Clinical neurologists have long known that some recovery of function after damage to the brain and spinal cord is possible, but the specific mechanisms mediating the process are still not completely understood. Part of the difficulty in defining the mechanisms of functional recovery stems from the fact that there may be multiple pathways leading to recovery. This is because brain and spinal cord injuries at the cellular and morphological level are not the result of a single causative event. Rather, they derive from an initial and relatively rapid biochemical cascade that then produces secondary cellular events leading to further destruction of nerve tissue. Many of the destructive events such as the breakdown of the blood—brain barrier, the excessive release of glutamate and other excitatory amino acids, dramatic changes in the levels of neurotransmitters such as gamma-aminobutyric acid (GABA) and norepinephrine, the production of oxygen free radicals, the release of arachidonic acid, lipid membrane peroxidation, and so forth are at the heart of much of the current research being conducted in university laboratories and pharmaceutical companies.


Brain Injury Receptive Field Middle Cerebral Artery Occlusion Superior Colliculus Somatosensory Cortex 
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© Springer Science+Business Media New York 2000

Authors and Affiliations

  • Donald G. Stein
    • 1
  1. 1.Brain Research Laboratory, Department of NeurologyEmory University School of MedicineAtlantaUSA

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