Background and Purpose-The association between hyperthermia and early neurological deterioration, increased morbidity, and mortality in acute ischemic stroke is well known. However, the timing at which the cerebral lesion may be aggravated by high temperature has not been firmly established. The aim of this study was to determine the prognostic value of body temperature measured at different times after onset of stroke. Methods-Axillary temperature was recorded every 2 hours for 72 hours in 260 patients with a hemispheric cerebral infarction of Ͻ24 hours' duration. A potential infectious focus was examined in all patients with hyperthermia (temperature Ͼ37.5°C in any of the assessments). Stroke severity was quantified with the Canadian Stroke Scale on admission. The relationship between the highest temperature recorded in each 6-hour interval from stroke onset and stroke outcome (Canadian Stroke Scale and Barthel Index at 3 months) or infarct volume was evaluated by correlation analyses. The importance of the time at which hyperthermia was first detected was assessed by logistic regression analysis. Results-During the first 72 hours, 158 patients (60.8%) had hyperthermia, and in 57.6% of them an infectious cause was identified. Mortality rate at 3 months was 1% in normothermic patients and 15.8% in hyperthermic patients (PϽ0.001).The correlation coefficients between the final infarct volume, Canadian Stroke Scale and Barthel Index scores at 3 months, and each temperature recording decreased progressively over time from symptom onset. Hyperthermia initiated within the first 24 hours from stroke onset, but not afterward, was independently related to larger infarct volume (odds ratio

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Our results support the excitotoxic activity of glutamate and glycine in patients with cerebral infarction.

The presence of glutamate increase in the CSF cannot be documented for greater than 6 hours in stable ischemic stroke. The sustained elevation of glutamate observed in progressing stroke suggests that the window to prevent neurological deterioration may be wider.

A current hypothesis for migraine suggests that neuroexcitatory amino acids may participate in the triggering of attacks. To investigate this possibility we measured glutamic and aspartic acid level in plasma and cerebrospinal fluid (CSF) of patients with common and classic migraine during attacks, making comparisons with controls suffering stress. Plasma levels of amino acids in migraine patients were lower than in controls. CSF concentrations of glutamic acid were higher in migraineurs than in controls. Our results suggest an excess of neuroexcitatory amino acids in the CNS of migraine patients during attacks, possibly favoring a state of neuronal hyperexcitability.