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We found that, after the initial demyelination and paraplegia, motor function recovered and was stable for up to 9 months, after which there occurred a slow deterioration of motor function accompanied by loss of motoneurons and loss of spinal white matter. A striking morphological feature was the appearance of large spheroids of calcium in the ventral and dorsal horns and occasionally in the white matter. Motor performance deterioration occurred earlier and was more severe in rats that had been exercised on a treadmill, but the same morphological changes occurred in both exercise\u2010 and nonexercise\u2010treated animals. Rats given treadmill exercise starting 3 weeks after toxin injection had a mean motor deficit score of 3.0 (i.e., paraplegia) at perfusion, whereas the nontreadmill\u2010treated rats had a mean score of 1.8 (SD 0.38; n = 6; <jats:italic>P<\/jats:italic> &lt; .05). These findings suggest that, in addition to the acute effects of the toxin\u2010induced demyelination from which there is recovery of motor function, there are chronic irreversible effects of the toxin, or the initial demyelination, that cause a slow progressive degeneration of the spinal cord. This model might therefore be useful in studying the long\u2010term effects of spinal insult of the type associated with conditions such as postpolio syndrome. \u00a9 2004 Wiley\u2010Liss, Inc.<\/jats:p>","DOI":"10.1002\/jnr.20143","type":"journal-article","created":{"date-parts":[[2004,5,5]],"date-time":"2004-05-05T22:08:00Z","timestamp":1083794880000},"page":"277-284","source":"Crossref","is-referenced-by-count":3,"title":["Recurrent paraplegia after remyelination of the spinal cord"],"prefix":"10.1002","volume":"77","author":[{"given":"Luc","family":"Jasmin","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Peter 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