No description available.

Background: Cognitive remediation is a behavioural intervention that aims to improve cognitive functioning with the goal of durability and generalisation. Although evidence suggests that computer-assisted cognitive remediation (CACR) improves cognitive functioning in individuals with schizophrenia, it remains unclear whether these effects generalise and lead to improvements in clinical symptoms and psychosocial functioning. The current study aimed to investigate the effects of CACR on clinical symptoms, cognitive functioning and psychosocial functioning in individuals with schizophrenia or schizoaffective disorder. Method: A systematic review was performed using the quality assessment criteria defined by Scottish Intercollegiate Guidelines Network (SIGN 50) to investigate the effects of CACR on clinical symptoms in individuals with a diagnosis of schizophrenia or schizoaffective disorder. Additionally, a within subjects repeated measures design was used to investigate the effects of CACR on cognitive functioning, functional capacity and everyday social functioning. Results: There was some evidence to suggest that CACR improves clinical symptoms, but the majority of studies reviewed did not report a significant effect, and a number of methodological weaknesses were identified in the literature. Results of the experimental study revealed improvements in speed of processing, reasoning and problem solving and the overall composite score for cognition, but these improvements could not be attributed solely to the CACR intervention. No improvements in functional capacity or everyday social functioning were observed. Conclusions: Further, more rigorous research is required to develop a clearer understanding of the effects of CACR on clinical symptoms. The results of the experimental study support previous literature which has identified that a pure CACR intervention does not improve psychosocial functioning. The results are discussed in relation to the relevant literature.

No description available.

Single nucleotide polymorphisms (SNPs) within the gene encoding the serine threonine kinase KIS (Kinase Interacting with Stathmin, also known as UHMK1) have recently been associated with schizophrenia. However, little is known about the neurobiology of KIS or the mechanisms through which disease-associated SNPs may increase susceptibility to schizophrenia. The studies presented in this thesis focus on the distribution of KIS and its mRNA, address the mechanisms through which KIS may confer susceptibility to schizophrenia, and investigate the physiological role(s) of KIS in the brain using two lines of knockout mice. The regional and cellular distribution of KIS was characterised in the brains of adult humans and mice, and through mouse neurodevelopment. The results of these experiments demonstrated that KIS is widely expressed in neurons in the brain regions examined in both species, its encoded protein is localised to the nucleus and cytoplasm, and KIS expression in mouse brain peaked around seven days after birth. KIS protein and mRNA was quantified in two large human post-mortem brain series to determine if KIS expression is altered in schizophrenia or bipolar disorder, or in relation to the leading schizophrenia-associated SNP (rs7513662). Using tissue from the superior temporal gyrus, dorsolateral prefrontal cortex, anterior cingulate cortex, and cerebellum, no difference in KIS expression (either mRNA or protein) was found between diagnostic or genotype groups in any brain region examined. Furthermore, KIS expression in lymphoblast cell lines also did not differ between diagnostic or genotype groups. Lastly, KIS expression (mRNA and protein) was characterised in two separate lines of KIS knockout mice. The results were complex, and left uncertainty as to whether either line was a true knockout or, conversely, whether any of the available KIS antibodies were specific. Nevertheless, the absence of KIS mRNA was robustly confirmed in one knockout mouse line, and brains from this line were subsequently used in three experiments. First, investigation of the quantity and phosphorylation state of the KIS targets stathmin and p27^kip1; no differences were found compared to wildtype mice. Second, quantification of mRNA expression of several other genes of interest with regard to schizophrenia; altered expression of GAP43, VGlut1, MAP2, spinophilin, and stathmin was found. Finally, stereological measurements were performed, and while no differences in whole or regional brain volumes in KIS knockout mice were found, there was a relative reduction in hippocampal volume. The results of these studies do not support the hypothesis that altered expression is the mechanism by which genetic variation of KIS may increase susceptibility to schizophrenia, nor that KIS expression is altered in the disease. However, the knockout mice data suggest that KIS may play a role in synaptic plasticity and function, providing novel information on the potential neurobiological roles of KIS.

The present study examines the relationship of diagnosis and denominational affiliation in light of the work of Charles Glock and Rodney Stark. The major hypothesis of the study was that diagnoses of first admissions to Timberlawn sanitarium would vary by denominational affiliation.

The purpose of this experiment was to investigate the modification of behavior of a thirty-five-year-old, hospitalized, chronic schizophrenic male. The hypothesis was that the patient's aggressive and self-injurious behavior could be modified through the use of aversion therapy.

No description available.

Class of 2007 Abstract / Objectives: This retrospective analysis compared the prescribing rates of typical versus atypical oral antipsychotics in the treatment of schizophrenia for 6 months before versus 6 months after the publication of the Phase 1 CATIE trial on September 22, 2005. Methods: Prescription and membership databases from COPE Behavioral Services in Tucson, AZ were utilized for determining prescribing rates of typical and atypical antipsychotics for pre- versus post-publication of the CATIE trial. Comparisons were made for gender, court order treatment, hospitalizations and length of stay, costs of services (case management, inpatient, lab, and other services), total number of prescriptions and number of tablets/capsules of typical and atypical antipsychotics, and cost of antipsychotic prescriptions. Results: There was no significant difference in prescribing rates for oral atypical and typical antipsychotics, cost of services, or hospitalization rates in the pre-publication (N=316) versus post-publication (N=336) groups. Atypical antipsychotics accounted for approximately 77% of antipsychotic prescriptions and for 98% of the total costs for antipsychotic therapy in the two time periods. During the 12-month study, the amount paid for atypical antipsychotic prescriptions was $ 1,026,004 versus $ 22,671 for typical antipsychotics. Conclusions: Prescribing patterns of oral typical and atypical antipsychotics for the treatment of schizophrenia did not change during the first six months after the publication of the phase I CATIE trail in this outpatient population. Atypical antipsychotics accounted for the majority of prescriptions and for the highest cost compared to other services provided despite similar efficacy to typical antipsychotics in the treatment of schizophrenia.

