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Interview with Dr. Paul Harch: the application of hyperbaric oxygen therapy in chronic neurological conditions



Introduction: Hyperbaric oxygen therapy (HBOT) remains a controversial and misunderstood therapy, especially when applied to chronic neuro-logical conditions and autism. This interview explores the science behind these applications. Methods: HBOT is defined as a pharmaceutical and its pharmacologic effects are reviewed in the context of the author's historical application of HBOT to neurology, including autism. Results: HBOT has a powerful drug effect in acute brain injury through inhibition of the acute inflammatory reaction of reperfusion injury (the injury caused by re-turn of blood flow after blood flow interruption—e.g. cardiac arrest at birth, near-drowning, etc.) The author's successful use of HBOT in divers with delayed treatment of brain decompression sickness led to the application to other types of chronic brain injury, including autism. HBOT is sug-gested to have common pharmaceutical actions on the pathology of chronic brain injury, including autism, that are reinforced by the author's proof of effectiveness in an animal model of chronic traumatic brain injury. Some of the author's 25 autistic patients seem to have significant birth insults that contributed to the diagnosis of autism. HBOT appears to be effective for these insults years later. Other physicians are now duplicating the author's findings in autism. There appears to be no identifiable body of information on HBOT in combination with chelation therapy. Conclusions: HBOT appears to be effective in the treatment of autism. The pathological targets of treatment are unknown at this time.
P. Harch, T. Small/Medical Veritas 2 (2005) 637–646 637
Interview with Dr. Paul Harch: the application of hyperbaric
oxygen therapy in chronic neurological conditions
Paul G. Harch, MD and Teri Small1
1AutismOne Radio
1816 Houston Ave.
Fullerton, CA 92833 USA
Phone: +1 714 680 0792
Introduction: Hyperbaric oxygen therapy (HBOT) remains a controversial and misunderstood therapy, especially when applied to chronic neuro-
logical conditions and autism. This interview explores the science behind these applications. Methods: HBOT is defined as a pharmaceutical and its
pharmacologic effects are reviewed in the context of the author’s historical application of HBOT to neurology, including autism. Results: HBOT
has a powerful drug effect in acute brain injury through inhibition of the acute inflammatory reaction of reperfusion injury (the injury caused by re-
turn of blood flow after blood flow interruption—e.g. cardiac arrest at birth, near-drowning, etc.) The author’s successful use of HBOT in divers
with delayed treatment of brain decompression sickness led to the application to other types of chronic brain injury, including autism. HBOT is sug-
gested to have common pharmaceutical actions on the pathology of chronic brain injury, including autism, that are reinforced by the author’s proof of
effectiveness in an animal model of chronic traumatic brain injury. Some of the author’s 25 autistic patients seem to have significant birth insults that
contributed to the diagnosis of autism. HBOT appears to be effective for these insults years later. Other physicians are now duplicating the author’s
findings in autism. There appears to be no identifiable body of information on HBOT in combination with chelation therapy. Conclusions: HBOT
appears to be effective in the treatment of autism. The pathological targets of treatment are unknown at this time.
© Copyright 2005 Pearblossom Private School, Inc.–Publishing Division. All rights reserved
Keywords: HBOT (hyperbaric oxygen therapy), autism, pharmaceutical, chronic brain injury, chelation therapy
Dr. Paul Harch is a graduate of Johns Hopkins University
School of Medicine and is a Diplomate of the Board of
Certification in Emergency Medicine and the American Board
of Hyperbaric Medicine. His clinical experience spans 20 years
of hospital-based emergency medicine and 18 years of hyper-
baric and diving medicine. Dr. Harch is a Clinical Assistant
Professor and Director of the Louisiana State University,
School of Medicine, Hyperbaric Medicine Fellowship Program
and Medical Director of the Hyperbaric Medicine Unit at the
Medical Center of Louisiana in New Orleans. His first applica-
tion of hyperbaric oxygen therapy and SPECT brain imaging to
the central nervous system began with divers with chronic brain
decompression sickness and boxers with dementia pugilistica.
He began using hyperbaric oxygen therapy and SPECT brain
imaging with chronic traumatic brain injury and stroke in the
early 1990s and with cerebral palsy and autistic children in the
early and mid-1990s. After improvement in people with chronic
brain injury, Dr. Harch’s research provided the first ever dem-
onstration of improvement of chronic brain injury in an animal
model in the history of science. In 2001, Dr. Harch completed a
study on SPECT brain imaging and toxic brain injury. He has
made three presentations to the U.S. House of Representatives,
Appropriations Sub-Committee on Labor, Health, Human Ser-
vices and Education and the Government Over-Sight Commit-
tee with regard to the application of hyperbaric oxygen therapy
in chronic neurological conditions. He has written or contrib-
uted to many articles and book chapters. In April 2004, Dr.
Harch was nominated for the NIH Directors Pioneer Award.
Dr. Harch it is a privilege to have you with us here today on
this most interesting topic.
Thank you. It’s a privilege to be here.
Dr. Harch, first of all, what is hyperbaric oxygen therapy?
Hyperbaric oxygen therapy is the use of greater than atmos-
pheric pressure oxygen by enclosing someone in a chamber and
using it as a drug to treat basic disease processes and hence the
diseases themselves.
So oxygen is considered a drug. What are the indications for
Well, there are a number of indications and the absolute
number somewhat depends on the country that you live in. In
the United States there is a list of typically reimbursed indica-
tions. And then there is a list that is reimbursed by Medicare
and Medicaid and there’s some overlap between those two or
there’s quite a bit of overlap. Outside the United States how-
ever, there is a much larger list—in Europe, in the Far East, and
in Russia. So asking about a list is somewhat dependent on
where you’re practicing. In the Unites States it’s fairly narrow
and outside the United States it is a much longer list, including
many neurological applications.
All right. So let’s differentiate between what is reimbursable
insurance wise and what conditions hyperbaric oxygen therapy
makes sense for. What would be the indications for use then if
we weren’t worried about who was paying what?
Well if we weren’t restricted, you would have likely some
additional indications, including the use in acute severe trau-
matic brain injury, the use in acute cardiac decompensation
usually in the setting of acute myocardial infarction, and a use
in cerebral palsy.
doi: 10.1588/medver.2005.02.00084
P. Harch, T. Small/Medical Veritas 2 (2005) 637–646
So, what’s holding up being able to use hyperbaric oxygen
therapy for situations where it would really benefit the patient?
That’s a great question. It’s a combination of what I like to
call the culture of medicine and medical politics. The typically
reimbursed indications have been compiled by a committee in
the Undersea and Hyperbaric Medical Society(UHMS). And
unfortunately, that list of indications, at least for probably six of
the thirteen indications, does not meet the standard for medical
proofing. In other words, there isn’t good clinical data to sup-
port the use of it. However, the list was compiled by tradition
and by the physician members of the Committee who had done
maybe some animal research and clinical treatment in that given
indication. And trying to get additional indications on that list
for reimbursement has a degree of arbitrariness to it. For exam-
ple, there is more evidence for the use of hyperbaric oxygen in
acute severe traumatic brain injury than for most of the indica-
tions on the reimbursed list. In cerebral palsy there is more data
now showing a benefit of hyperbaric oxygen than there are for a
number of the other indications on that list. So, the problem is
partly political. And I think it’s also rooted in doctor problems.
