By
David A. Steenblock, BS, MS, DO
This research paper was presented at the National Stroke Association
Conference in Boston, October 16-18, 1997.
Oxygen is Mother Nature's most natural drug, most important nutrient
and the element most essential to life. Hyperbaric oxygen therapy is
a unique and important treatment which uses oxygen under pressure
for the correction and healing of stroke and traumatically brain
injured (TBI) individuals. The first clinical use of hyperbaric
oxygen for the treatment of stroke patients was reported in 1965 and
many studies have been done since then proving its safety and
effectiveness.1,2
Most people believe that a stroke is due to the death of brain
cells. Brain cells are thought to die as a direct result of the
interruption of blood flow and the resulting lack of oxygen to a
part of the brain. This concept of what a stroke is has been dogma
for at least the last 100 years. This traditional concept of
infarction, that the brain tissue dies from a blood and oxygen
shortage lasting more than a few minutes, is no longer valid.1
A different
concept has been slowly evolving over the past 25 years that the
death of brain cells occurs only when the flow of blood falls below
a certain level (approximately 8-10 ml/100 gr./min.) while at
slightly higher levels the tissue remains alive but not able to
function. Thus in the acute stroke the affected central core brain
tissue may die while the more peripheral tissues remain alive for
many years after the initial insult, depending on the amount of
blood the brain tissue receives.
Those brain areas that are injured and are not receiving enough
blood flow as a result of the stroke or trauma are now referred to
as the "ischemic penumbra." This is the area that surrounds the
central core of infarcted (dead) tissue. These "rim" tissues do not
receive enough oxygen to function but do receive enough to stay
alive. These brain cells have been described as "sleeping beauties,"
"sleeping neurons," or "dormant" or "idling neurons." These neurons
are nonfunctional but anatomically intact and can be revived.
When I describe
this phenomena to my patients, I explain that some of the brain
cells are sick and just like we do when we are sick, we want to lie
down and not do anything. You also tend to be more grumpy, tired and
irritable than otherwise. These sick brain cells often are
responsible for the stroke or TBI patient being grumpy, irritable,
fatigued, depressed, etc. because cells in the emotional and
cognitive areas of the brain are not functioning effectively.
In the acute case as much as 85% of the brain injury involves those
tissues that surround the central core of dead brain tissue. It is
this ischemic penumbral tissue that the newly approved "clot
busting" drugs (tPA-tissue plasminogen activator) help to save if
they are given within the first three hours of the onset of a blood
clot type of stroke. Hyperbaric oxygen is being considered as a
treatment in conjunction with tPA in the acute stroke setting since
it will extend the period of time during which the tPA can be given.
A fundamental aspect of the pathology of chronic stroke and TBI
patients is that damaged blood vessels are the cause of the ischemic
penumbra. Unfortunately the brain has only limited healing
properties and these seem to run their course during the first year
after the traumatic brain injury. During this first year a number of
healing processes are occurring. A major damaging process that
occurs in the acute stroke or TBI is edema (swelling of the tissues
as a result of the damage). This swelling may take up to 9 to 12
months to resolve and during this time the swelling will be
compressing brain blood vessels Ð limiting the flow of blood to the
damaged tissues. As the swelling goes away, some of the blood
vessels will regain their original diameters and normal blood flow
will resume.
Another process that occurs during this first year is "neovascularization,"
also known as "angiogenesis." This is the process of forming new
capillaries which extend from the surrounding healthy brain tissue
into the areas of the ischemic penumbra. The outermost portions of
the ischemic penumbra (those portions closest to normal brain
tissue) are able to metabolize slightly since they are receiving
more blood than the more centrally located ischemic tissues. This
metabolism releases a breakdown product of ATP called adenosine.
Adenosine is
released from ischemic tissues when ATP is being utilized by the
cell for repair processes. Adenosine is a vasodilator and also
stimulates new capillaries to grow into the ischemic penumbra (neovascularization).
Thus during the first year after a stroke or TBI, new blood vessels
are stimulated to move into the ischemic penumbra to re-supply it
with a new blood supply.
Unfortunately, the ischemic penumbral tissues closer to the infarct
area usually are not receiving enough oxygen or nutrients to
generate ATP Ð either from aerobic or anaerobic metabolism. Due to
the lack of ATP formation, adenosine is not produced and the
formation of new capillaries does not occur. Thus the ischemic
penumbra remains ischemic because the process of neovascularization
is not able to be completed.
This often
results in a substantial amount of brain tissue that remains
ischemic and non-functioning in the chronic stroke and TBI patient's
brain. This failure of natural healing processes is due ultimately
to damaged blood vessels and their inability to provide oxygen and
nutrients to those portions of the brain that are damaged.
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