Abstract
Transection of the mammalian spinal cord results in a complete and permanent loss of voluntary motor function below the level of the lesion accompanied by an equally profound sensory loss. In many phylogenetically lower animals, massive axonal regeneration occurs and often results in some degree of functional restitution, despite the presence of scar formation within the site of injury (Bernstein and Bernstein 1967), but in mammalian forms regeneration of CNS axons is considered to be minimal and abortive (Ramon v Cajal 1928). A variety of treatment methods have been employed in an attempt to promote the regeneration of axons across the transection site (Puchala and Windle 1977). These have included the implanting of grafts of fetal brain tissue, degenerated sciatic nerve or muscle into the lesion site in order to improve the environment for optimal axonal growth (Sugar and Gerard 1940), administration of adrenocorticotrophic hormones (McMasters 1962), millipore cylinders (Campbell and Windle 1960), or Piromen, a pyrogenic bacterial polysaccharide thought to enhance regeneration by preventing the formation of a dense fibrous scar following injury (Clemente and Windle 1954, Littrell 1955). Application of Piro-men seemed to increase the number of regenerating fibers as shown by morphological and electrophysiological techniques, but the animals failed to demonstrate an improvement in their sensorimotor function.
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Matthews, M.A., Gelderd, J.B. (1986). Quantitative Studies of Reactive Events in the Site of Injury Following Transection of the Spinal Cord in the Rat. In: Das, G.D., Wallace, R.B. (eds) Neural Transplantation and Regeneration. Proceedings in Life Sciences. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-662-25264-2_6
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