Contrasting neuroendocrine responses in depression and chronic fatigue syndrome

Cleare, Anthony J.; Bearn, Jenny; Allain, Teresa; McGregor, A M; Wessely, Simon; Murray, Robin M.; O’Keane, Veronica

doi:10.1016/0165-0327(95)00026-j

Cited by 232 publications

(84 citation statements)

References 21 publications

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“…Fenfluramine, a serotonin-releasing agent, which also inhibits the reuptake of synaptic 5-HT and stimulates postsynaptic 5-HT 2A and 2C receptors (Newman et al, 1998) induces a rapid surge of PRL in laboratory animals and humans (Lu and Meites, 1973;Pinder et al, 1975;Slater et al, 1976). In contrast to healthy controls, a blunted PRL response occurs in some depressed patients when challenged with fenfluramine (Siever et al, 1984;Cleare et al, 1995;Coccaro et al, 1989;Mann et al, 1995;O'Keane and Dinan, 1991;Lopez-Ibor et al, 1988;Mitchell and Smythe, 1990), suggesting abnormal central serotonergic transmission in this condition. However, many studies have failed to show similar results (Asnis et al, 1988;Abel et al, 1997;Maes et al, 1991;Weizman et al, 1988;Kavoussi et al, 1998).…”

Section: The Ssris and Prolactinmentioning

confidence: 98%

From Galactorrhea to Osteopenia: Rethinking Serotonin–Prolactin Interactions

Emiliano

Fudge

2004

Neuropsychopharmacol

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The widespread use of the selective serotonin reuptake inhibitors (SSRIs) has been accompanied by numerous reports describing a potential association with hyperprolactinemia. Antipsychotics are commonly known to elevate serum prolactin (PRL) through blockade of dopamine receptors in the pituitary. However, there is little awareness of the mechanisms by which SSRIs stimulate PRL release. Hyperprolactinemia may result in overt symptoms such as galactorrhea, which may be accompanied by impaired fertility. Long-term clinical sequelae include decreased bone density and the possibility of an increased risk of breast cancer. Through literature review, we explore the possible pathways involved in serotonin-induced PRL release. While the classic mechanism of antipsychotic-induced hyperprolactinemia directly involves dopamine cells in the tuberoinfundibular pathway, SSRIs may act on this system indirectly through GABAergic neurons. Alternate pathways involve serotonin stimulation of vasoactive intestinal peptide (VIP) and oxytocin (OT) release. We conclude with a comprehensive review of clinical sequelae associated with hyperprolactinemia, and the potential role of SSRIs in this phenomenon.

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Section: The Ssris and Prolactinmentioning

confidence: 98%

From Galactorrhea to Osteopenia: Rethinking Serotonin–Prolactin Interactions

Emiliano

Fudge

2004

Neuropsychopharmacol

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“…However, there are a number of important differences between CFS and depression. Exploring the neurobiology of these conditions has thrown up interesting leads -such as the relative underactivity of the HPA axis in fatigue as opposed to the opposite overactivity of the axis in depression (Demitrack et al 1991 ;Cleare et al 1995). Hickie's paper demonstrates that depression, anxiety, psychological distress and fatigue are probably determined by different underlying genetic factors, with one uniquely contributing to fatigue.…”

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confidence: 99%

Chronic fatigue syndrome – mapping the interior

Hotopf

Wessely

1999

Psychol. Med.

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Over a century ago Beard referred to fatigue as the ‘Central Africa of medicine – an unexplored territory which few men enter’ (Beard, 1869). The last decade has seen major advances in our understanding of chronic fatigue syndrome (CFS). Much is now known of the epidemiology, clinical features and prognosis of the condition (Wessely et al. 1998), and a number of recent papers have reported randomized trials of successful treatments involving cognitive behaviour therapy (CBT) and graded exercise (Sharpe et al. 1996; Wearden et al. 1996; Deale et al. 1997; Fulcher & White, 1997). Despite these advances, which have defined some of the broad landmarks of the illness, and improved the care of patients, many areas remain uncharted. Several papers published in this issue of Psychological Medicine take us into such unexplored territory.

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“…Also hormonal blood levels have been found to be abnormal in the hypothalamus, pituitary glands or adrenal glands. The significance of these findings is unknown [29].…”

Section: Revised Fibromyalgia Impact Questionnaire (Fiqr)mentioning

confidence: 99%