A Specific Laboratory Test for the Diagnosis of Melancholia

Carroll, Bernard J.; Feinberg, Michael; Greden, John F.; Tarika, Janet; Albala, A. Ariav; Haskett, Roger F.; James, Norman McI.; Kronfol, Ziad; Lohr, Naomi E.; Steiner, Meir; Vigne, Jean Paul de; Young, Elizabeth A.

doi:10.1001/archpsyc.1981.01780260017001

Cited by 2,163 publications

(333 citation statements)

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“…Since cortisol is the main regulated end product of the HPA axis and it acts upon multiple systems of the brain, the persistence of a normal cortisol response in the face of elevated cortisol could have multiple consequences for the organism and further exacerbates the hypercortisolemia of depression. The resistance to the negative feedback effects of glucocorticoids seen with this stressor are in agreement with studies of dexamethasone glucocorticoid negative feedback using cortisol infusion challenges (Carroll et al 1981;Young et al 1991). Finally, several studies have examined the cortisol response to a cognitive stressor in depressed patients, and found elevated pre-stress cortisol but a smaller cortisol response to the cognitive challenge in the depressed patients compared to control subjects.…”

Section: Discussionsupporting

confidence: 80%

“…This increase in plasma cortisol is particularly evident in the evening, at the nadir of the circadian rhythm (Sachar et al 1973;Carroll et al 1976;Rubin et al 1987;Halbreich et al 1985;Pfohl et al 1985). Furthermore, a number of studies have investigated abnormal glucocorticoid feedback, typically using the synthetic steroid dexamethasone but also using the naturally occurring glucocorticoid cortisol (Carroll et al 1981;Young et al 1993Young et al , 1991. These studies generally support the view that there is significant dysregulation of steroid negative feedback mechanisms in major depression.…”

mentioning

confidence: 87%

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Hormonal Evidence for Altered Responsiveness to Social Stress in Major Depression

Young

López

Murphy-Weinberg

et al. 2000

Neuropsychopharmacology

135

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In patients with major depression, abnormalities in baseline cortisol secretion and resistance to negative feedback are well established. However, it is unclear if patients with major depression have alterations in the hypothalamicpituitary-adrenal (HPA) response to stressors. While other challenges to the HPA axis have used endocrine stimuli such as insulin-induced hypoglycemia, we now report of the response to a social stressor in patients withOver the last two decades, an extensive body of work has pointed to a close relationship between stress and major depression. Studies by numerous investigators including Frank et al. (1994) and Brown et al. (1994) have documented the role of stressful life events in the precipitation of depressive episodes. Studies in twins by Kendler et al. (1993) have demonstrated a clear interaction between genetic substrate and a recent stressful life event in the precipitation of a depressive episode. In addition, abnormalities in the hypothalamic-pituitary adrenal (HPA) axis are seen during depression. HPA measures have demonstrated different types of dysregulation at rest or following various endocrine challenges. For example, patients with major depression demonstrate elevated plasma cortisol levels at rest, a finding observed in approximately 50% of depressed patients. This increase in plasma cortisol is particularly evident in the evening, at the nadir of the circadian rhythm (Sachar et al. 1973; Carroll et al. 1976;Rubin et al. 1987;Halbreich et al. 1985;Pfohl et al. 1985). Furthermore, a number of studies have investigated abnormal glucocorticoid feedback, typically using the synthetic steroid dexamethasone but also using the naturally occurring glucocorticoid cortisol (Carroll et al. 1981;Young et al. 1993Young et al. , 1991. These studies generally support the view that there is significant dysregulation of NO . 4 steroid negative feedback mechanisms in major depression. Fewer studies have examined the activational circuits of the LHPA axis in depression, and these studies have been limited to endocrine challenges such as metyrapone, or insulin-induced hypoglycemia (Young et al. 1994;von Bardeleben et al. 1988;Kathol et al. 1992;Lopez et al. 1987). The metyrapone studies suggested increased central drive in the evening (Young et al. 1994), while insulin-induced hypoglycemia revealed elevated basal cortisol and an attenuated ACTH response to the challenge (Kathol et al. 1992;Lopez et al. 1987). Finally, there is evidence that corticotropin-releasinghormone, CRH, which represents the final common path of stress responsiveness in the brain, is elevated in CSF and hypothalamus, and that this elevation may contribute both to the endocrine and psychological profile seen in severe depression (Nemeroff et al. 1984;Roy et al. 1987;Raadsheer et al. 1995Raadsheer et al. , 1994Nemeroff, 1988;Nemeroff et al. 1988).In spite of these findings, it remains difficult to determine what these endocrine changes tell us about the alterations in key neuronal circuits which mediate stress resp...

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Section: Discussionsupporting

confidence: 80%

mentioning

confidence: 87%

Hormonal Evidence for Altered Responsiveness to Social Stress in Major Depression

Young

López

Murphy-Weinberg

et al. 2000

Neuropsychopharmacology

135

View full text Add to dashboard Cite

show abstract

“…The dexamethasone suppression test was performed as described by CARROLL et al, (1981). Briefly, 1 mg dexamethasone was administered orally at 2300 h and blood samples were collected the following day at both 0900 and 1600 h in order to determine plasma cortisol levels.…”

Section: Assessment Of Hormonal Variablesmentioning

confidence: 99%

Anhedonia, suicide ideation and Dexamethasone nonsuppression in depressed patients

Oei¹,

Verhoeven²,

Westenberg³

et al. 1990

Journal of Psychiatric Research

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“…A non-suppressive (i.e. abnormal) response to the dexamethasone suppression test (DST) helped to diagnose, it was alleged, primary 'endogenous' depression with high specificity (Carroll et al 1976(Carroll et al , 1981. Rudorfer & Clayton (1981), among others, claimed that the DST was useful in distinguishing organic and affective symptoms, but a growing number of reports, including one by Spar & Gerner (1982) who found abnormal DST results in 9 of 17 elderly patients with dementia but without major depressive illness, have cast doubt on earlier, enthusiastic claims, and the situation now remains more equivocal.…”

Section: 'True' and 'Pseudo' Dementia: Differences On Physical Investmentioning

confidence: 99%

Depression and dementia: the multi-faceted relationship

Mahendra¹

1985

Psychol. Med.

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A Specific Laboratory Test for the Diagnosis of Melancholia

Cited by 2,163 publications

References 31 publications

Hormonal Evidence for Altered Responsiveness to Social Stress in Major Depression

Hormonal Evidence for Altered Responsiveness to Social Stress in Major Depression

Anhedonia, suicide ideation and Dexamethasone nonsuppression in depressed patients

Depression and dementia: the multi-faceted relationship

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