- Title Pages
- Dedication
- Contributors
- Abbreviations
- 1 Death and survival in the nervous system
- 2 Axotomy and mechanical damage
- 3 Metabolic damage
- 4 Inflammation and demyelination
- 5 Infection
- 6 Neurodegenerative disease
- 7 Neuroprotection
- 8 Steroids
- 9 Trophic factors
- 10 Control of inflammation
- 11 Peripheral nerve regeneration
- 12 Failure of CNS regeneration
- 13 Anatomical plasticity
- 14 Biochemical plasticity
- 15 Remyelination
- 16 Coma
- 17 Motor, sensory, and autonomic function
- 18 Cognition
- 19 Psychiatric assessment
- 20 Pharmacological management
- 21 Neuropsychological rehabilitation
- 22 Axon regeneration in the CNS
- 23 Primary neuronal transplantation
- 24 Glial transplantation
- 25 Stem cells
- 26 Gene therapy
- Appendix 1 Alzheimer's disease
- Appendix 2 Amyotrophic lateral sclerosis (ALS)/Motor neurone disease
- Appendix 3 Creutzfeldt-Jakob disease (CJD)
- Appendix 4 Epilepsy
- Appendix 5 Huntington's disease
- Appendix 6 Multiple sclerosis
- Appendix 7 Parkinson's disease
- Appendix 8 Spinal-cord injury
- Appendix 9 Stroke
- References
- Index
Anatomical plasticity
Anatomical plasticity
- Chapter:
- (p.171) 13 Anatomical plasticity
- Source:
- Brain Damage, Brain Repair
- Author(s):
James W. Fawcett
Anne E. Rosser
Stephen B. Dunnett
- Publisher:
- Oxford University Press
In mammals, after damage to major axon tracts or large areas of neuronal tissue, there is permanent loss of function. Axons will not regenerate, and killed neurones are not replaced. This is in contrast to animals below the evolutionary level of the primitive amphibia, in which there is eventually an almost complete recovery of function, and early mammalian embryos have similar abilities. This is made possible by the regeneration of cut axons, and the replacement of lost neurones. The ability to regenerate central nervous system (CNS) axons over long distances and to replace large numbers of lost neurons is lost in evolutionary terms round the level of the primitive frogs, and in developmental terms around late limb-bud stages in mammalian embryos. However, even the mammalian CNS does have a considerable ability to readjust to functional loss. Thus, immediately after a stroke, patients will often have complete paralysis down one side of the body, but in the ensuing months a large proportion of the lost function may return.
Keywords: neuronal tissue, CNS regeneration, lost neurons, mammalian embryos, functional loss, stroke
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- Title Pages
- Dedication
- Contributors
- Abbreviations
- 1 Death and survival in the nervous system
- 2 Axotomy and mechanical damage
- 3 Metabolic damage
- 4 Inflammation and demyelination
- 5 Infection
- 6 Neurodegenerative disease
- 7 Neuroprotection
- 8 Steroids
- 9 Trophic factors
- 10 Control of inflammation
- 11 Peripheral nerve regeneration
- 12 Failure of CNS regeneration
- 13 Anatomical plasticity
- 14 Biochemical plasticity
- 15 Remyelination
- 16 Coma
- 17 Motor, sensory, and autonomic function
- 18 Cognition
- 19 Psychiatric assessment
- 20 Pharmacological management
- 21 Neuropsychological rehabilitation
- 22 Axon regeneration in the CNS
- 23 Primary neuronal transplantation
- 24 Glial transplantation
- 25 Stem cells
- 26 Gene therapy
- Appendix 1 Alzheimer's disease
- Appendix 2 Amyotrophic lateral sclerosis (ALS)/Motor neurone disease
- Appendix 3 Creutzfeldt-Jakob disease (CJD)
- Appendix 4 Epilepsy
- Appendix 5 Huntington's disease
- Appendix 6 Multiple sclerosis
- Appendix 7 Parkinson's disease
- Appendix 8 Spinal-cord injury
- Appendix 9 Stroke
- References
- Index