title: Nerve in reversal reaction.
abstract: 1. Much of the nerve destruction in leprosy takes place during the reactive phase, both during ENL reaction and RR. 2. The high risk patients expected to develop RR are borderline patients with generalized lesions (more than 10 skin lesions) and those presenting with three or more thickened nerve trunks. 3. In RR there is a sudden enhancement of already existing DTH to M. leprae and its antigens resulting in the release of excessive quantities of TNF alpha, INF gamma, and IL-2. The triggering mechanisms of this phenomenon is poorly understood. 4. The already existing granulomas suddenly increase considerably in size due to oedema and rapid influx of lymphocytes, Langhan's and foreign body giant cells. Fragments of M. leprae are also present in the granuloma of some patients. 5. In RR, the acute granulomatous inflammation can produce destruction of nerves even to the extent of causing caseous necrosis of the nerve tissue and irreversible paralysis. The swelling of the nerves due to sudden increase in inflammatory cells and oedema within an unyielding perineurium produce ischaemia and transient paralysis. 6. With prompt administration of anti-inflammatory drugs, paralysis recovers quickly, if it is of ischaemic origin; but will not recover if the Schwann cells and other nerve tissues are destroyed as a result of the immune granuloma. 7. A course of corticosteroids for six months along with anti-leprosy therapy is suggested in high risk patients as a preventive measure. 8. Further the serious problem of continuing nerve damage after clinical cure should be urgently tackled.
authors.affiliation: St Thomas Hospital, Chettupattu.
authors.forename: C K
authors.initials: CK
authors.lastname: Job
mesh_terms: D000818:Animals; D006801:Humans; D007918:Leprosy / Q000150:complications / Q000503:physiopathology*; D015439:Leprosy, Borderline / Q000503:physiopathology; D009443:Neuritis / Q000209:etiology; D010525:Peripheral Nerves / Q000503:physiopathology; D010523:Peripheral Nervous System Diseases / Q000209:etiology / Q000503:physiopathology*