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Neuropathies form an integral part of the symptomatology of leprosy. Neuropathies of leprosy take various forms and shapes. At one end is the cutaneous nerve involvement adjacent to the anaesthetic skin patch and the other is of symmetrical pansensory neuropathy and the devastating sensory ataxia of leprous ganglionits. Lepra reactions add to the spectrum. Hosts immunological status largely decides the clinical manifestations seen in nerves and skin. A wide array of diagnostic techniques like ultrasonography, magnetic resonance neurography, serological markers, molecular tests, skin biopsy and in selected cases, the nerve biopsy with special stains and electron microscopy are obtainable to help the clinical diagnosis. The unsuspecting clinician, lack of community awareness and limited availability of diagnostic tests are important adverse factors in the total outcome. Multi drug therapy is efficacious and corticosteroids reduce the impact of nerve damage in leprosy. The efficacy, dose and duration of corticosteroid therapy are presently inexact and other immune suppressants like azathioprine are being evaluated. Chronic disabilities and residual deficits require attention of multiple specialties. In the coming time, focus on prevention could lead to favourable results. This review will discuss the classification systems, common and uncommon clinical features, diagnostic armamentarium and therapeutic and preventive aspects of neuropathies of leprosy.

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The purpose of this study is to determine the extent of nerve involvement and to study the effect of corticosteroids combined with multidrug therapy on nerve damage in leprosy patients using sensory and motor nerve conduction studies. A cohort of 365 untreated multibacillary leprosy patients were prospectively studied using sensory and motor nerve conduction studies on upper and lower limb nerves. They were subgrouped as those to be treated with 12-week regimen of corticosteroids for reaction and/or neuritis or silent neuropathy of <6 months duration along with 12-month multidrug therapy (group A), and those with no reaction were treated with multidrug therapy only (group B). Analysis was performed using SPSS version 10.0. Significance of association was tested using chi(2) test. At registration, abnormality by nerve conduction studies was seen in 92% of patients and majority (65%) showing involvement of more than five sensory and motor nerves. Sensory nerve abnormalities were higher (52%) than motor (37%) (P < 0.001). Affection of sensory and motor nerves was higher in group A (P < 0.001). Notably, 40% nerves in group B also showed impairment at 0 month. This implies that almost all patients showed abnormal nerve conduction studies at onset regardless of reaction, proving nerve damage is more widespread than envisaged. At 18 months, overall percentile deterioration (23%) of nerves was higher than improvement (9%) (P < 0.001) indicating that corticosteroids combined with multidrug therapy failed to significantly improve the nerve status. Sensory nerve (57%) affection was significantly higher than motor (46%) (P < 0.001). Moreover, percentile deterioration of sensory nerves was higher in group A (P < 0.001) implying corticosteroids is not very efficacious in the prevention or reversal of nerve damage. Electrophysiological tests provide valuable information for detecting nerve function impairment and evaluating appropriate therapeutic regimens.