Proportion Of Schizophrenia Patients Research Articles

GABA Deficits Enhance the Psychotomimetic Effects of Δ9-THC.

Emerging evidence supports a number of associations between cannabis and psychosis/psychotic disorders, including schizophrenia. Acute exposure to both cannabis and synthetic cannabinoids (CBs) (including Spice and K2) can produce a range of transient psychotomimetic symptoms, cognitive deficits, and psychophysiological abnormalities that bear a striking resemblance to symptoms of schizophrenia (D'Souza et al, 2004; Radhakrishnan et al, 2014). Furthermore, epidemiologic studies suggest that early and heavy exposure to cannabis confers a higher risk for developing a psychotic disorder such as schizophrenia (Moore et al, 2007). However, only a minority of individuals exposed to CBs appear to be vulnerable to CB-related acute or persistent psychosis outcomes. In individuals with schizophrenia, CBs have been shown to transiently exacerbate symptoms (D'Souza et al, 2005), trigger relapse, and have negative consequences on the course of the illness (Linszen and van Amelsvoort, 2007). A number of lines of evidence suggest that schizophrenia patients are more vulnerable to some of the effects of CBs. In an experience sampling study, schizophrenia patients were more sensitive to the psychosis-inducing effects of cannabis than controls (Henquet et al, 2010). Epidemiologic studies also show that cannabis use is associated with greater negative consequences on the course and expression of schizophrenia (van Os et al, 2002). In an experimental study, despite receiving stable doses of antipsychotic medications and being clinically stable, 80% of schizophrenic patients, but only 25% of controls, experienced clinically significant psychosis (>3 points on the Positive and Negative Syndrome Scale (PANSS) positive subscale) with a low dose of delta-9-tetrahydrocannabinol (THC) (D'Souza et al, 2005). Finally, individuals who are psychosis prone as determined either psychometrically or by family history are more sensitive to the psychosis-inducing effects of cannabis (Arendt et al, 2008; GROUP, 2011). However, the basis of the enhanced vulnerability to the psychosis-inducing effects of CBs in schizophrenia patients is not clear. Several other mechanisms might explain vulnerability to THC effects including polymorphisms of genes for COMT (Henquet et al, 2006), AKT1, and DAT1 (Bhattacharyya et al, 2012, 2014), and γ-aminobutyric acid (GABA) deficits. Furthermore, it is conceivable that combinations of these factors may coexist and have additive or synergistic effects on increasing vulnerability to THC effects. GABA deficits have been observed in the dorsolateral prefrontal cortex in schizophrenia (Lewis et al, 2005), and furthermore, there is important interplay between the CB and GABA systems (Eggan et al, 2010). Indeed, converging lines of evidence, including post-mortem (Lewis et al, 2005), genetic (reviewed by Charych et al, 2009), and brain imaging studies (Busatto et al, 1997; Verhoeff et al, 1999) suggest that dysfunction of the GABA system contributes to the pathophysiology of schizophrenia. Although there is strong support for the existence of a GABA deficit in schizophrenia, the proportion of schizophrenia patients with this deficit is not known. The limited data available suggest that only 50% of schizophrenia patients have lower GABA levels compared with the lowest level found in healthy normal controls (Yoon et al, 2010). In several brain regions, particularly the cerebral cortex and hippocampus, CB1 receptors (CB1-Rs) are present on the axon terminals of cholecystokinin (CCK) containing GABA interneurons that target the perisomatic region of pyramidal cells (PCs) (Eggan et al, 2010). CB1-Rs are activated by endocannabinoids released postsynaptically by depolarized PCs (Wilson and Nicoll, 2002). The activation of CB1Rs inhibits the release of GABA by CCK-basket cells, leading to a disinhibition of postsynaptic PCs (Bartos and Elgueta, 2012; Klausberger et al, 2005). Thus, a CB1-R-mediated braking mechanism regulates the timing and release of GABA, and subsequently the overall inhibitory/excitatory balance in cortical networks (Farkas et al, 2010). This interplay between GABA and CB1-R systems provides a mechanism that could explain the higher vulnerability to CBs in schizophrenia. For instance, if CB1-R activation occurred in the presence of a pre-existing GABA deficit (as might be the case in schizophrenia), this could lead to further disinhibition and desynchronization of PC activity, leading to perturbations in gating, associative functions, and neurocognition, which could culminate in psychotic symptoms. This study tested the hypothesis that if, among other mechanisms, GABA deficits contribute to the increased vulnerability of schizophrenia patients to the psychosis-exacerbating effects of CBs, then inducing a GABA deficit in healthy subjects will increase the psychosis-inducing effects of THC. As described below, a GABA deficit was pharmacologically modeled by the administration of the GABAA inverse agonist, iomazenil.

Change of psychotropic drug prescription for schizophrenia in a psychiatric institution in Beijing, China between 1999 and 2008

To date, no study has investigated how prescription patterns change over time in Chinese patients with schizophrenia. This study aimed to determine psychotropic drug prescription patterns and the use of electroconvulsive therapy (ECT) for schizophrenia and their changes over time in a large psychiatric institution in Beijing, China. The case notes of inpatients with schizophrenia were scrutinized to identify psychotropic drug prescription patterns and the use of ECT on November 10, 1999 and the same calendar day in 2008 and to compare the two surveys. In 1999, 45.1% of inpatients with schizophrenia were on first-generation antipsychotic drugs (FGA), while 52.9% were on second-generation antipsychotic drugs (SGA). In 2008, the percentage of patients on FGAs decreased to 15.1%, while those on SGAs increased to 77.2%. The proportion of schizophrenia patients on mood stabilizers and antidepressants rose from 3.3% and 4.3% in 1999 to 18% and 9.5% by 2008, respectively. Use of ECT grew from 0.5% in 1999 to 5.6% by 2008. The proportion of schizophrenia patients not prescribed antipsychotic drugs changed from 5.6% in 1999 to 13.7% in 2008. The prescription pattern of psychotropic drugs changes considerably over time, even in the same clinical setting. Mental health professionals need to keep up with changes in the prescription patterns of psychotropic drugs in order to serve their patients at the best possible level. The socio-economic reasons for not prescribing antipsychotic drugs to schizophrenia patients should be further explored.

