The A allele of the 5-HT2A gene (–1438A/G polymorphism) has been associated with anorexia nervosa in four studies, but not in three others. One possibility to explain such a discrepancy is that the A allele acts as a modifying rather than a vulnerability allele. To test this hypothesis, we increased our initial sample of 102 trios [Mol. Psychiatry 7 (2002) 90] with 43 new patients with anorexia nervosa and 98 healthy controls. In addition to confirming the absence of association on the global sample of 145 patients, we found that patients with the A allele had a significantly later age at onset of the disease (P = 0.032). Furthermore, the A allele was also transmitted with an older age at onset (P = 0.023) using a quantitative-trait TDT approach. The A allele may thus act as a modifying factor (delaying onset), potentially explaining variations of allele frequency across samples, in which differences in average age at onset are not only possible, but also expected. Taking into account vulnerability genes, but also genes modifying the expression of the disorder, will help to disentangle the complexity of the etiological factors involved in anorexia nervosa.

Retrospective evaluation of patients admitted consecutively to the psychiatric units of two general hospitals in Florence, to evaluate the rate and risk factors of neuroleptic-induced dystonia (NDA). One hundred and fifty-nine patients out of 2354 reviewed charts were included. The incidence of NDA was 15.7%. Multivariate analyses revealed that both age and neuroleptization speed (NS)—a new variable—were related to the occurrence of dystonia.

The Kleine–Levin syndrome (KLS) is characterized by periodic, sudden-onset episodes of hypersomnia, compulsive hyperphagia, and behavioral–emotional symptoms, lasting from a few days to a few weeks, with complete remission in the intercritical periods. We report on efficacy of lithium treatment in a highly recurring form of the disorder in a 17-year-old male adolescent. The decreasing severity of the disorder paralleled the progressive increase of lithium dosage, up to 0.9 mEq l–1. Implications regarding the pharmacological treatment of this neglected disorder are discussed.