ABSTRACT AIM: The aim of this study was to determine, if any, the factors associated with relapse with a view to provide guidelines for prevention, early identification and management of relapse in a community setting. METHOD: The study is a retrospective record review of the patients attending seven randomly selected Community Mental Health Clinics in Southern Gauteng during the period January 1995 to June 2005. Two hundred and seventeen (217) patients aged 18 years with a diagnosis of schizophrenia were included in the study. Patients were excluded if the diagnosis of schizophrenia was made in the preceding six months of the study. Demographic and clinical variables including age, gender, marital status, source of income, highest level of education, non compliance, presence of substance abuse, co-morbid psychiatric condition, the presence and number of relapses and stressful life events were recorded on a data schedule. RESULTS: Two hundred and seventeen patients records were analysed: 61.8% have had at least one relapse. The only factors that provided a significant predictive factor for relapse included non compliance due side-effects, non compliance due to lack of insight, and the presence of depressive symptoms. 64.2% of the study population were non compliers and 27.1% have had depressive features. Demographic variables were not associated with relapse. CONCLUSION: These findings imply that interventions aimed at reducing relapse in schizophrenia should include improving medication compliance and early detection and treatment of depression.

M.Sc. (Med), Faculty of Health Sciences,University of the Witwatersrand, 2011 / Background: Many factors affect the prescribing of medication to patients with schizophrenia including variables that relate to physicians and may result in marked variance in the choice of drugs, dosages, drug combinations, route of administration and the use of antipsychotic, anticholinergic, sedative and other adjuvant drugs. Clinical practice guidelines were developed to address this variance and for other reasons, including the management of side-effects, drug innovation, rising costs, information overload, changes in treatment goals and the management of medication non-adherence. There are advantages and disadvantages to using clinical practice guidelines including those pertaining to context and cultural norms, but they remain the best method of assessing prescribing quality. Many guidelines are based on the results of randomised clinical trials (with a single drug) or are the consensus of experts in the field. Despite the development and publication of these guidelines over the past two decades, they are frequently not adhered to resulting in much variance in treatment. Aims and objectives: The aim of the study was to determine to what extent the prescribing of psychotropic drugs in the treatment of schizophrenia was consistent with the most recent version of each of five guidelines that originate outside South Africa (two from the United States and one each from Canada, the United Kingdom, and Australia and New Zealand); and one that was developed locally. Methodology: A retrospective, cross-sectional prescription chart review with data sampling at three time points (on hospital admission, at fourteen days thereafter and on hospital discharge) was undertaken. A sample population was drawn over a three year period during which the patients’ physician had access to the same drug formulary. Seventy patients met the study selection criteria in terms of age, diagnosis and receipt of antipsychotic medication during hospital stay and on discharge. Seventy patients met the study selection criteria, and their prescriptions for psychotropic medication (exclusively) were examined for a number of parameters including: drug class, drug name, dose, route of administration and whether the medication was to be administered routinely or ‘as needed’. Findings and discussion: As compared with the recommendations made in some or all of the guidelines, first generation antipsychotic agents were over-prescribed especially early on in the patients’ hospital stay, whereas second generation antipsychotics were under-prescribed. The profile changed after fourteen days and on discharge there were more patients on second generation drugs than on the older drugs. More patients were discharged on depot antipsychotic treatment than were admitted which is considered a favourable finding, however, many patients receiving the depot form continued to be prescribed the oral drug on a routine basis and for an indefinite period, resulting in antipsychotic polypharmacy. Anticholinergic drugs were prescribed as prophylaxis for the extra-pyramidal side-effects of the first generation antipsychotic drugs and more than a quarter of the sample received these drugs on discharge, after which they were to be taken routinely and indefinitely. A similar finding was made with the use of benzodiazepine sedatives, where nearly a quarter of patients received these drugs on discharge - again to be taken routinely and for an unspecified period. Sodium valproate was given increasingly to many patients in the sample and was prescribed to over a quarter of those upon discharge, without an indication of duration. Limitations: The study was retrospective in design, without the benefit of the patients’ clinical histories and treatment progress, and the findings were compared with guidelines whose age spanned more than a decade and some of which had become redundant. Conclusions: The study demonstrated some prescribing habits that were not in accord with the guidelines used for comparison in the study. The extent of the disagreement reveals the need for a prospective pilot study that will include the patients’ clinical progress in the study design which will provide greater insight into why specific medication parameters were chosen by the physician for the individual patient. If the findings justify it, then a programme promoting better adherence to the most current guidelines should be commenced.