Individuals with schizophrenia show significant visual dysfunction, including the inability to recognize whole objects when only fragments are presented. Sehatpour et al used multimodal (event-related potential and functional magnetic resonance imaging) imaging to trace sequential brain activation during this task. Deficits were demonstrated first in dorsal visual stream regions and subsequently in a larger network also involving the prefrontal cortex and hippocampus.
In a longitudinal functional magnetic resonance imaging study, Lui et al report that widespread increased regional synchronous neural activity occurs after antipsychotic therapy, accompanied by decreased integration of function across widely distributed neural networks. These findings contribute to the understanding of the complex systems-level effects of antipsychotic drugs.
Diazgranados et al conducted a randomized, placebo-controlled, double-blind crossover study to evaluate the antidepressant efficacy of an N-methyl-D-aspartate receptor antagonist (ketamine hydrochloride) in treatment-resistant bipolar depression. Subjects receiving ketamine showed significant improvement in depression compared with subjects receiving placebo within 40 minutes after injection, which remained significant through day 3.
Erk et al examined the effect of a genome-wide evidence–supported risk variant for bipolar disorder on brain function during episodic memory processing. Healthy carriers of the CACNA1C risk variant exhibited a pronounced reduction of bilateral hippocampal and subgenual anterior cingulate activation during recall that was accompanied by heightened psychopathology scores. Based on convergent preclinical and clinical evidence, the authors provide a neurogenetic risk mechanism for bipolar disorder backed by genome-wide evidence.
To examine the cost-effectiveness of a rural telemedicine-based collaborative care depression intervention, 395 patients at 7 small (serving 1000-5000 veterans) Veterans Health Administration community-based outpatient clinics serving rural catchment areas in 3 mid-South states were randomized to the intervention or usual care. Pyne et al report significantly better quality-adjusted life year outcomes in the intervention group and the mean base case incremental cost-effectiveness ratio was $85 634/quality-adjusted life year.
For offspring with a parental history of mental disorder, the risk of developing a clinically related disorder has been well established. In a population-based cohort study, Dean et al found that the impact of parental mental disorder was not confined to elevated risk for offspring of developing concordant disorders since risk was found to be elevated across a wide range of disorders. Risk was highest among individuals with 2 parents with mental disorders.
Mosconi et al examined neurobehavioral characteristics in unaffected first-degree relatives of individuals with autism. Family members demonstrated oculomotor deficits similar to those we previously reported in individuals with autism. The profile of findings suggests that autism is associated with familial bilateral prefrontal and cerebellar alterations and left lateralized striatal and frontoparietal circuitry dysfunction.
Using population-based longitudinal register data of children born in Finland from 1987 to 1989 (n = 175 869), Ekblad et al studied the association between prenatal smoking exposure and the prevalence of psychiatric morbidity and mortality into young adulthood. The risk for psychiatric morbidity was significantly higher in the exposed children than in the unexposed children. The risk was significantly increased for the majority of the psychiatric diagnoses.
Hamer et al report an association between mental health and objectively assessed secondhand smoke exposure in a nationally representative sample of 5560 nonsmoking adults. High secondhand smoke exposure (salivary cotinine level >0.70 and <15.00 μg/L) was associated with psychological distress cross-sectionally and a higher risk of a psychiatric hospital admission over 6 years' follow-up.
Lidstone et al investigated the placebo effect in 35 patients with Parkinson disease using positron emission tomography with [11C]raclopride. Verbal manipulation was used to modulate the patients' expectations of receiving active treatment (levodopa) when they actually received placebo. Maximal dopamine release occurred when the declared probability of receiving levodopa was 75%, indicating that the probability of anticipated improvement can profoundly modulate response to therapy.