Recent Studies in the Neuroendocrinology of Major Depressive Disorders

Sachar, Edward J.; Asnis, Gregory M.; Halbreich, Uriel; Nathan, Swami; Halpern, Frieda S.

doi:10.1016/s0193-953x(18)30968-7

Cited by 64 publications

(9 citation statements)

References 19 publications

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“…Even if these control mechanisms were clarified, the assumption of a direct relationship of biogenic amines with control of gonadotropin secretion would probably be very oversimplified. For example, although norepinephrine is certainly involved in GnRH secretion, the endocrine milieu at various times in the menstrual cycle is probably also of major significance, as it is for GH secretion (22). Similarly, the concept of a unitary biochemistry of depression is probably oversimplistic.…”

Section: Discussionmentioning

confidence: 99%

Pseudocyesis: Psychologic and Neuroendocrine Interrelationships

Starkman

Marshall

Ferla

et al. 1985

Psychosomatic Medicine

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There is a paucity of information concerning the interrelationship of psychiatric and neuroendocrine abnormalities in pseudocyesis. We have studied two patients using a multimodal investigatory approach, with particular attention to the association of depression and alterations in endocrine secretory patterns. Both patients had abnormal growth hormone secretory patterns, as demonstrated by lack of sleep-associated peaks and the absence of a response to L-dopa administration. Both patients had elevated testosterone and estradiol levels and normal prolactin levels. Only the patient who met DSM III criteria for a major depressive episode had abnormally elevated luteinizing hormone (LH) levels and large LH pulse amplitudes. These findings, together with a review of cases reported in the literature, suggest that no single neuroendocrine profile is common to all patients with pseudocyesis.

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Section: Discussionmentioning

confidence: 99%

Pseudocyesis: Psychologic and Neuroendocrine Interrelationships

Starkman

Marshall

Ferla

et al. 1985

Psychosomatic Medicine

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“…Although multiple endocrine abnormalities were studied for these purposes, two received particular attention: overactivity of the HPA axis, 22,23 with elevated circulating cortisol levels, blunting of the normal diurnal rhythm with increased nocturnal cortisol levels when normally quiescent, and failure to show inhibition of release by synthetic glucocorticoids such as dexamethasone; and hypoactivity of the hypothalamicpituitary-thyroid (HPT) axis with a decreased response of thyroid-stimulating hormone to an infusion of thyrotropinreleasing-hormone. Although multiple endocrine abnormalities were studied for these purposes, two received particular attention: overactivity of the HPA axis, 22,23 with elevated circulating cortisol levels, blunting of the normal diurnal rhythm with increased nocturnal cortisol levels when normally quiescent, and failure to show inhibition of release by synthetic glucocorticoids such as dexamethasone; and hypoactivity of the hypothalamicpituitary-thyroid (HPT) axis with a decreased response of thyroid-stimulating hormone to an infusion of thyrotropinreleasing-hormone.…”

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confidence: 99%

Electroconvulsive Therapy’s Mechanism of Action

Haskett

2014

The Journal of ECT

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Despite a range of etiological theories since the introduction of electroconvulsive therapy (ECT) more than 75 years ago, its mechanism of action remains poorly understood. The neuroendocrine hypothesis is based on the seizure-related release of hypothalamic hormones into the blood and cerebrospinal fluid and evidence of endocrine dysfunction in many patients with severe mood disorder. The specific effect of ECT was hypothesized to result from the transverse passage of current through the brain with direct stimulation of axial structures including the diencephalon. The prompt release of adrenocorticotropic hormone, cortisol, and prolactin into blood followed ECT with a return to pretreatment baseline levels in several hours. The elevated levels of hormones were absorbed by the cerebrospinal fluid, providing contact with brain cells and central nervous system structures. An apparently specific pattern of ECT-induced hormone changes, limited to prolactin and cortisol, suggested that ECT released a substance with dopaminergic antagonist and antipsychotic properties. As hypothalamic dysfunction is a key finding in endogenomorphic depression and the abnormal endocrine and physiological functions usually normalize with recovery, this led to a search for biological markers that would supplement clinical assessment of diagnosis and treatment response. One of these, the overnight dexamethasone suppression test found that 40% to 50% of melancholic depressed patients had abnormal results, whereas 90% of control patients suppressed normally. This was followed by a period of uncritical overenthusiasm followed by wholesale rejection of the clinical neuroendocrine strategies. Several key methodological issues received inadequate attention, and there have been calls to revisit this topic.

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“…DST abnormalities imply hypothalamic imbalance, and depression itself presents clinically with several symptoms suggesting hypothalamic dysfunction. It has also been demonstrated that the same neurotransmitters that have been implicated in depression, particularly norepinephrine and serotonin, also regulate the secretion of hypothalamic neuroendocrine cells 1 …”

mentioning

confidence: 99%

Dexamethasone Suppression Test as a Clinical Aid in Elderly Depressed Patients

Jenike

1983

J American Geriatrics Society

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Recent Studies in the Neuroendocrinology of Major Depressive Disorders

Cited by 64 publications

References 19 publications

Pseudocyesis: Psychologic and Neuroendocrine Interrelationships

Pseudocyesis: Psychologic and Neuroendocrine Interrelationships

Electroconvulsive Therapy’s Mechanism of Action

Dexamethasone Suppression Test as a Clinical Aid in Elderly Depressed Patients

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