02024nas a2200265 4500000000100000008004100001260001200042653002600054653002400080653002900104653001500133653003000148100001400178700001200192700001400204700001400218700001500232700001700247700001600264700001200280700001600292245006100308520137500369022001401744 2020 d c12/202010aPeripheral neuropathy10aaxonal degeneration10ademyelinating neuropathy10amorphology10aperipheral nervous system1 aAntunes S1 aFazan V1 aJardim MR1 aPereira M1 ada Costa E1 aPascarelli B1 aHacker MAVB1 aSarno E1 aBarreira AA00aMorphometric analysis of nerve fibers in neural leprosy.3 a

INTRODUCTION/AIMS: the present study assesses the contributions of axonal degeneration and demyelination in leprosy nerve damage. New clinical strategies can emerge from an in-depth understanding of the pathogenesis of neural leprosy. MET: Morphometric analysis of myelinated nerve fibers was performed on forty-four nerve biopsy samples collected from leprosy patients. Measures of density, diameter distribution, g-ratios, and the counting of axonal ovoids on the myelinated fibers were taken and compared to those in the control group.

RESULTS: The proportion of small myelinated fibers increased in the leprosy group while large fiber frequency decreased. Indicative of axonal atrophy, the g-ratio was lower in the leprosy group. The frequency of axonal ovoids was identical to that found in the non-leprosy neuropathies.

DISCUSSION: Axonal atrophy, Wallerian degeneration, and demyelination coexist in neural leprosy. Axonal degeneration predominates over demyelination in the chronic course of the disease; however, this may change during leprosy reactive episodes. This study regards demyelination and axon degeneration as concurrent mechanisms of damage to nerve fibers in leprosy. It also calls into question the view that demyelination is the primary and predominant mechanism in the complex pathogeny of neural leprosy.

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