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Showing papers by "Raymond J. Dolan published in 1984"


Journal ArticleDOI
TL;DR: Thirty-one of 68 patients with primary depression were found to have a blunted thyroid-stimulating hormone (TSH) response to thyrotropin-releasing hormone (TRH), and it is suggested that there may be more than one mechanism responsible for blunting of the TSH response in depressed patients.
Abstract: Thirty-one (43%) of 68 patients with primary depression were found to have a blunted thyroid-stimulating hormone (TSH) response to thyrotropin-releasing hormone (TRH). Increased thyroid activity, as measured by the free thyroxine index (FTI), was present in 16 (24%) of the patients. Patients with blunted responses had a higher mean FTI level than those with normal responses. Patients with blunted responses were significantly more likely to exhibit the symptoms of depersonalization, derealization and agitation. There was no clear association between blunting and any particular diagnostic category of depression. Patients with blunted responses and high FTI values were more likely to report significant long-term environmental difficulties than patients with blunted responses and normal FTI values. It is suggested that there may be more than one mechanism responsible for blunting of the TSH response in depressed patients. In some patients blunting may be due to negative feedback from increased output of thyroid hormones, possibly released as part of a stress response. In other patients blunting may be due to a different mechanism, possibly involving pituitary gland dysfunction. These mechanisms would not necessarily be mutually exclusive in any one patient.

50 citations


Journal ArticleDOI
TL;DR: Investigation of hypothalamic-pituitary-adrenal axis function in patients with primary depression raised doubts about the validity of using the dexamethasone suppression test as a diagnostic marker for a specific depressive syndrome.
Abstract: Hypothalamic–pituitary–adrenal axis function was investigated in 72 patients with primary depression. Forty-four per cent of the patients demonstrated abnormal suppression of their cortisol levels after a 1 mg overnight dexamethasone suppression test. Patients with abnormal suppression (‘non-suppressors’) were not clearly distinguished from ‘suppressors’ by the commonly used diagnostic classifications. They did not appear to be more severely depressed, but they were more likely than the ‘suppressors’ to be in-patients. Multivariate analysis of the data suggested that two clinical features were independently associated with non-suppression: the PSE syndromes of Slowness and General Anxiety. However, the association of these syndromes with non-suppression was relatively weak, indicating that the clinical significance of the dexamethasone suppression test is, as yet, unclear. The results raise doubts about the validity of using the dexamethasone suppression test as a diagnostic marker for a specific depressive syndrome.

32 citations


Journal ArticleDOI
TL;DR: TST results seem to be closely related in depression but not in other psychiatric disorders, so it is tempting to suggest that major depression might imply a specific limbic-hypothalamic dysfunction, common to the regulation of both the adrenal and the thyroid axis.
Abstract: TST results seem to be closely related in depression but not in other psychiatric disorders. Both endocrine tests are dependent on intact limbic-hypothalamic function involving several neurotransmitter systems (Carroll, 1982; Loosen & Prange, 1982), so it is tempting to suggest that major depression might imply a specific limbic-hypothalamic dysfunction, common to the regulation of both the adrenal and the thyroid axis. Further investigations are needed to explore this phenomenon.

5 citations