The United States Navy has dominated the field of hyperbaric
medicine for years and outsiders have had difficulty having
their ideas accepted. In particular, one of the individuals in the
United States, Dr. Richard Neubauer, who pioneered the use of
hyperbaric oxygen primarily for chronic neurological condi-
tions—how should I say this—has not had his scientific
thoughts properly evaluated. And he has been disparaged be-
cause he has had the nerve to treat outside of this accepted indi-
cations list. So to sum this all up, getting something on the typi-
cally reimbursed indications list is a matter of both science and
politics and that’s what has inhibited some of the applications to
neurological conditions.
Well, Dr. Harch, I think I jumped way ahead, but I’ve got to
tell you, that parents of children with autism are well ac-
quainted with the scenario that you have just described, that
Dr. Neubauer has faced. So we can commiserate, at least
speaking for myself.
Let me just interject one more quick thing. Unfortunately,
both the UHMS and another medical society have now issued
statements about punitive actions against their members who
treat outside their list. And this is contrary to the practice of
medicine, historically, and the Hippocratic Oath. It is also
what’s inhibiting the application to other indications. So what
we’re developing now is a speak-easy situation with hyperbaric
departments where I get phone calls from doctors around the
United States asking about how to treat a given patient in their
hospital hyperbaric unit, but the doctor is not willing to discuss
it or stand up and talk about it for fear of repercussions and re-
criminations from the medical societies. It’s a very big problem.
But, we’ll go on to the other things. I know you had a lot of
Okay. Let’s backtrack. Describe the pathogenesis of brain
injury, and the death or idling of neurons.
Any insult to the brain induces a primary immediate injury.
And the degree of damage is proportional to the degree of the
insult or the force of it such as in traumatic brain injury. You
can have a very mild traumatic brain injury or you can have a
very severe one. However, regardless of whether it is a trau-
matic brain injury or a cardiac arrest or an electrocution or a
toxin exposure— whatever—the immediate insult damages, or I
should say, kills some of the neurons and injures others. After
that immediate insult however, the body’s typical inflammatory
reaction is set in motion and part of that inflammatory reaction,
regardless of what the initial insult is, is an elaboration of
chemicals in the brain that damage neurons, dilate blood ves-
sels, make them leak, and cause leakage of fluid known as
edema or swelling. That swelling, once the liquid has leaked out
of the blood vessels, compresses tiny blood vessels and reduces
blood flow and hence oxygenation. So you have a secondary
insult that occurs and then the later part of the inflammatory
reaction is elaboration of white blood cells. In other words, they
come in, they are activated, they stick to the vessel walls, cause
further leakiness, discharge their enzymes and do further dam-
age. These secondary injury processes cause a stereotypic type
of pathology that leaves some cells dead but leaves others in a
state of low blood flow and oxygenation or a metabolically in-
jured state that can last for quite some period of time. The spe-
cialty of neurology has had the view for years and years and
years, if not hundreds of years, that there’s no such thing as a
stunned or injured neuron that can exist beyond, let’s say,
hours. In fact a lot of people originally thought it was six min-
utes. However, other tissues in the body have shown injury that
can last much longer and what is becoming apparent with the
application of hyperbaric oxygen to all these chronic neurologi-
cal conditions is that the thinking in neurology was wrong. In
fact, injured brain cells can last for a far greater time than what
was originally thought.
Is that the idling of neurons?
Correct. Those injured neurons are considered the idling
neurons and that was the Letter to the Editor of Lancet in 1990
that Dr. Neubauer published, where he described a 14 year post-
stroke, 60 year old woman, who was wheelchair bound,
couldn’t speak, couldn’t feed herself, drooled, etc. He did
SPECT brain blood flow imaging and was able to show before
and after a single hyperbaric treatment an improvement in
blood flow to what was thought to be a dead area of the brain.
Over the course of about 16 months or so giving hyperbaric
oxygen at a lower pressure than typically used and supplement-
ing it with face mask oxygen at a nursing home, they were able
to improve the function in this lady. The idea was that they may
have activated these idling neurons that had existed in this low
blood flow state in the stroked area.
Wow, that is really wonderful and that would be a person
who people would typically tend to give up on, too.
doi: 10.1588/medver.2005.02.00084
P. Harch, T. Small/Medical Veritas 2 (2005) 637–646 639
So let me just go over this and see if I have it right and cor-
rect me if I’m wrong. You have a primary or immediate injury
to the brain, such as from cardiac arrest or electrocution or
toxic injury. So you have an insult, then you have inflammation,
then you have chemical reactions in the brain, this dilates blood
vessels, this causes edema or swelling which compresses blood
vessels, that reduces oxygenation and then you have an elabo-
ration of white blood cells—that causes further damage such as
to the cell wall and correct me if I’m wrong and then this re-
sults in a chronically, metabolically injured state.
Correct. But I’m going to shorten the time frame there. The
white blood cell elaboration, chemical elaboration, and secon-
dary injury is all occurring within minutes to hours of the initial
insult and develops simultaneously. The white blood cell injury,
chemical injury, and leakage of fluid continues over the next 36
to 48 hours. This stereotypic reaction results in the stereotypic,
common pathological injury. That is what hyperbaric oxygen
therapy is treating in delayed fashion when we come in a year
or two later, as well as if you treat acutely.
Are there many examples or studies of the effectiveness of
hyperbaric oxygen therapy in a variety of acute injuries, includ-
ing acute brain injury?
Yes, but most of them are in animal models (if you limit
acute to the first 3-6 hours after injury). There are an increasing
number in humans. But for instance, the number of studies now
in animal models of acute brain injuries such as what is called
global ischemia, meaning you have stopped all the blood flow
to the brain or severely reduced it, as in cardiac arrest—the
numbers of these studies is multiplying and the results are uni-
form. What they’re showing is that in acute carbon monoxide
poisoning and acute global ischemia--even in some of the other
acute injuries—a single hyperbaric treatment within the first
few hours of injury can markedly reduce the injury and subse-
quent damage. By markedly I mean upto let’s say 90%, almost
a 100%, in some cases. The human examples of this, though,
have not been as well documented or researched. There have
been some in infants dating to 1963 in England and in Brazil in
I believe the early ‘90s. And there have been some reports of
coma cases in China and a group of near-hanging patients in
northern France, 170 near-hanging patients. So the human ex-
amples are not as common yet, but what it appears is that hy-
perbaric oxygen in the setting of acute brain injury is acting like
a generic drug.
Okay, so what is the common problem of all these injuries
that hyperbaric oxygen therapy seems to address?
That’s a great question. Many of the targets are not identi-
fied. But one of the targets is the white blood cells and it ap-
pears that the white blood cells are inhibited by the hyperbaric
oxygen, such that as they come through the blood vessels in the
damaged area, they don’t stick to the walls of the blood vessels.
