Nerve damage in leprosy: a continuing challenge to scientists, clinicians and service providers

This review focuses on nerve damage in leprosy. We present evidence to support the argument that leprosy is best seen as a chronic neurological condition rather than a simple skin disease. Nerve damage affects small dermal nerves and peripheral nerve trunks. Perineural inflammation is a characteristic and hallmark of early leprosy. T cell-mediated inflammation is the main pathological process in leprosy nerve damage. The level of nerve damage in leprosy is high with up to 60% of multibacillary patients having clinically apparent nerve damage at the time of diagnosis; 30% of patents may develop further nerve damage during treatment and 10% may develop new nerve damage after drug treatment. Since the nerve damage is immune mediated, the antibiotics used to treat Mycobacterium leprae infection have little effect on the accompanying nerve damage. This requires treatment with immunosuppressants to stop the inflammation. Treatment of nerve damage with steroids can be effective but about 50% of patients relapse and require a further course of steroids. Research is needed to refine steroid regimens to be used and define appropriate alternatives. Neuropathic pain is now being recognised as another late complication for leprosy patients. There are also service challenges relating to how best to identify patients who need steroid treatment and how to manage patients with established neuropathy who may require health services for many years.