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Original Article
2002:68:2;84-85
PMID: 17656885

Silent neuropathy in leprosy

S Jena, S Mishra, G Mohanty
 Department of Dermatology and Department of Neurology, VSS Medical College, Burla, Sambalpur - 768 017, India

Correspondence Address:
S Jena
Department of Neurology, VSS Medical College, Burla, Sambalpur - 768 017
India
How to cite this article:
Jena S, Mishra S, Mohanty G. Silent neuropathy in leprosy. Indian J Dermatol Venereol Leprol 2002;68:84-85
Copyright: (C)2002 Indian Journal of Dermatology, Venereology, and Leprology

Abstract

Twelve patients of silent neuropathy attending the OPD of Skin and VD, VSS Medical College Hospital during 1996 - 1998 were taken for study. On clinical analysis 5 cases were present as silent neuropathy, 4 cases during MDT and 3 cases after completion of MDT Seventy percent of cases showed good response to systemic steroid.
Keywords: Leprosy, Neuropathy - Silent

Introduction

Asymptomatic neuropathy in leprosy occurs in a proportion of patients without going through a stage of acute or sub acute neuritis. Clinically "neuritis" refers to acute or sub acute inflammatory state of nerve trunks associated with moderate to severe pain or tenderness, with or without paralysis. Impairment of sensory or motor nerve function without symptoms of neuritis has been described as a common phenomenon by a number of authors. Various terms have been used to describe this phenomenon, including ′quiet nerve paralysis.[1] (QNP), ′silent neuritis′[2] (SN), and ′nerve reaction′.[3] Reversibility of motor paralysis by steroid therapy in QNP has been described.[1] In this study we are reporting twelve cases of QNP and its response with systemic steroid.

Materials and Methods

Clinically diagnosed cases of leprosy attending the Skin and VD OPD, V.S.S Medical College Hospital during 1996 - 1998 were taken for the study. Cases with clinical impairment of sensory or motor nerve function were selected for presentation. All the routine investigations on blood, stool and urine, skin smear for AFB and nerve conduction test were done. They were treated with systemic steroid and MDT and advised for physiotherapy (Massage, active and passive exercise). Initially high dose of prednisolone (up to 60mg) was given and gradually reduced and stopped in course of 4-6 months. All the cases were kept under observation for 2 years.

Observation

Out of 12 cases of S.N. 5 cases presented as silent neuritis. They were new cases and not started on M. D. T. Four cases presented during M.D.T. and 3 reported after completion of M.D.T 50% of S.N. were found in BL cases, 33.3% in PNL and 16.7% in borderline tuberculoid leprosy as shown in [Table - 1]. The common clinical presentation was foot drop and clawing of hand. Other features like anaesthesia, trophic ulcer, trophic eczema, hypopigmented patches and thickened peripheral nerves were present. Nerve conduction test was found to be normal except in two cases where the conduction was slow.

As per [Table - 1] 66.6% of cases of SN were found in patients who were not on MDT Only 33.3% of cases were found among patients on MDT. It shows that the incidence of SN is low in patients who are under MDT. Thus antileprosy drugs have definite role in preventing the development of silent neuropathy.

High dose of prednisolone was given initially, gradually tapered to 10 mg daily, maintained for 6-8 weeks and then withdrawn. No side effects of steroids were found, but they were subsided after the dose of steroid was tapered. Majority of cases responded nicely. Improvement was excellent in patients who reported early as shown in [Table - 2]. Response to steroid was better in children than in old age group.

[Table - 2] shows that 83.3% of cases responded to systemic steroid and 16.6% of cases did not show any response. Relapse rate was 25%. Thus 58.3% of cases had complete clinical recovery. Early cases within 8 weeks of development of silent neuropathy had better response without any relapse than late cases of more than 2 months duration.

Discussion

This study shows that silent neuropathy may present at any stage of leprosy. Since nerve injury may occur after completion of MDT, monitoring at 3 months interval is necessary in paucibacillary patients for 2 years and in multibacillary patients for 5 years. Patients with more extensive clinical disease were at increased risk of development of SN.[4] Early diagnosis and treatment is necessary to prevent permanent deformities. Thus regular nerve function assessment using the most sensitive test available is essential to detect S.N. at an early stage and to prevent permanent nerve impairment.[4]

This study shows that in case of Quiet Nerve Paralysis steroid therapy for at least six months prevents establishment of motor paralysis and paralytic deformity in a high proportion of cases, especially if the condition is recognized early, before the nerve is completely paralysed.[1] Prognosis is good at an early age group than in older age group. Relapse rate is high in patients who started treatment late and in older age group.

References
1.
Srinivasan H, Roo K S, Shanmugan N. Steroid therapy in recent 'Quiet' nerve paralysis' in leprosy. Lepr India 1982;54:412-419.
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2.
Duncan ME, Pearson JMH. Neuritis in pregnancy and lactation. Int J Lepr 1982;50:31-38.
[Google Scholar]
3.
Barnetson R, Biune G, Pearson J M H, et al. Cell - mediated and humoral immunity in 'reversal reaction'. Int J Lepr 1976;44:267-274.
[Google Scholar]
4.
Van Brakel WH, Khawas IB. Silent neuropathy in leprosy: an epidemiological description. Lep Rev 1994;65:350-360.
[Google Scholar]
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