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A recent single-site study (Fisher et al., 2009. Am J Psychiatry. 166 (7) 805–11) showed that repeated training with the Brain Fitness Program (BFP) improved performance on a battery of neuropsychological tasks. If replicated these data suggest an important non-pharmacological method for ameliorating cognitive impairment in schizophrenia. Our study evaluated the BFP training effects in an open-label, multi-site, multinational clinical trial. Fifty-five stable adult patients with schizophrenia on regular antipsychotic medication completed ≥ 32 BFP training sessions over 8–10 weeks. Training effects on cognitive performance and functional capacity outcome measures were measured using CogState® schizophrenia battery, UCSD Performance based Skills Assessment (UPSA-2) and Cognitive Assessment Interview (CAI). BFP training showed a large and significant treatment effect on a training exercise task (auditory processing speed), however this effect did not generalize to improved performance on independent CogState® assessment. There were no significant effects on UPSA-2 or CAI scores. Our study demonstrated the feasibility of implementing BFP training in a multi-site study. However, BFP training did not show significant treatment effects on cognitive performance or functional capacity outcome measures despite showing large and significant effects on a training exercise. [ABSTRACT FROM AUTHOR]

Objective: To determine the efficacy of pharmacological treatment in the prevention of sudden cardiac death in hypertrophic cardiomyopathy (HCM). Design: Clinical outcome was assessed retrospectively in 293 patients with HCM, including 173 who were taking cardioactive medications. Setting: Department of Cardiology, University of Padua, Padua, Italy; a tertiary HCM Centre. Interventions: Medical treatment with 3 blockers, verapamil, sotalol and amiodarone. Main outcome measure: HCM-related sudden cardiac death. Results: 17 of 173 (10%) patients died suddenly or had aborted cardiac arrest, while being treated continuously with drugs having antiarrhythmic properties, over a period of 62 (56) months. Sudden death occurred in 20% of patients administered amiodarone (6/30), 9% each of patients taking verapamil (4/46) or 13 blockers (7/76), and 0% of those taking sotalol (0/21). Patients taking cardioactive drugs (n = 173) and those without pharmaceutical therapy (n = 120) did not differ with respect to sudden death mortality. Conclusion: Medical treatment is not absolutely protective against the risk of sudden death in HCM. The present data inferentially support the use of the implantable defibrillator as the primary treatment choice for prevention of sudden death in high-risk patients with HCM. [ABSTRACT FROM AUTHOR]