Family conflict, drug or alcohol use, and preexisting suicidal thoughts were associated with the occurrence of suicidal events among depressed adolescents who switched treatments after lack of response to a selective serotonin reuptake inhibitor (SSRI). Brent et al. (p. 418) report that the 334 patients were treated with a different SSRI or venlafaxine, with or without cognitive-behavioral therapy (CBT). Overall, the treatments did not differ in the frequency of suicidal events, which occurred a median of 3 weeks from treatment onset. However, among patients with high baseline levels of suicidal thoughts, those taking venlafaxine were more likely to have self-harm events. Benzodiazepine prescription was also associated with increased suicidal events. CBT did not have a protective effect on suicidality. During the trial, assessment of self-harm was changed from spontaneous patient reports to systematic monitoring, which revealed a higher number of overall suicidal events but a similar number of serious adverse events. Dr. Myrna Weissman discusses these findings in an editorial on p. 385.

A dimensional model is often proposed as an alternative to the current categories for diagnosing personality disorders. Rottman et al. (CME, p. 427) compared the current criteria in the Diagnostic and Statistical Manual (DSM-IV) with the Five-Factor Model (FFM), which covers 30 personality traits. Nearly 200 mental health professionals were asked to assign diagnoses to prototypical cases. Some case profiles used the symptom format of DSM-IV, and some used FFM descriptors. Diagnoses based on the FFM were less likely to be correct, and the participants rated the FFM as less clinically useful than DSM-IV for five of six functions. Andrew Skodol and Donna Bender examine the diagnosis of personality disorders in an editorial on p. 388.

Two family-based studies point toward genetic factors in schizophrenia for specific populations. Wratten et al. (p. 434) studied 24 Canadian families of Celtic or German descent that contained multiple relatives with schizophrenia. Testing focused on 60 variable regions in the NOS1AP gene, which influences synthesis of nitric oxide and thereby affects the neurotransmitter glutamate. Three of these regions were highly associated with schizophrenia, and a variant of one of these regions appears to increase the risk for the illness. An editorial on p. 392 by Drs. Susan Hodge and Robert Freedman explains the new statistical method used to identify this variant. The importance of a homogeneous population is illustrated by Escamilla et al. (p. 442), who conducted a genome-wide scan of 189 families of Latin American ancestry containing at least two siblings with a psychotic disorder. A region on chromosome 17q21 showed linkage to a diagnosis of schizophrenia or schizoaffective disorder, and it also showed suggestive linkage to the broader category of all psychotic disorders. A region on 15q22-24 showed a suggestive relationship to the narrower diagnosis.

A clue to the amygdale’s role in autism comes from the finding that patients with the disorder do not have the usual decrease in amygdala activity after repeated presentation of facial images. The amygdala is key to the mental processing of faces, and it has been proposed that dysfunction of the amygdala is related to the social deficits of autism. Kleinhans (CME, p. 467) found that habituation of the amygdala to faces was less in high-functioning adults with autism spectrum disorders than in IQ-matched healthy subjects. In addition, this lack of amygdala habituation was correlated with ratings of social impairment. An editorial by Michael Lombardo, Bhismadev Chakrabarti, and Simon Baron-Cohen on p. 395 highlights important facets of this study.