History of HBOT as a Stroke Therapy

The efficacy of HBOT in organ ischemia was first reported in the late 1950s in Boerema’s studies showing that exsanguinated pigs could survive when placed in a HBOT chamber, and that ischemic myocardial tissue could be saved with HBOT.  In 1961 Sir Charles Illingworth in Glasgow showed that cortical electrical activity could be sustained during cerebral ischemia with HBOT.  However, factors such as the timing, duration, optimal chamber pressure, type of stroke, etc. need much further investigation. HBOT’s role in the treatment of stroke remains controversial.

Stroke is the leading cause of long-term disability and the third leading cause of death in the US.  There are direct and indirect annual costs in excess of $56 billion.81 Two important therapeutic modalities have been tested over the last couple of decades.  One is “neuroprotection” with drugs that interrupt cell death after stroke, and the other is thrombosis, the dissolution of arterial clots that cause ischemic stroke.

The neuroprotective drugs have not shown success outside of animal studies.  Thrombolysis has proved successful and the use of intravenous tissue plasminogen activator (iv tPA) is approved in several countries.  Its use is limited to less than 5 percent of stroke patients because it must be given within three hours after stroke onset.  Later use of this therapy is associated with high rates of brain hemorrhage.

Possible reasons for the failure of previous HBO stroke trials:  the small number of patients in the trials, late onset of the initiation of HBOT, the amount of pressure used, etc.  As always, more and better studies are needed.

It appears that hyperoxia is a powerful neuroprotective therapy that can save ischemic brain tissue, extend the time for other stroke treatments and enhance post-stroke recovery.  More recent studies suggest that much benefit can be achieved even with normoboric therapy (NBO), which offers much more convenience and availability. The time window for NBO is 30 minutes.

“Stroke is now the second leading cause of death the most frequent cause of adult permanent disability in Western countries.  Ischemic infarcts account for about 80 % of all strokes and are originally caused by thromboembolic occlusion of a cerebral vessel.”82

Experiments have demonstrated that HBOT influences numerous common mechanisms of secondary brain injury.  It may be an effective treatment for several conditions including those not ischemic, such as hemorrhagic brain injury.

Randomized clinical trials of HBO have rarely been performed even for the conditions for which HBO is an accepted therapy.  Reports of observational data have been published on patients with CNS hemorrhage.  Surgical repair of ruptured cerebral aneurysms with oxygen at 1.6 to 2.0 ATA.  It was repeated from six to 15 times.83

“There is an increasingly strong body of pre-clinical data supporting the use of HBO in reducing secondary brain injury resulting from or causing bleeding in the CNS.  HBO seems to protect the neurovascular unit through multiple mechanisms including protection of the blood brain barrier, inflammation, cell death, etc.”84

Notes
81Zhang, 119.
82Ibid., 137.
83Ibid., 158.
84Ibid., 167.