Regeneration and Repair of the Nervous System: Clinical Aspects
In man, restoration of function after damage to the central nervous system (CNS) cannot be achieved by regeneration. It is, however, frequently accomplished by survival of the damaged neurons. This is only possible if the lesion is of a reversible nature. If the disease process or injury has caused irreversible damage, functional recovery can be achieved by compensatory mechanisms mediated by structures that have escaped damage. Restitution of function due to redundancy in a distributed system and substitution of function by the remaining part of the system represent further mechanisms underlying functional recovery after irreversible damage.
At the clinical level there are no reliable criteria for distinguishing reversible from irreversible lesions at the acute stage. It is therefore difficult to assess the extent of restoration of function after stroke or other acute lesions. Positron emission tomography seems to have the potential for making such a distinction. This would provide the basis for taking measures to prevent the progression of a potentially reversible into an irreversible lesion. The astonishing ability of the brain to survive complete ischemia for a time of as long as one hour and partial ischemia for much longer is an example of a potentially reversible lesion in acute stroke. The capacity for late structural repair is illustrated in the restoration of conduction in demyelinated central axons. At present, therapeutic strategies along these lines promise more benefit than attempts to achieve regeneration of destroyed tissue. However, the inroads made by experimental investigations into regeneration in the CNS justify intensive clinicopathological studies of this problem. In contrast to the poor regenerative capacity of the CNS, successful structural and functional repair mechanisms are illustrated by the remarkable ability of the peripheral neurons to regenerate.
KeywordsSchwann Cell Functional Recovery Human Central Nervous System Spinal Cord Transection Central Axon
Unable to display preview. Download preview PDF.
- (1).Aguayo, A.J.; Bray, G.M.? Perkins, C.S.; and Ducan, I.D. 1979. Axon-sheath cell interactions in peripheral and central nervous system transplants. 1979 Soc. Neurosci. Symp. 4: 361–383.Google Scholar
- (2).Aguayo, A.J.; Bunge, R.P.; Duncan, I.D.; Wood, P.M.; and Bray, G.M. 1979. Rat Schwann cells cultured in vitro can ensheath axons regenerating in mouse nerves. Neurology (Minneapolis) 29: 589.Google Scholar
- (5).Bostock, H., and McDonald, W.I. 1982. Recovery of function after demyelination. In Proceedings of the Dahlem Workshop on Neuronal-Glial Interrelationships: Ontogeny, Maintenance, Injury, Repair. Berlin: Springer.Google Scholar
- (9).Gilliatt, R.W. 1981. Physical injury to peripheral nerves. Physiologic and electrodiagnostic aspects. Mayo Clin. Proc. 56: 361–370.Google Scholar
- (11).Goldman, P.S. 1972. Developmental determinants of cortical plasticity. Acta Neurobiol. Exp. 32: 495–511.Google Scholar
- (17).Kennard, M.A. 1936. Age and other factors in motor recovery from precentral lesions in monkeys. Am. J. Physiol. 115: 138–146.Google Scholar
- (18).Kennard, M.A. 1940. Relation of age to motor impairment in man and in subhuman primates. Arch. Neurol. Psychiatr. 44: 377–397.Google Scholar
- (19).Kling, A., and Tucker, T.J. 1968. Sparing of function following localized brain lesions in neonatal monkeys. In The Neuropsychology of Development, ed. R.L. Isaacson, pp. 121–146. New York: John Wiley and Sons, Inc.Google Scholar
- (21).Kuypers, H.G.J.M. 1974. Recovery of motor function in rhesus monkeys. Neurosci. Res. Prog. Bull. 12/2: 240–244.Google Scholar
- (25).Sears, T.A., ed. 1982. Neuronal-glial Cell Interrelationships. Dahlem Konferenzen. Berlin: Springer.Google Scholar
- (27).Smith, K.J.; Blakemore, W.F.; and McDonald, W.I. 1979. Central remyelination restores secure conduction. Nature 280; 295–396.Google Scholar
- (28).Sunderland, S. 1978. Nerve and Nerve Injuries, 2nd ed. Edinburgh: Churchill, Livingstone.Google Scholar
- (30).Upton, A.R.M., and McComas, A.J. 1973. Double crush in nerve entrapment syndromes. Lancet II: 359–361.Google Scholar