Dexamethasone suppression test (DST) were performed in patients with dementia of the Alzheimer type and multiinfarct dementia. Test–retest reliability was found to be high in dementia patients if they were inpatients and environmental factors were dept stable. In this group 14% were non‐suppressors. If outpatients were investigated, admitted to hospital for only a few days, the test–retest reliability was low. In these patient groups 39–56% were non‐suppressors. Treatment with the serotonergic (5‐HT) uptake inhibitor citalopram significantly reduced the postdexamethasone cortisol levels as well at 08.00 am as at 03.00 pm the day after intake of 1 mg dexamethasone (after 10 h and 17 h respectively). Citalopram treatment also caused significant reduction of the cerebrospinal fluid (CSF) levels of 5‐hydroxyindolacetic acid (5‐HIAA) and 3‐methoxy 4‐hydroxyphenylglycol (HMPG). A correlation was seen between the citalopram‐induced reduction of 5‐HIAA levels in CSF and the degree of dexamethasone‐induced suppression of cortisol concentrations after the treatment period. Treatment with the 5‐HT uptake inhibitor alaproclate, with a regional selectivity principally to the limbic system, had little effect on the postdexamethasone cortisol levels. The results suggest a relation between the abnormal DST in dementia and a disturbed hypothalamic 5‐HT function.
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Balldin et al. (1988) studied this question.
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