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Showing papers by "David R. Rubinow published in 1999"


Journal ArticleDOI
TL;DR: This pilot study suggests that dehydroepiandrosterone is an effective treatment for midlife-onset dysthymia and shows no specific effects on cognitive function or sleep disturbance, although a type II error could not be ruled out.

179 citations


Journal ArticleDOI
TL;DR: The consensus of the group was that PMDD is a distinct clinical entity and potential treatments for this disorder can now be evaluated on this basis to meet the clear need for effective therapy.
Abstract: Does the evidence now available support the concept of premenstrual dysphoric disorder (PMDD) as a distinct clinical disorder such that the relative safety and efficacy of potential treatment can b...

151 citations


Journal ArticleDOI
TL;DR: It is found that both α 2 mRNA and protein levels are significantly increased by T treatment at embryonic day 20 (E20) and birth (P0), which indicates that the effects of T are developmental-stage-specific and may have an organizational impact on brain development.

24 citations


Journal ArticleDOI
TL;DR: It is suggested that the higher rate of major depression in patients with PMS during follow-up reflects the higher risk attendant to the history ofmajor depression that existed at baseline, and PMS appears to be a stable diagnosis over time.
Abstract: Background: Previous data suggest that premenstrual syndrome (PMS) and affective disorder are related. The purpose of this preliminary study was to ascertain (1) whether women with PMS have an increased risk for future major depressive episodes compared with controls and (2) whether PMS is a stable diagnosis over time. Method: Patients with prospectively confirmed PMS, along with retrospective DSM-IV premenstrual dysphoric disorder, and asymptomatic controls were studied at 5- to 12-year follow-up using a structured clinical interview. Additionally, those women who still had regular cycles and were medication-free were asked to complete 2 months of prospective daily ratings. Results: Women with PMS (N = 27) had a nonsignificantly higher incidence of new-onset depressive episodes (DSM-III-R and Schedule for Affective Disorders and Schizophrenia-Lifetime Version [SADS-L] criteria) during a 5- to 12-year follow-up compared with controls (N = 21). Differences in incidence disappeared when patients and controls without prior history of depression were compared. Prospective ratings completed during follow-up confirmed original diagnoses of PMS patients (N = 7) and controls (N = 11). Conclusion: While preliminary, these results suggest that the higher rate of major depression in patients with PMS during follow-up reflects the higher risk attendant to the history of major depression that existed at baseline. Additionally, at least in a small subsample, PMS appears to be a stable diagnosis over time.

20 citations


Journal ArticleDOI
TL;DR: The data support those from previous studies that found lower levels of CSFSS in MS during relapse and suggest that changes in CSF SS are related to the process responsible for diminished cognitive function in MS.

15 citations


Journal ArticleDOI
TL;DR: It is suggested that the context in which the neuro- regulatory actions of gonadal steroids occur determines the impact of steroid signaling on the regulation of affective state.
Abstract: Gonadal steroids seem to regulate affective state in some people (but not all), despite the absence of abnormal steroid hormone levels or dysfunction of the reproductive endocrine axis. In this article, we attempt to explain this paradox 1) by describing the molecular mechanisms by which gonadal steroids can regulate neuronal function; 2) by describing the specific regulatory impact of gonadal steroids on two systems im plicated in the pathophysiology of mood disorders; and 3) by defining the role of gonadal steroids in several mood disorders linked to periods of reproductive change. We suggest that the context in which the neuro- regulatory actions of gonadal steroids occur determines the impact of steroid signaling on the regulation of affective state. NEUROSCIENTIST 5:227-237, 1999

8 citations