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Hyperbaric oxygen therapy in the treatment of brain injury. (ucp Research Fact Sheet).

REPORT OF A MEETING

On July 25-28, 2001, a meeting was held in which clinicians, clinical investigators and family members reviewed the present status of information about the use of hyperbaric oxygen therapy (HBOT) in the treatment of brain injury. Nearly all participants in the meeting were advocates of the use of HBOT; there were no presentations by conferees who were either opposed to the use of the therapy for this purpose or whose position was as yet undecided. One of the major topics of discussion was the recent report of the "Montreal trial" that demonstrated significant functional improvement in many of the cerebral palsy children participating in the randomized double-blind HBOT trial, but with no differences in functional outcomes in children treated either with 1.35 ATA of air or 1.75 ATA of 100% oxygen (see Research Fact Sheet: Hyperbaric Oxygen Therapy (HBO) for Children with Cerebral Palsy: Report of a Clinical Trial).

The conferees participated in two broad areas of discussion: (1) reports of clinical experiences that appeared to preserve life and restore impaired function when HBOT was administered soon after brain injury (e.g. traumatic brain injury; drowning; birth hypoxia; meningitis); and (2) the clinical experience that HBOT appeared to restore function in persons (usually children) with disabilities following brain injury at sometime in the past (e.g. cerebral palsy).

At this meeting, the principal presentations were reports of clinical experience utilizing HBOT, either individual cases or case series. The reports described functional improvement in both the acute and chronic situations following brain injury. In the chronic situation (cerebral palsy), the results of the use of 100% oxygen administered at a variety of atmospheric pressures were discussed (1.75 ATA; 1.5 ATA; 1.35 ATA); all were reported to be associated with positive short term and long term results; no reports were presented that described poor results. The recognized danger of hyperbaric oxygen was discussed (i.e. seizures), as were the less well recognized behavioral manifestations of oxygen toxicity (e.g. agitation; aggressiveness). In the experience of the conferees, it appears that these complications are unusual, but when they do occur they are manageable by the termination of therapy and the use later of lower levels of hyperbaric oxygen.

One focused item of conference discussion was the Montreal trial and the "implication" that the control subjects receiving air at 1.35 ATA were receiving a "placebo" (a non-therapeutic intervention). It was stated by clinical participants at the conference that air at 1.35 ATA increased both the oxygen level of red blood cells and caused oxygen in the air to dissolve in the blood's fluid (plasma); both increased the availability of oxygen to body tissues-including the brain.

It was proposed by several conferees that the control group of the subjects in the Montreal study were also receiving an increased oxygen supply to the brain; thus explaining the similar clinical improvement in both segments of the study population. If this is true, should air administered at 1.35 ATA be used instead of HBOT? The question was asked, but not answered.

In support of the effects of HBOT on the brain, a number of brain imaging studies using SPECT before and after treatment were presented. SPECT provides images of regional cerebral blood flow; by inference, a change in blood flow implies but does not demonstrate a change in cerebral metabolism. In all of the cases presented, SPECT showed increase in cerebral blood flow in a variety of poorly perfused areas of the brain following HBOT. It was hypothesized that these areas of increased blood flow were metabolically more active than prior to HBOT.

COMMENT:

The reports presented at this meeting of improved function and cerebral circulation cannot be disregarded by labeling them as "observations by biased advocates". These observations by skilled clinicians and parents need to be explored by appropriate scientific studies that meet the standards of modem research. One study, the Montreal study, clearly indicates that room air delivered at a low level of increased atmospheric pressure (1.35 ATA) gives identical results to 100% oxygen delivered at increased pressure (1.75 ATA). At this time, there is still no scientifically acceptable evidence that HBOT is useful in the treatment of disabilities associated with cerebral palsy. The following questions remain to be answered:

* Is HBOT (oxygen level? pressure level?) useful in the treatment of disabilities associated with cerebral palsy?

* Is hyperbaria alone (pressure level?) useful in the treatment of disabilities associated with cerebral palsy?

* Is oxygen supplementation alone (oxygen level?) useful in the treatment of disabilities associated with cerebral palsy?

Sufficient clinical experience does exist to support the need for additional controlled studies exploring these questions in a scientifically acceptable manner (i.e. randomized, double-blind trials). Air delivered in a hyperbaric chamber at 1.0 ATA can serve as a control.

Another issue also requires study: the suggestion that there are "idling" neurones in the brain years after injury that become active after the use of HBOT. At this time, there is no evidence that this is true. However, there are methods available to test this hypothesis: PET brain imaging or metabolic magnetic imaging. These quantitative methods of measuring focal brain metabolism can be applied before and after HBOT and will answer the question.

Are the above studies do-able? They are. To be successful they must have the active participation of the children to be studied, their caregivers, clinicians, and scientists. They also require the organizational arrangements and financial resources that these studies demand in order to be successful. The UCP Research & Educational Foundation is attempting to see if the necessary personnel, the organizational and the financial requirements can be mobilized to initiate these needed studies to evaluate the usefulness of HBOT in treating children with disabilities due to cerebral palsy.

International Symposium on Hyperbaric Oxygen in Cerebral Palsy and the Brain-Injured Child. Boca Raton, Florida; July 25-28, 2001. Richard A. Neubauer, MD, Chairman
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Publication:The Exceptional Parent
Geographic Code:1USA
Date:Mar 1, 2002
Words:989
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