Premium
Peripheral nerve lesions in HTLV‐I associated myelopathy (HAM/TSP)
Author(s) -
Bhigjee Ahmed I.,
Bill Pierre L. A.,
Wiley Clayton A.,
Windsor Isobel M.,
Matthias Denise A.,
Amenomori Tatsuhiko,
Wachsman William,
Moorhouse David
Publication year - 1993
Publication title -
muscle and nerve
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.025
H-Index - 145
eISSN - 1097-4598
pISSN - 0148-639X
DOI - 10.1002/mus.880160106
Subject(s) - sural nerve , remyelination , myelopathy , pathology , pathogenesis , medicine , nerve root , myelin , immunology , peripheral neuropathy , atrophy , fibrosis , spinal cord , central nervous system , psychiatry , anatomy , diabetes mellitus , endocrinology
Abstract Peripheral nerve dysfunction (PND) was found in as many as 43% of our patients with human T‐cell lymphotropic virus type I (HTLV‐I)–associated myelopathy (HAM/TSP). To evaluate the PND further we biopsied the sural nerve in 6 patients. The histological features were varying degrees of demyelination, remyelination, axonal atrophy and degeneration, and perineurial fibrosis. “Globule” or “sausage” formation was prominent in two of the specimens. Inflammatory infiltrates were absent. No deposits of IgG, IgM, IgA, or complement were detected in the biopsies. No viral antigen or proviral DNA was detected. It is proposed that the PND and the histological findings noted are part of HTLV‐I–associated disease and not an unrelated disorder. The pathogenesis of the PND remains unclear. There was no evidence of direct viral infection. The histological findings could represent primary changes induced by viral‐triggered release of soluble factors, such as cytokines or secondary changes to more proximal disease, e.g., root involvement. © 1993 John Wiley & Sons, Inc.