Neuroaxonal dystrophy in HTLV-1-associated myelopathy/tropical spastic paraparesis: neuropathologic and neuroimmunologic correlations |
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Authors: | Elizabeth Wu Dennis W. Dickson Steven Jacobson Cedric S. Raine |
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Affiliation: | (1) Department of Pathology (Neuropathology), Albert Einstein College of Medicine, 1300 Morris Park Avenue, 10461 Bronx, NY, USA;(2) Department of Neurology, Albert Einstein College of Medicine, 1300 Morris Park Avenue, 10461 Bronx, NY, USA;(3) Department of Neuroscience, Albert Einstein College of Medicine, 1300 Morris Park Avenue, 10461 Bronx, NY, USA;(4) the Rose F. Kennedy Center of Research in Mental Retardation and Human Development, Albert Einstein College of Medicine, 1300 Morris Park Avenue, 10461 Bronx, NY, USA;(5) Neuroimmunology Branch, NINDS, National Institutes of Health, Bethesda, Maryland, USA |
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Abstract: | Summary Detailed neuropathologic and immunohistologic analysis of a case of serologically and polymerase chain reaction-confirmed human immunodeficiency virus type I (HTLV-I)-associated myelopathy/tropical spastic paraparesis (HAM/TSP) is reported in a 73-year-old North American black woman. In addition to the usual neuropathologic features of HAM/TSP, including tractal degeneration of the spinal cord, leptomeningeal and perivascular fibrosis, perivascular demyelination and chronic inflammation, neuroaxonal spheroids were prominent in the spinal cord. Neuroaxonal dystrophy was characterized by neurofilamentous masses that were immunoreactive for phosphorylated neurofilament epitopes, but not ubiquitin. Neuroimmunologic analysis of the inflammatory reaction revealed a prevalence of CD8+ T cells and class I major histocompatibility molecules (MHC) (HLA-ABC and 2-microglobulin), but very few CD4+ T cells. Microglia were highly reactive for class II MHC (HLA-DR ) and this was attributed to activation, rather than CD4 interaction, since CD4 presence was minimal. Inflammatory cytokine immunoreactivity was also detected in glia. It is concluded that the cumulative effects of cytotoxic T cell (CD8) infiltration and the possible involvement of cytokines were responsible for the unusual degree of neuroaxonal dystrophy and vascular fibrosis, as well as the observed demyelination in this case.Supported in part by grants NS 07098, NS 08952, NS 11920 and MH 47667 from the NIH; and RG 1001-G-7 from the National Multiple Sclerosis Society. |
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Keywords: | Neuroaxonal dystrophy Cytokines HTLV-I Myelopathy HTLV-I-associated myelopathy/tropical spastic paraparesis |
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