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Official Journal of the , the International Union of Phlebology and the
Indexed/Abstracted in: BIOSIS Previews, Current Contents/Clinical Medicine, EMBASE, PubMed/MEDLINE, Science Citation Index Expanded (SciSearch), Scopus
Impact Factor 0,899
Koszewicz M., Gosk-Bierska I., Bilin´ska M., Podemski R., Budrewicz S., Adamiec R., S/lotwin´ski K.
1 Department of Neurology, Medical University of Wrocl/aw, Poland
2 Department of Angiology, Hypertension, and Diabetology, Medical University of Wrocl/aw, Poland
Aim. The pathogenesis of Raynaud’s phenomenon is still unclear. Neural and intravascular mechanisms are thought to be involved in the pathological process. The role of the autonomic nervous system is continually discussed, with particular attention to over-reactivity of the sympathetic part. The aim of this study was the clinical and electrophysiological analysis of autonomic nervous system function in patients with primary Raynaud’s phenomenon.
Methods. Thirty four patients with primary Raynaud’s phenomenon and 31 sex and age-matched controls were examined. Neurological examination, modified Low’s Questionnaire, orthostatic and sustained handgrip tests, conduction velocity study in three nerves, sympathetic skin response (SSR), and heart rate variability (HRV) during deep breathing and at rest with the fast Fourier transform were performed.
Results. In the clinical examinations, 35.3% of the primary Raynaud’s patients presented sensory neuropathy, but this was not confirmed in the standard conduction velocity tests. The modified Low’s Questionnaire revealed dysautonomy in 82% of the patients. Autonomic regulation during the orthostatic and handgrip tests were within the normal limits. HRV at rest and the E/I ratio were significantly lower in the patient group than in the controls, while HRV spectrum analysis revealed the predominance of the low-frequency band in the patients.
Conclusion. These results indicate the presence of sympathetic dysregulation and impairment of parasympathetic modulation of heart function in primary Raynaud’s patients. The different cardiovascular and sudomotor functions are not affected to the same degree. These observations might support the theory of a central impairment of autonomic function in primary Raynaud’s phenomenon. Peripheral nerve lesion as a coexisting cause of the observed dysautonomy remains uncertain.