HBOT and Stroke - TBI

David A. Steenblock, D.O.
Inc
Personalized Regenerative Medicine
Hyperbaric Oxygen Research

for Stroke and TBI
Dr. David A. Steenblock

Personalized Regenerative Medicine
Mission Viejo, CA 92691
1-800-300-1063
Definition
Hyperbaric oxygen is Supercharged Oxygen! Hyperbaric (hyper – high; baric – pressure)
oxygen can be defined as inhaling 100% inside a chamber that is pressured to greater than the
pressure at sea level or 1 ATA (atmospheres absolute). Dr. Steenblock uses 100% oxygen by
mask with pressurized air (21%) rather than 100% pressureized oxygen for greater safety. He
also uses pressures of about 1.5 ATA to 2.0 ATA that are recommended by experts in the field
such as Dr. K.K. Jain, as being safe as well as effective for brain injured patients. Using higher
pressures can result in increased oxidative stress that is counterproductive to tissue repair and
healing
Jain, K.K. Textbook of Hyperbaric Medicine, 5th Edition, Hogrefe Publishing, Cambridge,
MA, 2009.
Oxygen is Life!
A continuous, sufficient oxygen supply is essential for cell function. The brain is about 2% of
the body’s mass and utilizes 20% of the body’s oxygen. Oxygen delivery to the brain is highly
dependent on the flow of blood. A lack of oxygen to the brain cells, that lasts for a couple of
minutes, can lead to brain damage. A lack of oxygen beyond five or six minutes, can lead to the
person’s death. The neurons are the most vulnerable to hypoxia (a lack of oxygen) and ischemia
(a lack of blood flow). The second most vulnerable brain cells to a lack of oxygen are the
oligodendrocytes that produce myelin for the nerves. Multiple sclerosis is considered to be a
disorder of the myelin. The third most vulnerable cells are the astrocytes (white matter) that
support the neurons. Next are the microglia that play a protective role in the brain as immune
cells. However, when they become activated, as with hypoxia, ischemia, or inflammation, they
can also be destructive to the brain cells.
Shen J, Liu KJ, Liu S, Miyake M. Chapter 3: Cerebral Tissue Oxygenation: Transportation,
Metabolism, Measurement, and Significance in the Ischemic Brain. In Zhang, John (Ed),
Hyperbaric Oxygen for Neurological Disorders, Best Publishing Company, Flagstaff, AZ, 2008;
pp 67 – 84.
Back to the Future!

David A Steenblock, D.O. 1
For a consultation, call us at 1-800-300-1063
According to Dr. Jain, the history of increased pressure for healing dates back to Alexander the
Great in 320 BC when he was lowered into the Bosphorus Straits in a glass barrel to give him a
“secret weapon” in battles. (The Textbook of Hyperbaric Medicine).
There have been various attempts through the centuries to use oxygen under pressure for
increased healing and well-being. More recently, in 1960, Dr. Ita Boerema at the University of
Amsterdam, Netherlands was able to keep pigs alive in a hyperbaric chamber after the
hemoglobin had been removed from their bodies. As his fame grew, Dr. Boerema was given the
latitude to construct a surgical room inside a hyperbaric chamber where he proceeded to treat
3,300 patients (including infants, the elderly and the comatose) with conditions that included
respiratory distress, gas and drug poisoning, shock, and gas gangrene.1 The hyperbaric chamber
also extended the possibilities for cardiovascular surgery. After hyperbaric oxygen was
introduced to the surgical procedures, the mortality rate for surgery dropped from 66% to 23%.
The world then began to take notice. 2
1) Boerema I. Use of hyperbaric oxygen. American Heart Journal. 1965; 69:289-292.
2)Leopardi LN, Metcalfe MS, Forde A, Maddern GJ. Ite Boerema – surgeon and engineer
with a double-Dutch legacy to medical technology. Surgery 2004; 135(1): 99-103.
In 2009, a paper on HBOT from the Department of Neurosurgery, University Hospital of

Münster in Germany was published on the benefits of HBOT to help support brain oxygen levels
in damaged tissue. http://www.ncbi.nlm.nih.gov/pubmed/19277461
Where in the world is HBOT now?

