Neuroendocrine Evaluation of Depression in Borderline Patients

Carroll, Bernard J.; Greden, John F.; Feinberg, Michael; Lohr, Naomi E.; James, Norman McI.; Steiner, M.; Haskett, Roger F.; Albala, A. Ariav; DeVigne, Jean-Paul; Tarika, Janet

doi:10.1016/s0193-953x(18)30938-9

Cited by 161 publications

(37 citation statements)

References 16 publications

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“…Previous studies using the dexamethasone suppression test (DST) have revealed divergent findings. Earlier studies in patients with BPD have found nonsuppression rates to 1 mg DST ranging from 9.5% to 62% [17,18]. De la Fuente and Mendlewicz [19] carefully excluded coexisting MDD in their sample of patients with BPD and found a non-suppression rate of 25% to 1 mg DST.…”

Section: Endocrinologymentioning

confidence: 97%

New developments in the neurobiology of borderline personality disorder

Bohus

Schmahl²,

Lieb³

2004

Curr Psychiatry Rep

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Within the past several years, research on the clinical phenomena and neurobiology of borderline personality disorder has increased substantially. Borderline personality disorder is currently best thought of in terms of dimensions rather than as a categorical disorder. This article reviews the most recent findings on two of the core dimensions--affective dysregulation and impulsivity. Most of the neuropsychologic, physiologic, endocrinologic, and neuroimaging data support the theory that a dual brain pathology, affecting prefrontal and limbic circuits, may underlie this hyperarousal-dyscontrol syndrome.

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Section: Endocrinologymentioning

confidence: 97%

New developments in the neurobiology of borderline personality disorder

Bohus

Schmahl²,

Lieb³

2004

Curr Psychiatry Rep

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“…During the 1980s, a series of dexamethasone suppression test (DST) studies have been conducted in BPD patients. Most of these studies were not conclusive, because the potential effects of MDD and/or PTSD on the outcome were not taken into account (for an overview see Lahmeyer) (Baxter et al, 1984;Carroll et al, 1981b;Kontaxakis et al, 1987;Krishnan et al, 1984;Lahmeyer et al, 1989;Soloff et al, 1982;Steiner et al, 1984;Sternbach et al, 1983).…”

Section: Introductionmentioning

confidence: 99%

Fluvoxamine Reduces Responsiveness of HPA Axis in Adult Female BPD Patients with a History of Sustained Childhood Abuse

Rinne

Kloet

Wouters

et al. 2003

Neuropsychopharmacol

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The aim of the study is to test whether fluvoxamine affects the function of the hypothalamic pituitary adrenal (HPA) axis in female borderline (borderline personality disorder, BPD) patients with and without a history of sustained childhood abuse. Special attention is given to the presence of comorbid major depressive disorder (MDD) and post-traumatic stress disorder (PTSD). The HPA axis of 30 female BPD patients with (n ¼ 17) and without (n ¼ 13) a history of sustained childhood abuse was challenged with a combined dexamethasone and corticotropin releasing hormone test (DEX/CRH test) before and after 6 (n ¼ 14) and 12 (n ¼ 16) weeks of fluvoxamine treatment (150 mg/day). Both 6-and 12-week fluvoxamine treatments were associated with a significant and robust reduction of the adrenocorticotrophic hormone (ACTH) and cortisol response to the DEX/CRH test. The magnitude of the reduction was dependent on the presence of sustained childhood abuse, but not on the presence of comorbid MDD or PTSD: patients with a history of sustained childhood abuse showed the strongest reduction in ACTH and cortisol. In conclusion, Fluvoxamine treatment reduces the hyperresponsiveness of the HPA axis in BPD patients with a history of sustained childhood abuse. This effect is likely to be obtained in the first 6 weeks of treatment.

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“…A significant proportion of depressed patients display altered activity of the HPA axis, and stress generally leads to hypersecretion of corticosteroids, which imposes an increased risk for depression (Carroll et al, 1981;Nemeroff et al, 1984;Strohle and Holsboer, 2003;Brown et al, 2004;de Kloet et al, 2005;Antonijevic, 2006;Hen, 2006, 2004). Chronic treatment of rodents with corticosterone effectively induces multiple anxiety-and depression-like changes in behavior, neurochemistry and brain morphology (Ardayfio and Kim, 2006;Gourley et al, 2008;Murray et al, 2008;David et al, 2009).…”

Section: Non-response/resistance In the Corticosterone Modelmentioning

confidence: 99%