03073nas a2200409 4500000000100000008004100001260001300042653001500055653001000070653000900080653002200089653001000111653002100121653001900142653001100161653001100172653001400183653001200197653002000209653000900229653001600238653001000254653002700264653003900291653001500330653002600345653001700371100001800388700001500406245006600421856005900487300001100546490000700557050002200564520206300586022001402649 1994 d c1994 Dec10aAdolescent10aAdult10aAged10aAged, 80 and over10aChild10aChild, Preschool10aCohort Studies10aFemale10aHumans10aIncidence10aleprosy10aLogistic Models10aMale10aMiddle Aged10aNepal10aNeurologic Examination10aPeripheral Nervous System Diseases10aPrevalence10aRetrospective Studies10aRisk Factors1 avan Brakel WH1 aKhawas I B00aSilent neuropathy in leprosy: an epidemiological description. uhttp://leprev.ilsl.br/pdfs/1994/v65n4/pdf/v65n4a08.pdf a350-600 v65 aVANBRAKEL1994 (2)3 a

This paper presents epidemiological data on silent nerve function impairment in leprosy based on a retrospective study of 536 patients registered at Green Pastures Hospital, Pokhara, West Nepal. Because of the multiple possible aetiologies it is proposed that the clinical phenomenon should be named 'Silent Neuropathy' (SN). We defined this as sensory or motor impairment without skin signs of reversal reaction or erythema nodosum leprosum (ENL), without evident nerve tenderness and without spontaneous complaints of nerve pain (burning or shooting pain), paraesthesia or numbness. The functioning of the main peripheral nerve trunks known to be affected in leprosy was assessed using a nylon filament to test touch thresholds and a manual voluntary muscle test to quantify muscle strength. Almost 7% of new patients had SN at first examination. 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 occurred during the first year of treatment. During steroid treatment the sensory and motor function in nerves affected by SN improved significantly (p = 0.012, Wilcoxon matched-pairs signed ranks test) over a period of 3 months. The patients with more extensive clinical disease (3/9 or more body areas involved, more than 3 enlarged nerves or a positive skin smear) were found to be at increased risk of developing SN. We discuss 4 different possible aetiologies of SN: 1, Schwann cell pathology; 2, nerve fibrosis; 3, cell-mediated immune reaction; and 4, intra-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 nerve function assessment at every visit to the clinic at least during their first year of treatment. Regular nerve function assessment is essential to detect SN at an early stage and to prevent permanent impairment of nerve function.

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