2001 Clinical and Scientific Meeting

A. McGrath, G. C. Scroop, C. Sargent, R. B. Burnet and B. Chatterton

Adelaide Chronic Fatigue Syndrome Research Group
Department of Physiology,
University of Adelaide,
South Australia,
Australia

No evidence of hypotension or impaired cognitive function with acute orthostatic stress in Chronic Fatigue Syndrome

Fatigue, cognitive dysfunction and short-term memory impairment are features common to both CFS and idiopathic orthostatic intolerance (Freeman and Komaroff, 1997; Mathias et al., 1999), suggesting that the shared symptomatology may have a similar mechanism, namely postural hypotension leading to reduced cerebral perfusion and hypoxic dysfunction. There is some evidence to support this suggestion in CFS patients (Freeman and Komaroff, 1997; Bou-Holaigah et al., 1995), but while disordered autonomic cardiovascular innervation, a low blood volume and physical deconditioning with a loss of skeletal muscle tone (Streeten et al. 2000; Freeman and Komaroff, 1997; Streeton and Anderson, 1992) have all been proposed as possible mechanisms, none has been systematically investigated nor has the impact of orthostatic stress on cognitive function been quantified in CFS.

The present study examined the effect of two orthostatic stressors, namely active standing and lower body negative pressure (LBNP, at minus 50 mmHg), each for 10 minutes, on a series of cardiovascular and cognitive function markers in 10 female CFS patients and 10 healthy sedentary controls matched for age and body mass index. Total blood volume and lean body mass were measured in both subject groups prior to testing and fell within normal limits. Only 3 subjects, all healthy controls, exhibited pre-syncopal signs (hypotension and bradycardia) and symptoms (sweating, nausea and anxiety) in response to orthostatic stress, and in each case this was during the last two minutes of LBNP. Apart from this, blood pressure was well maintained in both subject groups during each orthostatic stress, and both subject groups responded to LBNP with a similar increase in forearm muscle vascular resistance, suggesting that baro-reflex function is normal in CFS patients. While resting heart rate was not different between CFS patients and controls and increased in response to both orthostatic stressors, the increase in heart rate in response to active standing, but not LBNP, was significantly larger in CFS patients (CFS, 20 ± 3, Controls, 11 ± 2, beats/min, n=10). The responses to a battery of cognitive function tests, used previously in CFS studies (La Manca et al. 1998), were not altered in either group in response to active standing.

It is concluded that postural hypotension does not occur in response to short-term orthostatic stress in CFS, and further, that acute orthostatic stress does not affect cognitive function.

Bou-Holaigah, I., Rowe, P.C., Kan, J. and Calkins, H. (1995). The relationship between neurally mediated hypotension and the chronic fatigue syndrome. Journal of the American Medical Association, 274: 961-967.
Freeman R. and Komaroff A.L. (1997). Does the chronic fatigue syndrome involve the autonomic nervous system? Review of Infectious Diseases, 13: s8-s11.
Streeton D.H. and Anderson G.H. Jr. (1992). Delayed orthostatic intolerance. Archives of Internal Medicine, 152: 1066-1072.
Streeten, D.H., Thomas, D. and Bell, D.S. (2000). The roles of orthostatic hypotension, orthostatic tachycardia, and subnormal erythrocyte volume in the pathogenesis of the chronic fatigue syndrome. American Journal of the Medical Sciences, 320: 1-8.
LaManca, J.J., Sisto, S.A., DeLuca, J., Johnston, S.K., Lange, G., Pareja, J., Cook, S. and Natelson, B.H. (1998). Influence of exhaustive treadmill exercise on cognitive functioning in chronic fatigue syndrome. American Journal of Medicine 105: 59S-65S.

 

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