Dexamethasone suppression test in dementia

Abstract

The performance of the Dexamethasone Suppression Test (DST) was investigated in 60 demented patients including 14 patients admitted to a psychogeriatric assessment ward, 29 electively admitted patients and 17 long‐stay patients in comparison with 37 normal control subjects. It was shown that acutely admitted patients had the highest rate of DST non‐suppression (86%), whilst electively admitted patients had the lowest rate (55%) in comparison with normal controls (11%). In the electively admitted group abnormal DST results and Cortisol Suppression Index and DST non‐suppressors showed depressive signs more frequently than suppressors. There was no association between DST results and age, weight, cognitive, behavioural, cortical dysfunction and degree of cerebral atrophy as determined by CT scan results.

Relationship between DST and the serotonergic system. Results from treatments with two 5‐HT reuptake blockers in dementia disorders

“…This indicates that the abnormal DST in demented patients may not only be due to the disorder itself but might also be explained by effects of environmental factors ('stress factors'). A similar effect of hospitalization on the DST has also been reported for emergently admitted patients with dementia by Abou-Saleh et al (1987) but also for other psychiatric disorders (Coccaro et al, 1984;Baumgartner et al, 1986), thus further strengthening the concept of environmental factors, at least partly, affecting the results of the DST.…”

“…The dexamethasone suppression test (DST) was designed as a laboratory test in patients with melancholia (Carroll et al, 1981) but it has been shown that 50-70% of patients with dementia disorders are also nonsuppressors, i.e. d o not demonstrate the normal suppression of serum cortisol concentrations after a dexamethasone load (Raskind et al, 1982;Spar and Gerner, 1982;Coppen et al, 1983;Balldin et al, 1983;McKeith, 1984;Jenike and Albert, 1984;Alexopoulos et al, 1985;McAllister and Hays, 1987;Abou-Saleh et al, 1987). The DST findings in dementia have, however, been debated (Rudorfer and Clayton, 1981;Carnes et al, 1983).…”

HPA axis function in depression and dementia: A review

“…In patients with AD the observation of both HPA axis dysfunction and severe hippocampal changes has led to speculation that, even if the glucocorticoid cascade hypothesis is not important in normal ageing, it may play some role in accelerating cell loss in AD. Some evidence for this comes from studies showing a positive correlation between postdexamethasone cortisol levels and dementia severity (Jenike and Albert, 1984;Molchan et al, 1990;, although not all have found this (Greenwald et al, 1986;Abou-Saleh et al, 1987) One possible explanation for such contradictory findings may be the effect of dexamethasone levels on results. As noted above, some have shown dexamethasone concentrations to be positively correlated with dementia severity (Molchan et al, 1990).…”

Somatotropic-pituitary function in Alzheimer's disease and depression in old age

“…The earliest studies exam ined the hypothalam ic± pituitary± adrenal axis through the dexam ethasone suppression test and showed a high frequency of early escape from dexam ethasone suppression in senile and presenile form s of Alzheim er' s disease (Abou-Saleh et al, 1987). High basal levels of GH and thyroid stim ulating horm one (TSH ) (Christie et al, 1987) and an am pli® ed G H response to G HRH reported in Alzheim er' s disease patients of early onset are linked to a reduced hypothalam ic content of somatostatin (C acabelos et al, 1988).…”