Cortisol suppression and hearing thresholds in tinnitus after low-dose dexamethasone challenge
1 Cognitive Brain Research Unit, Cognitive Science, Department of Behavioural Sciences, University of Helsinki, Helsinki, P.O. Box 9 00014, Finland
2 Finnish Centre of Excellence in Interdisciplinary Music Research, Department of Music, University of Jyväskylä, Jyväskylä, Finland
3 BRAMS, International Laboratory for Brain, Music, and Sound research, Montreal, Canada
4 École d'orthophonie et d'audiologie, Faculté de médecine, Université de Montréal, Canada, and Centre de recherche de l'Institut universitaire de gériatrie de Montréal, Montréal, Canada
5 Université de Montréal BRAMS, Pavillon 1420, Mont-Royal C.P. 6128, succ. Centre-ville, Montréal, QC H3C 3J7, Canada
BMC Ear, Nose and Throat Disorders 2012, 12:4 doi:10.1186/1472-6815-12-4Published: 26 March 2012
Tinnitus is a frequent, debilitating hearing disorder associated with severe emotional and psychological suffering. Although a link between stress and tinnitus has been widely recognized, the empirical evidence is scant. Our aims were to test for dysregulation of the stress-related hypothalamus-pituitary adrenal (HPA) axis in tinnitus and to examine ear sensitivity variations with cortisol manipulation.
Twenty-one tinnitus participants and 21 controls comparable in age, education, and overall health status but without tinnitus underwent basal cortisol assessments on three non-consecutive days and took 0.5 mg of dexamethasone (DEX) at 23:00 on the first day. Cortisol levels were measured hourly the next morning. Detection and discomfort hearing thresholds were measured before and after dexamethasone suppression test.
Both groups displayed similar basal cortisol levels, but tinnitus participants showed stronger and longer-lasting cortisol suppression after DEX administration. Suppression was unrelated to hearing loss. Discomfort threshold was lower after cortisol suppression in tinnitus ears.
Our findings suggest heightened glucocorticoid sensitivity in tinnitus in terms of an abnormally strong glucocorticoid receptor (GR)-mediated HPA-axis feedback (despite a normal mineralocorticoid receptor (MR)-mediated tone) and lower tolerance for sound loudness with suppressed cortisol levels. Long-term stress exposure and its deleterious effects therefore constitute an important predisposing factor for, or a significant pathological consequence of, this debilitating hearing disorder.