Brain, Vol 121, Issue 12 2239-2247, Copyright © 1998 by Oxford University Press
P Facer, R Mathur, SS Pandya, U Ladiwala, BS Singhal and P Anand
Loss of nociception and hypohidrosis in skin are hallmarks of leprosy,
attributed to early invasion by Mycobacterium leprae of Schwann cells
related to unmyelinated nerve fibres. We have studied skin lesions and
contralateral clinically unaffected skin in 28 patients across the leprosy
spectrum with a range of selective quantitative sensory and autonomic
tests, prior to biopsy of both sites. Unaffected sites showed normal skin
innervation, when antibodies to the pan-neuronal marker PGP (protein gene
product) 9.5 were used, with the exception of intraepidermal fibres which
were not detected in the majority of cases. Elevation of thermal thresholds
and reduced sensory axon-reflex flare responses in affected skin correlated
with decreased nerve fibres in the subepidermis, e.g. axon-reflex flux
units (means+/-SEM) for no detectable innervation; decreased innervation;
and clinically unaffected skin, were 23+/-3.1; 41.2+/-7.3; and 84.5+/-4.0,
respectively. Reduced nicotine-induced axon-reflex sweating was correlated
with decreased innervation of sweat glands. Where methacholine-induced
direct activation of sweat glands was affected, there was inflammatory
infiltrate and loss of sweat gland structure. This study demonstrates a
correlation between selective nerve dysfunction on clinical tests and
morphological changes in skin, irrespective of the type of leprosy, and is
the first to show that loss of sweating in leprosy may result either from
decreased innervation and/or involvement of the sweat glands. The findings
have implications for the selection and monitoring of patients with leprosy
in clinical trials which aim to restore cutaneous function.
ARTICLES
Correlation of quantitative tests of nerve and target organ dysfunction with skin immunohistology in leprosy
Academic Department of Neurology, St Bartholomew's and The Royal London School of Medicine and Dentistry, UK.
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