[Cerebral protection. The role of nutritional therapy]

Prevention of secondary cerebral insults has the highest priority as far as therapeutic interventions of the patient with brain lesions are concerned. Patients with cerebral lesions have to overcome both, cerebral and systemic insults. The intensity of the neuronal injury determines the grade of hypermetabolism. Optimal metabolic and nutritional therapy for patients with cerebral lesions should be accomplished to minimize secondary brain damage. Frequently, the systemic hypermetabolic response is associated with cerebral ischemic metabolism. Therefore systemic blood glucose levels should be less than 150 mg/dl to prevent intracellular anaerobic accumulation of lactate. Individual utilization capacity of substrates is determined by the grade of hypermetabolism. Substrate load has to be adapted to the individual utilization capacity to avoid side effects of nutritional therapy like substrate and volume overload, imbalances of electrolytes as well as enhanced application of excitatoric substrates. In addition, whenever possible enteral nutrition should be applied to profit from reduced bacterial translocation and improved glucose hemostasis. Oxygen radical production and lipid peroxidation are important pathophysiologic mechanisms concerning cerebral lesions. More recent data show reduced antioxidative status in patients with brain injuries which favors lipid peroxidation. Further studies must be carried out to evaluate the potential neuro-protective effect of an antioxidative nutritional regimen in patients with cerebral lesions.