Patients ages 7 to 18 years old whose depression responded to 12 weeks of fluoxetine treatment were more likely to avoid relapse during the next 6 months if they continued to take fluoxetine than if they were switched to placebo. The relapse rates during continuation treatment were 42% for the 50 patients randomly assigned to fluoxetine and 69% for the 52 assigned to placebo. Emslie et al. (CME, p. 459) also found that the time to relapse was longer for the fluoxetine group. Relapse rates were similar in children and in adolescents, but the impact of continued fluoxetine treatment was greater for boys than for girls. These findings are the subject of an editorial by Dr. Neal Ryan on p. 411.

Improvement was greater for 65 patients with borderline personality disorder who received standard treatment plus a group program with cognitive-behavioral, skills training, and systems components than for 59 patients who received standard treatment only. Blum et al. (p. 468) describe the group treatment, known as Systems Training for Emotional Predictability and Problem Solving, or STEPPS. It consists of 20 weekly sessions for patients and one session for family members and significant others on how to respond to the patient. At the end of treatment, the patients who received STEPPS plus treatment as usual had greater improvements in impulsive, affective, cognitive, and interpersonal domains, as well as overall global measures, compared to those who received usual treatment only. Most gains were maintained over 1 year of follow-up. Dr. Kenneth Silk discusses treatment for borderline personality disorder in an editorial on p. 413.

Longitudinal measurements of brain volume in patients with recent-onset schizophrenia revealed that those who used cannabis during 5 years of follow-up lost more gray matter volume than patients who did not use cannabis. The cannabis users also had greater increases in volumes of the lateral and third ventricles. Rais et al. (p. 490) report that the 19 cannabis users had less symptomatic improvement during follow-up than the 32 nonusers, but functional outcomes and days of hospitalization were similar in the two groups. Hashimoto et al. (p. 479) extended the finding of altered gene expression affecting γ-aminobutyric acid (GABA) in schizophrenia, from the dorsolateral prefrontal cortex to the anterior cingulate, primary motor, and primary visual cortices. Seven GABA-related transcripts were expressed at lower levels in the postmortem brains of 12 subjects with schizophrenia than in normal subjects, and the magnitude of the differences was indistinguishable across the four brain regions. Since the areas represent different functions, GABA-related abnormalities may contribute to multiple features of schizophrenia. Dr. Robert Freedman examines these findings in an editorial on p. 416.

Systematic testing of 648 variants in 14 genes did not confirm the relationships to schizophrenia shown in previous smaller studies. Sanders et al. (p. 497) determined genotypes of common single-nucleotide polymorphisms (SNPs) in 1,870 people with schizophrenia or schizoaffective disorder and 2,002 comparison subjects. Although 30 of the 648 tests showed nominal statistical significance, they did not meet the stricter threshold required for the large number of tests. The 14 candidate genes have drawn great interest because they are involved in pathways that can plausibly be related to hypothesized mechanisms in schizophrenia. Although small effects cannot be definitively ruled out, it is unlikely that these common SNPs account for a substantial proportion of the genetic risk for schizophrenia. Dr. Steven Hamilton reflects on the genetics of schizophrenia in an editorial on p. 420.