ClinicalTrials.gov identifier: NCT01280305.

Two previous randomized controlled trials (RCTs) suggested that adjunctive aspirin is efficacious in treating schizophrenia. We conducted two 16-week double-blind randomized placebo-controlled RCTs of adjunctive 1000 mg aspirin vs placebo in schizophrenia. Study 1 included 200 patients, with Positive and Negative Syndrome Scale (PANSS) total score as the primary outcome. Study 2 included 160 patients with C-reactive protein (CRP) >1 mg/L at baseline; the primary outcome was PANSS-positive score. Dropout rates for aspirin/placebo were 12% in study 1 and 20% in study 2. Differences in outcome between aspirin and placebo were calculated with linear regression, adjusting for the baseline value of the outcome. No statistically significant between-group differences were found in primary or secondary outcomes in either study. Study 1: mean difference in PANSS at 16 weeks was −3.9 (95% CI: −8.4 to 0.5, P = .10, effect size (ES) = −0.25) and at 8 weeks was −3.5 (95% CI: −7.5 to 0.5, P = .11, ES = −0.22). Study 2: mean difference in PANSS at 16 weeks was 0.3 (95% CI: −4.1 to 4.7, P = .90, ES = 0.02) and in positive PANSS was 0.5 (95% CI: −1.0 to 2.1, P = .50, ES = 0.11). A meta-analysis of these data with the existing studies, excluding one with large baseline differences in total PANSS, found that the overall estimate of the effect of adjunctive aspirin on the PANSS total score comparing group means at the end of the study was −2.9 (95% CI: −6.6 to 0.7; P = .21), favoring aspirin. Our studies and meta-analysis failed to find a statistically significant improvement in the symptoms of schizophrenia from adjunctive aspirin therapy in comparison to placebo in schizophrenia. Trial registration: study 1: Clinicaltrials.gov: NCT01320982; study 2 (high CRP): EudraCT Number: 2014-000757-36.

Valnoctamide was well tolerated at 1500 mg/d but lacked efficacy in the treatment of symptoms in patients with acute mania. Possible differences between the biological mechanisms of action of valproic acid and valnoctamide are discussed.

Background and Hypothesis Meta-analyses have shown that the majority of patients with schizophrenia who have not improved after 2 weeks of treatment with an antipsychotic drug are unlikely to fully respond later. We hypothesized that switching to another antipsychotic with a different receptor binding profile is an effective strategy in such a situation. Study Design In total, 327 inpatients with an acute exacerbation of schizophrenia were randomized to double-blind treatment with either olanzapine (5–20 mg/day) or amisulpride (200–800 mg/day). Those patients who had not reached at least 25% Positive-and-Negative-Syndrome-Scale (PANSS) total score reduction from baseline after 2 weeks (the “non-improvers”) were rerandomized double-blind to either staying on the same compound (“stayers”) or to switching to the other antipsychotic (“switchers”) for another 6 weeks. The primary outcome was the difference in the number of patients in symptomatic remission between the combined “switchers” and the “stayers” after 8 weeks of treatment, analyzed by logistic regression. Study Results A total of 142 nonimprovers were rerandomized at week two. 25 (45.5 %) of the ‘stayers' compared to 41 (68.3 %) of the “switchers” reached remission at endpoint (p = .006). Differences in secondary efficacy outcomes were not significant, except for the PANSS negative subscore and the Clinical-Global-Impression-Scale. “Switchers” and “stayers” did not differ in safety outcomes. Conclusions Switching “non-improvers” from amisulpride to olanzapine or vice-versa increased remission rates and was safe. The superiority in the primary outcome was, however, not paralleled by significant differences in most secondary efficacy outcomes and the effect was only apparent at the last visit making replications of longer duration necessary.

Purpose: Patients with severe mental illness (SMI) and alcohol use disorder (AUD) are at higher risk for contracting coronavirus-19 (COVID-19) and for poor outcomes of COVID-19 infection. One reason for this could be the lack of knowledge regarding preventive measures against COVID-19 and the inability of the psychiatric patients to discern misinformation from facts. Patients and Methods: The study design was cross-sectional. We applied one questionnaire that evaluated knowledge of prevention measures and information about COVID-19 (comprised of two sections, each with five questions). The first section evaluated knowledge regarding the official WHO prevention measures against COVID-19, and the second consisted of false information about COVID-19 which examined the ability to identify misinformation about COVID-19. These questionnaires were applied face-to-face to psychiatric male inpatients from a tertiary psychiatric hospital in Bucharest diagnosed with SMI or severe alcohol disorder (SAUD) and to male controls from the community, matched by age and education. Mean scores of patients and controls were compared using Mann-Whitney test. Results: There were 115 male psychiatric patients in total (65 SMI and 50 SAUD) and 57 controls included after the matching procedure. We found statistically significant lower (P<0.05) scores for psychiatric patients compared to controls regarding the prevention and general knowledge of COVID-19 (P<0.001), the WHO information about prevention measures (P=0.041), and the ability to identify misinformation about COVID-19 (P<0.001). The fact that psychiatric patients have less knowledge about prevention measures against COVID-19 and a reduced capacity to discern misinformation suggests that we need to identify new methods to convey correct information to these patients and also to better equip them to handle misinformation regarding COVID-19. Conclusion: Patients with SMI and SAUD are less informed regarding COVID-19 infection and preventive measures compared to controls, while being prone to believing false information about COVID-19 as well.