The burden, the coping strategies and the social network of a sample of 236 relatives of patients with schizophrenia, living in five European countries, were explored by well-validated assessment instruments. In all centres, relatives experienced higher levels of burden when they had poor coping resources and reduced social support. Relatives in Mediterranean centres, who reported lower levels of social support, were more resigned, and more often used spiritual help as a coping strategy. These data indicate that family burden and coping strategies can be influenced by cultural factors and suggest that family interventions should have also a social focus, aiming to increase the family social network and to reduce stigma.
The impact of social and clinical factors on the choice of coping strategies of a sample of 236 relatives of patients with schizophrenia, living in five European countries, was explored using well-validated questionnaires. The adoption of problem-focused coping strategies was more frequent among young relatives and among relatives of younger patients, and was associated with higher levels of practical and emotional social support and of professional help. In contrast, emotion-focused strategies were more frequently adopted by relatives who had been living longer with the patient and who had poorer social support. It is suggested that supportive and educational interventions should be provided as early as possible to relatives of patients with schizophrenia, which, in addition to having a practical focus, should also have a social focus, aiming at extending the family's social network.
In the search for genetic factors contributing to tardive dyskinesia, dopamine receptor genes are considered major candidates. The dopamine D3 receptor is of primary interest as dopamine D3 receptor knock-out mice show locomotor hyperactivation resembling extrapyramidal side-effects of neuroleptic treatment. Furthermore, Steen and colleagues (1997) recently reported an association between tardive dyskinesia and a dopamine D3 receptor gene variant. In the present study we tried to replicate this finding. We investigated 157 patients with schizophrenia or schizoaffective disorder receiving long-term neuroleptic medication who never or persistently displayed tardive dyskinesia. As advanced age is a main risk factor for tardive dyskinesia, we also compared older patients with a long duration of schizophrenia not displaying tardive dyskinesia to younger patients with a shorter duration of the illness displaying tardive dyskinesia. However, we found no evidence that the dopamine D3 receptor gene is likely to confer susceptibility to the development of tardive dyskinesia.
Treatment for schizophrenia is best provided by integrating the various and specific psychosocial intervention strategies in addition to the optimal use of medication. Methods for implementing these strategies in outpatient settings include the use of a comprehensive assessment and treatment plan, the training of mental health professionals, and periodic review with assessment packages.
Tardive dyskinesia (TD) is a common side effect of long-term medication with typical neuroleptics. TD presents itself by abnormal involuntary movements and may lead to a potentially disabling and chronic clinical course. A vast majority of patients suffering from schizophrenia are smokers. Smoking has been reported to induce the activity of the CYP1A2 enzyme, which is an established metabolic pathway within the disposition of antipsychotics. Recently, a C-->A genetic polymorphism in the first intron of the CYP1A2 gene was reported to influence CYP1A2 activity in smokers. Subsequently, a pharmacogenetic study in 85 U.S. patients with schizophrenia (44 smokers, 41 individuals with unknown smoking status) showed the C/C genotype to be associated with higher TD severity (measured by the Abnormal Involuntary Movement Scale, AIMS) than the A/C or A/A genotype. This finding prompted us to investigate whether this effect was also present in a larger German sample of 119 patients with schizophrenia (82 smokers, 37 individuals with unknown smoking status). However, we could not replicate the reported association. The median AIMS scores did not differ between individuals with the A/A, A/C, or C/C genotypes. In an additional analysis, we compared the genotypic and allelic distribution among individuals grouped according to the criteria established by Schooler and Kane [1982: Arch Gen Psychiatry 39:486-487] (persistent TD vs. absent TD). We did not observe a differential genotypic or allelic distribution between the two diagnostic groups. Thus, our results do not support the hypothesis that the C-->A polymorphism in the CYP1A2 gene is involved in the etiology of TD in the German population.
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