Recent studies are focusing on the biological pathways of depressive
symptoms rather than the syndrome. Tremblay et al (SEE 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 (SEE 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 (SEE 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 (SEE 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 (SEE 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 (SEE 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 (SEE 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.
