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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
Online ISSN 1827-1839
Koszewicz M. 1, Gosk-Bierska I. 2, Jerzy G. 3, Biliƒska M. 1, Podemski R. 1, Budrewicz S. 1, Adamiec R. 2
1 Department of Neurology, Wrocław Medical University, Wrocław, Poland;
2 Department of Angiology, Hypertension, and Diabetology; Wrocław Medical University, Wrocław, Poland; 3 Department of Traumatology and Hand Surgery, Wrocław Medical University, Wrocław, Poland
AIM: Different mechanisms (neural and intravascular) are thought to be important in the pathogenesis of Raynaud’s phenomenon (RP). In a previous study we confirmed autonomic nervous system impairment in patients with primary RP, but the pathogenic role of peripheral nerves remained unclear. The aim of the current study was an electrophysiological analysis of peripheral nerves using both standard conduction velocity and the conduction velocity distribution (CVD) in patients with primary RP in order to investigate the causes of dysautonomia.
METHODS: We examined 34 patients with primary RP and dysautonomia and 31 sex- and age-matched controls. Standard motor and sensory conduction tests in ulnar and peroneal (sural) nerves and a CVD test in the same nerves were performed.
RESULTS: Clinically, none of the patients had motor symptoms, while 35.3% of them presented sensory neuropathy. Standard neurographic tests were within the normal limits except for the significant prolongation of mean sensory latency in both examined nerves. CVD revealed significant slowing of motor conduction velocity in all the conduction values, e.g. in the 10th, 50th, and 90th percentiles of velocity. There were no differences in the width of the velocity distribution in the patient group and controls.
CONCLUSION: The results of CVD indicated the presence of generalized subclinical peripheral motor nerve impairment (subclinical polyneuropathy) in patients with primary RP and dysautonomia. Based on the present and previous studies, we conclude that the mechanism of autonomic dysfunction in primary RP is mixed, resulting from both central and peripheral neural abnormalities.