{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,13]],"date-time":"2026-02-13T16:18:43Z","timestamp":1770999523770,"version":"3.50.1"},"reference-count":27,"publisher":"SAGE Publications","issue":"5","license":[{"start":{"date-parts":[[2005,10,1]],"date-time":"2005-10-01T00:00:00Z","timestamp":1128124800000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Mult Scler"],"published-print":{"date-parts":[[2005,10]]},"abstract":"<jats:p>\n                    The objectives of this study were (1) to determine how cerebrospinal fluid (CSF)                 neurofilament heavy chain (NfH\n                    <jats:sup>SMI34<\/jats:sup>\n                    and NfH\n                    <jats:sup>SMI35<\/jats:sup>\n                    ) levels                 relate to clinical outcome in optic neuritis (ON) and multiple sclerosis (MS)                 relapse patients treated with high dose oral methylprednisolone; and (2) to                 correlate neurofilament and myelin basic protein (MBP) concentrations, particularly                 as the latter was previously associated with clinical disability. Fifty subjects                 participated in two double-blind, randomized, placebo-controlled clinical trials.                 Eight\/18 patients in the ON trial and 15\/32 subjects in the MS attack trial were                 treated with oral methylprednisolone. In the MS attack trial group, CSF                 NfH\n                    <jats:sup>SMI34<\/jats:sup>\n                    and NfH\n                    <jats:sup>SMI35<\/jats:sup>\n                    measured at week 3 and DCSF                 NfH\n                    <jats:sup>SMI34<\/jats:sup>\n                    levels from baseline to week 3 were predictive of clinical                 outcome at week 8 and 52. In the ON group, no such association was seen. When both                 groups were combined, baseline CSF NfH\n                    <jats:sup>SMI34<\/jats:sup>\n                    and NfH\n                    <jats:sup>SMI35<\/jats:sup>\n                    correlated positively with baseline enhancing lesion volume (ELV)                 (r\n                    <jats:sub>s<\/jats:sub>\n                    =0.50, p&lt;0.01 and r\n                    <jats:sub>s<\/jats:sub>\n                    =0.53, p&lt;0.01,                 respectively). Levels of NfH\n                    <jats:sup>SMI35<\/jats:sup>\n                    at baseline and week 3 also strongly                 correlated with the MBP concentration. This study supports the view that acute                 inflammation in ON and MS results in axonal pathology and that the latter has a role                 in determining functional impairment.\n                  <\/jats:p>","DOI":"10.1191\/1352458505ms1218oa","type":"journal-article","created":{"date-parts":[[2005,8,20]],"date-time":"2005-08-20T17:32:16Z","timestamp":1124559136000},"page":"532-536","source":"Crossref","is-referenced-by-count":30,"title":["Acute axonal damage predicts clinical outcome in patients with multiple sclerosis"],"prefix":"10.1177","volume":"11","author":[{"given":"E T","family":"Lim","sequence":"first","affiliation":[{"name":"Department of Neuroinflammation, Institute of Neurology, University                         College London, Queen Square, London, WC1N 3BG, UK,"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"F","family":"Sellebjerg","sequence":"additional","affiliation":[{"name":"Department of Neurology, University of Copenhagen, Glostrup, Copenhagen,                         DK-2600, Denmark"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"C V","family":"Jensen","sequence":"additional","affiliation":[{"name":"Danish Research Centre of Magnetic Resonance, Copenhagen University                         Hospital, Hvidovre Hospital, Hvidovre, DK-2650, Denmark"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"D R","family":"Altmann","sequence":"additional","affiliation":[{"name":"Department of Neuroinflammation, Institute of Neurology, University                         College London, Queen Square, London, WC1N 3BG, UK, Medical Statistics Unit,                         London School of Hygiene and Tropical Medicine, Keppel Street, London, WC1E                         7HT, UK"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"D","family":"Grant","sequence":"additional","affiliation":[{"name":"Department of Neuroinflammation, Institute of Neurology, University                         College London, Queen Square, London, WC1N 3BG, UK"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"G","family":"Keir","sequence":"additional","affiliation":[{"name":"Department of Neuroinflammation, Institute of Neurology, University                         College London, Queen Square, London, WC1N 3BG, UK"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"E J","family":"Thompson","sequence":"additional","affiliation":[{"name":"Department of Neuroinflammation, Institute of Neurology, University                         College London, Queen Square, London, WC1N 3BG, UK"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"G","family":"Giovannoni","sequence":"additional","affiliation":[{"name":"Department of Neuroinflammation, Institute of Neurology, University                         College London, Queen Square, London, WC1N 3BG, UK"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"179","published-online":{"date-parts":[[2005,10]]},"reference":[{"key":"e_1_2_1_1_1","doi-asserted-by":"publisher","DOI":"10.1093\/brain\/120.3.393"},{"key":"e_1_2_1_2_1","first-page":"323","article-title":"Axonal transection in the lesion of multiple sclerosis","volume":"338","author":"Trapp BD","year":"1988","unstructured":"Trapp BD , Peterson J , Ransohoff RM , Rudick R , Mork S , Bo L. 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