Hyperbaric oxygen for cerebral vasospasm and brain injury following subarachnoid hemorrhage

Robert P Ostrowski1, John H Zhang

  • 1Department of Physiology and Pharmacology, Loma Linda University, 11041 Campus Street, Loma Linda, CA 92350, USA.

The impact of acute brain injury and delayed neurological deficits due to cerebral vasospasm (CVS) are major determinants of outcomes after subarachnoid hemorrhage (SAH). Although hyperbaric oxygen (HBO) had been used to treat patients with SAH, the supporting evidence and underlying mechanisms have not been systematically reviewed. In the present paper, the overview of studies of HBO for cerebral vasospasm is followed by a discussion of HBO molecular mechanisms involved in the protection against SAH-induced brain injury and even, as hypothesized, in attenuating vascular spasm alone. Faced with the paucity of information as to what degree HBO is capable of antagonizing vasospasm after SAH, the authors postulate that the major beneficial effects of HBO in SAH include a reduction of acute brain injury and combating brain damage caused by CVS. Consequently, authors reviewed the effects of HBO on SAH-induced hypoxic signaling and other mechanisms of neurovascular injury. Moreover, authors hypothesize that HBO administered after SAH may "precondition" the brain against the detrimental sequelae of vasospasm. In conclusion, the existing evidence speaks in favor of administering HBO in both acute and delayed phase after SAH; however, further studies are needed to understand the underlying mechanisms and to establish the optimal regimen of treatment.

Related Concept Videos

Hemorrhagic Stroke ll: Pathophysiology01:29

Hemorrhagic Stroke ll: Pathophysiology

A hemorrhagic stroke develops when a cerebral blood vessel ruptures, allowing blood to escape into the surrounding brain tissue, as in intracerebral hemorrhage (ICH), or into the subarachnoid space, as in subarachnoid hemorrhage (SAH). Because the skull is a rigid compartment, the sudden presence of extravascular blood rapidly increases intracranial pressure and compresses adjacent neural structures, leading to immediate tissue injury and impaired cerebral perfusion.Mass Effect and Primary...
Cerebral Edema ll: Pathophysiology01:22

Cerebral Edema ll: Pathophysiology

Vasogenic edema is a major form of cerebral edema characterized by abnormal accumulation of fluid in the brain’s extracellular space due to disruption of the blood–brain barrier (BBB). The BBB is a specialized structure composed of endothelial cells connected by tight junctions, supported by astrocytic endfeet and a basement membrane. Under normal conditions, it tightly regulates the movement of ions, proteins, and solutes between the bloodstream and brain parenchyma. When this barrier loses...
Increased Intracranial Pressure l: Introduction01:14

Increased Intracranial Pressure l: Introduction

Intracranial hypertension is a sustained elevation of intracranial pressure (ICP) above 22 mm Hg. In supine adults, normal ICP is ~7–15 mm Hg.The rigid, nonexpandable cranium contains three components—brain tissue, blood, and cerebrospinal fluid (CSF)—that total ~1,700 mL in a typical adult: 1,400 mL brain (~80%), 150 mL blood (~10%), and 150 mL CSF (~10%). According to the Monro–Kellie doctrine, total intracranial volume is effectively fixed. When one component expands, CSF and venous blood...