As a result, they don’t initiate much of the secondary injury.
There are other effects that are likely occurring on the cells
and in particular the DNA. During a low blood flow, low oxy-
gen insult there is a type of injury to the DNA and it appears
that hyperbaric oxygen may be reducing or preventing that in-
jury if it’s delivered early enough.
Okay. Is the impact of a lack of blood flow and the impact of
a lack of oxygen equal?
No. It appears that low blood flow is a more severe injury. In
other words, low oxygen by itself, as a purely individual form
of brain insult is fairly well tolerated for a certain period of
time. But eventually, with low enough oxygen you affect the
heart and you will decrease the heart’s pumping ability and so
you eventually end up with low blood flow. So low blood flow
has the insult of not only low oxygen, but you deprive the tissue
of all of the other nutrients, and especially for the brain that’s
glucose or sugar. It appears that the insult of low oxygen, low
glucose, and low nutrients is a more damaging form of injury.
How does this relate to what happens to children with au-
tism? Is the brain injury in autism considered chronic or acute
and does the hyperbaric oxygen therapy fit both?
Well, that is more difficult to answer because no one knows
with certainty the exact cause of autism. It appears that autism
has many different causes and if you could pinpoint the cause at
the time the cause was elaborated, then hyperbaric oxygen ren-
dered immediately may have some impact on the insult that’s
going to generate the autism injury or diagnosis. But most of
the children that we’re seeing we are unable to couple the hy-
perbaric oxygen with the insult, unless it occurs at birth. So for
instance a number of the autistic children that I have treated
have had very obvious birth insult with low blood flow, low
oxygen insults, very poor APGARs, resuscitation, etc. Hyper-
baric oxygen therapy potentially delivered at that time may
have a big benefit. But most of the children we’re seeing are
two years and beyond and of course by that time it is a chronic
brain injury. What you’re treating at that point is a little bit
more speculative because the exact pathology has not been
Okay. Are there birthing events that can cause or act as a
set-up for autism?
It appears so. Part of the problem is the inexactness or I
should say the non-reproducability of the diagnosis. In other
words, a lot of different pediatric neurologists will give a diag-
nosis of autism or autism-spectrum and some of the time it may
not be completely along the guidelines of certain rating scales.
But the children nevertheless are called autistic based on a pre-
dominance of certain behaviors. Many of the children I’ve seen
or, I should say, a good number of the children have deficits in
addition to the typical autistic ones that may be motor, sensory
or appear to be sensory, coordination problems and so on which
suggests that there is a global brain injury such as would occur
with low blood flow at birth.
Okay. So are you saying that the mechanics of certain birth-
ing injuries are consistent with symptoms displayed by some
children who have autism such as it looks like it happened to a
doi: 10.1588/medver.2005.02.00084
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trauma site in the brain or they’re displaying emotions or be-
haviors that are consistent with birthing injuries?
What I’m saying is that birthing injuries can result in a pat-
tern of injury to the brain that gives you the constellation of
signs and symptoms that result in a diagnosis of autism. Essen-
tially, in some autistic children you can’t implicate necessarily a
vaccine problem or let’s say another toxin because from day
one of birth these children are abnormal after the birth insult.
And yet later they are given a diagnosis of autism. So it appears
that that insult is causing an injury to the brain that is mechanis-
tically different from a toxic injury, but may injure the same
areas of the brain and, hence, give you the same constellation of
signs and symptoms that result in the diagnosis.
Okay, so let’s talk about these children for a moment. What
can you do about this, and how effective might hyperbaric be if
it’s started days or years after the injury?
Well, it can be very effective and it has a range of effective-
ness. For some children it’s a small effect. For others it’s a
fairly dramatic effect. I can’t say that we have cured any of
these children. What we’re doing is correcting, or I should say,
repairing a chronic wound in their brain with hyperbaric oxygen
much like we do for chronic extremity wounds in diabetics or
chronic radiation wounds or any of the other chronic indications
that hyperbaric oxygen has typically been applied to.
All right. Now let’s talk about the children who have docu-
mented toxicity issues such as mercury poisoning. I think we’ve
already mentioned the fact that hyperbaric oxygen therapy can
help with toxic brain injury. How does it do that?
It’s unclear in the case of mercury.
Okay, well, all right. What kinds of results have been seen
with those children?
The same range of results, a variable range. Some of them,
again presuming that those children have a toxic injury and
that’s very hard to prove at least in the individual patient, but
assuming that they do, they have a range of responses also. See,
I think that the key that needs to be understood here is that the
discovery I made in the late 1980s and 1990s was in our divers
with brain decompression sickness and in the boxers in whom
my partners had started a program attempting to treat. These
were boxers who had brain damage from boxing and of course
all of these cases of the boxers were chronic. The divers were
acute, subacute and then we had some chronic cases. What ap-
peared to me is that when we were treating the time-honored,
traditional HBO application, i.e., decompression sickness, that
we were not treating bubbles in these patients, especially the
farther we got out from the injury. It rang a bell and alerted me
to the fact that possibly we were just treating chronic brain in-
jury that could be treated in other patients with other diagnoses.
So I started extending a lower dose protocol of HBO to patients
with old stroke, old trauma, etc. and in the process got referred
in 1992 what was to become the first cerebral palsy child
treated in North America with hyperbaric oxygen. And then
what followed were more children, including autistic children
What I started doing was applying in a very stereotypic manner
SPECT brain imaging to document the changes seen with low
pressure hyperbaric oxygen and running a fairly rigid protocol.
What I found was these autistic children were responding just
like all of the other diagnoses we were treating. Basicly, the 23
or so children with autism, autism spectrum, Asperger’s Syn-
drome, and children with neurological abnormalities and strong
autistic traits or behaviors, improved just like the adults and
other pediatric diagnoses. Some of them I’m sure are due to
toxins, some clearly were due to birth injuries. and some due to
causes that we don’t know. But the great majority were re-
sponding fairly similarly. And now what’s happened is two
other sites in the United States have duplicated this. One in Los
Angeles (the physician there is now retired), treated nine of
these children in the late 1990’s and early 2,000’s. In New York
there are approximately 20 children that have also been treated.
Both of these doctors were claiming an improvement very simi-
lar to what I was seeing.
Okay. So those are studies, right?
They are not true studies, really. They are children who were
referred and were clinically treated. Many of mine were actu-
ally treated on a protocol that was approved by the Human Ex-
perimentation Committee (Institutional Review Board-IRB) of
our local hospital. So mine was a formal study, initially. But
now we don’t have that protocol and I’m back to treating the
children clinically. What I’m saying is that all of the results are
very similar .
Tell us about SPECT imaging and how the computer devel-
ops the pictures.
All right. SPECT is an acronym for Single Photon Emission
Computed Tomography. It is CT scanning technology applied
to nuclear medicine. SPECT measures brain blood flow and
indirectly gives you information on metabolism. What happens
is, instead of shooting the x-rays through the tissue like you do
with a CT scan, you inject a very small amount of a radioactive
material, 5% of which is taken up into the brain. And it stays in
the brain for hours. It is distributed and taken up in brain pro-
portional to blood flow. So you’re able to measure blood flow.
