Massive persistent release of excitatory amino acids following human occlusive stroke.
BACKGROUND
Animal stroke models demonstrate excitatory amino acid (EAA) release in ischemic tissue, as measured by microdialysis. Currently glutamate antagonist drugs are being developed to protect brain tissue after ischemic events. However, the role of EAAs in human occlusive stroke is not well known. We therefore measured glutamate and aspartate release in a patient after occlusive stroke.


METHODS
We describe a case of occlusive stroke in a 50-year-old man. A partial temporal lobectomy was done to remove infarcted tissue and to prevent brain stem compression as well as uncal herniation. A microdialysis probe was placed into the cortex to measure EAAs. Massively increased levels of glutamate and aspartate were detected in the extracellular fluid in this patient (> 300 times normal levels 6 days after infarction).


CONCLUSIONS
These findings indicate that EAAs are tremendously increased in brain tissue after occlusive stroke. The time course of the release of EAAs is much longer than animal studies have suggested previously. Administration of EAA antagonists to patients with ischemic stroke may therefore be beneficial.
D001224:Aspartic Acid / Q000378:metabolism; D002343:Carotid Artery, Internal / Q000473:pathology; D016893:Carotid Stenosis / Q000150:complications*; D002561:Cerebrovascular Disorders / Q000209:etiology / Q000378:metabolism* / Q000473:pathology; D018846:Excitatory Amino Acids / Q000378:metabolism*; D018698:Glutamic Acid / Q000378:metabolism; D006801:Humans; D008297:Male; D008875:Middle Aged
D018846:Excitatory Amino Acids; D001224:Aspartic Acid; D018698:Glutamic Acid