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

討論小組

書目名稱Brain Injury and Recovery影響因子(影響力)




書目名稱Brain Injury and Recovery影響因子(影響力)學科排名




書目名稱Brain Injury and Recovery網絡公開度




書目名稱Brain Injury and Recovery網絡公開度學科排名




書目名稱Brain Injury and Recovery被引頻次




書目名稱Brain Injury and Recovery被引頻次學科排名




書目名稱Brain Injury and Recovery年度引用




書目名稱Brain Injury and Recovery年度引用學科排名




書目名稱Brain Injury and Recovery讀者反饋




書目名稱Brain Injury and Recovery讀者反饋學科排名

他去就結束

Studies in Computational Intelligence isomorphic relationship between the neurological and behavioral, how could the behavior return without a parallel regrowth of the neural tissue? And if other parts of the brain also have an isomorphic relationship with other sets of behaviors, how is it possible for one or more of these neurological areas to take on new behaviors?

Kinetic

Automatic Translation of Multi-word Labelsed with the host brain, and, under the right conditions, is capable of mediating significant recovery from central nervous system (CNS) injury (Sladek and Gash, 1984; Bjorklund and Stenevi, 1985; Gash ., 1985).

insert

Arguments against Redundant Brain Structures,efect can only be ascertained if all of the possible functions are known and have been studied. Perhaps that is why the problem usually is avoided in research papers that are concerned with restricted themes. Nevertheless, the idea of overabundant neurons in the brain is an old one.

Solace

Self-Help-Group

ONYM

粘

fibroblast

Mass Action and Equipotentiality Reconsidered, as explanations for recovery of function. We revisit the concepts by briefly looking at the history before considering their current forms. We then examine the question of whether they are useful concepts to consider as explanations of recovery of function.

浸軟

Is Dendritic Proliferation of Surviving Neurons a Compensatory Response to Loss of Neighbors in the in the chemical composition of the neuron’s immediate surround, its afferent supply, its targets, or in its neighboring neurons and glia. The plastic response(s) to such perturbations may include alteration in dendritic and/or axonal morphology, in synapses, receptors, metabolism, even in genetic expression (e.g., Black ., 1984: Davis ., 1986).