Copyright 2001 American Medical Association. All Rights Reserved. Applicable FARS/DFARS Restrictions Apply to Government Use.2001
People with panic disorder (PD) may be oversensitive to a mild suffocatory stimulus, but the mechanism underlying laboratory-induced panic remains undescribed. Battaglia et alArticle found that the anxious reaction to CO2 inhalation in PD patients becomes blunted when brain cholinergic muscarinic receptors are temporarily blocked by biperiden. Brain muscarinic receptors may partially control sensitivity to CO2 inhalation, a trait that may vary among individuals.
A commentary by Roy-Byrne and Stein is included.Article
Gorman et alArticle found that although patients with panic disorder do have panic attacks more frequently than normal volunteers or patients with major depression, the exaggerated respiratory responses observed are more a function of if a panic attack occurs than the diagnostic group of an individual.
Theories that the primary deficit in schizophrenia is a loss of functional connectivity have drawn attention to the thalamus, with its important links to frontal-temporal cortex. Magnetic resonance imaging (MRI) studies have described diminished size of both the frontal and temporal lobes. Volume loss could also characterize their primary thalamic relay nuclei, the mediodorsal nucleus, and the pulvinar. Using a reliable intensity-gradient delineation filter, Byne et alArticle found significant volume loss in schizophrenia. These findings of the first MRI evidence of a structural abnormality in these thalamic nuclei have implications for the neural circuitry impairments in schizophrenia.
Mathalon et alArticle compared change in brain volume over an average of 4 years in men with schizophrenia and controls. Cortical sulci, lateral ventricles, and gray matter in the frontotemporal cortex deteriorated faster in patients than in controls, with greater clinical severity associated with faster rates of frontotemporal brain volume decline.
The outbreak of a first psychotic episode of schizophrenia is often preceded by cognitive and affective changes, which strain the person affected and might lead to social deficits, but, as based on retrospective studies, were regarded as too unspecific for an early detection of psychoses. Klosterkötter et al's prospective study of such patients Article showed a good predictive accuracy for some of these prodromal symptoms, especially certain thought, language, and perception disturbances.
People with schizophrenia differ greatly in how their illness affects them. Kirkpatrick et alArticle propose that one group of patients may have a disease separate from other forms of schizophrenia, with differences in signs and symptoms, course of illness, biological correlates, treatment response, and risk factors. They outline a research plan for testing the competing hypotheses of a single vs multiple diseases.
Psychiatric symptoms associated with anabolic steroid abuse are well described, but underlying biological mechanisms remain poorly understood. In the first reported study of CSF changes during anabolic steroid use, Daly et alArticle observed significant changes in levels of the neurotransmitter metabolites 5-HIAA and MHPG during high-dose administration of the anabolic steroid methyltestosterone to normal male volunteers. The changes in 5-HIAA levels correlated with some of the behavioral symptom changes observed. The findings suggest a role for serotonergic systems in the development of adverse psychological responses to anabolic steroids.
Simon et alArticle evaluated the cost-effectiveness of a systematic outpatient depression management program for high utilizers of general medical care and found that those participating in the depression management program experienced significantly less time depressed and had higher health care costs (especially for follow-up visits and antidepressant medications). The balance of benefits and costs compares favorably with several generally accepted medical interventions.
In a family study, Heun et alArticle observed a clustering of primary progressive dementia in families of patients with Alzheimer disease, of late-onset depression (onset age ≥60 years) in relatives of patients with late-onset depression, and of early-onset depression in families of patients with early-onset depression. The lack of overlap of familial aggregations suggest that the disorders represent clinical entities with distinct inheritance. Other reasons must be investigated to explain the observed comorbidity and symptomatic similarities.
This Month in Archives of General Psychiatry. Arch Gen Psychiatry. 2001;58(2):113. doi:10.1001/archpsyc.58.2.113