Multicenter Studies Of Oral Ziprazidone For The Treatment Of Patients With Schizophrenia And Schizoaffective Disorder [estudos Multicêntricos Da Ziprasidona Oral No Tratamento De Pacientes Com Esquizofrenia Ou Transtorno Esquizoafetivo]

Background: The oral ziprasidone efficacy, safety, and tolerability on Brazilian patients with schizophrenic and schizoaffective disorder were evaluated through two sequential clinical trials. Methods: Prospective open studies. At the first 6-week trial patients received 80 to 160 mg/day of ziprasidone, and were evaluated using the Positive and Negative Symptom Scale (PANSS), Clinical Global Impression-Severity Scale (CGI-S), Intensity Care Questionnaire (ICQ) e Patient Preference Scale (PPS). Safety and tolerability were evaluated by clinical, EKG, and laboratorial analysis, Extrapyramidal Symptom Rating Scale (ESRS), and Barnes Akathisia Scale (BAS). Responsive patients were included on one up to 12-month second trial. Results: 162 patients were analyzed regarding drug efficacy, and 164 regarding tolerability at first clinical trial. From baseline to endpoint treatment decreased PANSS scores from 94.3 to 76.2 (P<.0001). Either scores on CGI-S and ICQ showed significantly reduction. Ziprasidone had the patient's preference (64.8%) compared to the last medication used through the PPS application. Neither, extrapyramidal symptoms or EKG alterations were found. From 106 included patients at the second trial, 86 were analyzed regarding efficacy. The median of treatment duration was 5.6 months, and the mean of PANSS was kept during the evaluation. The adverse events profiles from both studies were similar. Conclusion: Oral ziprasidone is an effective and safe drug for chronic treatment of patients with schizophrenic and schizoaffective disorder. © Copyright Moreira Jr. Editora.644170176Kane, J., Honigfeld, G., Singer, J., Meltzer, H., Clozapine for the treatment-resistant schizophrenic. A double-blind comparison with chlorpromazine (1988) Arch Gen Psychiatry, 45, pp. 789-796Freedman, R., Schizophrenia (2003) N Engl J Med, 349, pp. 1738-1749Meltzer, H.Y., Clinical studies on the mechanism of action of clozapine: The dopamine-serotonin hypothesis of schizophrenia (1989) Psychopharmacology (Berl), 99, pp. S18-S27Kane, J.M., Oral ziprasidone in the treatment of schizophrenia: A review of short-term trials (2003) J Clin Psychiatry, 64 (SUPPL. 19), pp. 19-25Gunasekara, N.S., Spencer, C.M., Keating, G.M., Ziprasidone: A review of its use in schizophrenia and schizoaffective disorder (2002) Drugs, 62 (8), pp. 1217-1251Glassman, A.H., Bigger Jr., J.T., Antipsychotic drugs: Prolonged QTc interval, torsade de pointes, and sudden death (2001) Am J Psychiatry, 158, pp. 1774-1782Diagnostic and Statistical Manual of Mental Disorders, 4th ed.: DSM-IV. Washington, D.C.: American Psychiatric Association, 1994Chaves, A.C., Shirakawa, I., Escala das síndromes negativa e positiva - PANSS e seu uso no Brasil (1998) Rev Psiq Clín, 25 (6), pp. 337-343Clinical Global Impression Severity Scale (1976) ECDEU Assessment Manual of Psychopharmacology, , National Institute of Mental Health, Guy W Ed, Washington, DC: U. S. Government Printing OfficeChouinard, G., Margolese, H.C., Manual for the Extrapyramidal Symptom Rating Scale (ESRS) (2005) Schizophr Res, 76 (2-3), pp. 247-265Barnes, T.R., A rating scale for drug-induced akathisia (1989) B J Psychiatry, 154, pp. 672-676Awad, A.G., Hogan, T.P., Subjective response to neuroleptic drugs and the quality of life: Implication for treatment outcome (1994) Acta psychiatr Scand, p. 89. , spplm 380 27-32Arato, M., O'Connor, R., Meltzer, H.Y., A 1-year, double-blind, placebo-controlled trial of ziprasidone 40, 80 and 160 mg/day in chronic schizophrenia: The Ziprasidone Extended Use in Schizophrenia (ZEUS) study (2002) Int Clin Psychopharmacol, 17, pp. 207-215Hirsch, S.R., Kissling, W., Bauml, J., Power, A., O'Connor, R., A 28-week comparison of ziprasidone and haloperidol in outpatients with stable schizophrenia (2002) J Clin Psychiatry, 63, pp. 516-523Weiden, P.J., Simpson, G.M., Potkin, S.G., O'Sullivan, R.L., Effectiveness of switching to ziprasidone for stable but symptomatic outpatients with schizophrenia (2003) J Clin Psychiatry, 64, pp. 580-588Harvey, P.D., Meltzer, H., Simpson, G.M., Potkin, S.G., Loebel, A., Siu, C., Romano, S.J., Improvement in cognitive function following a switch to ziprasidone from conventional antipsychotics, olanzapine, or risperidone in outpatients with schizophrenia (2004) Schizophr Res, 66, pp. 101-113Weiden, P.J., Daniel, D.G., Simpson, G.M., Romano, S.J., Improvement in indices of health status in outpatients with schizophrenia switched to ziprasidone (2003) J Clin Psychopharmacol, 23, pp. 595-600Lieberman, J.A., Stroup, T.S., McEvoy, J.P., Swartz, M.S., Rosenheck, R.A., Perkins, D.O., Effectiveness of antipsychotic drugs in patients with chronic schizophrenia (2005) N Engl J Med, 353, pp. 1209-1223Kingsbury, S.J., Fayek, M., Trufasiu, D., Zada, J., Simpson, G.M., The apparent effects of ziprasidone on plasma lipids and glucose (2001) J Clin Psychiatry, 62, pp. 347-349Cohen, S., Fitzgerald, B., Okos, A., Khan, S., Khan, A., Weight, lipids, glucose, and behavioral measures with ziprasidone treatment in a population with mental retardation (2003) J Clin Psychiatry, 64, pp. 60-6

