The metabolic response to brain injury

Every year several million people sustain brain injury. The development of an optimal metabolic and nutritional support program for brain-injured patients relies on an understanding of the metabolic response and nutritional complications that occur with brain injury. Severely brain injured patients have increased serum and urine levels of norepinephrine, epinephrine, and cortisol. These patients also have increased oxygen consumption and urinary nitrogen excretion. This group has observed hypozincemia, hyperzincuria, increased serum C-reactive protein and copper concentrations, and hypoalbuminemia in nonsteroid-treated severely brain-injured patients. Experimental head injury produces interleukin-1 (IL-1) of brain origin. This cytokine mediates many of the aspects of the acute phase response, including all of the metabolic abnormalities reported by our group. IL-1, when administered intracerebroventricularly to experimental animals, appears to have enhanced biological activity compared to that administered systemically. Interleukin-1 activity has been found in significant amounts in the intraventricular fluid of head-injured patients. We suggest that IL-1 acts in concert with traditional stress hormones such as epinephrine, norepinephrine, and cortisol to produce the profound metabolic disturbances observed in the head-injured patient.