The etiology, biology, and evolving pathology of premenstrual syndromes

Halbreich, Uriel

doi:10.1016/s0306-4530(03)00097-0

Cited by 251 publications

(217 citation statements)

References 204 publications

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“…Thus, the possibility exists that failure to recover from stressors or failure to mount an appropriate allopregnanolone response to stress reflects the price of repeated biological adaptations to the increased life stress that is well documented in PMDD women and may contribute to the greater emotional and behavioral impact of daily stressors in the large subgroup (45−60%) of PMDD with histories of depression. If confirmed, these results are consistent with more recent conceptualizations of PMDD as a heterogeneous disorder with respect to pathophysiological mechanisms (Halbreich, 2003).…”

Section: Alterations In Allopregnanolone Responses To Stress In Priorsupporting

confidence: 91%

Neurosteroids in the context of stress: Implications for depressive disorders

Girdler

Klatzkin

2007

Pharmacology & Therapeutics

132

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Animal models indicate that the neuroactive steroids 3α,5α-THP (allopregnanolone) and 3α,5α-THDOC (allotetrahydroDOC) are stress responsive, serving as homeostatic mechanisms in restoring normal GABAergic and hypothalamic-pituitary-adrenal (HPA) function following stress. While neurosteroid increases to stress are adaptive in the short term, animal models of chronic stress and depression find lower brain and plasma neurosteroid concentrations and alterations in neurosteroid responses to acute stressors. It has been suggested that disruption in this homeostatic mechanism may play a pathogenic role in some psychiatric disorders related to stress. In humans, neurosteroid depletion is consistently documented in patients with current depression and may reflect their greater chronic stress. Women with the depressive disorder, premenstrual dysphoric disorder (PMDD), have greater daily stress and a greater rate of traumatic stress. While results on baseline concentrations of neuroactive steroids in PMDD are mixed, PMDD women have diminished functional sensitivity of GABA A receptors and our laboratory has found blunted allopregnanolone responses to mental stress relative to non-PMDD controls. Similarly, euthymic women with histories of clinical depression, which may represent a large proportion of PMDD women, show more severe dysphoric mood symptoms and blunted allopregnanolone responses to stress versus never-depressed women. It is suggested that failure to mount an appropriate allopregnanolone response to stress may reflect the price of repeated biological adaptations to the increased life stress that is well documented in depressive disorders and altered allopregnanolone stress responsivity may also contribute to the dysregulation seen in HPA axis function in depression.

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Section: Alterations In Allopregnanolone Responses To Stress In Priorsupporting

confidence: 91%

Neurosteroids in the context of stress: Implications for depressive disorders

Girdler

Klatzkin

2007

Pharmacology & Therapeutics

132

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“…Up to 18 % of women have severe PMS and 3-8 % qualify for a diagnosis of premenstrual dysphoric disorder (PMDD) (2). PMDD is classified as a "depressive disorder not otherwise specified" in the American Psychiatric Association's Diagnostic and Statistical Manual of Mental Disorders, fourth edition (DSM-IV).…”

Section: Introductionmentioning

confidence: 99%

Reduced parasympathetic activity during sleep in the symptomatic phase of severe premenstrual syndrome

Baker

Colrain

Trinder

2008

Journal of Psychosomatic Research

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Objective-Severe premenstrual syndrome (PMS) is a common, distressing disorder in women that manifests during the premenstrual (late-luteal) phase of the ovulatory menstrual cycle. There is some evidence that altered autonomic function may be an important component of PMS but few studies have used heart rate variability (HRV), as a sensitive marker of autonomic activity, in severe PMS and findings are conflicting.Methods-We investigated HRV during sleep, a state relatively free of external disruptions, in nine women with severe PMS and twelve controls.Results-The normal-to-normal (NN) RR-interval was shorter during the sleep period in women with PMS than in controls in both the follicular and late-luteal phases of the menstrual cycle. The standard deviation of all NN intervals (SDNN), a measure of total variability in the inter-beat interval, was lower during the sleep period in the late-luteal phase than in the follicular phase in women with PMS. The square root of the mean of the sum of the squares of differences between adjacent NN intervals (rMSSD), a measure reflecting high frequency activity, showed a similar pattern. High frequency power, a marker of parasympathetic activity, was lower during non-rapid eye movement (non-REM) and REM sleep in the late-luteal phase than in the follicular phase in women with severe PMS. Controls had a shorter NN-interval, but similar HRV measures, in the late-luteal phase compared with the follicular phase.Conclusion-These results suggest that women with severe PMS have decreased parasympathetic activity during sleep in association with their premenstrual symptoms compared to when they are symptom-free.

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“…Luteinizing hormone is also well known to affect the central nervous system [19]. The patient still comes to our hospital for relief from premenstrual syndrome related to the plasma levels of ovarian steroid hormones [20]. Her central nervous system thus may be more highly sensitive to sex hormones than those of other women.…”

Section: Discussionmentioning

confidence: 99%

A Case of Ovulatory Cycle-dependent Symptoms in Woman with Previous Interferon .BETA. Therapy

Nakamura

Hino

2005

Endocr J

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Abstract. A woman with a menstrual cycle-dependent fever (more than 38°C) and severe fatigue that disrupted her ability to work was referred to our hospital. Six years ago, the patient received interferon b injections (6,000,000 IU day -1 × 48 days) for the treatment of hepatitis C virus. Although the treatment was successful against the virus, the symptomatic fever occurred monthly since the third year after receiving the treatment. The symptoms occurred a few days after ovulation in every menstrual cycle. When the ovarian function was suppressed by GnRH agonist (GnRHa), the symptoms disappeared. While in anovulation, the patient received estrogen followed by estrogen with progestogen, which resembles the sex hormone milieu of a normal menstrual cycle without the LH surge; this treatment did not induce the symptoms. When human CG (hCG) was injected on the beginning day of estrogen with progestogen following treatment with estrogen alone, the previous symptoms reappeared. However, the hCG injection without estrogen priming did not induce the symptoms. These studies indicated that the LH surge after estrogen priming induced the symptoms. Changes in serum inflammatory cytokine levels (interleukin-1, interleukin-6, and tumor necrosis factor-a) were examined during the ovulatory cycle and the interleukin-1 levels during the treatment. There were no significant changes on these levels in the febrile period. The patient experienced normal menstrual cycles after finishing the five-month GnRHa treatment. Although her symptoms still occur, they are mild and do not require further medical treatment.

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The etiology, biology, and evolving pathology of premenstrual syndromes

Cited by 251 publications

References 204 publications

Neurosteroids in the context of stress: Implications for depressive disorders

Neurosteroids in the context of stress: Implications for depressive disorders

Reduced parasympathetic activity during sleep in the symptomatic phase of severe premenstrual syndrome

A Case of Ovulatory Cycle-dependent Symptoms in Woman with Previous Interferon .BETA. Therapy

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