Hyperbaric oxygenation for the treatment of stroke

K K Jain MD (Dr. Jain is a consultant in neurology and has no relevant financial relationships to disclose.)
Originally released June 24, 1997; last updated May 19, 2017; expires May 19, 2020

This article includes discussion of hyperbaric oxygenation for the treatment of stroke, acute ischemic stroke, chronic poststroke stage, poststroke depression, and rehabilitation after stroke. The foregoing terms may include synonyms, similar disorders, variations in usage, and abbreviations.


Hyperbaric oxygen is an established form of therapy, but its use in stroke remains controversial. Several animal experimental studies laid down the rational basis for this treatment, and over 2500 stroke patients have been treated with hyperbaric oxygen. Part of the controversy arising from lack of efficacy is the poor design of studies. Evidence in favor of hyperbaric oxygen is accumulating. As a neuroprotective, hyperbaric oxygen should be applied for acute stroke within the same window as thrombolytic therapy, ie, 3 to 6 hours. Late application and use of pressures higher than 1.5 to 2 ATA may even be harmful. Beneficial effect is also obtained by a combination of hyperbaric oxygen and physical therapy in the chronic poststroke stage for neurologically stable patients.

Key points


• Oxygen under pressure greater than at sea level is approved for the treatment of several disorders, particularly those characterized by ischemia or hypoxia.


• Despite experimental evidence and rationale for neuroprotective effect as well as considerable clinical experience, the use of hyperbaric oxygen has not been officially approved.


• Some of the controlled clinical trials have not shown beneficial effects, and further studies are ongoing to resolve the controversy.


• Hyperbaric oxygen therapy is safe, and its use continues to increase as an adjunct to the management of stroke.

Historical note and terminology

Development of hyperbaric oxygen or its therapeutic use is closely tied to diving medicine. Compressed air was used for the treatment of a variety of medical disorders in 17th-century Europe prior to the discovery of oxygen by Priestley in 1775. Toward the end of the 19th century, hyperbaric chambers were used in the United States for the treatment of nervous disorders. In 1928, the largest and sole functioning hyperbaric chamber (the tank) in the world was that of Cleveland's Dr. Cunningham, who was repeatedly requested by the Bureau of Investigations of the American Medical Association to document his claims regarding the effectiveness of hyperbaric therapy. Cunningham failed to produce any publication. He was eventually censured by the American Medical Association that same year in a report that stated:


Under the circumstances, it is not to be wondered that the Medical Profession looks askance at the "tank treatment" and intimates that it seems tinctured much more strongly with economics than with scientific medicine. It is the mark of the scientist that he is ready to make available the evidence on which his claims are based (Trimble 1974).

The year 1937 saw the demise of hyperbaric air therapy in the United States. The scrap metal of Cunningham's hyperbaric chamber was used for armament construction for World War II. The same year saw the birth of hyperbaric oxygen therapy for the treatment of decompression sickness in divers. In 1960, a landmark study showed that hyperbaric oxygen could maintain life in pigs in the absence of blood (Boerema et al 1960). The pigs were exsanguinated and transfused with plasma after the separation of red blood cells and placed in a hyperbaric chamber breathing 100% oxygen at 6 atmospheres absolute. Some of the earlier conditions treated with hyperbaric oxygen were carbon monoxide poisoning and infections. The use of hyperbaric oxygen has expanded, and now there are more than 500 hyperbaric facilities in the United States alone.

During the past 30 years, hyperbaric oxygen has been applied in the treatment of acute stroke patients; more than 2500 patients have been documented in various publications (Jain 2017). All of these studies were uncontrolled and reported favorable results. There were some publications of controlled clinical trials. Anderson and colleagues' findings point to an outcome trend favoring sham treatments and indicate that hyperbaric oxygen might worsen outcome (Anderson et al 1991). A double-blind study by Nighoghossian and colleagues detected an outcome trend favoring hyperbaric oxygen therapy (Nighoghossian et al 1995). One clinical trial found hyperbaric oxygen to be ineffective (Rusyniak et al 2003). This has raised the level of controversy surrounding this method of treatment and will be discussed in more detail later in this article.

Although hyperbaric oxygen is an approved method of treatment for several conditions, such as decompression illness and nonhealing wounds, it has not yet won general recognition in the United States for the management of stroke patients. Considerable progress has occurred since the condemnation of Cunningham, and hyperbaric oxygen has been placed on a scientific footing by thousands of publications and a textbook (Jain 2017). The cost-effectiveness of hyperbaric oxygen has been demonstrated, but this method of treatment remains controversial.

Definitions. Hyperbaric oxygenation involves the use of 100% oxygen under pressure greater than that found on earth's surface at sea level. Several units are used to denote barometric pressure, the most common being atmospheres absolute (ATA). The treatment is applied in a specially constructed chamber. Hyperbaric air involves the use of room air, rather than 100% oxygen, and is used as a control "sham treatment" in clinical trials.

Evaluation of a new method of treatment for stroke should be considered separately for acute and chronic phases of the disease. Although acute stroke is easy to define and most strategies are aimed at treatment during the first few hours, the definition of chronic poststroke stage remains a problem. This term should be used when the patient has reached a stable state after the acute phase and no further recovery is seen. It is difficult to fit this in a time scale. For some patients, recovery stops after a few months following the stroke. One year is an arbitrary limit. A patient who does not recover within this period may be labeled as having a chronic poststroke stage; however, some patients may continue to recover up to 2 years following the stroke. Viability of neurons in the penumbra zone surrounding the infarct has been demonstrated up to several years.

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