By Alan C. Swann (auth.), J. John Mann M.D., David J. Kupfer M.D. (eds.)
This moment of 2 elements compares and contrasts the biology of melancholy with different, clinically overlapping problems resembling alcoholism and consuming issues.
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Additional info for Biology of Depressive Disorders: Part B Subtypes of Depression and Comorbid Disorders
They can help validate these diagnoses in children and adolescents. They may help distinguish various subtypes of depression which may allow more accurate prediction in treatment response, relapse, or recurrence. These measures may, in the future, prove to have value as diagnostic or confirmatory tests. They may identify subgroups among depressed children who are at particularly high risk of violence, suicide, or homicide (particularly measures of serotonergic systems). , "high-risk" children).
HPA Ax1s-CRH STIMULATION TEST Corticotropin-releasing hormone (CRH) is a synthetic analog to an endogenously produced hypothalamic peptide which physiologically stimulates pituitary release of ACTH (with subsequent adrenal secretion of cortisol). , 1988), have found that CRH infusion tests provide further evidence for HPA axis abnormalities associated with depression in adults. These studies have shown blunted ACTH response to CRH despite normal to high cortisol response (Amsterdam, Maislin, Winokur, Kling, Gold, 1987; Holsboer, Gerken, & Stalla, 1987).
Episodes: Animal Models Animal models for depression generally are based on repeated inescapable stressors ("learned helplessness"). The resulting behavioral deficits are generally reversed by treatments that are antidepressive in man. Olfactory bulbectomy produces similar effects (Jesberger & Richardson, 1985). Inescapable shock reduces cerebral NE and SHT but not cerebral blood flow (Hughes, Kent, Campbell, Oke, Croskell, & Preskom, 1984). Inescapable stress in normal humans produces changes inCA and cortisol interpreted as resembling those in depression (Breier, Albus, Picklar, Zahn, Wolkowitz, & Paul, 1987).