{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,19]],"date-time":"2026-09-19T09:44:34Z","timestamp":1789811074981,"version":"4.0.1"},"reference-count":30,"publisher":"Wiley","issue":"5","license":[{"start":{"date-parts":[[2017,11,8]],"date-time":"2017-11-08T00:00:00Z","timestamp":1510099200000},"content-version":"vor","delay-in-days":7,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"name":"Intramural research program at NIH"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Annals of Neurology"],"published-print":{"date-parts":[[2017,11]]},"abstract":"<jats:sec><jats:title>Objective<\/jats:title><jats:p>Previous work measures spinal cord thinning in chronic progressive myelopathies, including human T\u2010lymphotropic virus 1 (HTLV\u20101)\u2010associated 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.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>Spinal cord cross\u2010sectional area was measured in individuals (24 healthy controls [HCs], 17 asymptomatic carriers of HTLV\u20101 (AC), 47 HAM\/TSP, 74 relapsing\u2010remitting MS [RRMS], 17 secondary progressive MS [SPMS], and 40 primary progressive MS [PPMS]) from C1 to T10. Clinical disability scores, viral markers, and immunological parameters were obtained for patients and correlated with representative spinal cord cross\u2010sectional area regions at the C2 to C3, C4 to C5, and T4 to T9 levels. In 2 HAM\/TSP patients, spinal cord cross\u2010sectional area was measured over 3 years.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>All spinal cord regions are thinner in HAM\/TSP (56\u2009mm<jats:sup>2<\/jats:sup> [standard deviation, 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 (Expanded Disability Status Scale [<jats:italic>p<\/jats:italic>\u2009=\u20090.009] and Instituto de Pesquisas de Cananeia [<jats:italic>p<\/jats:italic>\u2009=\u20090.03]) and CD8<jats:sup>+<\/jats:sup> T\u2010cell frequency (<jats:italic>p<\/jats:italic>\u2009=\u20090.04) correlate with T4 to T9 spinal cord cross\u2010sectional area in HAM\/TSP. Higher cerebrospinal fluid HTLV\u20101 proviral load (<jats:italic>p<\/jats:italic>\u2009=\u20090.01) was associated with thinner spinal cord cross\u2010sectional area. Both HAM\/TSP patients followed longitudinally showed thoracic thinning followed by cervical thinning.<\/jats:p><\/jats:sec><jats:sec><jats:title>Interpretation<\/jats:title><jats:p>Group average spinal cord cross\u2010sectional area in HAM\/TSP and progressive MS show spinal cord atrophy. We further hypothesize in HAM\/TSP 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. Ann Neurol 2017;82:719\u2013728.<\/jats:p><\/jats:sec>","DOI":"10.1002\/ana.25072","type":"journal-article","created":{"date-parts":[[2017,10,10]],"date-time":"2017-10-10T18:45:35Z","timestamp":1507661135000},"page":"719-728","source":"Crossref","is-referenced-by-count":41,"title":["Imaging spinal cord atrophy in progressive myelopathies: HTLV\u2010I\u2010associated neurological disease (HAM\/TSP) and multiple sclerosis (MS)"],"prefix":"10.1002","volume":"82","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-8884-3525","authenticated-orcid":false,"given":"Shila","family":"Azodi","sequence":"first","affiliation":[{"name":"Viral Immunology Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health (NIH) Bethesda MD"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Govind","family":"Nair","sequence":"additional","affiliation":[{"name":"Translational Neuroradiology Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health (NIH) Bethesda MD"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yoshimi","family":"Enose\u2010Akahata","sequence":"additional","affiliation":[{"name":"Viral Immunology Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health (NIH) Bethesda MD"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Emily","family":"Charlip","sequence":"additional","affiliation":[{"name":"Viral Immunology Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health (NIH) Bethesda MD"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ashley","family":"Vellucci","sequence":"additional","affiliation":[{"name":"Viral Immunology Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health (NIH) Bethesda MD"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Irene","family":"Cortese","sequence":"additional","affiliation":[{"name":"Neuroimmunology Clinic, National Institute of Neurological Disorders and Stroke, National Institutes of Health (NIH) Bethesda MD"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jenifer","family":"Dwyer","sequence":"additional","affiliation":[{"name":"Neuroimmunology Clinic, National Institute of Neurological Disorders and Stroke, National Institutes of Health (NIH) Bethesda MD"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"B. 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