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Med Hypotheses. 2004;62(2):203-6.

Dysautonomia in chronic fatigue syndrome: facts, hypotheses, implications.

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  • 1Department of Internal Medicine A, Bnai Zion Medical Center and Bruce Rappaport Faculty of Medicine, Technion - Israel Institute of Technology, PO Box 4940, Haifa 31048, Israel. naschitz@tx.technion.ac.il

Abstract

The diagnosis of chronic fatigue syndrome (CFS) is based on patient history and treatment on cognitive behavior therapy and graded exercise. There is increasing evidence that dysautonomia occurs in CFS manifest primarily as disordered regulation of cardiovascular responses to stress. We impart our experience relating to diagnosis, monitoring, and treatment of CFS based on identification and management of dysautonomia. Recently proposed methods for assessment of the cardiovascular reactivity, the 'hemodynamic instability score' (HIS) and the 'Fractal and Recurrence Analysis-based Score' (FRAS), served for this purpose. On HUTT, a particular dysautonomia is revealed in CFS patients that differ from dysautonomia in several other disorders. This distinct abnormality in CFS can be identified by HIS >-0.98 (sensitivity 84.5% and specificity 85.1%) and FRAS > +0.22 (sensitivity 70% and specificity 88%). Therefore, the HIS and FRAS may be used, in the appropriate clinical context, to support the diagnosis of CFS, which until now, could only be subjectively inferred. A pilot study suggested that midodrine treatment, directed at the autonomic nervous system in CFS, results first in correction of dysautonomia followed by improvement of fatigue. This finding implies that dysautonomia is pivotal in the pathophysiology CFS, at least in a large part of the patients, and that manipulating the autonomic nervous system may be effective in the treatment of CFS.

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