TY - JOUR
T1 - Relationship of endogenous cortisol to gait in idiopathic parkinsonism
AU - Dobbs, R. J.
AU - Purkiss, A. G.
AU - Charlett, Andre
AU - Peterson, D.
AU - Weller, C.
AU - Dobbs, S. M.
PY - 1997
Y1 - 1997
N2 - Serum cortisol concentration is higher by, on average, 17 % in idiopathic parkinsonism (Purkiss AG et al. Br Clin Pharmac 1996; 42:in press). The relationship of resting cortisol to gait is examined, in 93 subjects with diagnosed idiopathic parkinsonism and 167 without, to explore any association with severity, as well as with presence, of parkinsonism. Cortisol was measured by radioimmunoassay: the between-assay coefficient of variation being 6, 5 and 3 % at serum concentrations of 77, 399 and 1086 nmol.l-1. Mean stride length at free walking speed, after rest, was obtained using die gait-assessment trolley (Bowes SG et al. Br Clin Pharmac 1991;31:295-304) in the same empty corridor (in a therapeutic window in parkinsonians). After standardisation for covariates found to be significant in the controls (sampling time, height and gender in the case of cortisol; age, height and die Modified Tooting Bec cognitive function score for stride length), there was a significant (P<0.01) interaction between presence/absence of parkinsonism and stride length with respect to cortisol. Between controls, cortisol was greater by 0.49 (95% C.I. 0.08, 0.89) % per cm longer stride (P=0.02). Between parkinsonians, cortisol tended (P>0.05) to be greater the shorter the stride by, on average, 0.18 %. cm-1. A persistently active immune mechanism in the pathogenesis, may disrupt and, in the absence of treatment, reverse the normal relationship between resting cortisol and performance.
AB - Serum cortisol concentration is higher by, on average, 17 % in idiopathic parkinsonism (Purkiss AG et al. Br Clin Pharmac 1996; 42:in press). The relationship of resting cortisol to gait is examined, in 93 subjects with diagnosed idiopathic parkinsonism and 167 without, to explore any association with severity, as well as with presence, of parkinsonism. Cortisol was measured by radioimmunoassay: the between-assay coefficient of variation being 6, 5 and 3 % at serum concentrations of 77, 399 and 1086 nmol.l-1. Mean stride length at free walking speed, after rest, was obtained using die gait-assessment trolley (Bowes SG et al. Br Clin Pharmac 1991;31:295-304) in the same empty corridor (in a therapeutic window in parkinsonians). After standardisation for covariates found to be significant in the controls (sampling time, height and gender in the case of cortisol; age, height and die Modified Tooting Bec cognitive function score for stride length), there was a significant (P<0.01) interaction between presence/absence of parkinsonism and stride length with respect to cortisol. Between controls, cortisol was greater by 0.49 (95% C.I. 0.08, 0.89) % per cm longer stride (P=0.02). Between parkinsonians, cortisol tended (P>0.05) to be greater the shorter the stride by, on average, 0.18 %. cm-1. A persistently active immune mechanism in the pathogenesis, may disrupt and, in the absence of treatment, reverse the normal relationship between resting cortisol and performance.
UR - http://www.scopus.com/inward/record.url?scp=33748972124&partnerID=8YFLogxK
M3 - Article
AN - SCOPUS:33748972124
SN - 0009-9236
VL - 61
SP - 179
JO - Clinical Pharmacology and Therapeutics
JF - Clinical Pharmacology and Therapeutics
IS - 2
ER -