Pharmacophilia and pharmacophobia: determinants of patients' attitudes towards antipsychotic medication.

OBJECTIVE: To identify factors that influence attitudes towards psychopharmacological treatment in patients suffering from schizophrenia and schizoaffective psychoses. METHODS: Ninety-two participants in an outpatient psychoeducational program, classed as "pharmacophobic" or "pharmacophilic" according to the Drug Attitude Inventory scale, were compared with regard to sociodemographic variables, clinical characteristics, subjective deficit syndrome, illness concepts, knowledge, locus of control, and quality of life. RESULTS: The 59 pharmacophilic and the 33 pharmacophobic patients did not differ significantly with regard to most sociodemographic variables, symptoms, or classic personality traits such as locus of control, self-concept, and quality of life. The only differences concerned hospitalization history ( P < 0.05) and statements on the actual, subjective experience of desired and undesired effects of medication ( P < 0.01). CONCLUSIONS: The impact of subjective experiences with drug treatment on attitudes towards medication and compliance needs to be a main focus of interventions targeting attitudes towards pharmacological treatment.

Possible association between childhood absence epilepsy and the gene encoding GABRB3.

BACKGROUND: Childhood Absence Epilepsy (CAE) is considered to have a predominantly, perhaps exclusively, genetic background. To date, genes responsible for susceptibility to CAE have not been identified. The object of the present study was to test association between CAE and the genes encoding the gamma-aminobutyric acid (GABA) type-A receptor subunits alpha 5 (GABRA5) and beta 3 (GABRB3) located on the long arm of chromosome 15 (15q11-q13). METHODS: A family-based candidate gene approach was applied: 50 Austrian nuclear families ascertained for the presence of an affected child were investigated. GABRA5 and GABRB3 subunit genes were genotyped using DNA gained from peripheral blood samples by Polymerase Chain Reactions (PCR). Genetic association was tested using a Monte Carlo Version of the multi-allele Transmission-Disequilibrium Test (TDT). RESULTS: The TDT displayed significant overall association with GABRB3 (p = .0118). CONCLUSIONS: The present data suggest that the tested polymorphism may be either directly involved in the etiology of CAE or in linkage disequilibrium with disease-predisposing sites.

Bright light therapy stabilizes the antidepressant effect of partial sleep deprivation.

Partial sleep deprivation (PSD) results in a pronounced decrease of depressive symptoms in the majority of patients with major depressive disorder. Generally this acute antidepressant effect is not stable, relapse usually occurs after one night of recovery sleep. We therefore studied whether light therapy, beginning in the morning after PSD, is able to prevent the relapse after sleep deprivation, using a controlled, balanced, parallel design. All patients received an antidepressant medication, which was kept constant before and during the study period. Fourteen of 20 patients (70%) showed a reduction of at least 40% in the Hamilton Depression Rating Scale (HDRS) in the morning after PSD and were classified as PSD responders. Responders as well as nonresponders were randomly assigned to receive either bright light (BL/3000 lux) or dim light (DL/100 lux) therapy during the following 6 days after PSD. In the responder group BL therapy prevented significantly (p = 0.005) the relapse after the next night of sleep and prolonged significantly (p = 0.011) the antidepressant effects of PSD up to 7 days. In contrast, patients in the DL condition relapsed after the recovery night and showed no further improvement of the depressive syndrome after 1 week of DL therapy. PSD nonresponders did not benefit from light treatment. These findings indicate that BL therapy might be efficacious to prevent relapse after PSD.