According to Dr. Jain’s Textbook of Hyperbaric Medicine, 2nd Edition, published in 1996, about
40% of the world’s hyperbaric chambers were found in the USSR, 12% were found in both
South Korea and the People’s Republic of China, and 11% were found in Europe, Japan and the
U.S. Dr. Jain’s recent 5th edition (2009) shows 37% of the world’s hyperbaric chambers in
China, 26% in Russia, 10% in both Europe and Japan, 8% in South Korea and 7% are found in
the U.S. Four of these 7% of the world’s chambers are located at Dr. Steenblock’s clinic.
1) Jain, K.K. Textbook of Hyperbaric Medicine, 2nd Edition, Hogrefe Publishing, Kirkland,
WA, 1996.
2) Jain, K.K. Textbook of Hyperbaric Medicine, 5th Edition, Hogrefe Publishing, Cambridge,
MA, 2009.
Stroke statistics
Stroke is the leading cause of long-term disability and now the second leading cause of death in
the U.S. 1 The direct and indirect costs of stroke exceed $56 billion a year. 2
1) Veltkamp R, Schwab S, Sun L. Chapter 6: HBO for Stroke: Basic Science Studies. In Zhang,
John (Ed), Hyperbaric Oxygen for Neurological Disorders, Best Publishing Company, Flagstaff,
AZ, 2008; pp 135-154.
2) Singhal AB, Lo EH. Chapter 5: Oxygen Therapy for Ischemic Stroke: Clinical Aspects. In
Zhang, John (Ed), Hyperbaric Oxygen for Neurological Disorders, Best Publishing Company,
Flagstaff, AZ, 2008; pp 115-134
Stroke is a brain attack

A heart attack is also called a cardiac infarction. Likewise, stroke involves an infarct zone of
dead tissue as well as the tissue that surrounds the infarct zone, called the ischemic penumbra.
(The image in brain tomography is that of light, representing the penumbra, that surrounds a
darkened central area, the infarct zone of dead tissue, similar to the “penumbra” image of the sun
being eclipsed by the moon). In the hours, days, and weeks following a stroke, the neurons in
this area usually suffer a delayed death from partial oxygen and increased inflammation and
oxidative stress. A recent scenario is that neurons in this penumbra area that have enough
oxygen to survive but not enough to function, may be “idling” or “asleep” for months and even
years after a stroke. The salvaging of this surrounding area is associated with improved clinical
outcome. Hyperbaric oxygen’s supercharged oxygen is able to revitalize these idling neurons
that have been deficient in oxygen but not enough to die yet.
Neubauer R.A, Gottlieb SF, Kagan RL. Enhancing idling neurons. (Letter). Lancet, March 3.
1990, pg. 542.
What are the benefits of HBOT for stroke?

Matchett and associates provide a summary of the benefits of hyperbaric oxygen treatment in
animal models of cerebral ischemia (stroke), many of which have evaluated energy metabolism
in the ischemic penumbra region. Most of these studies conclude that hyperbaric oxygen
improves neurological outcome. In fact, these positive outcomes are described as “a rather robust
beneficial effect.”
Matchett GA, Martin RD, Zhang JH. Hyperbaric oxygen therapy and cerebral ischemia:
neuroprotective mechanisms. Neurological Research 2009; 31: 114-121.
http://www.ncbi.nlm.nih.gov/pubmed/19298750
Hyperbaric oxygen provides the following neuroprotective benefits:
1. Sustains cell viability in acute hypoxic tissue, especially in the ischemic penumbra
area that surrounds the infarct core. (Matchett)
One of Neubauer’s early studies on idling neurons:
2. Increases oxygen (pO2) from 34 mmHg (air-about 21% oxygen) to 90 mmHg (100%
oxygen). HBO also increases the diffusion distance for oxygen1 so the oxygen can reach
the cell from farther distances away. HBO increases oxygen in the plasma tenfold. 2 This
is important in areas where there is blood vessel damage that limit tissue access to the red
blood cells.
1) Ostrowski RP, Zhang JH. Chapter 4: Mechanisms of HBO for Neurological
Disorders. In Zhang, John (Ed), Hyperbaric Oxygen for Neurological Disorders, Best
Publishing Company, Flagstaff, AZ, 2008; pp 85-114.
2) Singhal AB, Lo EH. Chapter 5: Oxygen Therapy for Ischemic Stroke: Clinical
Aspects. In Zhang, John (Ed), Hyperbaric Oxygen for Neurological Disorders, Best
Publishing Company, Flagstaff, AZ, 2008; pp 115-134
3. Improves tissue metabolism

The mitochondria in cells are the energy factories. They produce the energy needed for
the cell to function. An increase in oxygen delivery to ischemic areas improves local
tissue metabolism. Anerobic metabolism, utilized when oxygen is deficient, produces
about 2 moles of ATP (cell energy from the mitochondria). Aerobic metabolism, that
requires oxygen, results in over ten times the anerobic amount of energy. Preservation of
ATP and other high energy phosphate compounds help to maintain mitochondrial function
as well as cell survival and function. (Matchett; Ostrowski)
4. Reduces excitotoxic effects.