Analysis of structural brain asymmetries in attention-deficit/hyperactivity disorder in 39 datasets

OBJECTIVE: Some studies have suggested alterations of structural brain asymmetry in attention-deficit/hyperactivity disorder (ADHD), but findings have been contradictory and based on small samples. Here, we performed the largest ever analysis of brain left-right asymmetry in ADHD, using 39 datasets of the ENIGMA consortium. METHODS: We analyzed asymmetry of subcortical and cerebral cortical structures in up to 1,933 people with ADHD and 1,829 unaffected controls. Asymmetry Indexes (AIs) were calculated per participant for each bilaterally paired measure, and linear mixed effects modeling was applied separately in children, adolescents, adults, and the total sample, to test exhaustively for potential associations of ADHD with structural brain asymmetries. RESULTS: There was no evidence for altered caudate nucleus asymmetry in ADHD, in contrast to prior literature. In children, there was less rightward asymmetry of the total hemispheric surface area compared to controls (t = 2.1, p = .04). Lower rightward asymmetry of medial orbitofrontal cortex surface area in ADHD (t = 2.7, p = .01) was similar to a recent finding for autism spectrum disorder. There were also some differences in cortical thickness asymmetry across age groups. In adults with ADHD, globus pallidus asymmetry was altered compared to those without ADHD. However, all effects were small (Cohen's d from -0.18 to 0.18) and would not survive study-wide correction for multiple testing. CONCLUSION: Prior studies of altered structural brain asymmetry in ADHD were likely underpowered to detect the small effects reported here. Altered structural asymmetry is unlikely to provide a useful biomarker for ADHD, but may provide neurobiological insights into the trait