03090nas a2200457 4500000000100000008004100001260001300042653001000055653000900065653002600074653003000100653002200130653002100152653001100173653002200184653001100206653001400217653002300231653001200254653002500266653000900291653001600300653003900316653001700355653002600372653002000398653002100418653003000439653001700469653002200486100001800508700001400526700001600540245006900556856005100625300001100676490000700687050003200694520189200726022001402618 2003 d c2003 Dec10aAdult10aAged10aDisability Evaluation10aDrug Therapy, Combination10aElectrophysiology10aErythema Nodosum10aFemale10aFollow-Up Studies10aHumans10aIncidence10aLeprostatic Agents10aleprosy10aLeprosy, lepromatous10aMale10aMiddle Aged10aPeripheral Nervous System Diseases10aPrednisolone10aRetrospective Studies10aRisk Assessment10aSampling Studies10aSeverity of Illness Index10aTime Factors10aTreatment Outcome1 aRosenberg N R1 aFaber W R1 aVermeulen M00aUnexplained delayed nerve impairment in leprosy after treatment. uhttps://leprosyreview.org/article/74/4/35-7365 a357-650 v74 aInfolep Library - available3 a

The objective of this study was to examine the clinical signs, symptoms and course of neuropathies in patients with leprosy who after treatment developed nerve impairment, not explained by relapse or reversal reactions. We searched the case-records of leprosy patients, seen between 1985 and 2002 at the department of dermatology at our centre. Included in the study were patients who had developed nerve impairment after treatment of leprosy in the absence of relapse, erythema nodosum leprosum, or reversal reactions, and who were referred to a neurologist. In these patients, we recorded age, onset of leprosy, type of leprosy, treatment of leprosy, signs and symptoms of delayed nerve impairment, results of electrophysiological studies, responses to treatment and course. Included were 14 patients, of whom eight had a (sub)acute multiple mononeuropathy (group I); and six had a slowly progressive multiple mononeuropathy (group II). Patients in group I had limited improvement of nerve impairment after treatment with corticosteroids, and recurrence of symptoms and signs (usually of the motor nerves) when corticosteroids were tapered off. Patients in group II had slowly progressive predominantly sensory nerve impairment. Initially, they had only subjective symptoms, after at least 3 years objective signs became detectable. These patients were not treated with immunosuppressants. Two groups of patients with unexplained delayed nerve impairment could be distinguished. One group had a multiple mononeuropathy resembling reversal reactions with insufficient response to corticosteroids. In these patients, more aggressive and prolonged immunosuppressive treatment should be considered. The aetiology for the neuropathy in the other group remains unclear and further investigations are needed to understand the pathogenesis before treatment recommendations can be given.

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