Toxicity of Plasticity. Lessons from a model of developmental learning disorder

Abstract

It is generally recognized that brain plasticity works at least as a mechanism for recovery of function after brain injury. Thus, for instance, the recovery of speech after an aphasia-producing stroke is thought to reflect brain changes of reorganization with beneficial results. Plasticity is thought to exert a useful function in degenerative conditions as well as in injury, which may explain why symptoms of disorders such as Alzheimer’s and Huntington’s disease take a long time to become clinically visible after a clear latency following the onset of neuropathologic changes. The commonly silent growth of brain tumors in terms of cognitive dysfunction is also attributed to brain plasticity changes that serve to compensate for the slow loss attributable to the tumor. Finally, the often cognitively silent cortical injury after a difficult gestation or perinatal complications is thought to result from the unusually active brain plasticity that occurs early in life (Aoki et al. 1988; Cotman et al. 1993; Freed et al. 1985; Milner 1974; Rauschecker 1995; Schneider 1979; Zilles 1992). However, regarding early brain plasticity (Schneider 1979), and occasionally after brain pathology later in life (Cotman et al. 1993), there has been a debate as to the positive and negative effects of brain plasticity. In the present chapter I will present evidence from my laboratory concerning a particular example of brain plasticity after early cortical injury that brings with it negative cognitive effects.