Background Within 2 min of severe ischemia, spreading depolarization (SD) propagates like
a wave through compromised gray matter of the higher brain. More SDs arise over hours in …

Background When a patient arrives in the emergency department following a stroke, a
traumatic brain injury, or sudden cardiac arrest, there is no therapeutic drug available to help …

Neuronal injury following focal cerebral ischemia is widely attributed to the excitotoxic effects
of gluta‐mate. However, critical analysis of published data on glutamate toxicity in vitro and …

Cerebral microdialysis has enabled the clinical characterization of excitotoxicity (glutamate>
10 μM) and non-ischemic metabolic crisis (lactate/pyruvate ratio [LPR]> 40) as important …

Recent findings have provided insights into pathogenic mechanism (s) that may complement
and add to the traditional glutamatergic mechanisms to which ischemic brain injury is …

Secondary brain injury is a well-demonstrated contributor to the morbidity and mortality of
severe head injury. At least ten new compounds which antagonize the effects of glutamate in …

Glutamate-mediated excitotoxicity is an important mechanism leading to post ischemic
stroke damage. After acute stroke, the sudden reduction in cerebral blood flow is most …

Excitotoxicity, the specific type of neurotoxicity mediated by glutamate, may be the missing
link between ischemia and neuronal death, and intervening the mechanistic steps that lead …

Spreading depolarization (SD) has emerged as an important contributor to the enlargement
of acute brain injuries. We previously showed that the N‐methyl‐D‐aspartate receptor …

Brain injury following cerebral ischaemia (stroke) involves a complex combination of
pathological processes, including excitotoxicity and inflammation leading to necrotic and …