Hyperbaric oxygen reduces the need for glucose, pyruvate, and lactate. Sufficient
oxygen reduces the glutamate stimulation of the cell and it’s excitotoxic effects. Too
much glutamate leads to sodium and calcium entry into the cell and a greater need for
ATP production to remove these minerals. An imbalance of charges between the inside
and outside of the cell in sodium-potassium and calcium-phosphorus can lead to
depolarization and eventual cell death. (Matchett)
A supportive article by Yang and associates:
5. Reduces risk of infection.

Oxygen is required for the leukocyte killing of microorganisms. Hyperbaric oxygen is
reported to double (or more) leukocyte bacteriocidal activity and control bacterial and
fungal infections. (Ostrowski)
Supportive free article by Bitterman: http://www.ncbi.nlm.nih.gov/pubmed/19291278
6. Reduces oxidative stress.

At 1.5 ATA, HBO inhibits hydroxyl radical in the brain, a reactive oxygen species (ROS)
that causes oxidative stress and tissue damage. At 2 ATA, HBO upregulates manganese-
superoxide dismutase (SOD) and decreases NADPH oxidation (that increases ROS). In
addition, thioredoxins, antioxidants that are increased by oxygen, have been found to
prevent programmed cell death. (Ostrowski)
Free article: http://www.ncbi.nlm.nih.gov/pubmed/16556878
7. Reduces inflammation.
Hyperbaric oxygen reduces pro-inflammatory cyclooxygenase-2 mRNA (COX-2). COX-
2 stimulates pro-inflammatory prostanoids, prostaglandins, prostacyclins and throm-
boxane. Hyperbaric oxygen also reduces inflammatory mediators such as Tumor
Necrosis Factor-alpha, Interleukin 1 and Interleukin 6. (Matchett)
Supportive article by Vlodavsky and associates:
8. Decreases size of the cerebral infarction

The secondary factors that result in cell death in the penumbra and thereby increase the
size of the infarction include inflammation, degradation of the extracellular matrix (that
stabilizes the brain cells), oxidative damage, sodium influx, edema (swelling), glutamate
excitotoxicity, depolarization and programmed cell death (apoptosis). The size of the
infarction has been associated with the amount of blood-brain barrier breakdown, which
is associated with an increase in extracellular matrix degeneration and edema.
Extracellular matrix degradation is also a factor in promoting hemorrhage and neural
death by apoptosis. Hyperbaric oxygen helps to repair the extracellular matrix and the
blood-brain barrier. (Veltkamp)
One of his other articles: http://www.ncbi.nlm.nih.gov/pubmed/15777761
9. Reduces edema (swelling)

By improving oxygen delivery to the cell’s energy factories, the mitochondria, ATP is
able to help sustain ionic pump function in the cells to counteract sodium influx and
eventual cell death. 1 In addition, by protecting the integrity of the blood brain barrier
and reducing inflammation, HBO reduces swelling. 2 (Ostrowski; Matchett)
A supportive free article by Qin and associates:
10. Reduces intracranial pressure.

HBO reduces cerebral blood volume and edema, resulting in reduced ICP. (Ostrowski)
A supportive free article from Ren and associates:
11. Reduces breakdown of the blood-brain barrier

The blood-brain barrier (BBB) is formed by endothelial cells (that build the blood
vessels), the extracellular matrix and astrocytes (white matter). Edema and secondary
hemorrhages result from BBB damage. Hyperbaric oxygen reduces MMP-9 (matrix
metalloproteinase-9) that degrades the extracellular matrix. (Matchett; Ostrowski)
A supportive Veltkamp free article: http://www.ncbi.nlm.nih.gov/pubmed/16020761
12. Reduced programmed cell death (apoptosis).