Behavioral Assessment of the Dysexecutive Syndrome Battery (BADS) in Schizophrenia

The purposes of this study were to explore the diagnostic features of the behavioral assessment of the dysexecutive syndrome battery (BADS) in the Spanish population of chronic schizophrenia patients, its concurrent validity with other classic neuropsychologic tests of executive dysfunction, and its correlates with clinical variables. A cross-sectional study was conducted in a sample of 61 patients with chronic schizophrenia and in a control group of 35 healthy participants. The diagnostic characteristics of the test were studied. An evaluation was performed of the association of BADS with a gold standard battery of executive dysfunction, with the symptoms, and with functional performance. Several regression models were tested to assess the clinical effect of executive impairment in schizophrenia. BADS seems to offer good reliability, a 1-dimensional structure, and good convergent validity. The proportion of schizophrenia patients with impaired executive functioning in our sample was 47%. It was a risk factor for the inpatient status and for more illness severity. Executive functioning in schizophrenia can be reliably and validly assessed with BADS. The diagnosis of impaired executive functioning may be of clinical usefulness as a marker of more illness severity and poorer functional status.

Trends in psychiatric hospitalisation of people with schizophrenia: A register-based investigation over the last three decades

The number of psychiatric beds has declined considerably in many countries over the past decades. Long-term studies on the impact of these health care changes for the severely mentally ill, however, are still scarce. This epidemiological study investigates the use of inpatient psychiatric services by people with schizophrenia, compared to that by people with other mental disorders. We used psychiatric register data of the Swiss canton Zurich to establish the annual treatment prevalence in the period 1977–2004. For patients with psychoses, the length of inpatient episodes decreased by half. The annual number of inpatient admissions doubled. The proportion of schizophrenia patients, which accounted for 36%–41% of all inpatient treatments up to 1993, dropped to 20% in 2004, while that of other psychoses remained about the same (8%–10%) throughout the study period. This contrasts with a 2–3 fold increase in other patient groups. The annual treatment prevalence for people with schizophrenia declined from 7.3 to 2.2 per 10 000 population since the 1990s and affected patients of all ages and of both sexes equally. The treatment prevalence for other psychoses remained virtually unchanged (1.3 per 10 000). For all other mental disorders, there was an up to twofold increase. The study suggests that the downsizing of psychiatric hospitals has resulted in a far-reaching redistribution of overall inpatient treatment resources. The considerable decrease in inpatient treatment for people with schizophrenia emphasizes the need to further investigate the current state of coverage for and the appropriateness of health care available to this patient group.

Deviant Strategy on the Modified Six Elements Test in Patients with Schizophrenia

Impaired executive functioning is found in a considerable proportion of schizophrenia patients. Neuropsychological tests are originally designed to measure the behavior of neurological patients and may therefore miss psychiatry-related cognitive deficits. Qualitative information on tests for executive functioning is important in psychiatric populations. The Modified Six Elements Test (MSET) is a planning test that consists of 6 tasks, for which subjects have limited time and have to obey to switching rules. This study concerns a qualitatively different approach schizophrenia patients use on the MSET, and its relationship with cognitive measures. MSET scores and strategies of schizophrenia patients were compared to those of healthy controls, closed-head-injury patients, and peripheral injury patients. Also, schizophrenia patients and healthy controls were compared on verbal memory and vigilance. Schizophrenia patients finish fewer assignments on the MSET, receive a lower profile score compared to healthy controls, and use a different strategy on the test compared to the other groups. They also perform below healthy controls on the tests for verbal memory and vigilance. Use of the different strategy in schizophrenia patients was related to impaired cognitive functioning. An interesting strategy used by schizophrenia patients on the MSET appears to be indicative of impaired cognitive functioning. This strategy may be a compensatory strategy to spare cognitive resources. It could also be the result of a concrete interpretation of the test instructions.

Effects of neurocognitive enhancement therapy in schizophrenia: Normalisation of memory performance

Introduction. A preponderance of research indicates that cognitive function in schizophrenia can be improved through cognitive remediation. However, few studies have attempted to characterise the extent of improvement relative to nonpsychiatric controls. Method. Cognitive performance on reaction time, digit recall, and word recall of 58 schizophrenia patients at baseline and after 6 months of cognitive remediation was compared to the performance on these tasks of 39 community controls. Schizophrenia patients participated in Neurocognitive Enhancement Therapy (NET) and received hierarchical training on the memory tasks, but not on the reaction time task, which was only administered at intake and follow‐up. Results. The schizophrenia sample showed significantly poorer performances than the community control sample on all three tasks at baseline. NET led to significant improvements in performance on trained memory tasks, but not the untrained reaction time task. There was a significant increase in the proportion of schizophrenia patients who achieved normal range performance on the memory tasks. Conclusions. 52% of schizophrenia patients who were impaired on at least one of the memory tasks normalised their performance on at least one of those tasks as a result of cognitive training. Results suggest that clinically meaningful improvement may be possible using cognitive remediation.

Estimating the proportion of schizophrenia patients for whom QTC prolonging antipsychotics may be contraindicated

Estimating the proportion of schizophrenia patients for whom QTC prolonging antipsychotics may be contraindicated