EPIDEMIC NEUROPATHY IN CUBA - MORPHOLOGICAL CHARACTERIZATION OF PERIPHERAL-NERVE LESIONS IN SURAL NERVE BIOPSIES

被引:39
作者
BORRAJERO, I
PEREZ, JL
DOMINGUEZ, C
CHONG, A
CORO, RM
RODRIGUEZ, H
GOMEZ, N
ROMAN, GC
NAVARROROMAN, L
机构
[1] NATL REF CTR PATHOL ANAT,PATHOL LAB,HAVANA,CUBA
[2] DEPT INTERNAL MED,HAVANA,CUBA
[3] HERMANOS AMEIJEIRAS HOSP,HAVANA,CUBA
[4] NINCDS,NEUROEPIDEMIOL BRANCH,BETHESDA,MD
[5] NCI,HEMATOPATHOL SECT,PATHOL LAB,BETHESDA,MD 20892
关键词
AXONAL NEUROPATHY; BERI BERI; CUBA; EPIDEMIC NEUROPATHY; MORPHOMETRY; MYELIN; NEUROTOXICITY; NUTRITIONAL NEUROPATHY; SURAL NERVE BIOPSY; TROPICAL MYELONEUROPATHIES;
D O I
10.1016/0022-510X(94)90137-6
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
More than 50 000 patients were affected in Cuba during an epidemic outbreak of peripheral neuropathy from January 1992 until September 1993. The disease presented as either a retrobulbar optic neuropathy, a predominantly sensory peripheral neuropathy, a dorsolateral myeloneuropathy, or as mixed forms. The morphological findings in sural nerve biopsies from 34 patients with various forms of the disease are presented here. Frozen, paraffin and semi-thin sections were prepared for light and electron microscopy, immunohistochemistry and morphometric analysis. Every case presented morphological alterations ranging from mild axonal dystrophy (9 cases, or 27%) to moderate and severe atonal damage (25 cases, or 73%). In 6 cases (18%), axonal damage was accompanied by perineural fibrosis and vascular abnormalities. Axonal regeneration was noted in 8 cases (23%) and remyelination in 9 (26%). Morphometric analysis showed a predominant loss of myelinated fibers in 92% of the patients. Quantification of myelinated fiber loss in 11 patients revealed a remarkable decrease in large caliber fibers. Scarce mononuclear cells were observed in 17 cases. No virus-like elements were seen. The morphological features found in this study indicate that, regardless of the clinical presentation, peripheral nerve lesions of the epidemic neuropathy in Cuba correspond to an axonal neuropathy. These lesions are compatible with nutritional, toxic, or metabolic etiologies. An inflammatory etiology would be unusual with these lesions.
引用
收藏
页码:68 / 76
页数:9
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