A focus of neurorehabilitation is restoration of function. Recovered function utilizes existing neurological structures, as in unmasking, or relies upon the creation of new structures via neurogenesis, synaptogenesis, gliogenesis and angiogenesis. Neurorehabilitation facilitates, recruits and/or co-opts plasticity for re-acquisition of function. Recently, increased emphasis on disease processes initiated or accelerated by and disease management following traumatic brain injury (TBI) has been proposed, fundamentally restructuring how TBI is approached. A more comprehensive approach to neurorehabilitation and disease management following TBI may include the development of trophic, plasticity, metabolic, endocrine, neuromodulatory, and orthonutrient strategies that act to optimize neurophysiological function after TBI.
Neurodegenerative processes after TBI include microglial activation, increased oxidative stress, ROS production, increased hyperphosphorylation of tau protein, and cytokine activation which interact to impact overall mitochondrial stress. These processes may be influential in bioenergetic function during periods of high physiological demand such as during intense cortical reorganization. Additionally, strategies for residual and emerging neurological structures in the injured brain may be warranted and/or beneficial to either immediate function or to long-term neurophysiological health. For example, it appears that tau protein may be a factor for some genotypes in chronic traumatic encephalopathy (CTE). Surveillance for testosterone insufficiency or deficiency might constitute a long-term endocrine intervention targeting slowing or preventing the development of tauopathy associated with CTE.
Novel adjuvant therapeutic approaches during chronic rehabilitation might include cellular metabolic targets such as ROS production, cytokine production, microglial activation and deactivation and organelle biosynthesis. Targets relative to metabolic stress management might include protection from oxygen and/or glucose deprivation, oxidative stress, CA+ loading and increased hyperphosphorylation of tau protein. Outcome goals might include prevention of disease processes such as seizures, lipid metabolism disorders, neuroendocrine insufficiencies or deficiencies, dementia or other neurodegenerative conditions.