As it gives off these radioactive counts you lay underneath
what’s a sophisticated Geiger counter, if you will, and the best
of these machines have three Geiger counter-like cameras
around the head that rotate around over the course of about 16
minutes. They collect all of the counts and then the computer
reconstructs it and a technologist processes it to give you a pic-
ture of brain blood flow. What you’re able to see is each area of
the brain’s blood flow or function in relation to the other areas
in the brain. So the way the computer does this is it takes the
brightest spot in the brain where the highest amount of radioac-
tive counts are, which means the highest amount of blood flow,
and gives it a relative value of a 100. All the rest of the areas of
the brain are then scaled to that and you get a picture showing
on this type of scale how much blood flow there is in all of
these areas in a relative fashion. What it allows you to do is see
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how the brain is working as opposed to looking at just a road
map of the brain like CT or MRI gives you.
Wow. So you do a SPECT scan and then you perform hyper-
baric oxygen therapy and repeat scan.
Yes. And the way this began was in it’s application to the
divers. What we would do is image them as soon after they had
their initial treatment to see what their brain looked like. Then
we either treated them another time and repeated the imaging
right afterwards to see if we were further improving the brain
and it matched them clinically, or we would repeat the imaging
once the diver said, okay I’m feeling pretty good, I’m not get-
ting any better with successive treatments. At that point we
we’d see how the imaging looked. What we found was it corre-
lated very highly and strongly with the diver’s clinical reports
of his improvement and our demonstration of that on our physi-
cal exam.
So we then took that sequence of SPECT, one HBOT, repeat
SPECT, and thought well maybe we could use this as a test in
the divers, like Dr. Neubauer had done in the Lancet with the
stroke patient. We decided to look at it in a very rigid fashion
for anyone with a chronic brain injury and we chose chronic
brain injury because we didn’t want anybody to say that the
cases had improved on they’re own because they were only
three weeks out from an injury. So we made people wait a
minimum of one year and then I would examine them, video
examine them, take a detailed history from them, and do a
SPECT brain scan. The following day or two days later they
would go in the chamber a single time and then within hours we
would repeat the brain scan and look to see if there were im-
provements. Whether or not we did, we went ahead and offered
the patient treatment and at the end of treatment we sat down
and I repeated all the exams, history, videos, etc. and we re-
peated the SPECT scans. What we found was that second
SPECT scan after a single treatment was predicting and show-
ing injured brain that would cause clinical improvement with
repetitive treatment. Furthermore, the clinical improvements
were documented by improvements on SPECT brain imaging
after a course of treatment. And so the autistic children, the
cerebral palsy children, the adults with trauma, stroke, and toxic
brain injury were all put in there, or I should say, were all part
of this study, which ran for nearly six years and involved a cou-
ple hundred patients.
Wow. That is really exciting.
Now what we found though is that we didn’t need the imag-
ing. It was a leverage tool. Statistically, if you looked at all the
patients the vast majority of them showed some improvement
with repetitive low pressure hyperbaric oxygen treatment.
Eventually, the imaging was only necessary if people wanted to
try to see what their brain looked like, the dysfunction, or see
the injury in their child and/or use it as evidence in application
for insurance reimbursement of hyperbaric oxygen. Or they
needed it for documentation in litigation when there was some
question about whether there was a brain injury or not. In these
instances if you have the imaging showing an abnormality and
then after treatment an improvement and simultaneously im-
proved patient, you knew that there was an injury there in fact
to begin with.
Okay but you’re feeling that the scan wasn’t absolutely
mandatory is that because of your previous work showing that
when someone said they had improved clinically it was evi-
denced by their scans.
But I’m saying the imaging, now because of the large ex-
perience between 1993 and 2000, is optional. We’re no longer
on a rigid protocol by a hospital experimental committee and an
experimental protocol mandating the imaging. We now know
that we have a very good chance of improving a patient clini-
cally without having to prove it on the imaging. But if people
want the imaging I’m happy to do it.
Okay. So I think I heard you say that you have a way, and
I’m not telling people that this is 100% reliable ( that’s not up
to me,) but you can prognosticate or test the amount of recov-
erable tissue in the brain of an autistic patient by scanning?
By scanning.
By that sequence. Interestingly, something very important
happened in here. When I was showing the imaging around the
country and even internationally at meetings and lectures I
ended up in contact with a very, highly respected nuclear radi-
ologist who offered to take the imaging on a number of the
children I had treated and analyze it by a very sophisticated
method. I sent him all of the imaging on the first 18 children
that I had treated beginning in 1992 through I guess it was 1998
or so. What he did was take all of the first scans, baseline scans,
average them, take all of the scans after a single treatment and
average them, and then all of the scans after a course of treat-
ment and average them. And then we subtracted. We took the
second scan which is after that first treatment that was trying to
look at injured brain’s responsiveness to hyperbaric oxygen and
we subtracted it from the final scan after a course of treatment.
What we found was the areas of the second scan that had
showed improvement were some very important areas of the
brain that had to do with memory or cognition, vision, emotion,
aggressivity, etc. And those areas that showed up on that second
scan were the same areas that showed improvement after a
course of treatment so that when you subtracted the second one
from the final scan there were almost no changes. The subset of
patients where it was really proven was the cerebral palsy chil-
dren. So, when we looked at a homogeneous diagnosis, cerebral
palsy, we found this very tight correlation which proved that
what Dr. Neubauer had shown in that idling neuron letter was
true. In other words, like Dr. Neubauer, we proved that you
doi: 10.1588/medver.2005.02.00084
P. Harch, T. Small/Medical Veritas 2 (2005) 637–646
could identify damaged areas in the brain with SPECT brain
imaging before and after a single treatment that would respond
to repetitive hyperbaric oxygen.
Okay. So you’re not saying there wasn’t any change in the
amount of restoration between the second scan and the final
scan. You’re saying that the areas that were improved in the
final scan were those areas that were improved in the second
scan, is that correct?
Yes. it’s not quantitative, really. I mean you can’t correlate
the exact amount of change on the scan with exact amount of
change in functions. All we saw was that by this statistical and
mathematical method that the areas that showed significant im-
provements in blood flow after a single hyperbaric treatment
were the same areas showing significant improvement in blood
flow after a full course of hyperbaric oxygen.
Simultaneously the children were improving.
Were improving in clinically from the second to the final
Okay. Good enough. And some of the areas that you said
had improved in those patients were memory, cognition, vision,
emotion and aggressivity.
Yes, well in more general sense, areas that control emotion
and behavior, irritability, this type of thing.
Tell me the difference between low and high dose and
whether you use the same dose of hyperbaric oxygen therapy
for chronic illness as you do for acute injury.
