Cortisol is higher in parkinsonism and associated with gait deficit
Article first published online: 29 JAN 2009
Acta Neurologica Scandinavica
Volume 97, Issue 2, pages 77–85, February 1998
How to Cite
Charlett, A., Dobbs, R. J., Purkiss, A. G., Wrighe, D. J., Peterson, D. W., Weller, C. and Dobbs, S. M. (1998), Cortisol is higher in parkinsonism and associated with gait deficit. Acta Neurologica Scandinavica, 97: 77–85. doi: 10.1111/j.1600-0404.1998.tb00614.x
- Issue published online: 29 JAN 2009
- Article first published online: 29 JAN 2009
- Accepted for publication October 13, 1997.
- endogenous cortisol;
Introduction– We propose an active pathogenic mechanism, involving circulating cortisol, in parkinsonism. Materials and methods– Serum cortisol was measured in 96 subjects with idiopathic parkinsonism, 170 without, and in 17 spouses and 36 siblings of elderly sufferers with double the number of controls, all obeying inclusion/exclusion criteria. Results– Cortisol, adjusted for sampling time, was greater (17%, on average, P < 0.001) in parkinsonians, but not in relatives. The central cortisol lowering effect of anti-muscarinics was seen (P=0.025). Selegiline may attenuate the disease, and parkinsonism is less frequent in tobacco smokers. Selegiline was associated with a lower cortisol (P=0.03): chronic smoking appeared (P=0.08) to be, irrespective of parkinsonism. Bowel stasis has been implicated in the pathogenesis: cortisol was higher in parkinsonians requiring laxatives (P=0.05). In controls, cortisol was lower, the longer the stride (P=0.02): in parkinsonians, this relationship was numerically reversed. A similar (P=0.01) group performance interaction was seen for deterioration, over 4 years, in gait. Conclusion– Cortisol is doing harm or mirroring something which is. A common pathway for neuronal protectiodrescue emerges.