Neuroprotection in Critical Care Neurology

Menno R. Germans; Hieronymus D. Boogaarts; R. Loch Macdonald

doi:10.1055/s-0036-1592359

Seminars in Neurology, Inhaltsverzeichnis

Semin Neurol 2016; 36(06): 642-648
DOI: 10.1055/s-0036-1592359

Review Article

Thieme Medical Publishers 333 Seventh Avenue, New York, NY 10001, USA.

Neuroprotection in Critical Care Neurology

Menno R. Germans

¹Department of Neurosurgery, Radboud University Medical Center, Nijmegen, The Netherlands

,

Hieronymus D. Boogaarts

¹Department of Neurosurgery, Radboud University Medical Center, Nijmegen, The Netherlands

,

R. Loch Macdonald

²Division of Neurosurgery, Department of Surgery, Keenan Research Centre for Biomedical Science and Li Ka Shing Knowledge Institute, University of Toronto, Toronto, Ontario, Canada

› Institutsangaben

Abstract

Ischemic stroke, intracerebral hemorrhage, subarachnoid hemorrhage, and traumatic brain injury—all have in common early brain injury due to brain tissue destruction, reduced cerebral blood flow and oxygen delivery, and overall substantial morbidity and mortality. The pathophysiology of brain tissue damage likely includes common cellular mechanisms. Neuroprotection has seldom, if ever, been shown to reduce early brain injury. Secondary brain injury develops after these conditions due to macroscopic events such as increased intracranial pressure and reduced cerebral blood flow, as well as cellular processes including vascular damage, inflammation, and apoptotic/necrotic cell death. Preclinical as well as some human studies show successful neuroprotection with, for example, hypothermia for cardiac arrest. Nevertheless, there remains much room for improvement that will require randomized clinical trials of emerging neuroprotective strategies.

Keywords

cerebral ischemia - neuroprotection - subarachnoid hemorrhage - traumatic brain injury

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Referenzen

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