AN IMMUNOHISTOCHEMICAL STUDY ON CUTANEOUS SENSORY RECEPTORS AFTER CHRONIC MEDIAN NERVE COMPRESSION IN MAN

Citation
G. Ramieri et al., AN IMMUNOHISTOCHEMICAL STUDY ON CUTANEOUS SENSORY RECEPTORS AFTER CHRONIC MEDIAN NERVE COMPRESSION IN MAN, Acta anatomica, 152(3), 1995, pp. 224-229
Citations number
26
Categorie Soggetti
Anatomy & Morphology
Journal title
ISSN journal
00015180
Volume
152
Issue
3
Year of publication
1995
Pages
224 - 229
Database
ISI
SICI code
0001-5180(1995)152:3<224:AISOCS>2.0.ZU;2-9
Abstract
Carpal tunnel syndrome represents the most frequent chronic compressiv e neuropathy in man and hence may be investigated as a spontaneous mod el of peripheral nerve damage and repair. In the present report the fa te of nerve fibers in the digital skin after long-lasting median nerve compression has been investigated immunohistochemically in comparison to normal digital skin, with special consideration to sensory endings and encapsulated receptors, The presence has been documented of the n eurospecific marker PGP 9.5, the glia-associated protein S-100, and th e neuropeptides CGRP and CPON which are mainly associated with the sen sory and sympathetic nerve fibers respectively, The morphology and dis tribution of nerve fibers and corpuscles appeared comparable to that o f normal digital skin; a reduction in the density of sensory receptors has, however, been observed, although not to the degree that was expe cted to explain the clinical deficits, It has been also demonstrated t hat at least part of the CGRP-containing sensory and CPON-containing s ympathetic axons may survive unaltered even in patients with a long cl inical history of profound sensorial impairment, An apparent discrepan cy between the maintenance of nerve fibers and the sensory disturbance s and the frequent observation of prompt postoperative recovery even a fter years of compression results from this investigation. The correla tion of immunohistochemical observations and functional scores may not be considered conclusive. It must, however, be discussed If the senso rial impairment in this syndrome might have, at least in some cases, n ot only an anatomical but also an electrophysiological basis.