The Effect of Dexamethasone on Cerebrospinal Fluid Monoamine Metabolites and Cortisol in Psychiatric Patients

Abstract

The effect of 1 mg dexamethasone on CSF levels of 5-hydroxyindoleacetic acid (5 HIAA), homovanillic acid (HVA) and cortisol (CS) was investigated in 100 psychiatric inpatients: 45 subjects had their lumbar punctures 1-4 days following dexamethasone administration, and the results were compared with those from 55 other patients investigated before drug ingestion. All patients were women, and none had received psychotropic medication for at least two weeks before the study. Seven subjects consented to two LPs both before and after dexamethasone. As expected, cortisol in the CSF significantly decreased after dexamethasone: the decrease was greatest 10 hours following the drug. HVA showed a weak and transient elevation after 10 hours only. CSF 5 HIAA was found to be significantly increased in postdexamethasone samples and high levels were still found even after 82 hours. Diagnostic differences (major or minor depression, schizophrenia, alcohol abuse or dependence) did not account for the observed differences. Repeated CSF examinations in seven subjects corroborated these findings: all cortisol values were decreased and all 5 HIAA values were increased after dexamethasone while HVA values showed random changes. The data may suggest that serotonergic mechanisms may be involved in dexamethasone action in the CNS. In addition, dexamethasone administration can alter CSF 5 HIAA level, a possible factor which should be taken into consideration in CSF studies.

Neuroendocrine effects of l-tryptophan and dexamethasone

“…Millard et al (1972) reported that IV administration of L-tryptophan to rats produced an increase in cerebral serotonin levels, and this increase was doubled by prior administration of corticosterone. Banki et al (1983) found increased levels of the serotonin-metabolite 5-hydroxyindoleacetic acid (5-HIAA) in cerebrospinal fluid after dexamethasone in a group of psychiatric patients. Similarly, Rothschild et al (1985) reported increased serotonin and 5-HIAA levels in the hypothalamus of rats after one dosage of dexamethasone IP.…”

Circadian Patterns of Plasma Immunoreactive Corticotropin, Beta-Endorphin, Corticosterone and Prolactin after Immunoneutralization of Corticotropin-Releasing Hormone

“…These data suggest a suppressive effect of glucocorticoids on PRL secretion. The relatively short duration of PRL suppression in DEX-treated rats is parallel to the time course of increased dopamine turnover [42]. The re bound increase in PRL observed might reflect the increase in serotonin turnover, which lasts longer than the dopaminergic effect [42].…”

“…The relatively short duration of PRL suppression in DEX-treated rats is parallel to the time course of increased dopamine turnover [42]. The re bound increase in PRL observed might reflect the increase in serotonin turnover, which lasts longer than the dopaminergic effect [42]. Direct glucocorticoid effects or modulation of neurotransmitter-receptor functions might be involved in the attenu ated PRL responses to selective serotonin agonists after chronic cortisol treatment [43].…”

Long-Term Cortisol Treatment Impairs Behavioral and Neuroendocrine Responses to 5-HT₁ Agonists in the Rat

“…Recently, strong GC immunoreactivity was found in all areas of the rat brain stem rich in 5-hydroxytryptamine (5-HT) cell bodies 118], The approximate coexistence of GC receptors and 5-HT neurons was reported by Fuxe et al 117] to be 100% in the B1-B9 brain stem raphe areas. After GC administration, changes in seroto nin (5-HT) metabolism have been shown in both rats (2K 30, 55] and humans [9]. GC administration has also been demon strated to reduce myoclonus responses to the 5- HT precursor, and behavioral responses to the 5-HT-releasing drug, /j-chloroamphetamine, and the nonselective 5- HT agonist,.…”