Patients were compared to 15 age and sex-matched healthy controls. Both average and maximum amplitude of absolute gamma (37-41Hz) synchrony were measured, and differences between groups were calculated using independent samples t-tests. Due to sample size limitations, stability of gamma synchrony was assessed as a mean change at follow-up that was within one-half of the baseline standard deviation. Correlational analyses were then conducted on the change in PANSS scores and change in gamma synchrony between sessions. At baseline and follow-up, a trend for raised gamma synchrony was observed in the psychosis group compared to controls.
Stability of gamma synchrony was observed across all regions despite a significant improvement in symptoms. In the left-frontal region, there was a significant positive correlation between the reduction in gamma synchrony and improvement in the PANSS general and total scores. However, this result did not persist after correction for multiple comparisons. The stability of absolute gamma synchrony despite significant clinical improvement implies that abnormal neuronal synchrony is a trait feature of psychosis. This supports the proposition that altered gamma synchrony may be an endophenotype for schizophrenia. Future research with a larger sample size is warranted to clarify these preliminary findings.
Impaired functional connectivity, as measured by synchronous gamma activity, has been observed in both the early and chronic stages of schizophrenia, as well as in unaffected first-degree relatives. This suggests gamma synchrony may be a trait-like marker of psychosis susceptibility, and not just a state-dependant characteristic. To conduct a pilot study into the short-term temporal stability of gamma synchrony and its relationship to symptomatic improvement in young patients who have been treated for recent onset psychosis. 20 medicated subjects underwent both clinical (PANSS) and electrophysiological (auditory oddball task during EEG) evaluation at both baseline and 8 weeks follow-up.
The diagnosis of schizophrenia lacks a broadly accepted biological basis and its heterogeneity may well represent a group of disorders with different aetiologies. Even so, brain imaging can map and quantify structural brain abnormalities in vivo as an intermediate (or endo-) phenotype of the disorder. To identify the degree of regional grey matter deficits in relation to age, the severity of psychopathology and cognitive/ neurological impairment, and treatment response in schizophrenia. Eighteen schizophrenia patients (32.2 years [SD 14.3], meeting DSM-IV criteria were examined. Eighteen pair-wise age (±2 years) and gender-matched healthy volunteers (31.9 years [SD 14.3]) served as control group.
Individuals with psychosis have an elevated risk for heart disease and are more likely to die prematurely from heart disease than the general population. The age at which cardiovascular risk indicators are first elevated relative to the general population is unknown. Mean waist circumference, BMI, blood pressure, fasting blood glucose, triglycerides, LDL, HDL and total cholesterol were plotted by age and sex in a representative sample of 1,642 individuals with psychosis (aged 18+) who were in contact with mental health services and 11,247 controls (aged 25+) from the general population. Correlations between risk indicators were compared between samples.
Dysregulation of the epidermal growth factor (EGF) system, implicated in synaptic plasticity, long-term potentiation and dendritic spine connectivity has been linked to schizophrenia. For instance, in patient brain and blood low EGF levels resulting in compensatory up-regulation of the EGF receptor (ErbB1) is postulated to represent a hypofunctioning signalling state. Consistent with this hypothesis our preclinical in vitro and in vivo data demonstrate that the antipsychotic drug clozapine increases ErbB1 signalling via G-protein coupled receptor (GPCR) transactivation in prefrontal cortex and striatum1,2,3. The clozapine induced increase in ErbB1 signalling results in delayed activation of the extracellular signal regulated kinase (ERK) pathway with downstream activation of the transcription factors, p90RSK and c-Fos.
Ketamine is a potent antagonist of the N-methyld-aspartate receptor that induces positive psychotic symptoms in healthy individuals reminiscent of those seen in people with schizophrenia. Ketamine is believed to act by imposing a broad modulatory effect on brain networks, particularly cortico-striatothalamic circuitry. To investigate the effect of a sub-anaesthetic dose of ketamine on the resting-state functional connectivity of dorsal and ventral corticostriatal circuits, structures that have strongly been implicated in the emergence of psychotic symptoms, and to characterize the symptom correlates of putative changes in cortico-striato-thalamic functional connectivity induced by ketamine infusion.
People suffering from psychiatric illness have alarmingly higher smoking rates than the general population, up to 80% in some cases. This has previously been attributed to measures of social disadvantage and poor economic well-being. This study aimed to identify factors associated with the high rates of tobacco smoking amongst people with psychosis living in a disadvantaged region in Adelaide, South Australia. We hypothesised that whilst tobacco use by people with psychosis living in this region was primarily associated with mental illness, smoking prevalence would be further increased by the disadvantaged conditions existing within this context. Data were collected from 402 people with psychosis aged 18-64 who resided in the Northern suburbs of Adelaide. Demographic data and lifestyle variables were assessed that may be accountable for smoking prevalence. 74% of men and 71% of women with psychosis were current smokers. Factors including unemployment, lower education, and receiving government welfare known to be associated with smoking in the general population, were more prevalent in the Northern region.
People with psychotic disorders have higher rates of CVD risk factors compared to the general community. To our knowledge, this is the first RCT of its kind. To determine the efficacy of a multi-component intervention (smoking, diet and activity) delivered face to face compared to a largely telephone delivered intervention (smoking) among smokers with psychotic disorders. Participants with psychotic disorders residing in the community and smoking =15 cigarettes/day (CPD) were randomly assigned to either condition.