Transient glucose hypermetabolism after acute subdural hematoma in the rat.

Abstract

Ischemic brain damage occurs in most patients with acute subdural hematoma, yet many aspects of the distribution and extent of this damage remain unexplained. Previous studies in rat model, which produces a region of infarction under the hematoma, have implicated an "excitotoxic" mechanism, suggesting that high concentrations of excitatory amino acids may exacerbate ischemic damage. A study is described in which local glucose utilization is measured 2 or 4 hours after induction of acute subdural hematoma in the rat. These changes are compared to those produced by introducing the same volume of inert silicone gel into the subdural space. Massive increases (up to 142%) in glucose utilization occurred throughout both hippocampi and in a variable zone around the ischemic core, but these had normalized by 4 hours after blood injection. Hippocampal hypermetabolism was not seen after introduction of the silicone mass, suggesting that diffusible substances from the clotted blood may be responsible for these changes. This transient hypermetabolism accords with an excitotoxic process, which may amplify brain damage after acute subdural hematoma.