title: Recurrent paraplegia after remyelination of the spinal cord.
abstract: We have conducted a long-term study of spinal cord morphology and motor function recovery in rats that have undergone lumbar spinal demyelination induced by the B-fragment of cholera toxin (CTB)-saporin. 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- and nonexercise-treated 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-treated rats had a mean score of 1.8 (SD 0.38; n = 6; P <.05). These findings suggest that, in addition to the acute effects of the toxin-induced 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-term effects of spinal insult of the type associated with conditions such as postpolio syndrome.
authors.affiliation: Department of Neurological Surgery, University of California San Francisco, San Francisco, California 94143-0452, USA.
authors.forename: Luc
authors.initials: L
authors.lastname: Jasmin
authors.forename: Peter T
authors.initials: PT
authors.lastname: Ohara
mesh_terms: D000818:Animals; D002114:Calcinosis / Q000473:pathology / Q000503:physiopathology; D002772:Cholera Toxin; D002908:Chronic Disease; D020278:Demyelinating Autoimmune Diseases, CNS / Q000473:pathology / Q000503:physiopathology*; D004195:Disease Models, Animal; D005260:Female; D009046:Motor Neurons / Q000473:pathology; D009069:Movement Disorders / Q000209:etiology / Q000473:pathology / Q000503:physiopathology; D009410:Nerve Degeneration / Q000209:etiology / Q000473:pathology / Q000503:physiopathology*; D009416:Nerve Regeneration / Q000502:physiology*; D010264:Paraplegia / Q000473:pathology / Q000503:physiopathology* / Q000517:prevention & control; D010805:Physical Conditioning, Animal / Q000009:adverse effects*; D010940:Plant Proteins; D016262:Postpoliomyelitis Syndrome / Q000473:pathology / Q000503:physiopathology; D051381:Rats; D017207:Rats, Sprague-Dawley; D020127:Recovery of Function / Q000502:physiology*; D054789:Ribosome Inactivating Proteins, Type 1; D000076985:Saporins; D055502:Secondary Prevention; D013116:Spinal Cord / Q000473:pathology / Q000503:physiopathology
chemical_list: D010940:Plant Proteins; D054789:Ribosome Inactivating Proteins, Type 1; C420112:cholera toxin B-saporin conjugate; D002772:Cholera Toxin; D000076985:Saporins