The difference is somewhat arbitrary. You’ll have a hard
time finding people who will define it. But in the K.K. Jain
Textbook of Hyperbaric Medicine, in one of the chapters I
wrote, I defined low pressure HBOT and we have talked about
it in terms of being less than two atmospheres of absolute pres-
sure. .So generally two atmospheres of pressure and greater is
considered higher pressure hyperbaric oxygen or traditional
hyperbaric oxygen. Less than two atmospheres is considered
low pressure. And then what’s crept in also is this term “mild
hyperbaric” which they’ve used to describe treatment in the
portable chambers where hyperbaric air or oxygen supple-
mented hyperbaric air is pressurized to 1.3 atmospheres. But
generally, when we talk about low pressure hyperbaric oxygen
it is less that two atmospheres and it’s generally in the range of
an atmosphere and a half.
Okay. So what do you use?
I’m in that low pressure range for the chronic conditions. For
acute conditions it is different; the responsiveness of tissue is
mainly at higher pressures, but you can’t usually treat as much
at these higher pressures acutely. Meaning you can’t go on for
many, many treatments like we can at lower pressure.
So for acute injuries do you switch from higher to lower or
do you just stop?
Well you have to adjust the dose based on the patient’s re-
sponse. Often though if you get to patients quick enough, for
instance with decompression sickness, you only need the first
treatment. When they did a review of the world Navy’s experi-
ence with HBOT in decompression sickness, they found that,
the first treatment was curative in 90% of cases if they deliv-
ered it within one to two hours. And that’s a generally high
pressure treatment. So, if you get someone quick enough a high
pressure treatment can be curative on the first treatment and you
don’t need a lot more additional treatments.
Okay. And speaking of you mentioned the word “mild” and
you talked about portable chambers. Now are portable cham-
bers as efficacious as going to a center that does not have port-
able chambers or is there a safety concern?
Well, the first part of that nobody knows. The safety concern
is always there and depends on the knowledge and experience
of whomever is delivering the treatment and using the cham-
bers. We know from the Collet Study in 2001 of the Montreal
cerebral palsy children, where they made a mistake in the de-
sign of the experiment and they gave the control group of chil-
dren 1.3 atmospheres of air, that this had a beneficial effect. In
fact it was equivalent to and in some cognitive measures a little
bit better than the hyperbaric oxygen group that got 1.75 at-
mospheres. The 1.75 I felt was too much so there may have
been both an overdose effect with the 1.75 and who knows,
maybe the proper dose or even an under dose at 1.3 atmos-
pheres of air. But what happened is it appears that 1.3 atmos-
pheres of compressed air or 30% increase in oxygen was
enough to cause a very measurable benefit in those children. So
that is the one study we know that has some evidence for “mild
hyperbaric air.” Beyond that there’s claimed widespread use,
especially in the Far East but there’s very little data on this. Dr.
Heuser out in California had some SPECT imaging and other
data that he showed in children and sent as a letter to the Lancet
that followed the Collette article, but beyond these instances
there’s very little published information on the “mild hyper-
baric” to make a really solid statement about effectiveness in
many conditions.
And I guess the other part of my question was: is it safer to
go for hyperbaric oxygen therapy in a center rather than using
a portable unit?
Well, we always think it’s safer to go to a center where
you’ve got medically knowledgeable people. What people for-
get is that hyperbaric oxygen therapy is a medical treatment. It
always has been and it always will be. It’s just that in this neu-
rological field now, it’s pushed underground partly by these
punitive statements or threatening statements that have been
made by medical societies and some of their doctors so that we
have people forced to be their own doctors, buy portable cham-
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bers and so on. But you can have problems with any medical
treatment and especially with pure oxygen. So we recommend
that this be done at a facility where there are medically trained
people. In fact if you go back to I believe 2001 there was an
article published in the online edition of Pediatrics and it was
the doctors from the hospital-based facility in Vancouver re-
porting on two complications that occurred at a free-standing
facility delivering low-pressure hyperbaric oxygen in Vancou-
ver. We wrote a rebuttal to that article because it just was scien-
tifically inaccurate. The point is though, they had some compli-
cations at this facility and the level of medical expertise and
care there may not have been adequate. In other words, they had
to send the patients to the hospital and these children were
treated for pretty severe conditions, some of which may have
been preventable. So we recommend that it be done in a facility
where there are medically knowledgeable people because acci-
dents and side effects occur, untoward effects of hyperbaric
oxygen, complications etc., like with any medical treatments.
Okay. So it’s not that this is a particularly or even as risky
procedure but it just needs to be done right, is that correct?
Absolutely correct. This is one of the lowest risk procedures
in all of medicine.
Okay. In an autistic child with mercury-induced brain dam-
age, will hyperbaric oxygen therapy produce any lasting
growth and restoration of function without chelation also being
I can’t answer that exactly. That’s not known. Of the 23 chil-
dren that I have treated a good number of them have had chela-
tion therapy either before, during or after hyperbaric oxygen.
And because the numbers are small it’s hard to dissect out
enough patients in each little group to make a statement such as
that. It seems to me, and it makes good sense, that if you have a
toxin that’s embedded in tissues that is inhibiting tissue growth
that you would want to remove it to get lasting changes. How-
ever, hyperbaric oxygen therapy may be able to induce some of
the changes in the absence of removing it or may even stimulate
removal of it. We don’t know for sure.
How much may the efficiency and effectiveness of either
therapy (and I understand that this may be educated specula-
tion)—chelation or hyperbaric oxygen therapy—be increased?
By using both, may it shorten the overall time of therapy?
Nobody knows that answer. That was the projected thought
and that was the protocol that we were wanting to design and
set up at the University of Oklahoma. And it was the thought
that stimulated me to make some very, very positive statements
about the potential for this at the Congressional Hearing in
2004. In other words, we had taken Dr. Buttar’s reports of im-
provement in the autistic children he had chelated and coupled
them with the reports of improvement in these children by my-
self and other hyperbaric oxygen practitioners to make the
statement that combining the therapies made the most sense and
potentially could have the greatest benefits. And what we were
hoping to do and what I was hoping to do by making what
maybe even a little hyperbolic statement was to stimulate inter-
est and funding to get this whole process rolling at the Univer-
sity of Oklahoma. We wanted to put it in an online format and
be able to collect massive amounts of data from patients all
over the country who are getting chelation therapy, hyperbaric
oxygen, or a combination of both and allow them to sign up on
a formal protocol where we would put them in one arm or an-
other. It make sense. I think it would be the best way to do it, in
other words, chelation plus hyperbaric in some combination,
but we don’t have solid proof that it would work. It’s more a
theoretical possibility.
So is the International Hyperbaric Medical Association still
collaborating with the American Board of Clinical Metal Toxi-
cology under the supervision of Oklahoma University Health
Science Center to study this? What is the status of this project?
Well, yes, but it’s gotten mired in some administrative de-
lays in trying to set it up. Part of it is a funding issue. It takes a
number of thousands of dollars to actually set up the Institu-
tional Review Board application, get all of the online program-
ming done and roll this out as a formal program. So it is await-
ing funding and some more administrative maneuvering.
So let’s talk about the exact mechanisms—I’m backtracking
a little bit again—the exact mechanisms which hyperbaric oxy-
gen therapy actually helps, restores and cleans up the areas of
the brain. Thinking back on what you said earlier, does it do
things like restore the brain tissue metabolism of oxygen and
nutrients or you know you said it woke up the idling neurons?
