Monitoring Brain Activity in Human Brain Injury

Aneurysmal Subarachnoid Hemorrhage, Cerebral Hemorrhage, Cerebral Infarction, Traumatic Brain Injury

Spreading depression, Seizures, Blood-brain barrier

The outcome of brain injury (physical or stroke) may be related to a brain electrical phenomenon known as Cortical Spreading Depression (CSD). This is a brief cessation of function in a local region of brain tissue. It has been hypothesized that CSD may occur after brain injury and may expand the damage to adjacent brain areas. Our aim is to detect CSD by means of intracranial electrodes in patients with brain injuries and asses how these events alter the outcome of the patients.

Cortical spreading depression (CSD) is a wave of mass neuronal firing and neuronal and glial depolarisation which propagates through grey matter in the central nervous system in response to a pathologic stimulus, at a rate of between 1 and 5 mm per minute. First described by Leão in 1944 as a sudden depression of ECoG amplitude spreading across the cortex of the rabbit (Leao, A. A. P. 1944), CSD can be elicited in experimental animals by chemical, electrical, and mechanical stimuli, with varying degrees of ease. CSD provoked in healthy, normally perfused neural tissue does not induce persistent metabolic stress or cellular damage, and indeed such induction of CSD in animal experiments may confer protection against the adverse effects of a subsequent ischaemic insult (Kobayashi, S. et al. 1995). In animal models of focal cerebral ischaemia, usually induced by occlusion of the middle cerebral artery, a spontaneous phenomenon occurs around the periphery of the core territory, with electrophysiological features essentially identical with CSD, and similar capacity to propagate across cerebral cortex. Designated peri-infarct depolarisation (PID), this event is associated with infarct expansion, or recruitment of at-risk cortical territory into the expanding core, and has been shown capable of causing this expansion, in the absence of therapeutic intervention. Indeed it has been hypothesized that glutamate release may be involved in PID generation, and that excitotoxicity may accomplish detrimental effects via this route (Hossmann, K. A. 1994), (Obrenovitch, T. P. and Urenjak, J. 1997). Some experimental neuroprotection treatments for stroke act to decrease the incidence of PID (Iijima, T. et al. 1992;Chen, Q. et al. 1993;Busch, E. et al. 1996). In traumatic and ischaemic (especially in middle cerebral artery occlusion and aneurysmal subarachnoid haemorrhage) brain injury in humans, a phase of delayed deterioration often associated with severe and refractory brain swelling develops between 2 and 5 days after the initial ictus, and is associated with poor or fatal outcome. The cause and mechanism of this deterioration remain poorly understood, and the possibility exists that CSD/PID events might contribute to deterioration. To date, CSD or PID have been reported in only ten human subjects in two papers (Mayevsky, A. et al. 1996; Strong, A. J. et al. 2002). Strong et al. reported that transient ECoG suppressions suggestive of depolarisations are common - but by no means universal - after brain injury in humans. Sub-dural ECoG electrode strips were placed in 14 patients who had undergone craniotomy for trauma or intracranial hemorrhage; monitoring was for up to 60 h following the injury. Five of these patients (36%) showed patterns of ECoG depression consistent with PID/CSD in brain regions adjacent to the primary injury.

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Germany, Israel