ELECTROPHYSIOLOGICAL EVIDENCE OF NERVE ENTRAPMENT SYNDROMES AND SUBCLINICAL PERIPHERAL NEUROPATHY IN PROGRESSIVE SYSTEMIC-SCLEROSIS (SCLERODERMA)

Citation
M. Mondelli et al., ELECTROPHYSIOLOGICAL EVIDENCE OF NERVE ENTRAPMENT SYNDROMES AND SUBCLINICAL PERIPHERAL NEUROPATHY IN PROGRESSIVE SYSTEMIC-SCLEROSIS (SCLERODERMA), Journal of neurology, 242(4), 1995, pp. 185-194
Citations number
36
Categorie Soggetti
Clinical Neurology
Journal title
ISSN journal
03405354
Volume
242
Issue
4
Year of publication
1995
Pages
185 - 194
Database
ISI
SICI code
0340-5354(1995)242:4<185:EEONES>2.0.ZU;2-D
Abstract
We report the electrophysiological findings and the management of 5 su bjects with progressive systemic sclerosis (PSS) and clinical evidence of nerve entrapment. Three had carpal tunnel syndrome (CTS), I bilate ral CTS and right tarsal tunnel syndrome (TTS) and 1 Guyon's canal syn drome. Only 1 patient (with CTS) showed significant clinical improveme nt after surgical decompression; the other 4 demonstrated a slight rec overy of conduction without lasting clinical relief after conventional treatment. To explain these failures we hypothesized that these entra pment syndromes were the clinical expression of underlying diffuse dam age to the peripheral nervous system (PNS). The conduction values of n erves unaffected by entrapment syndromes were within normal limits, bu t almost all distal velocities were below the mean of controls. Such s ubclinical distal peripheral neuropathy was also verified in a selecte d sample of 17 patients with PSS, without clinical symptoms or signs o f PNS involvement. In these 17 cases the mean distal sensory and motor conduction findings of the median, ulnar, sural and tibial nerves wer e significantly lower than those of a control group, while no signific ant differences were found in the more proximal tracts of the same ner ves. Furthermore, 3 of the 17 patients showed classical electrophysiol ogical evidence of TCS and TTS without any clinical symptoms. We concl uded that the subjects with PSS had subclinical polyneuropathy which m ay become plain polyneuropathy or nerve entrapment syndromes perhaps i nduced by other risk factors.