Abstract
Local cerebral glucose utilization (LCGU) was studied in 23 awake rats following fluid percussion injury (cerebral contusion). In this system, percussion energy was created by a hammer hitting a vinyl chloride membrane with thickness of 0.5 mm and diameter of 100 mm. This system produced a biphasic impact, which would do no unfavorable damage to the brain stem, but cause a reproducible localized cerebral contusion. The LCGU was quantitatively measured by the [14C]deoxyglucose autoradiographic method (Sokoloff). Six rats were controls. LCGU was studied at 1, 2, 4, and 24 hours following injury. [14C]deoxyglucose uptake was remarkably decreased at the center of the contusion and LCGU was mildly decreased at 1 and 4 hours, and definitely at 24 hours over the ipsilateral hemisphere. Interestingly there were two different types of behavior in LCGU changes at 2 hours after injury; no change or slight decrease in 4 of 6 rats (Group A) and remarkable increase (more than 150%) all over the cortex and the hippocampus of the ipsilateral side in 2 of 6 rats (Group B). This unique phenomenon in Group B—“hypermetabolic state”—resembles the autoradiographic findings in cortical spreading depression, which reportedly show remarkable increase of extracellular K+ and negative shift of direct current (DC) potential, associated with increased glucose uptake of the brain. Persistent oligemia was also reported following cortical spreading depression. The authors observed negative shift of DC potential between 1 and 4 hours, most frequently around 2 hours, after fluid percussion injury (unpublished data). If this hypermetabolic state following experimental head injury is associated with persistent oligemia, as reported in cortical spreading depression, cerebral metabolism would be trapped in a vicious cycle. Secondary brain damage is quite possible due to the above reason, and 2 hours after injury would be the critical period for any trial of treatment.
