Human brain plasticity: an emerging view of the multiple substrates and mechanisms that cause cortical changes and related sensory dysfunctions after injuries of sensory inputs from the body.

Injuries of peripheral inputs from the body cause sensory dysfunctions that are thought to be attributable to functional changes in cerebral cortical maps of the body. Prevalent theories propose that these cortical changes are explained by mechanisms that preeminently operate within cortex. This paper reviews findings from humans and other primates that point to a very different explanation, i.e. that injury triggers an immediately initiated, and subsequently continuing, progression of mechanisms that alter substrates at multiple subcortical as well as cortical locations. As part of this progression, peripheral injuries cause surprisingly rapid neurochemical/molecular, functional, and structural changes in peripheral, spinal, and brainstem substrates. Moreover, recent comparisons of extents of subcortical and cortical map changes indicate that initial subcortical changes can be more extensive than cortical changes, and that over time cortical and subcortical extents of change reach new balances. Mechanisms for these changes are ubiquitous in subcortical and cortical substrates and include neurochemical/molecular changes that cause functional alterations of normal excitation and inhibition, atrophy and degeneration of normal substrates, and sprouting of new connections. The result is that injuries that begin in the body become rapidly further embodied in reorganizational make-overs of the entire core of the somatosensory brain, from peripheral sensory neurons to cortex. We suggest that sensory dysfunctions after nerve, root, dorsal column (spinal), and amputation injuries can be viewed as diseases of reorganization in this core.