Several studies have indicated that patients with bipolar disorder (BD) who respond well to lithium prophylaxis constitute a biologically distinct subgroup. Lithium is thought to stablize mood by acting at the phosphoinositide cycle. We have investigated a polymorphism located in the gene (PLCG1) that codes for a ␥-1 isozyme of phospholipase (PLC), an enzyme that plays an important role in the phosphoinositide second messenger system. A population-based association study and a family-based linkage study were carried out on patients who were considered excellent responders to lithium prophylaxis. Response to lithium was evaluated prospectively with an average follow-up of 14.4 ± 6.8 years. The PLCG1 polymorphism was investigated in 136 excellent lithium responders and 163 controls. In addition, the segregation of this marker was studied in 32 families ascertained through lithium-responsive bipolar probands. The allele distributions between lithium-responsive bipolar patients and controls were different, with a higher frequency of one of the PLCG1 polymorphisms in patients ( 2 = 8.09; empirical P = 0.033). This polymorphism, however, confers only a small risk (OR = 1.88, CI 1.19-3.00). Linkage studies with the same marker yielded modest support for the involvement of this gene in the pathogenesis of BD when unilineal families were considered (Max LOD = 1.45; empirical P = 0.004), but not in the whole sample. Our results provide preliminary evidence that a PLC isozyme may confer susceptibility to bipolar disorder, probably accounting for a fraction of the total genetic variance. Whether this polymorphism is implicated in the pathogenesis of BD or in the mechanism of lithium response remains to be determined.

The aim of the present study was to develop a Swedish self-rating instrument for clinical aggression research based on the American Aggression Questionnaire (AQ), which measures physical aggression, verbal aggression, anger, and hostility. To test this adapted Aggression Questionnaire--revised Swedish version (AQ-RSV), it was mailed to 781 randomly selected individuals, aged 20-40 year. A total of 497 (64%) evaluable AQ-RSV inventories were obtained and analyzed statistically. Drop-out analysis showed that non-responders were most often male and significantly older than responders. Among the responders, AQ-RSV showed significant sex differences in all aggression subscales except Hostility. Aggression was found to vary with age, geographical region, and size of home community. The AQ and the AQ-RSV were comparable in correlations between the four aggression subscales and in alpha coefficients, which indicated considerable internal consistency. Development of the aggression-measuring instrument for Swedish conditions is important not only to study subtraits of aggression but to enable analyses of their relationships to neurobiological and psychiatric variables.

Objective:  To study the impact of torture on symptomatology among mass displaced adults. Method: A sample (total 131; 70 females, 61 males) of mass displaced adults from Kosovo, in Sweden, completed 3 months after a baseline study on trauma experiences and perceived symptoms, self‐rated instruments measuring psychiatric symptoms, aggression and coping. Results:  Torture is associated with poor coping (manageability); depression, anxiety and aggression are associated with post‐traumatic stress disorder. All psychiatric symptoms and poor coping (but not aggression) are associated with being female. Limitations of the study include a relatively small sample. Ongoing trauma and stress before repatriation may also influence the responses. Several lessons learnt for prevention are discussed. Conclusion: Anger and hostility are important consequences of torture. Further research is necessary to understand the associations among coping strategies, psychiatric symptoms, aggression, torture experience and gender over time after repatriation or applying for asylum.

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Corticotropin-releasing hormone (CRH) and proenkephalin (PENK) are hypothalamic peptides involved in the stress response and hypothalamic-pituitary axis regulation. Previous research has implicated these peptides in the pathogenesis of affective disorders. In this study we investigated two polymorphisms located in the genes that code for CRH and PENK by means of association and linkage analyses. A total of 138 bipolar patients and 108 controls were included in the association study. In addition, 24 families were available for linkage analysis, including six families of probands with documented periodic positivity of dexamethasone suppression tests (DST) during remission. We found no association of bipolar disorder with either gene. Similarly, we did not find any evidence of linkage (P = 0.56 for CRH and 0.52 for PENK) in the entire sample or in the subsample of families of DST positive probands. In conclusion, our study does not support the hypothesis that genes coding for CRH or PENK contribute to the genetic susceptibility to bipolar disorder. Am. J. Med. Genet. (Neuropsychiatr. Genet.) 96:178-181, 2000.