Yes, well if we go back to my definition, it is the use of high
pressure oxygen as a drug to treat basic disease processes and
hence the disease itself. In acute situations as I talked about
we’re affecting that inflammatory reaction. We’re also able to
oxygenate these low oxygen areas and that seems to have some
kind of metabolic benefit, acutely and some type of effect on
reversing the abnormal or injury physiology. In a chronic situa-
tion with a chronic wound what has become apparent is that
hyperbaric oxygen is acting as a DNA signaling drug. And
there are now multiple molecular biochemical experiments
showing this in animals. Even in the acute situation actually
hyperbaric oxygen is acting on the DNA to stimulate the DNA
to begin elaboration—the process actually is called “transcrip-
tion,” of gene sequences that code for repair hormones. And
this has now been measured. Various hormone levels have been
elevated with hyperbaric oxygen and they’re measuring those
transcription products— called messenger RNA—and also
showing up-regulation of certain types of growth hormone re-
ceptors on the cells. So in the chronic situation what we’re do-
ing is we are repairing the wound. And to my knowledge, ex-
cept for Regranex the isolated platelet-derived growth factor
that’s available for application to diabetic foot wounds, HBO is
the only prescription repair drug that we know of. In other
words, we are stimulating the repair process through hormonal
elaboration and the eventual result is growth and replication of
healing tissue cells and of new blood vessels.
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Yes. And that’s what we were able to show indirectly in an
animal model. In the early ‘90s as I started showing this at vari-
ous types of meetings in the chronic patients that we were treat-
ing, the complaint was that I didn’t have an animal model. And
so we went to a well-known acute animal model and we just let
the injury mature until it was a chronic one. Then I went and
applied the human protocol to the animals (it was a trauma
model) and what we found was an increase in blood vessel den-
sity in the damaged area of the brain that was causing the be-
havioral or the cognitive defects in memory and a simultaneous
improvement in that memory function in the hyperbaric treated
rats. Importantly, the two of those, the blood vessel density and
the improvement in cognition, were highly correlated. This
manuscript is done and it’s been a long time in the making and
we’re very near to submitting it.
Wow. That is just dynamite.
Well it is and that’s what has allowed me to make some of
the bold statements that I have made in the textbook chapters
and in public appearances, namely, that we have a treatment for
chronic brain injury. I mean normally the FDA drug approval
process is that you do test tube work, small animals, large ani-
mals, then the foreign human trials and finally in the United
States they do the clinical trials. What we had done is found this
worked, just serendipitously if you will, in the treatment of the
age old indication for hyperbaric oxygen—divers’ disease or
decompression sickness—and then extended the findings to a
variety of different human clinical situations and then go back-
ward and apply the human protocol to animals and prove that it
worked. What it suggests is what I talked about earlier in the
application of hyperbaric oxygen to the acute animal situation,
that HBO is acting as a somewhat generic drug on generic pa-
thology in animals and humans.
Can you please repeat what you said about transcription
gene sequences, messenger RNA, regulation of growth hor-
mone, etc.?
Okay. Hyperbaric oxygen in both acute, but especially in
chronic situations, is acting as a DNA signaling drug to turn on
the transcription process of DNA and specifically the genes that
are coding for growth and repair hormones. The transcription
process, which means taking the DNA to messenger RNA, pro-
ceeds to translation where the messenger RNA gets translated
into proteins. It’s those proteins that are growth and repair hor-
mones. Simultaneously, there is a stimulation and up-regulation
of the surface receptors on the cells that accept some of these
growth hormones. So you’re making more hormones and
you’re also having the cell be able to respond to these hormones
better. The net result is growth of tissue—in particular blood
Wow. Now the results you saw in your animal model with
improved memory, etc. are, is that the same type of result that
an autistic child might experience?
Yes. Or cerebral palsy. Now granted the mechanisms may be
different. As we talked about we could be treating all sorts of
different things and many different causes in an autistic child.
But if we just look at it in the setting and with the perspective
that I was treating 40 to 50 different neurological diagnoses
over these years and we were seeing the patients—some diag-
noses more than others—respond in a similar fashion it implies
that we may be inducing the same effect in all of these different
diagnoses. In other words, the patients were showing improve-
ment in their injury and when we took that same protocol and
applied it to an animal with an injury, we got the same re-
sponse. So what it suggested was that at least some of the
mechanisms that were active in the humans or I should say,
some of the mechanisms of hyperbaric oxygen that were in the
humans we were treating were the same mechanisms in the ani-
mal model. And vice versa.
What kinds of functional areas do autistic children show
improvement in? What kind of reports do you hear from par-
Well, we hear reports of improvements in their autistic fea-
tures, in other words the socialization, the language, and the
repetitive behaviors. We see the children making eye contact,
we’ll see them advance some in speech where they’ll either
start to say some words or make sentences. And this is not all of
them, I’m just saying there’s a range of them. The general one
is you have improvement in some or all of these functions. And
the third thing is that we’ll see improvement in their repetitive
behaviors, their “stemming”.
And other countries are using hyperbaric oxygen therapy
with success it sounds like?
Yes, but I don’t know how much or how many of them have
applied it to autistic children. What we saw at a number of the
International Symposia were doctors applying this to children
with cerebral palsy after the reports here in the United States
and Canada. And what those doctors were reporting was a gen-
eral positive experience in those cerebral palsy children. Now
how many are treating autism and other pediatric neurological
diagnoses is not clear because the information hasn’t been pub-
lished. And what is in the symposia are often some more acute
types of studies.
Dr. Harch what are the different kinds of chambers and fa-
cilities. I know we talked about having a portable unit in your
driveway or going to a center. How many children are allowed
in a chamber? Are there any safety risks to having too many
people in a chamber?
Well, yes. There are safety risks. There are a number of dif-
ferent types of chambers. There are the single person ones, both
the portable and the more hard shell, actually they’re divided
into the soft chambers with the canvas-like exteriors and then
most of those are considered portable and collapsable. Then
there are the hard shell chambers, the typical single person
ones. And actually these single person ones can have more than
one person in them; you don’t like to do that but it’s been a
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habit. In other words a lot of times the mother or parent may
want to go in the chamber with the child so you will have two
of them in there at once. Those chambers are also portable even
though they’re hard shell. Typically I mean they are portable—
you can put them on a truck, they’re on rollers and you can roll
them around. The bigger ones of those however are not so port-
able. One of them in particular weighs 5,000 pounds. The next
level up are the “multi-place chambers that can accommodate
multiple persons because of the size of them and they can be
30, 40, 50 feet long. In the 1920s Cunningham’s Chamber I
think was nearly 100 feet long. They can make, you can make
them as big as you want to. But those multi-place chambers are
usually so heavy they are fixed, they’re not really portable ex-
cept with a crane and a big truck and they can accommodate a
fairly large number of patients. Those, because of their size, are
not economical to pressurize with oxygen so they’re pressurized
with air and then you breath oxygen from a mask or a little
hood tent that’s placed over the head. Whether or not you are in
a portable chamber or a hard shell monoplace chamber or the
larger multi-place one, as long as you’re at the given pressure,
at the same pressure and getting oxygen at that pressure or the
same mix of oxygen and air, you’re getting the same hyperbaric
You don’t have to worry about too many people being in a
chamber and breathing out gases?
