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

Balldin, Jan; Gottries, C. G.; Karlson, Ingvar; Lindstedt, Göran; Lérngström, Göran; Svennerholm, Lars

doi:10.1002/gps.930030104

Cited by 17 publications

(7 citation statements)

References 51 publications

(58 reference statements)

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“…The patients were in long-term care at follow-up but at index DST were in a variety of settings including psychogeriatric assessment units and day-care settings. Balldin et al, (1988) have shown low rates of DST nonsuppression in chronically hospitalized ATD patients but much higher rates when the patients were in circumstances similar to the index DST situation in the present study.…”

Section: Discussionmentioning

confidence: 58%

A follow‐up study of elderly depressives and Alzheimer‐type dementia—relationship with DST status

Ferrier

Lister

Riordan

et al. 1991

Int J Geriat Psychiatry

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SUMMARYSeventy-three elderly patients (38 with Alzheimer-type dementia (ATD) and 35 with major depressive disorder) were followed up 2-5 years after an index admission during which a dexamethasone suppression test (DST) had been performed. Clinical state, cognitive function, neurological status and repeat DST were assessed where possible. The death rate was high in both groups (greater in the ATD group) but was not influenced by original DST status. Original DST status did not predict on survival time, development of physical illness or admission rate in either group, but DST non-suppression in the depressed group was associated with significant cognitive decline and abnormal neurological features. Possible mechanisms of the association are discussed.KEY wows-Alzheimer-type dementia, major depression, dexamethasone suppression test.Extensive studies have revealed that many depressed patients exhibit state-dependent hypothalamic-pituitary adrenal axis dysregulation with an increase in mean 24-hour plasma cortisol levels, a blunting of the normal diurnal rhythm of cortisol secretion and increased 24-hour urinary 17-hydroxy corticosteroid excretion (Carroll et al., 1981). More recently attention has focused on the observation that depressed patients show relative resistance to the suppressive effects of synthetic corticosteroids such as dexamethasone and a significant proportion of depressed patients fail to suppress on the dexamethasone suppression test (DST, Carroll et al., 1981). Initially it was suggested that the DST may distinguish between those elderly patients with depression and those with dementia (Carnes et al., 1983;Rudorfer and Clayton, 1982). However, recent studies have cast doubt on the DST as a diagnostic discriminator in elderly psychi- (1983) and McKeith (1984) found rates of DST non-suppression of51% and 58% respectively in Alzheimer-type dementia (ATD). In 1987 we reported a 47% rate of DST non-suppression in a group of ATD patients (Ferrier et al., 1988) although many fewer ATD patients than depressed patients exhibited basal hypercortisolaemia in our study.Therefore the DST has limited utility in routine diagnostic clinical practice in the psychiatry of old age. However, there are some outstanding issues to resolve. One of these is whether DST non-suppression identifies groups of demented andlor depressed patients with particular clinical characteristics and whether there are prognostic implications of DST non-suppression. This question is particularly important in view of the hypothesis put forward by Sapolsky (1987) that elevated glucocorticoids may induce selective hippocampal damage. Animal evidence indicates that the hippo-

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Section: Discussionmentioning

confidence: 58%

A follow‐up study of elderly depressives and Alzheimer‐type dementia—relationship with DST status

Ferrier

Lister

Riordan

et al. 1991

Int J Geriat Psychiatry

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“…In a group of 16 demented outpatients the effect of treatment with a 5-HT re-uptake blocker (citalopram) on the DST was studied (16). Ten of the patients were diagnosed as AD/SDAT and six as multi-infarction dementia (MID).…”

Section: Neuroendocrinological Studies In Dementiamentioning

confidence: 99%

Biological markers in dementia

Gottfries¹

1988

Nordisk Psykiatrisk Tidsskrift

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Gottfries C.G. Biological markers in dementia. Nord Psykiatr Tidsskr 1988;42: 147-153.As biopsies are not usually carried out in the diagnosis of dementia disorders, biological markers for dementia must be searched for in the body fluids. Although no changes are found in the concentrations of active amines and minor metabolites of the monoamines in CSF, the major metabolites, homovanillic acid (HVA) and 5-hydroxyindolacetic acid (5-HIAA), are significantly reduced in patients with Alzheimer's disease (AD) and senile dementia of Alzheimer type (SDAT). The findings from CSF concur with postmortem brain tissue investigations in demented patients. Significant correlations are found between reduced concentrations of monoamine metabolites in CSF and behavioural disturbances as rated by the GBS-scale. Neuroendocrinological studies in dementia show that there is a pathological response to the dexamethasone suppression test in patients with AD, SDAT and multi-infarction dementia (MID). Also, when assessing the postsynaptic NA-sensitivity by giving clonidine, a blunted growth hormone response was recorded. The challenge with the thyrotropin-releasing hormone (TRH) gives a blunted TSH-response in demented patients. It is of interest that there are considerable similarities between neuroendocrinal disturbances in melancholia and in dementia disorders. The investigation of blood is also of value in the diagnosis of dementia disorders. In an investigation of 155 patients admitted to a hospital for suspected dementia it was found that 23% of the patients with late onset primary dementia (SDAT) had low concentrations of vitamin B12, in the blood, high MAO-activity in the platelets and normal concentrations of HVA in CSF. 0 Biological markers, Dementia Monoamines, Neuroendocrine studies.

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“…Some patients were furthermore retested after treatment with the selective 5-HT uptake inhibitor citalopram, which may have a secondary effect also on the NA neurotransmission (Balldin et al, 1987a).…”

Section: Introductionmentioning

confidence: 99%

“…The findings mentioned above of changed concentrations of NA and the metabolite HMPG in certain brain areas from patients with AD/ SDAT prompted us to investigate this patient group using the clonidine-GH test to assess the postsynaptic NA sensitivity and compare data with the results from clinical ratings of the patients and with the CSF monoamine metabolite data. Some patients were furthermore retested after treatment with the selective 5-HT uptake inhibitor citalopram, which may have a secondary effect also on the NA neurotransmission (Balldin et al, 1987a).…”

Section: Introductionmentioning

confidence: 99%

The clonidine test in patients with dementia disorders: Relation to clinical status and cerebrospinal fluid metabolite levels

Balldin

Gottfries

Lindstedt

et al. 1988

Int J Geriat Psychiatry

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SUMMARYClonidine loading tests (100 pg i.v.) for growth hormone (GH) release were performed in eight patients with dementia of the Alzheimer type and four with multi-infarct dementia. Clonidine did not stimulate GH but depressed blood pressure levels. Basal GH levels correlated to clinical variables of affective symptomatology but not with monoamine levels in the cerebrospinal fluid. Treatment with a 5-HT uptake inhibitor (citalopram) did not affect the outcome of the loading tests.

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

Cited by 17 publications

References 51 publications

A follow‐up study of elderly depressives and Alzheimer‐type dementia—relationship with DST status

A follow‐up study of elderly depressives and Alzheimer‐type dementia—relationship with DST status

Biological markers in dementia

The clonidine test in patients with dementia disorders: Relation to clinical status and cerebrospinal fluid metabolite levels

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