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31 - Rehabilitation of dementia

from Section B3 - Cognitive neurorehabilitation

Published online by Cambridge University Press:  04 August 2010

Michael Selzer
Affiliation:
University of Pennsylvania
Stephanie Clarke
Affiliation:
Université de Lausanne, Switzerland
Leonardo Cohen
Affiliation:
National Institute of Mental Health, Bethesda, Maryland
Pamela Duncan
Affiliation:
University of Florida
Fred Gage
Affiliation:
Salk Institute for Biological Studies, San Diego
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Summary

There is a neural substrate to support rehabilitation in those with dementia

When the central nervous system is abruptly injured, such as from stroke or traumatic brain injury, the premorbid neural reserve determines how the brain responds spontaneously without explicit therapeutic intervention. This concept also is relevant to those who have neurodegenerative diseases such as dementia, in that even though the neural substrate can be considered in continuous state of decline, the brain spontaneously may attempt to salvage or repair damaged tissue without exposure to treatments. Given exposure to rehabilitative treatments, it has been postulated that the brain will respond at a neural level to support its attempts to salvage/repair damaged tissue and even recover when exposed to these behaviorally based treatments. What remains elusive is when treatments as applied during rehabilitation are either supportive or possibly detrimental to spontaneous neural recovery. Moreover, in the context of dementia, at which point in the disease trajectory that the neural reserve capacity is completely depleted such that even the most passive learning situations are fruitless, is similarly elusive.

The work of Katzman et al. (1989) and Satz (1993) has supported the concept of the determinism of neural repair/recovery by the brain's reserve tissue capacity in their studies of Alzheimer's disease. Reserve capacity has been associated with brain size. Katzman et al. (1989) reported the histopathologic features of a small group of octogenarians who were cognitively intact and healthy. The surprising finding was that these individuals had neuropathological findings consistent with Alzheimer's disease.

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Publisher: Cambridge University Press
Print publication year: 2006

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