Glucose hypermetabolism after acute subdural hematoma is ameliorated by a competitive NMDA antagonist.

Intracranial hematomas occur in almost half of patients who sustain a severe head injury, and outcome is particularly poor in patients with acute subdural hematoma. We have measured regional cerebral glucose metabolism (2-deoxyglucose autoradiography) in a new rat model of acute subdural hematoma and compared the changes to those seen in sham-operated control animals and animals pretreated with a high-affinity competitive NMDA antagonist, D-CPP-ene. At 2 h after inducing the hematoma, a severe reduction in glucose use was seen in the cortex beneath the hematoma (less than 5 mumol/100g/min) consistent with a zone of histologic infarction seen in other studies. A band of markedly increased glucose use was seen in the periischemic zone, surrounding this infarcted tissue and throughout the hippocampus bilaterally (up to 142% increase). Both the zone of reduced glucose use and the volume of tissue with increased glucose metabolism were significantly reduced in the animals pretreated with D-CPP-ene. These data indicate that the neuroprotective effect of NMDA antagonists, seen in this and other models, may be mediated by reducing the increased metabolism that occurs probably due to glutamate release.