Alcohol withdrawal is a clinically and etiologically heterogeneous syndrome caused by a complex interaction of environmental (e.g., amount of ethanol) and genetic factors. Multiple genes are considered to be involved in various components of the syndrome, each of them contributing only modestly to withdrawal vulnerability. Association studies using candidate genes of the dopamine, serotonin, gabaergic and opioidergic systems are reviewed and methodological limitations are discussed.

The introduction of atypical antipsychotics has triggered a reevaluation of treatment strategies in schizophrenia. Although research findings inform about the efficacy and safety of drugs, it is the decisions made daily in ordinary practice that affect the vast majority of patients. The aim of this paper was to examine the use of atypical antipsychotics in clinical care, by means of a survey of prescribing practices for clozapine, risperidone, olanzapine, sertindole and quetiapine for all patients treated for DSM-IV schizophrenia within a psychiatric service. Seventy-five (26%) of the 286 patients identified were on atypical antipsychotics. Patients on clozapine were mostly male, had more than 15 years of contact with psychiatric services and were poor responders. Patients prescribed other atypicals had responded to prior treatment with typical neuroleptics and had less than five years of contact with psychiatric services. Gender distribution was equal in this group. The use of research criteria for treatment resistance identified only one patient, as prolonged use of high-dose neuroleptics was uncommon. The new atypical antipsychotics appear to be replacing older neuroleptics as the first-line treatment of schizophrenia while clozapine is mostly reserved for poor responders. Clinicians' definition of treatment resistance was variable and below the threshold used in research.

All drugs abused by humans increase dopamine in the shell of nucleus accumbens, which implicate the neurons of this structure in their hedonic and reinforcing properties. Among the various dopamine receptor subtypes, the D1 (D1R) and D3 (D3R) receptors co-localise in accumbal shell neurons. Synergistic D1R/D3R interactions at this level were found on gene expression and during induction and expression of behavioral sensitisation to levodopa in rats bearing unilateral lesions of dopamine neurons. Behavioral sensitisation to abused drugs is a component of their long-term effects. Converging pharmacologic, human postmortem and genetic studies suggest the involvement of the D3R in reinforcing effects of drugs; D3R agonists reduced cocaine self-administration in rats, without disrupting the maintenance of self-administration. These data suggest the use of D3R agonists as partial substitutes to treat cocaine dependence, by affecting its reward component. However, substitution therapies maintain dependence and may be inefficient on drug craving and relapse, which are the unsolved and critical problems in the treatment of drug addiction. Recently, a highly selective and partial D3R agonist was shown to reduce cocaine-associated cue-controlled behaviour in rats, without having any primary intrinsic effects. As drug-associated cues maintain drug-seeking in animals and elicit craving and relapse in humans, such D3R agents have potential therapeutic applications.

Torture has been a widespread experience in the twentieth century. Acute and chronic psychological sequelae are common among victims of torture. To our knowledge, there are few reports about eating disorders as a psychological sequela of torture. We report a female patient who developed an eating disorder following torture. A case of weight loss from food avoidance and vomiting in a young adult Turkish torture victim is described, and possible etiological factors discussed.