The Frontier of Electrophysiologic Monitoring in Acute Brain Injury

Excerpt

In 1944, Leão reported his observations on the spreading depression of activity in the cerebral cortex of rabbits after electrical stimulation [1]. Today, we understand this phenomenon as the result of spreading depolarizations (SDs): massive depolarization of injured or irritated neurons with the nearly complete loss of their resting electrochemical gradient, resulting in the influx of water into cells and the depression of electrical activity [2]. This phenomenon has been observed after multiple forms of acute brain injury, such as subarachnoid hemorrhage, ischemic stroke, and traumatic brain injury (TBI). Substantial observational data indicate that SDs result in secondary brain injury and unfavorable neurologic outcomes resulting from cytotoxic edema and infarct development [2]. Leão also noted the relationship between spreading depression and ictal activity [1], which is associated with secondary brain injury. Much of the work establishing the relationship between seizures and secondary brain injury comes from TBI. Seizures occurring within the first 7 days after TBI are known as early posttraumatic seizures (EPSs) and are associated with intracranial hypertension and brain tissue hypoxia [3]. Cerebral microdialysis studies have linked EPS with disturbances in cerebral energy metabolism reflective of metabolic crisis [4]. Furthermore, EPSs are associated with higher mortality, worse functional outcomes, hippocampal atrophy, and posttraumatic epilepsy [3, 5, 6]. There is now compelling evidence for the cooccurrence of SDs and seizures after multiple forms of acute brain injury [7‐9], but their relative importance as instigators of secondary brain injury is largely unknown. …