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Pharmacological Modulation of Spreading Depolarizations

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Neurovascular Events After Subarachnoid Hemorrhage

Part of the book series: Acta Neurochirurgica Supplement ((NEUROCHIRURGICA,volume 120))

Abstract

Spreading depolarization (SD) is a wave of almost complete depolarization of the neuronal and glial cells. Nowadays there is sufficient evidence demonstrating its pathophysiological effect in migraine with aura, transient global amnesia, stroke, subarachnoid hemorrhage, intracerebral hemorrhage, and traumatic brain injury. In these cases, occurrence of SD has been associated with functional neuronal damage, neuronal necrosis, neurological degeneration, and poor clinical outcome. Animal models show that SD can be modulated by drugs that interfere with its initiation and propagation. There are many pharmacological targets that may help to suppress SD occurrence, such as Na+, K+, Cl, and Ca2+channels; Na+/K+-ATPase; gap junctions; and ligand-based receptors, for example, adrenergic, serotonin, sigma-1, calcitonin gene-related peptide, GABAA, and glutamate receptors. In this regard, N-methyl-d-aspartate (NMDA) receptor blockers, in particular, ketamine, have shown promising results. Therefore, theoretically pharmacologic modulation of SD could help diminish its pathological effects.

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Correspondence to Renán Sánchez-Porras MD .

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Sánchez-Porras, R., Zheng, Z., Sakowitz, O.W. (2015). Pharmacological Modulation of Spreading Depolarizations. In: Fandino, J., Marbacher, S., Fathi, AR., Muroi, C., Keller, E. (eds) Neurovascular Events After Subarachnoid Hemorrhage. Acta Neurochirurgica Supplement, vol 120. Springer, Cham. https://doi.org/10.1007/978-3-319-04981-6_26

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  • DOI: https://doi.org/10.1007/978-3-319-04981-6_26

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