Objective: Previous work measures spinal cord thinning in chronic progressive myelopathies, including HTLV-1 associated myelopathy/tropical spastic paraparesis (HAM/TSP) and multiple sclerosis (MS). Quantitative measurements of spinal cord atrophy are important in fully characterizing these and other spinal cord diseases. We aimed to investigate patterns of spinal cord atrophy and correlations with clinical markers.

Methods: Spinal cord cross sectional area was measured in individuals (24 healthy controls (HC), 17 asymptomatic carriers of HTLV-1 (AC), 47 HAM/TSP, 74 RRMS, 17 SPMS, and 40 PPMS) from C1 to T10. Clinical disability scores, viral markers, and immunological parameters were obtained for patients and correlated with representative spinal cord cross sectional area regions at the C2-C3, C4-C5, and T4-T9 levels. In two HAM/TSP patients, spinal cord cross sectional area was measured over three years.

Results: All spinal cord regions are thinner in HAM/TSP (56 mm2 [SD 10], 59 [10], 23 [5]) than in HC (76 [7], 83 [8], 38 [4]) and AC (71 [7], 78 [9], 36 [7]). SPMS (62 [9], 66 [9], 32 [6]) and PPMS (65 [11], 68 [10], 35 [7]) have thinner cervical cords than HC and RRMS (73 [9], 77 [10], 37 [6]). Clinical disability scores (EDSS (p=0.009) and IPEC(p=0.03)) and CD8+ T cell frequency (p=0.04) correlate with T4-T9 spinal cord cross sectional area in HAM/TSP. Higher CSF HTLV-1 proviral load (p=0.01) was associated with thinner spinal cord cross sectional area. Both HAM/TSP patients followed longitudinally showed thoracic thinning followed by cervical thinning.

Interpretation: Group average spinal cord cross sectional area in HAM/TSP and progressive MS show spinal cord atrophy. We further hypothesize that is possible that neuroglial loss from a thoracic inflammatory process results in anterograde and retrograde degeneration of axons, leading to the temporal progression of thoracic to cervical atrophy described here. This article is protected by copyright. All rights reserved.


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