AbdelMalik et al (SEE ARTICLE) investigated the role of childhood head injury in the development of schizophrenia in Canadian families with a familial form of the disorder. Age at onset of psychosis was significantly younger in individuals who had a history of mild head injury (eg, concussion) before age 11 years. History of childhood head injury was also twice as likely in individuals with schizophrenia than their unaffected siblings.
Lencz et al (SEE ARTICLE) report results of a visual delayed match-to-sample task that was designed to separate the roles of 2 cognitive functions: initial representation of the stimulus (perceptual competence) and maintenance of the representation over delay. Patients in the first episode of schizophrenia, including antipsychotic-naive patients, had impairments in perceptual competence when compared with healthy controls. These patients also demonstrated maintenance deficits, suggesting 2 dissociable abnormalities.
Mathalon et al (SEE ARTICLE) investigated whether patients comorbid for schizophrenia and alcoholism suffer compounded brain volume deficits. They compared structural magnetic resonance imaging scans from comorbid, schizophrenic, alcoholic, and healthy control men. All patient groups showed cortical gray matter volume deficits; however, the comorbid group showed significantly greater deficits in the prefrontal cortex, despite matching the schizophrenic group in illness severity and duration and having 5 times less lifetime alcohol consumption than the alcoholic group.
Families with varying maternal histories of depression were studied by Hammen and Brennan (SEE ARTICLE) . Severity of maternal depression in the child's first 10 years predicted youth depressive disorders by age 15 years; major depressive episodes of even 1 to 2 months' duration significantly increased children's risk. Nondepressive disorders in youth appeared to be more predicted by maternal chronicity than severity. Timing of maternal depression, disaggregated from severity and chronicity, did not differentially affect risk.
Judd et al (SEE ARTICLE) described the naturalistic weekly symptom status of patients with biopolar II disorder (BP-II) during the long-term course of their illness. Longitudinally, BP-II is a chronic affective disorder; patients were symptomatic over half the time. The disorder is expressed within each patient as a fluctuating dimensional continuum that includes the full severity range of depressive and hypomanic symptoms. Depression dominates BP-II, primarily at the minor and subsyndromal levels. Hypomanic episodes of long (
7 days) vs short duration (2-6 days) appear to be a part of the same disease process.
The precise molecular mechanisms associated with suicidal behavior remain unclear. The transcription factor CREB regulates the expression of many genes in neurons that mediate critical physiological functions.Dwivedi et al (SEE ARTICLE) report that activation as well as expression of CREB are reduced in the prefrontal cortex and hippocampus of all suicide victims, irrespective of psychiatric diagnosis. Given the role of CREB in regulating physiological functions through gene transcription, decreased activation and expression of CREB could be of pathophysiological significance.
Orr et al (SEE ARTICLE) used an identical co-twin control design to clarify the origin of larger heart rate responses to sudden, loud tones in posttraumatic stress disorder (PTSD). Pairs of Vietnam combat veterans diagnosed as having PTSD or non-PTSD and their non–combat-exposed, monozygotic twins were studied in the psychophysiology laboratory. The larger average heart rate responses observed in the veterans with PTSD were not shared by their non–combat-exposed co-twins, suggesting that this biological PTSD marker represents an acquired sign of PTSD rather than a familial vulnerability factor.
Breslau et al (SEE ARTICLE) examined whether traumatic events increased the risk for substance use disorders independent of posttraumatic stress disorder (PTSD). They found elevated risk of nicotine dependence and drug disorder in trauma victims with PTSD but not in the absence of PTSD, compared with unexposed persons. Trauma did not predict alcohol disorder either in the presence or the absence of PTSD. Posttraumatic stress disorder might be a causal factor in nicotine and drug use disorders.
Chronic high-frequency stimulation of the subthalamic nucleus is a relatively new therapy in the treatment of advanced stages of Parkinson disease. Schneider et al (SEE ARTICLE) investigated the acute effects of this stimulation on emotional, cognitive, and motor functions in patients with Parkinson disease and compared them with a dopaminergic challenge. They found that subthalamic nucleus stimulation selectively improved emotional memory, mood induction effect, and self-reported well-being, as well as motor functions. Cognitive functions remained unaffected.
Toomey et al (SEE ARTICLE) used a co-twin control research design to examine whether there are residual deficits in neuropsychological functioning 1 year past cessation of heavy stimulant abuse. Twins were administered a neuropsychological test battery assessing attention, executive functioning, motor skills, intelligence, and memory. Abusing twins demonstrated deficits in motor skills and attention, but also showed a strength on one measure of attention, visual vigilance.
Calcyon is a member of a novel group of dopamine D1 receptor interacting proteins capable of modifying the function of this receptor. In a postmortem study, Koh et al (SEE ARTICLE) report that the levels of calcyon are nearly doubled in the prefrontal cortex in individuals with schizophrenia as compared with controls or individuals with bipolar disorder or depression.
