Titlebook: Brain Injury and Recovery; Theoretical and Cont Stanley Finger,T. E. Levere,Donald G. Stein (Dean Book 1988 Plenum Press, New York 1988 Ar

Indent

Assumptions about the Brain and Its Recovery from Damage,ry long way from understanding how the brain as an entity, or its subdivisions, acts to produce the mental and behavioral characteristics of people. Yet without any firm foundation of this knowledge, as scientists, we must proceed in our research programs to generate an empirical basis for the under

積習難改

Misnomer

saturated-fat

Infant Brain Injury,e expected following injury sustained early in life as compared to brain injury sustained later in life?” Although the answers “l(fā)ess recovery,” “about the same recovery,” or “more recovery” would seem simple enough, establishing one alternative over the others has proven difficult (see Finger and Al

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indecipherable

Another Look at Vicariation,one part of the brain to substitute for the function of another. Vicariation has been the source of much debate in neuroscience and lies at the heart of the enduring controversy known as localization of function. The idea that another area of the brain can take over the function of a damaged area fo

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財產

Trophic Hypothesis of Neuronal Cell Death and Survival, of the organism at the time of the damage, several different mechanisms have been proposed for the observed recovery. These mechanisms include regeneration, collateral sprouting, receptor supersensitivity, and enzymatic hyperactivity (Aguayo, 1985; Marshall, 1984; Cotman and Nieto-Sampedro, 1984).

演繹

不在灌木叢中

Is Dendritic Proliferation of Surviving Neurons a Compensatory Response to Loss of Neighbors in thety. The view taken here is that the plastic capacity of the developing brain does not suddenly cease as some developmental landmark is reached but that some degree of residual plasticity is maintained to the end of the developmental continuum (death). Functionally, this residual plasticity may be ma