Aggravation of Acute Ischemic Stroke by Hyperthermia Is Related to an Excitotoxic Mechanism

Abstract

Objective: To examine whether hyperthermia aggravates cerebral injury in acute ischemia by an excitotoxic mechanism, we studied the relationship between body temperature on admission and CSF concentrations of neuroexcitatory amino acids in 128 patients with acute ischemic stroke of less than 24 h duration. Methods: Stroke worsening was defined as the percent change between the Canadian Stroke Scale (CSS) at 48 h and the CSS on admission. Infarct volume was measured on days 4–7 on cranial computed tomography. Excitatory amino acids were analyzed using HPLC. Results: Glutamate concentration [median (min.-max.)] was 11 (2–19) µmol/l in hyperthermic patients (body temperature >37.5°C) and 5 (2–22) µmol/l in normothermic patients (p < 0.0001). Glycine concentration in hyperthermic and normothermic patients was 16 (3–21) µmol/l and 9 (3–50) µmol/l, respectively (p < 0.0001). Glutamate was significantly higher in patients with hyperthermia only during the first 12 h after the onset of symptoms. The CSF concentrations of glutamate (r = 0.52; p < 0.0001) and glycine (r = 0.62; p < 0.0001) correlated with body temperature. Body temperature was significantly related to stroke worsening and infarct size, but this effect was dependent on the glutamate effect. Conclusion: Glutamate and glycine release during the acute phase of cerebral ischemia could be responsible for the increased brain damage in hyperthermia.

Comprehensive Overview of Nursing and Interdisciplinary Care of the Acute Ischemic Stroke Patient

“…These all worsen overall patient outcome. 13,82,[122][123][124][125][126][127][128][129][130][131] To provide high-quality care, nurses must coordinate the activities of the multidisciplinary team. Clinical pathways or physician standing orders can guide the team in managing stroke patients and are useful for coordinating diagnostic tests and appropriate therapies and care issues.…”

Effect of Hyperthermia on Prognosis After Acute Ischemic Stroke

“…Гипертермия вызывает физиологические и структурные изменения вещества мозга, в т. ч. изменение активности ферментов и по-вреждение белков, составляющих основу цитоскеле-та. Повреждение вещества мозга также происходит за счет высвобождения токсичных возбуждающих нейромедиаторов (глутамата и глицина) и образова-ния свободных радикалов при гипертермии [18][19][20][21][22].…”

A novel mechanism of neuroprotection: Blood glutamate grabber

“…35 Moreover, high levels of glutamate in the plasma for at least 24 h were associated with early neurological deterioration, whereas in patients with stable ischemic stroke, glutamate levels dropped to normal values less than 6 h from onset. 35 All of these clinical data demonstrated for the first time the critical role of glutamate in stroke pathology and suggested a source of new strategies for the research of new protective therapies based on the inhibition of glutamate toxicity.…”

“…[32][33][34][35][36][37] Ischemic patients presented higher blood and cerebrospinal fluid (CSF) glutamate levels than control subjects at admission, 37 suggesting that glutamate concentrations above 200 mM in plasma acted as an important predictor of neuronal damage progression at 48 h, with a sensitivity of 85% and a specificity of 97%. 35 Moreover, high levels of glutamate in the plasma for at least 24 h were associated with early neurological deterioration, whereas in patients with stable ischemic stroke, glutamate levels dropped to normal values less than 6 h from onset. 35 All of these clinical data demonstrated for the first time the critical role of glutamate in stroke pathology and suggested a source of new strategies for the research of new protective therapies based on the inhibition of glutamate toxicity.…”