SILENT NEUROPATHY IN LEPROSY - AN EPIDEMIOLOGIC DESCRIPTION

Citation
Wh. Vanbrakel et Ib. Khawas, SILENT NEUROPATHY IN LEPROSY - AN EPIDEMIOLOGIC DESCRIPTION, Leprosy review, 65(4), 1994, pp. 350-360
Citations number
27
Categorie Soggetti
Tropical Medicine",Pathology,"Dermatology & Venereal Diseases
Journal title
ISSN journal
03057518
Volume
65
Issue
4
Year of publication
1994
Pages
350 - 360
Database
ISI
SICI code
0305-7518(1994)65:4<350:SNIL-A>2.0.ZU;2-#
Abstract
This paper presents epidemiological data on silent nerve function impa irment in leprosy based on a retrospective study of 536 patients regis tered at Green Pastures Hospital, Pokhara, West Nepal. Because of the multiple possible aetiologies it is proposed that the clinical phenome non should be named 'Silent Neuropathy' (SN). We defined this as senso ry or motor impairment without skin signs of reversal reaction or eryt hema nodosum leprosum (ENL), without evident nerve tenderness and with out spontaneous complaints of nerve pain (burning or shooting pain), p araesthesia or numbness. The functioning of the main peripheral nerve trunks known to be affected in leprosy was assessed using a nylon fila ment to test touch thresholds and a manual voluntary muscle test to qu antify muscle strength. Almost 7% of new patients had SN at first exam ination, The incidence rate of SN among the 336 new patients who were available for follow-up was 4.1 per 100 person years at risk. In total , 75% of all SN episodes diagnosed after the start of chemotherapy occ urred during the first year of treatment. During steroid treatment the sensory and motor function in nerves affected by SN improved signific antly (p = 0.012, Wilcoxon matched-pairs signed ranks test) over a per iod of 3 months. The patients with more extensive clinical disease (3/ 9 or more body areas involved, more than 3 enlarged nerves or a positi ve skin smear) were found to be at increased risk of developing SN. We discuss 4 different possible aetiologies of SN: 1, Schwann cell patho logy; 2, nerve fibrosis; 3, cell-mediated immune reaction; and 4, intr a-neural ENL. Some epidemiological evidence is presented that suggests that SN cannot be equated with a 'reversal reaction expressing itself in the nerves'. It is recommended that all patients should have a ner ve function assessment at every visit to the clinic at least during th eir first year of treatment. Regular nerve function assessment is esse ntial to detect SN at an early stage and to prevent permanent impairme nt of nerve function.