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.