Recent studies are focusing on the biological pathways of depressive symptoms rather than the syndrome. Tremblay et al Article hypothesized that the brain reward system, the neural pathways that mediate pleasure and motivation, may represent a neural substrate of specific depressive symptoms such as anhedonia. In this study, patients diagnosed as having major depressive disorder exhibited a hypersensitive response to a dopaminergic probe's rewarding effects, which was dependent on the severity of depression. Brain reward system dopaminergic pathways may develop into a future therapeutic target in major depressive disorder.
Disrupted attention is characteristic of schizophrenia. Event-related potential (ERP) studies have found abnormalities in auditory attention in schizophrenia, but results from visual attention studies have been inconsistent. Potts et al Article demonstrated a specific reduction of attention-related ERP components (the frontal P2a and posterior N2b) in patients with schizophrenia in a visual (location/feature) selective attention task, indicating a disruption in the neural systems supporting visual attention. The topographic distribution of these components suggested dysfunction in frontal cortex or disconnection between frontal executive functions and perceptual representations in posterior brain regions in patients with schizophrenia.
Although medication and psychosocial interventions have been developed to treat anxiety disorders, it is unclear how such treatments modify brain activity. Furmark et al Article used positron emission tomography to study cerebral blood flow during an anxiety-provoking speaking task in patients with social phobia, before and after treatment with citalopram or cognitive-behavioral therapy. Both treatments were equally effective and, regardless of treatment approach, symptom improvement was associated with reduced neural activity in the medial temporal lobe, including the amygdala and hippocampus. Citalopram and cognitive-behavioral therapy may thus exert their anxiety-reducing effects through a common pathway in the brain.
The importance of investigating the effect of comorbid personality disorders on the outcome of anxiety disorders has been addressed by few prospective longitudinal studies. Massion et al Article report that the presence of a personality disorder predicted a lower likelihood of remission from generalized anxiety disorder and social phobia, but not panic disorder. A lower likelihood of remission from generalized anxiety disorder was predicted by the presence of avoidant personality disorder or dependent personality disorder. The findings suggest a differential effect of personality disorders on the course of anxiety disorders.
Intramuscular (IM) typical antipsychotics are commonly used to treat acute agitation in schizophrenia, but may cause parkinsonian side effects. Breier et al Article report a dose-response relationship for IM olanzapine (2.5, 5.0, 7.5, and 10.0 mg per injection) in reducing acute agitation in schizophrenia. At 2 hours after the first injection, IM olanzapine was superior to placebo and as effective as IM haloperidol (7.5 mg per injection) in reducing agitation. The IM olanzapine was generally well tolerated and had a more favorable safety profile than IM haloperidol.
Are childhood developmental impairments specific to later schizophrenia? Cannon et al Article investigated childhood development between ages 3 and 11 years in relation to schizophreniform disorder, mania, and anxiety/depression at age 26 years in the Dunedin birth cohort. Motor, language, and cognitive impairments were associated only with later schizophreniform disorder, while emotional and interpersonal difficulties were associated with all adult psychiatric outcomes assessed. These findings support developmental etiological models of schizophrenia.
Evidence suggests that schizophrenia may be due to altered brain development early in life. In the largest study to date, McGrath et al Article have shown that people with psychosis tend to have slight alterations in the shape of their head, face, and palate compared with healthy individuals. While these changes do not allow diagnosis, the changes provide clues to early brain development. A relative overgrowth of the temporal lobes during early life may explain these new findings. While phrenology has long been discredited, perhaps the skull does provide a persisting record of early brain development in psychosis.
This Month in Archives of General Psychiatry. Arch Gen Psychiatry. 2002;59(5):407. doi:10.1001/archpsyc.59.5.407