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Biomedical subjects

Carla M Canuso

Publications and source records attributed to Carla M Canuso.

5 recordsLinked to original sources
PubMed2006

Effects of risperidone augmentation in patients with treatment-resistant depression: Results of open-label treatment followed by double-blind continuation.

Approximately one-third of persons with depression do not respond to antidepressant monotherapy. Studies suggest that atypical antipsychotic augmentation may benefit these patients. We investigated the longer-term efficacy of risperidone augmentation of serotonin-selective reuptake inhibitor treatment for resistant depression. In 57 in- and outpatient centers in three countries, we conducted a three-phase study with 4-6 weeks of open-label citalopram monotherapy, 4-6 weeks of open-label risperidone augmentation, and a 24-week double-blind, placebo-controlled discontinuation phase. A total of 489 patients with major depressive disorder and 1-3 documented treatment failures entered the citalopram monotherapy phase (20-60 mg/day). Patients with <50% reduction in HAM-D-17 scores entered the risperidone augmentation phase (0.25-2.0 mg/day). Patients with HAM-D-17< or =7 or CGI-S < or = 2 were randomized to risperidone or placebo augmentation. The primary outcome was time to relapse during the double-blind phase. During citalopram monotherapy, 434 patients had <50% HAM-D-17 reduction; 299 (68.9%) were fully nonresponsive (<25% reduction) and 135 were partially nonresponsive (25-49% reduction). Of the 386 nonresponders who entered the augmentation phase, 243 remitted and 241 entered the double-blind phase. Median time to relapse was 102 days with risperidone augmentation and 85 days with placebo (NS); relapse rates were 53.3 and 54.6%, respectively. In a post hoc analysis of patients fully nonresponsive to citalopram monotherapy, median time to relapse was 97 days with risperidone augmentation and 56 with placebo (p = 0.05); relapse rates were 56.1 and 64.1%, respectively (p < or = 0.05). Open-label risperidone augmentation substantially enhanced response in treatment-resistant patients, but the longer-term benefits of augmentation were not demonstrated in this study.

Adolescent↗
PubMed2006

An open-label extension trial of risperidone monotherapy in the treatment of bipolar I disorder.

The primary objective of this 9-week open-label extension trial was to assess the effects of risperidone monotherapy in patients with acute bipolar I disorder who completed treatment in two preceding 3-week double-blind trials. Patients with DSM-IV bipolar I disorder, experiencing an acute manic episode, received a flexible dose of risperidone (1-6 mg/day) or placebo in two independent double-blind, randomized, 3-week monotherapy trials. Completers who required ongoing treatment were eligible to enter this open-label 9-week extension trial during which all patients received risperidone. The primary efficacy measure was the mean change in the Young Mania Rating Scale (YMRS) total score. Secondary efficacy measures included the Clinical Global Impressions-Severity Scale, Montgomery-Asberg Depression Rating Scale, Positive and Negative Syndrome Scale and Global Assessment Scale. Safety assessments included adverse event reports, laboratory tests, and the Extrapyramidal Symptom Rating Scale (ESRS). Of the 283 patients who entered the extension study, 160 had previously received risperidone (RIS/RIS) in the acute treatment trial and 123 had received placebo (PLA/RIS). This study was completed by 71% of these patients. The mean+/-SE modal dose of risperidone was 4.6+/-1.5 mg/day. Patients in both the RIS/RIS and PLA/RIS groups improved significantly at the endpoint of the 9-week open-label study compared to their open-label baseline scores (-5.2+/-0.69, P<0.001 and -9.12+/-1.44, P<0.001, respectively) on the YMRS. Furthermore, changes from double-blind baseline to open-label endpoint were -29.4+/-1.0 in the RIS/RIS group and -23.9+/-1.4 in the PLA/RIS group. Significant improvements from both double-blind and open-label baseline were seen at week 1 of the open-label trial (P<0.001) and at each subsequent timepoint. A similar pattern was observed on the secondary measures of efficacy. Most frequent adverse events were extrapyramidal disorder (18%) and somnolence (12%). Most adverse events were mild or moderate in severity. The mean score for the Parkinsonism subscale of the ESRS was 1.1 at open-label baseline, and decreased by 0.1 at endpoint. Mean increase in body weight from open-label baseline was 0.6 kg in patients treated with placebo in the preceding double-blind trial and 1.2 kg in patients previously treated with risperidone. Risperidone treatment was well tolerated and resulted in further improvement during the 9-week extension, beyond the 3 weeks of acute treatment. Patients switched from placebo to risperidone improved markedly. Risperidone treatment did not induce depression.

Adult↗
PubMed2003

Detection and management of comorbidity in patients with schizophrenia.

Approximately half of patients with schizophrenia have at least one comorbid psychiatric or medical condition, worsening prognosis and contributing to the high rate of morbidity and mortality. Depression is associated with suicide, the leading cause of premature death in patients with schizophrenia; obsessive-compulsive symptoms may worsen prognosis; alcohol and substance use disorders are associated with a poor outcome; and comorbid medical conditions, including cardiac and pulmonary disease, infectious diseases, diabetes, hyperlipidemia, hypogonadism, and osteoporosis, are often underrecognized and undertreated. The new generation of antipsychotic medications has improved the potential outcome of patients with schizophrenia. Providing optimal treatment for patients and fully realizing the potential of these new agents require focused attention on detection, recognition, and treatment of comorbid psychiatric and medical conditions in patients with schizophrenia.

Age of Onset↗
PubMed2002

Antipsychotic medication, prolactin elevation, and ovarian function in women with schizophrenia and schizoaffective disorder.

Some, but not all, antipsychotics elevate serum prolactin. Antipsychotic-induced hyperprolactinemia is thought to account for high rates of menstrual dysfunction and diminished estrogen levels in women with schizophrenia. However, few studies have directly assessed the relationships between prolactin, menstrual function, and ovarian hormone levels in this population. Sixteen premenopausal women with schizophrenia and schizoaffective disorder, eight treated with an antipsychotic with prolactin-elevating potential (five with typical antipsychotics and three with risperidone) and eight treated with an antipsychotic with prolactin-sparing potential (seven with olanzapine and one with clozapine), were studied for eight weeks. Data were collected on menstrual functioning and on serum prolactin, estradiol, and progesterone levels, and were compared between subjects who received an antipsychotic with prolactin-elevating potential and an antipsychotic with prolactin-sparing potential, and between subjects with hyperprolactinemia (N=6) and normoprolactinemia (N=10). Additionally, peak ovarian hormone levels were compared to normal values. While mean prolactin levels of subjects who received an antipsychotic with prolactin-elevating potential were significantly greater than those of subjects who received an antipsychotic with prolactin-sparing potential, there were no differences in rates of menstrual dysfunction or in ovarian hormone values between the two groups. Additionally, similar rates of menstrual dysfunction and ovarian hormone values were observed between the hyperprolactinemic and normoprolactinemic subjects. Moreover, irrespective of medication type or prolactin status, most subjects had peak estradiol levels below normal reference values for the periovulatory phase of the menstrual cycle. While our sample size is small, warranting the need for further investigation, the findings of this preliminary study suggest that antipsychotic-induced hyperprolactinemia, alone, may not adequately explain the observed ovarian dysfunction in women with schizophrenia.

Adult↗