No, well that’s another issue. In the air chambers that have
hood tents or face masks there is an exhaust line so that when
you breathe out you’re not breathing into the chamber. You
don’t want elevated levels of oxygen in an air chamber; that’s
in fact how many of the fires have occurred. Normally it is ex-
hausted outside the chamber. But the chamber fires that have
occurred have been in air chambers where they have oxygen
leaks and simultaneously someone brought in some type of fire
hazard, hand-warmers, or something that had a spark to them
and it started to burn. Of course once you’re above about 23
and a half percent oxygen, fire rate is accelerated. The other risk
regarding having too many people in a chamber you talked
about is if you should have problems. I mean if you had 20
people in a chamber and no inside attendant or one inside atten-
dant and had some kind of problem you may be under-manned
to take care of it.
Right, but generally I hear that the risks are minimal., I’ve
heard some children have problems with their ears. Are any
problems to any children’s eyes or anything?
The main problem is ear clearing, in other words adjusting
the pressure like you do when you go up on an airline flight.
And there are ways to minimize that, but that’s the most com-
mon one. In children with seizure disorders you have to be care-
ful. You have to adjust the dose with that because they are more
sensitive to the oxygen. Beyond that the risks are really mini-
mal and in the hundreds of cases we’ve treated at least half of
which are children, we have treated extremely ill children, and
the complication and problem rate is very, very low. I mean you
need to select your patients and be careful and make accommo-
dations when they have airway problems in particular.
Well I guess that’s another good reason to have knowledge-
able medical providers on hand and doing an evaluation and
assessment as with any significant therapy for your child.
Yes. I mean we’ve had aspirations in children who were
very ill. And that was one of the cases up in Vancouver also. So
again it’s a medical treatment. You like to have people who are
medically knowledgeable and adept, who are delivering it. And
since we are dosing a drug, you want to carefully be following
the patients. You could have too much, other times you’re not
doing enough.
Yes, I would want to be really careful when I was doing
things that would change my child’s brain for the better, but
still I’d want to be careful.
Let’s come full circle around to the beginning of the inter-
view and tell us why is this protocol more fiscally logical for
government than not using this protocol—in a utopian world?
In a utopian world if you could treat sooner than later, you
have a better chance of reversing, correcting or ameliorating a
problem. The second reason is, if we can improve these chil-
dren and if by all indications we are, the long-term economic
impact will be far less. In other words, children that require
one-on-one attention for their entire adult life are a massive
problem in the United States. And not only from just the man-
power necessary to accommodate them, but it’s a big financial
problem from lost productivity in society. And we haven’t even
talked about the very personal damage to that individual.
If you’re really looking at just cost-effectiveness, the cost of
caring for this entire generation of damaged children is phe-
nomenal. If we can reverse this early on or ameliorate it, it will
pay a long term dividend.
Yes and even more important than the money is the health of
the child so in a utopian world this wouldn’t even have hap-
pened to our children.
So, why isn’t there more widespread use of hyperbaric oxy-
gen therapy by the medical profession?
That’s the million dollar question.
Well it really sounds like this is an exciting and viable road
to look into for the field of neurology.
It is. I’ll tell you where the problem lies. It gets back to the
culture of medicine issue and the problems with medical socie-
ties and doctors and so on. A lot of this is also rooted in an in-
adequate definition of hyperbaric oxygen. Traditionally hyper-
baric oxygen was defined as a therapy used for intractable, in-
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curable and otherwise hopeless medical conditions. Of course
that definition which went through to as far as almost 2003.
Today, it’s still in much of that original form except for the
addition of the verb “is”. The inadequacy of this definition has
been responsible for a misunderstanding of what hyperbaric
oxygen is. The definition I gave you at the start, in other words,
its existence as a drug is very different from what the traditional
concept has been. So it has been an unknown therapy that’s
been used for hopeless medical conditions. Well, that list of
accepted indications or typically reimbursed indications put
together by the medical society is a group of disjointed diagno-
ses. Decompression sickness, chronic bone infection, compro-
mised flaps and grafts, carbon monoxide poisoning, brain ab-
scess. When practitioners look at this, they look at it and say
this makes no sense. Why this list of seemingly unconnected
diagnoses? When you look at hyperbaric oxygen in terms of a
drug that acts on basic disease processes common to many dif-
ferent diagnoses you now can go back and look at each diagno-
sis and say, oh wow it is effective on the hypoxia and the reper-
fusion injury in this one and this one and this one, it’s effective
on growing new blood vessels in this one and this one. And
pretty soon the list starts to make sense. Then the obvious ques-
tion comes about, why not many other diagnoses with similar
disease processes?
Well what happened in the 1970s was Dr. Richard Neubauer
said, guess what guys? I applied a lower dose of this than what
was traditionally used in chronic wounding and treatment of
divers by the U.S. Navy to a few multiple sclerosis (MS) pa-
tients and they got better. Next thing you know it got politi-
cized. The MS Society was apparently very upset over claims
that this worked on MS.
They funded a study done in New York City which was pub-
lished in the New England Journal of Medicine that proved that
hyperbaric oxygen was effective in MS. However, due to vari-
ous political problems coupled with the fact that the hyperbaric
physicians could not explain and defend how this worked—
what the mechanisms of action maybe--and they couldn’t give
an adequate definition that might explain it, i.e., acting like a
drug—it was criticized. In the face of unchallenged and unan-
swered criticism, it became discredited. And then reports sur-
faced that doctors were applying it to a variety of other condi-
tions much like Dr. Cunningham did in the 1920’s when he
found it was effective for his initial indication. He thought, the
pathology in this condition is such, and here is the same pathol-
ogy or pathophysiology in another condition, therefore, it
should work in this other condition. When he applied this think-
ing and the HBOT, he got in trouble with the AMA because he
didn’t report his results. Similarly, in the 1970s and ‘80s doc-
tors expansively began to apply HBOT to a variety of other
conditions. When criticisms were leveled at them they couldn’t
explain why it was effective. So in this wave of criticism, hy-
perbaric oxygen was suppressed and died back. A good exam-
ple of this was in 1978 in medical school, when I was at Johns
Hopkins and asked one of our fellows or one of our residents
when I had heard of hyperbaric oxygen, “Well what is hyper-
baric oxygen?” He said, “Oh, it’s a fraudulent, snake oil treat-
ment that is worthless—don’t even give it another thought.”
And I didn’t give it another thought until diving medicine—my
introduction to this in 1985 and ’86. So the point is, there is this
massive, misperception and misunderstanding of hyperbaric
oxygen from the ‘70s and ‘80s which has poisoned the whole
generation of doctors. That is now what we we’re fighting
against as people are realizing that this is a drug with very pro-
found and far-reaching effects on human pathophysiology,
acute and chronic. As the experiments are showing this, it’s a
matter of disseminating the information, applying it appropri-
ately, and explaining the best we can how this is working.. And
that’s where we are.
