As psychiatry has become increasingly dominated by the neurosciences,
the role of psychoanalytic treatments within psychiatry has become more and
more controversial. Psychoanalytic treatments may be necessary when other
treatments are not effective, or for the residual, often less manifest, problems
that persist after brief interventions. After reviewing existing evidence
on the efficacy and effectiveness of psychoanalytic
treatments, Gabbard et al (SEE ARTICLE) propose a research agenda for
21st-century psychiatry that will answer the still-unresolved questions about
these treatments.
Several postmortem studies showed an elevation of serotonin 5-HT1A receptor density in schizophrenia. In the first study examining those
receptors in schizophrenic patients in vivo using positron emission tomography
and [11C]WAY-100635, Tauscher et al (SEE ARTICLE) demonstrate a higher 5-HT1A receptor binding
potential in the cortex of schizophrenic patients as compared with an age-matched
healthy control group. While the biological significance of elevated 5-HT1A receptor density in schizophrenia remains unclear, this finding needs
to been seen in the light of preclinical evidence supporting a role for 5-HT1A receptors in mediating antipsychotic action and extrapyramidal side
effects of drugs.
Heckers et al (SEE ARTICLE) studied
messenger RNA (mRNA) expression of glutamic acid decarboxylase (GAD), the
hallmark enzyme of GABAergic neurons, in the hippocampus of bipolar and schizophrenic
patients. The number of GAD mRNApositive neurons was markedly reduced
in bipolar disorder and showed a more subtle decrease in schizophrenia. The
cellular expression of GAD65 mRNA was significantly reduced in one hippocampal
sector, CA4, in bipolar disorder. These findings confirm previous reports
of an abnormal GABA system in both disorders, and provide novel evidence for
an abnormal regulation of GAD in hippocampal neurons in bipolar disorder.
This is the first prospective longitudinal study of the natural history
of the weekly symptomatic status of bipolar I disorders. During a mean of
13.2 years of follow-up, bipolar I emerged as a chronic illness in which patients
were symptomatic 47% of the time. Judd et al (SEE ARTICLE) also found the weekly symptom status is primarily depressive
rather than manic (3:1 ratio, respectively). Subthreshold affective symptoms
were 3 times more common than symptoms at the manic and major depressive level.
Longitudinally, symptom severity and polarity fluctuate frequently within
the same patient.
There are questions about long-term outcomes of cocaine-dependent patients
following discharge. Simpson et al (SEE ARTICLE) found that only 1 in 4 patients admitted to a national sample of treatment
programs still used cocaine on a weekly basis 5 years latercomparable
to rates reported in the first year after treatment. Greater severity of drug
use and related problems at intake as well as more limited treatment contact
were related to poorer outcomes on drug use and criminal activity.
Johnson et al (SEE ARTICLE) found
that adolescents with eating disorders were at substantially elevated risk
for anxiety disorders, cardiovascular symptoms, chronic fatigue, chronic pain,
depressive disorders, limitations in activities, infectious diseases, insomnia,
neurological symptoms, and suicide attempts during early adulthood after adolescent
health problems, psychiatric comorbidity, body mass index, socioeconomic status,
and worries about health during adulthood were controlled statistically. These
findings suggest that adolescent eating disorders may contribute to the development
of physical and mental health problems during early adulthood.
Several recent magnetic resonance imaging (MRI) studies have reported
progressive changes in the size of various brain structures, supporting speculation
about neurodegeneration. Weinberger et al (SEE ARTICLE) question the meaning of the progressive changes found with MRI and the improbability
that they reflect neurodgeneration, including that the pattern of changes
are inconsistent from one study to another, that most patients actually improved
clinically while these apparent progressive changes emerged, and that the
magnitude of the changes rivals that found in neurodegenerative disorders
such as Alzheimer disease, yet that evidence of neurodegeneration is conspicuously
absent from postmortem tissue studies. It is concluded that MRI evidence of
progressive changes probably reflects something other than irreversible neurodegeneration.