognitive impairment and brain structure abnormalities. Difficulties during delivery are associated with a higher risk of birth asphyxia leading to brain structural abnormalities, such as ventriculomegaly, which has been related to cognitive disturbances.
We examined differences in ventricular size between 142 FEP patients and 123 healthy control participants using magnetic resonance imaging. Obstetric complications were evaluated using the Lewis–Murray scale. We examined the impact of obstetric difficulties during delivery on ventricle size as well as the possible relationship between ventricle size and cognitive impairment in both groups.
FEP patients displayed significantly larger third ventricle size compared with healthy controls. Third ventricle enlargement was associated with diagnosis (higher volume in patients), with difficulties during delivery (higher volume in subjects with difficulties), and was highest in patients with difficulties during delivery. Verbal memory was significantly associated with third ventricle to brain ratio.
Our results suggest that difficulties during delivery might be significant contributors to the ventricular enlargement historically described in schizophrenia. Thus, obstetric complications may contribute to the development of psychosis through changes in brain architecture.
Psychotic disorders are associated with metabolic abnormalities including alterations in glucose and lipid metabolism. A major challenge in the treatment of psychosis is to identify patients with vulnerable metabolic profiles who may be at risk of developing cardiometabolic co-morbidities. It is established that both central and peripheral metabolic organs use lipids to control energy balance and regulate peripheral insulin sensitivity. The endocannabinoid system, implicated in the regulation of glucose and lipid metabolism, has been shown to be dysregulated in psychosis. It is currently unclear how these endocannabinoid abnormalities relate to metabolic changes in psychosis. Here we review recent research in the field of metabolic co-morbidities in psychotic disorders as well as the methods to study them and potential links to the endocannabinoid system. We also describe the bioinformatics platforms developed in the EU project METSY for the investigations of the biological etiology in patients at risk of psychosis and in first episode psychosis patients. The METSY project was established with the aim to identify and evaluate multi-modal peripheral and neuroimaging markers that may be able to predict the onset and prognosis of psychiatric and metabolic symptoms in patients at risk of developing psychosis and first episode psychosis patients. Given the intrinsic complexity and widespread role of lipid metabolism, a systems biology approach which combines molecular, structural and functional neuroimaging methods with detailed metabolic characterisation and multi-variate network analysis is essential in order to identify how lipid dysregulation may contribute to psychotic disorders. A decision support system, integrating clinical, neuropsychological and neuroimaging data, was also developed in order to aid clinical decision making in psychosis. Knowledge of common and specific mechanisms may aid the etiopathogenic understanding of psychotic and metabolic disorders, facilitate early disease detection, aid treatment selection and elucidate new targets for pharmacological treatments.
For rare blood groups the recruitment of donor relatives, for example siblings, is expected to be effective, since the probability of a similar rare blood group is likely. However, the likelihood differs between blood groups and is not commonly available. This paper provides a unified mathematical formulation to calculate such likelihoods. From a mathematical and probabilistic point of view, it is shown that these likelihoods can be obtained from the computation of a stationary genotype distribution. This, in turn, can be brought down to a system of quadratic stochastic operators. A generic mathematical approach is presented which directly leads to a stationary genotype distribution for arbitrary blood groups. The approach enables an exact computation for the effectiveness of recruiting next of kin for blood donorship. Next to an illustration of computations for ‘standard’ ABO and Rhesus-D blood groups, it is particularly illustrated for the extended Rhesus blood group system. Also other applications requiring next of kin blood group associations can be solved directly by using the unified mathematical formulation.
Thalamic volume deficits are associated with psychosis but it is unclear whether the volume reduction is uniformly distributed or whether it is more severe in particular thalamic regions.
To quantify whole and regional thalamic volume in males with early-onset psychosis and healthy male controls.
Brain scans were obtained for 80 adolescents: 46 individuals with early-onset psychosis with a duration of positive symptoms less than 6 months and 34 healthy controls. All participants were younger than 19 years. Total thalamic volumes were assessed using FreeSurfer and FSL-FIRST, group comparisons of regional thalamic volumes were studied with a surface-based approach.
Total thalamic volume was smaller in participants with early-onset psychosis relative to controls. Regional thalamic volume reduction was most significant in the right anterior mediodorsal area and pulvinar.
In males with minimally treated early-onset psychosis, thalamic volume deficits may be most pronounced in the anterior mediodorsal and posterior pulvinar regions, adding strength to findings from post-mortem studies in adults with psychosis.
Adolescents with first-episode psychosis have increased severity of
neurological soft signs when compared with controls, but it is unclear
whether increased severity of neurological soft signs is an expression of
specific structural brain deficits.
To examine whether increased severity of neurological soft signs was
associated with decreased brain volumes in adolescents with first-episode
Brain scans were obtained for 70 adolescents (less than 18 years of age)
with first-episode psychosis (duration of positive symptoms less than 6
months). Volumes were assessed using voxel-based morphometry and through
segmentation of anatomical structures.
Increased severity of sensory integration neurological soft signs
correlated with smaller right and left thalamus volume, whereas increased
severity of sequencing of complex motor acts neurological soft signs
correlated with smaller right caudate volume.
Neurological soft signs may be an easy-to-assess marker of
region-specific structural brain deficits in adolescents with
Background. Current cognitive models of positive symptoms of psychosis suggest a mechanism of defective self-monitoring that may be relevant for (i) expression of psychosis at the clinical and subclinical level and (ii) transmission of risk for psychosis.
Method. The study included 41 patients with psychosis, 39 non-psychotic first-degree relatives, 39 subjects from the general population with a high level of positive psychotic experiences, and 52 healthy controls with an average level of positive psychotic experiences. All subjects performed a speech attribution task in which single adjectives with a complimentary or derogatory meaning were presented to them on a computer screen; subjects had to read aloud and determine the source (self/other/uncertain) of the words they heard. In some of the trials, participants’ speech was distorted, in others they heard someone else's voice (alien feedback condition) that could also be distorted.
Results. No large or significant differences in errors in the speech attribution task were found between the four groups in any of the conditions.
Conclusions. Contrary to previous work using this paradigm, this study found no evidence that either expression of psychosis or risk for psychosis was associated with impairment in self-monitoring.
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