Very, very well put. And parents of children who have au-
tism are well acquainted with logic not being well accepted by
mainstream entities. So we can again commiserate with that
situation. Where should a parent look for more general infor-
mation about hyperbaric oxygen therapy and to contact an ex-
perienced provider?
I’m going to have to tell you that some of the best general
information is probably on the internet. There are various books
that are for sale on the subject and Best Publishing Company
out of Flagstaff, Arizona is a good source of HBO books. For a
wide-ranging, open-minded, scientific view of the literature of
hyperbaric oxygen the textbook of Hyperbaric Medicine which
is edited by Dr. K.K. Jain and published by Hogrefe & Huber
Publishers out of Germany and the United States is an excellent
source. And beyond that the medical societies provide some
information but you’re going to get a very narrow view with
some of them. And so I don’t think they’re the best source.
So where can a parent find information about an experi-
enced provider?
Well experienced providers—that is another good question.
Julie Gordon with the MUMS network maintains a list of pro-
viders without offering opinions on the given site. And she en-
courages people to do their own homework. Cerebral Palsy
Magazine has just come out with a list of recommended provid-
ers for their readership and children with cerebral palsy; that
was just published in the June issue. Beyond that it is very dif-
ficult to find information on the best place to get hyperbaric
oxygen for let’s say a neurological application, just as it is try-
ing to find information on the best medical care for any condi-
tion in the United States. It involves a lot of homework and
research and talking to other patients. I encourage patients to
access their support groups. Autism One, and the DAN People.
Also, the various autism conferences are becoming excellent
sites for exchange of information and identification of providers
of services who appear to be operating in an ethical and appro-
priate medical fashion.
Dr. Harch I’d like to thank you for providing us with all of
this most interesting information and for researching this area
that shows promise for helping to move our children forward on
the road towards recovery.
Well thank you very much. It’s been my pleasure and I ap-
preciate the opportunity.
doi: 10.1588/medver.2005.02.00084
... However , very few of these types of treatments have been critically evaluated. Starting around 2005, some investigators speculated that HBOT may be useful in improving behavioral and physiological abnormalities found in some children with ASD4445464748. This manuscript will review the current evidence for HBOT as a treatment for ASD. ...
... This child also had chronic diarrhea and had the first normal bowel movement in his life with HBOT treat- ment [99]. In another report, 23 patients with ASD had various improvements in social interaction, language and repetitive behaviors with HBOT at 1.5 atm [47]. Finally, one prospective study of 20 children with ASD reported improvements in communication, social interaction and stereotypical behaviors after 20 HBOT sessions at 1.5 atm/ 100% oxygen [118]. ...
Full-text available
Traditionally, hyperbaric oxygen treatment (HBOT) is indicated in several clinical disorders include decompression sickness, healing of problem wounds and arterial gas embolism. However, some investigators have used HBOT to treat individuals with autism spectrum disorders (ASD). A number of individuals with ASD possess certain physiological abnormalities that HBOT might ameliorate, including cerebral hypoperfusion, inflammation, mitochondrial dysfunction and oxidative stress. Studies of children with ASD have found positive changes in physiology and/or behavior from HBOT. For example, several studies have reported that HBOT improved cerebral perfusion, decreased markers of inflammation and did not worsen oxidative stress markers in children with ASD. Most studies of HBOT in children with ASD examined changes in behaviors and reported improvements in several behavioral domains although many of these studies were not controlled. Although the two trials employing a control group reported conflicting results, a recent systematic review noted several important distinctions between these trials. In the reviewed studies, HBOT had minimal adverse effects and was well tolerated. Studies which used a higher frequency of HBOT sessions (e.g., 10 sessions per week as opposed to 5 sessions per week) generally reported more significant improvements. Many of the studies had limitations which may have contributed to inconsistent findings across studies, including the use of many different standardized and non-standardized instruments, making it difficult to directly compare the results of studies or to know if there are specific areas of behavior in which HBOT is most effective. The variability in results between studies could also have been due to certain subgroups of children with ASD responding differently to HBOT. Most of the reviewed studies relied on changes in behavioral measurements, which may lag behind physiological changes. Additional studies enrolling children with ASD who have certain physiological abnormalities (such as inflammation, cerebral hypoperfusion, and mitochondrial dysfunction) and which measure changes in these physiological parameters would be helpful in further defining the effects of HBOT in ASD.
... This in turn should lead to improved clinical outcomes. Some physicians have begun using HBOT in autistic children and anecdotal reports indicate that HBOT has improved symptoms in autistic children including enhancements in socialization, language, and repetitive behaviors [78,128] . A recent retrospective case series also indicates that low pressure HBOT may improve symptoms in autistic children (see Appendix A). ...
Autism is a neurodevelopmental disorder that currently affects as many as 1 out of 166 children in the United States. Recent research has discovered that some autistic individuals have decreased cerebral perfusion, evidence of neuroinflammation, and increased markers of oxidative stress. Multiple independent single photon emission computed tomography (SPECT) and positron emission tomography (PET) research studies have revealed hypoperfusion to several areas of the autistic brain, most notably the temporal regions and areas specifically related to language comprehension and auditory processing. Several studies show that diminished blood flow to these areas correlates with many of the clinical features associated with autism including repetitive, self-stimulatory and stereotypical behaviors, and impairments in communication, sensory perception, and social interaction. Hyperbaric oxygen therapy (HBOT) has been used with clinical success in several cerebral hypoperfusion syndromes including cerebral palsy, fetal alcohol syndrome, closed head injury, and stroke. HBOT can compensate for decreased blood flow by increasing the oxygen content of plasma and body tissues and can even normalize oxygen levels in ischemic tissue. In addition, animal studies have shown that HBOT has potent anti-inflammatory effects and reduces oxidative stress. Furthermore, recent evidence demonstrates that HBOT mobilizes stem cells from human bone marrow, which may aid recovery in neurodegenerative diseases. Based upon these findings, it is hypothesized that HBOT will improve symptoms in autistic individuals. A retrospective case series is presented that supports this hypothesis.
Hyperbaric oxygen treatment (HBOT) has been reported to improve cerebral hypoperfusion, inflammation, and mitochondrial dysfunction, all of which have been observed in some individuals with autism spectrum disorders (ASD). In several studies, HBOT improved cerebral hypoperfusion, decreased a marker of inflammation, and did not worsen oxidative stress markers at pressures commonly used in children with ASD. Most studies of HBOT in children with ASD reported improvements in several behavioral domains, although many of these studies were not controlled. The two studies employing a control group appear to have conflicting results. However, this may have been due to different sample sizes and frequencies of HBOT sessions, with the larger study reporting improvements in several domains using a greater intensity of treatments. All studies reported that HBOT had minimal adverse events. Additional studies of HBOT in individuals with ASD are warranted to determine optimal treatment protocols.
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