Physiopsychotherapy?

We sought to compare four different definitions of control groups in studies of the coaggregation between two disorders (A and B) on: 1) their ability to detect valid familial coaggregation; 2) their liability to artifactual evidence for familial coaggregation; and 3) their robustness to the overselection of comorbid cases. Using a quantitative genetic model of transmission, we simulated sibling pairs with familial and nonfamilial sources of comorbidity. Four different definitions of controls were tested to predict disorder B in siblings of cases vs. controls: 1) unscreened controls included subjects with A or B as well as subjects with either A or B; 2) in the symmetrical selection method, controls included only subjects without A; 3) supernormal controls included only subjects without A or B; and 4) in the pure proband method, cases included subjects with A only, and controls included only subjects without A or B. In the absence of selection bias, 1) the unscreened control and the symmetrical selection methods did not yield spurious evidence for familial coaggregation and could detect familial coaggregation; 2) the supernormal controls yielded spurious evidence of familial coaggregation; and 3) the pure proband method sometimes yielded spurious evidence for negative familial coaggregation, and had limited power to detect familial coaggregation. However, the pure proband method was the only one unaffected by overselection of comorbid cases. In the absence of selection bias, both the unscreened control and the symmetrical selection methods are appropriate, and the robustness of the pure proband method to overselection of comorbid cases may be an interesting feature in studies using clinical samples. Moreover, quantitative genetics methods may offer important advantages in the study of familial coaggregation.

Anxiety Disorders↗

PubMed1997

Positron emission tomography measurement of cerebral metabolic correlates of yohimbine administration in combat-related posttraumatic stress disorder.

BACKGROUND: We have previously reported an increase in symptoms of anxiety in patients with posttraumatic stress disorder (PTSD) following administration of the beta 2-antagonist yohimbine, which stimulates brain norepinephrine release. Preclinical studies show decreased metabolism in the neocortex and the caudate nucleus with high-dose yohimbine-induced norepinephrine release, but low levels of norepinephrine release result in an increase in metabolism in these areas. METHODS: We used positron emission tomography and fludeoxyglucose F 18 to measure brain metabolism in Vietnam combat veterans with PTSD (n = 10) and healthy age-matched control subjects (n = 10), following administration of yohimbine (0.4 mg/kg) or placebo in a randomized, double-blind fashion. RESULTS: Yohimbine resulted in a significant increase in anxiety in the patients with PTSD, but not in healthy subjects. There was a significant difference in brain metabolic response to yohimbine in patients with PTSD compared with healthy subjects in prefrontal, temporal, parietal, and orbitofrontal cortexes. Metabolism tended to decrease in patients with PTSD and increase in healthy subjects following administration of yohimbine. CONCLUSION: These findings are consistent with our previous hypothesis of enhanced norepinephrine release in the brain with yohimbine in patients with PTSD.

Anxiety Disorders↗