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We examined the relationship between perceived quality of life (QOL) and subjective quality of sleep among schizophrenia patients, and its relation to symptom severity, side effects and emotional distress. One hundred and forty five schizophrenia patients were comprehensively evaluated with standardized measures of symptom severity, adverse effects, emotional distress, QOL, and sleep quality (the Pittsburgh Sleep Quality Index, PSQI). Partial correlation and multiple regression analyses were performed. Poor sleepers reported lower mean scores on all QOL domains, they were more depressed and distressed, and had more adverse effects to medications with concomitant distress than good sleepers. The negative relationship between complaints of poor sleep quality and QOL measures remained significant when the confounding effect of depression, side effects, and distress was partialled from the correlation matrix. Daytime dysfunction (a component of the PSQI) accounted for 12.6% of the variance in QOL index scores. Thus, poor QOL reported by schizophrenia patients is substantially associated with poor sleep quality. This association appears both independently and synergistically with depression, distress and side effects of medications.

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This study compared the manifest dream content of 20 schizophrenic adolescent inpatients whose medications were stable for at least four weeks, 21 adolescent inpatients with other mental disorders (nonschizophrenic group) matched for age and gender, and 31 matched community controls. All participants were administered the standardized Formal Dream Content Rating Scale (FDCRS), which evaluates dream-related anxiety, cognitive disturbance, implausibility, involvement, primitivity, and recall, as well as two additional scales measuring emotional expression and duration of dream report. The Positive and Negative Symptoms Scale (PANSS) was administered to the two inpatient groups. The community controls demonstrated more involvement and emotional expression than the schizophrenic patients; furthermore, they demonstrated more implausibility and had a greater duration of dream report compared with the nonschizophrenic group. In the schizophrenic patients only, elevated scores on the negative subscale of the PANSS were significantly correlated with lower scores on involvement, emotional expression, and dream recall. No relationship was found between the positive subscale of the PANSS and any of the FDCRS subscales. These results suggest that psychopathology per se, rather than the specific psychiatric disturbance, may be associated with impoverishment of dream content, and that negative, rather than positive, schizophrenic symptomatology may be influential in the dream content of schizophrenic youngsters.

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Olanzapine is a substrate of the cytochrome P450 enzyme (CYP) 1A2. In this study, pharmacokinetic interactions and clinical effects of adding the CYP1A2 inhibitor fluvoxamine to steady-state olanzapine was examined in patients suffering from schizophrenia. Eight patients had been treated for at least 3 months with 10 to 20 mg/day olanzapine. Fluvoxamine (100 mg/day) was added (week 0) to the olanzapine treatment and continued for 8 weeks. Concentrations of olanzapine and its metabolite N-desmethylolanzapine and of fluvoxamine were analyzed at weeks 0, 1, 4, and 8. Addition of fluvoxamine resulted in a 12% to 112% ( < 0.01) increase of olanzapine from 31 +/- SD 15 ng/mL (week 0) to 56 +/- 31 ng/mL (week 8) in all patients. N-desmethylolanzapine concentrations were not significantly changed ( > 0.05). Fluvoxamine concentrations were 48 +/- 26 ng/mL on week 1 and 83 +/- 47 ng/mL on week 8. It is concluded that fluvoxamine affects olanzapine degradation and thus increases olanzapine concentrations. Although the combination was well tolerated in this sample and the negative symptom response appeared to be favorable in at least five patients, the combination therapy of olanzapine and fluvoxamine should be used cautiously and should be controlled by therapeutic drug monitoring to avoid olanzapine-induced side effects or intoxications.

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The records of 52 patients with major depression who were treated with bilateral electroconvulsive therapy (ECT) were reviewed. Responders and nonresponders were compared on demographic, clinical, and treatment parameters. ECT nonresponders had a longer duration of current depressive episode as well as a greater initial severity of depression. The groups did not differ in age, sex, polarity, presence of psychosis, pre-ECT pharmacotherapy, and treatment parameters other than total electrical charge administered. Patients with long episode duration and greater severity of illness may represent a subgroup of major depressives relatively refractory to ECT and warranting novel therapeutic approaches.