In seriously ill patients a number of variables (blood pressure, arterial oxygen and carbon dioxide levels, intracranial pressure, etc.) are routinely monitored with the underlying aim of preventing brain damage. This objective might be achieved more effectively by monitoring the function of the cerebral cortex itself ( Prior.19.8.5; Grundy ...1995). Both EEG and evoked potentials are sensitive to reduction in cerebral blood flow, and two important thresholds have been identified ( Prior 1985).
The first threshold is the blood flow level at which EEG alteration first appears during gradual flow reduction. This occurs when regional cortical blood flow falls to 20 ml/min/100 g, and is manifest in the EEG by an increase in the proportion of low frequencies (below 8 Hz) and the disappearance of higher frequencies. Alternatively, if the reduction in cerebral blood flow is rapid, a burst-suppression pattern dominates the EEG at flow levels below 20 ml/min/100 g. At about the same flow level the waveform of the cortical somatosensory evoked potential changes, with an increase in latency.
The second threshold is the disappearance of spontaneous EEG activity, which occurs when regional cerebral blood flow falls to approximately 15 ml/min/100 g. If flow remains below this level for more than 45 min, neuronal activity does not return with adequate reperfusion and histology demonstrates selective neuronal loss. Evoked potentials disappear when flow falls to about 12 ml/min/100 g, and infarction results if flow is maintained at this level for 2 to 3 h.
Therefore progressive reduction of cerebral blood flow is reflected in the EEG and evoked potentials by a sequence of changes which appear before irreversible damage has occurred. EEG recognition of ischemia is particularly significant in patients in whom the lower limit of cerebral autoregulation is elevated above its usual level of 60 to 70 mmHg, so that arterial blood pressure is no longer a reliable guide to adequate cerebral perfusion.
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