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Psychotherapy for children and adolescents has advanced considerably in light of decades of empirical research. Even so, very little is known about why and for whom treatment works or the conditions of delivering treatment that optimize therapeutic change. KazdinArticle proposes a research plan that identifies the goals of therapy research, how they can be attained, and how to monitor progress toward the accumulation of knowledge. The plan emphasizes the importance of understanding the mechanisms through which therapeutic change occurs, connecting treatment to what is known about childhood and adolescent disorders, and expanding the range of questions that guide treatment research.
Commentaries by WeiszArticle and KendallArticle are included.
In a 4-week, double-blind, placebo-controlled study, Tohen et alArticle report that olanzapine was significantly more effective than placebo in reducing the symptoms of mania.
Using positron emission tomography, Yatham et alArticle found that depressed patients had a significant decrease in serotonin2 receptors in various brain regions. The findings suggest that the decrease in serotonin2 receptors could be a compensatory response of the brain to the state of depression.
Lieb et alArticle investigated a representative community sample of adolescents and their parents and found a strong association between parental social phobia and social phobia among offspring. Other forms of parental psychopathology, as well as parental overprotection and rejection, also were associated with social phobia in offspring. The findings suggest that multiple familial factors are involved in the development of social phobia.
Birmaher et alArticle evaluated whether growth hormone (GH) secretion after the administration of growth hormone–releasing hormone (GHRH) is altered in never-depressed youth at high risk to develop depression. Compared with normal controls, the high-risk subjects secreted significantly less GH. These results indicate that the decreased GH response found in high-risk subjects may represent a trait marker for depression in youth.
Increased platelet reactivity likely underlies the increased vulnerability of depressed patients to atherosclerotic heart disease and/or stroke. Musselman et alArticle sought to determine whether the increased platelet reactivity associated with major depression is reduced after antidepressant treatment. In comparison with normal control subjects, patients with major depression exhibited greater platelet procoagulant activity; ie, increased platelet binding of the monoclonal antibodies anti-LIBS and GA6 and increased plasma concentrations of platelet factor 4. After 6 weeks of open-label treatment with paroxetine, the depressed patients exhibited significant reduction in all 3 parameters.
Why do people differ in their liability to tobacco use? Kendler et alArticle address this question in a study of male-male and female-female pairs from the Swedish Twin Registry, raised together and apart. In males, genetic factors play a strong role in influencing risk for tobacco use in all cohorts. In females born before 1925, tobacco use was infrequent and risk was largely environmental. In later cohorts of women, rates of tobacco use increased, as did heritability.
In a controlled magnetic resonance imaging study of patients with schizophrenia, alcoholism, and schizophrenia combined with alcoholism, Sullivan et alArticle found that those with schizophrenia alone had enlarged fourth ventricles but no cerebellar tissue volume deficits, whereas patients with both diseases had cerebellar volume deficits (also observed in alcoholism) and fourth ventricular enlargement. Severity of brain dysmorphology in the comorbid group exceeded that observed in either single diagnosis and suggests that alcohol abuse may be especially damaging to brain already compromised by schizophrenia.
Inconsistencies exist in the schizophrenia literature concerning intellectual decline, premorbid deficits, and preserved abilities. In a large series of patients, Weickert et alArticle found 50% demonstrated marked intellectual decline from premorbid levels with executive function, episodic memory, and attention deficits; 25% exhibited premorbid intellectual impairment with global deficits; and 25% displayed preserved intellect with subtle executive function and attention deficits.
This Month in Archives of General Psychiatry. Arch Gen Psychiatry. 2000;57(9):827. doi:10.1001/archpsyc.57.9.827