The Dexamethasone Suppression Test in Patients With Mood Disorders

Aj, Rush; De, Giles; Ma, Schlesser; Pj, Orsulak; Cr, Parker; Je, Weissenburger; Gt, Crowley; Khatami, Manoochehr; N, Vasavada

doi:10.4088/jcp.v57n1006

Cited by 156 publications

(74 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…For example, the HPA axis is resistant to suppression by dexamethasone in the dexamethasone suppression test (DST) (Carroll et al, 1981), the release of adrenocorticotrophic hormone (ACTH) after CRH challenge is diminished (Thalen et al, 1993), and CRH-induced release of ACTH and cortisol is increased after dexamethasone in the Dex-CRH test (Heuser et al, 1994). In, on average, 30-50% of depressed patients the HPA axis is not suppressed in the DST, with the highest rates of nonsuppression being found in patients with melancholic, endogenous, familial or psychotic subcategories of depression (Nelson and Davis, 1997;Rush et al, 1996). The failure to suppress the HPA axis may be because of reduced negative feedback via glucocorticoid receptors, facilitation of CRH-induced ACTH release, or both.…”

Section: Introductionmentioning

confidence: 99%

Anxious–Retarded Depression: Relation with Plasma Vasopressin and Cortisol

Winter

Hemert

DeRijk

et al. 2003

Neuropsychopharmacol

105

View full text Add to dashboard Cite

Dysregulation of the hypothalamus-pituitary-adrenal (HPA) axis is related to melancholic or endogenous depression; however, the strength of this relationship depends on the definition of the specific depression subcategory. A two-dimensionally defined subcategory, anxious-retarded depression, is related to melancholic depression. Since arginine vasopressin (AVP) activates the HPA axis, and both major depression and the melancholic subcategory are associated with elevated plasma AVP levels, we investigated whether the plasma AVP level is also elevated in anxious-retarded depression, melancholic depression and anxious-retarded melancholic depression, and whether plasma AVP and cortisol levels are correlated in these subcategories. A total of 66 patients with major depression not using oral contraception were investigated. Patients with anxious-retarded depression had a highly significant AVP-cortisol correlation, while no such correlation was found in patients with nonanxious-retarded depression. Log-transformed mean plasma AVP values were higher in patients with anxious-retarded depression than in patients with nonanxious-retarded depression. Patients with anxious-retarded melancholic depression also had a significantly elevated level of plasma AVP and a highly significant correlation between plasma AVP and cortisol levels. The correlation was low in patients with melancholic depression. Anxious-retarded depression may be a useful refinement of the melancholic subcategory with regard to dysregulation of the HPA axis and plasma AVP release.

show abstract

Section: Introductionmentioning

confidence: 99%

Anxious–Retarded Depression: Relation with Plasma Vasopressin and Cortisol

Winter

Hemert

DeRijk

et al. 2003

Neuropsychopharmacol

105

View full text Add to dashboard Cite

show abstract

“…This notion is supported by neuroendocrine studies which have shown that 43% of depressed bipolar patients are DST nonsuppressors (Rush et al, 1996) and that the dexamethasone/corticotropin releasing hormone (dex/CRH) test is abnormal during relapse, recovery (Rybakowski and Twardowska, 1999;Schmider et al, 1995;Watson et al, in press) and in apparently healthy subjects with genetic loading for mood disorders (Lauer et al, 1998). It is also supported by post-mortem studies which show evidence of reduced GR mRNA expression in post-mortem brain tissue samples from patients with bipolar disorder (Knable et al, 2001;Lopez et al, 2003;Webster et al, 2002).…”

Section: Discussionmentioning

confidence: 76%

“…In mood disorders, the greatest incidence of HPA axis abnormalities are found in bipolar and psychotic unipolar disorder (Rush et al, 1996) and reduction of cortisol levels in these conditions may therefore ameliorate depression and improve neurocognitive functioning (Reus and Wolkowitz, 2001). In keeping with this view, preliminary data suggests that cortisol synthesis inhibitors may be antidepressant (Brown et al, 2001).…”

Section: Introductionmentioning

confidence: 99%

Improvements in Neurocognitive Function and Mood Following Adjunctive Treatment with Mifepristone (RU-486) in Bipolar Disorder

Young

Gallagher

Watson

et al. 2004

Neuropsychopharmacol

292

159

View full text Add to dashboard Cite

High cortisol levels are found in severe mood disorders, particularly bipolar disorder. Hypercortisolaemia may cause or exacerbate both neurocognitive impairment and depressive symptoms. We hypothesized that antiglucocorticoid treatments, particularly corticosteroid receptor antagonists, would improve neurocognitive functioning and attenuate depressive symptoms in this disorder. To test this hypothesis, 20 bipolar patients were treated with 600 mg/day of the corticosteroid receptor antagonist mifepristone (RU-486) or placebo for 1 week in a double-blind crossover design. Over the total 6 weeks of the study, neurocognitive and neuroendocrine function were evaluated at baseline, days 21 and 42. Mood symptoms were evaluated weekly. Nineteen subjects completed the protocol; there were no drop-outs due to adverse events. Following treatment with mifepristone, selective improvement in neurocognitive functioning was observed. Spatial working memory performance was significantly improved compared to placebo (19.8% improvement over placebo). Measures of verbal fluency and spatial recognition memory were also improved after mifepristone. Beneficial effects on mood were found; Hamilton Depression Rating Scale scores were significantly reduced compared to baseline (mean reduction of 5.1 points) as were Montgomery-Asberg Depression Rating Scale scores (mean reduction of 6.05 points). No significant change occurred after placebo. These data require replication but provide preliminary evidence that glucocorticoid receptor antagonists may have useful cognitive-enhancing and possibly antidepressant properties in bipolar disorder.

show abstract

“…However, in a subset of patients with MDD, cortisol alterations persist and may constitute a biological risk for relapse. 94,95 Divergent results in HPA axis measures in mood disorders may be due to some variability of clinical characteristics such as subtypes of depression (endogenous vs psychoses vs atypical), 75,96,97 chronicity of illness, 98 the presence of anxiety symptoms, 68,99 recurrence of depressive episodes, 100 severity of symptoms, 96,101 age-dependent 102 and sampling factors (in-patients vs outpatients). 67,75,[103][104][105][106] HPA axis hyperactivity may play an important role in the pathogenesis of major depression.…”

Section: Neuroendocrine Dysregulations In Patients With Mddmentioning

confidence: 99%

Brain-immune interactions and disease susceptibility

2005

View full text Add to dashboard Cite

Many studies have established the routes by which the immune and central nervous (CNS) systems communicate. This network of connections permits the CNS to regulate the immune system through both neuroendocrine and neuronal pathways. In turn, the immune system signals the CNS through neuronal and humoral routes, via immune mediators and cytokines. This regulatory system between the immune system and CNS plays an important role in susceptibility and resistance to autoimmune, inflammatory, infectious and allergic diseases. This review focuses on the regulation of the immune system via the neuroendocrine system, and underlines the link between neuroendocrine dysregulation and development of major depressive disorders, autoimmune diseases and osteoporosis.

show abstract

The Dexamethasone Suppression Test in Patients With Mood Disorders

Cited by 156 publications

References 0 publications

Anxious–Retarded Depression: Relation with Plasma Vasopressin and Cortisol

Anxious–Retarded Depression: Relation with Plasma Vasopressin and Cortisol

Improvements in Neurocognitive Function and Mood Following Adjunctive Treatment with Mifepristone (RU-486) in Bipolar Disorder

Brain-immune interactions and disease susceptibility

Contact Info

Product

Resources

About