01884nas a2200217   4500000000100000008004100001260001300042653001100055653001200066653002500078653001300103653002200116100001200138245009400150856004300244300001100287490000700298050001300305520133400318022001401652       2001                            d  c2001 Jun10aHumans10aleprosy10aMycobacterium leprae10aNeuritis10aPeripheral nerves1 aJob C K00aPathology and pathogenesis of leprous neuritis; a preventable and treatable complication.  uhttp://ila.ilsl.br/pdfs/v69n2s1a05.pdf  aS19-290 v69  aJOB 20013 a<p>In conclusion, it may be said that many advances have been made in the diagnosis, treatment and prevention of nerve damage. It is now a well accepted fact that the affinity of M. leprae for Schwann cells and the property of M. leprae to grow in cooler sites of the body have made certain segments of nerve trunks vulnerable. Trauma that supervenes the inflammation and swelling severely aggravates the nerve damage. The reactive phase in all forms of leprosy, the etiology of which is not clearly understood, produces intraneural caseous necrosis in tuberculoid disease and microabscesses in lepromatous disease, causing much irreversible damage to nerves. The steroid treatment that is administered during the reactive phase has helped greatly to stop further damage, although the damage already done to nerves is not always reversible. Preventive measures like detecting the disease before nerve trunks are infected and offering prompt and adequate antileprosy therapy as early as possible have helped to reduce the prevalence of deformities. It is hoped that administering steroids along with antileprosy therapy to prevent active inflammation and or fibrosis of the nerve will reduce the prevalence of nerve damage significantly. Measures which provide rest for the infected nerve to prevent trauma should be explored.</p>  a0148-916X