Apoptosis is initiated by both mitochondrial dysfunction (resulting in reduced ATP and
increased oxidative damage) and degradation of the extracellular matrix. Hyperbaric
oxygen can inhibit these processes. HBOT inhibits hypoxia-inducible factor-1alpha
(HIF-1a), improves the Bcl-2/Bax ratio in favor of anti-apoptosis and reduces cytochrome
C release from the mitochondria. There is also evidence that HBOT reduces PARP
cleavage, reduces cleaved caspase 3 and reduces DNA fragmentation which contribute to
cell death. (Matchett)
Supportive article by Yin and associates: http://www.ncbi.nlm.nih.gov/pubmed/12843789
13. Promotes the development of new blood vessels

Short term use reduces vascular endothelial growth factor (VEGF) and helps preserve the
blood brain barrier. However, the daily use of HBOT stimulates VEGF and the
development of new capillaries in the brain that will eventually provide a consistent
supply of oxygen to the cells. Oxygen is also necessary for fibroblast differentiation to
produce collagen, which supports capillary formation. (Ostrowski)
Supportive free article by Sheikh and associates:
14. Promotes peripheral nerve regeneration

Hyperbaric oxygen stimulates the regeneration of the peripheral nerves after injury.
(Matchett)
Supportive article by Bradshaw and associates:
15. Promotes white matter growth in the CNS.
Hyperbaric oxygen can stimulate the growth of oligodendrocytes and myelin basic
protein (white matter) in the brain.
Yang YJ, Wang XL, Yu XH, Wang X, Xie M, Liu CT. Hyperbaric oxygen induces
endogenous neural stem cells to proliferate and differentiate in hypoxic-ischemic brain
damage in neonatal rats. Undersea Hyperbaric Medicine 2008, 35(2): 113-29.
Hyperbaric oxygen therapy stimulates the production of glial cell derived neurotrophic
factor in a rat model of spinal cord injury.
Tai PA, Chang CK, Niu KC, Lin MT, Chiu WT, Lin CM. Attenuating experimental
spinal cord injury by hyperbaric oxygen: stimulating production of vasculendothelial and
glia cell line-derived neurotrophic growth factors and interleukin-10. J Neurotrauma.
2010, 27(6): 1121-7. http://www.ncbi.nlm.nih.gov/pubmed/20334467
16. Promotes bone marrow stem cell mobilization.

In humans, HBOT was shown at 2ATA to stimulate stem cell mobilization from the bone
marrow. With animal studies, hyperbaric oxygen increased nitric oxide, which was
shown to promote the mobilization.
Thom SR, Bhopale VM, Velazquez OC, Goldstein LJ, Thom LH, Buerk DG. Stem cell
mobilization by hyperbaric oxygen. Am J Physiol Heart Circ Physiol 2006; 290(4):
H1378-86. http://www.ncbi.nlm.nih.gov/pubmed/16299259
17. Promotes axonal growth.

Nogo-A is increased after cerebral ischemia which reduces axonal regrowth. HBOT is
associated with reduced levels of Nogo-A, which may be a factor in how HBOT
promotes nerve regeneration. (Matchett)
Supportive article by Zhou and associates:
18. Promotes new neurons

(lab study) Newborn rat neural stem cells were given HBOT of different pressures and
exposure times. The highest percentage of neurons differentiated from the neural stem
cells were found for the one hour of HBOT at 2 ATA.
Note: This is the protocol generally used by Dr. Steenblock’s clinic.
19. The sooner the better for Stroke and TBI.

According to animal research, beginning hyperbaric oxygen within 6 hours of stroke onset
was most effective and treatment after 24 hours also showed benefit in acute cerebral
ischemia. In cerebral hemorrhage studies, hyperbaric oxygen should to be initiated
immediately after the hemorrhage onset to produce benefits. (Matchett)
20.. Oxidative Stress can result from higher pressures.

The major concern about hyperbaric oxygen is the potential damage from oxidative stress.
However, this generally occurs with hyperbaric pressures at 2.5 ATA and higher. HBOT
at 1.5 ATA is reported to inhibit hydroxyl radical in the brain.. The Guidelines for
hyperbaric oxygen recommend pressures no greater than 3 ATA. HBO at lower pressures
(2 ATA and below for one hour on a daily basis) does not increase lipid peroxidation.
After reviewing the literature, Dr. Jain recommends 1.5 to 2ATA for neurological patients
who are more susceptible to seizures. (Textbook of Hyperbaric Medicine)
Hyperbaric Oxygen Therapy for Stroke

Update Feb, 2011
Stroke after cardiac surgery

HBOT is recommended for patients who have a stroke after open cardiac surgery.
Stroke and secondary damage

Experimental and clinical studies have reported positive effects of HBOT in ischemic stroke.
Survival rates have increased and neurological outcome has improved with hyperbarix
oxygenation. http://www.ncbi.nlm.nih.gov/pubmed/19485935
Integrative medicine program for stroke

Long term HBOT is safe and holds great promise for ischemic stroke.
Delayed hyperbaric oxygenation compared to normobaric hyperoxia

(rat study) HBOT was more effective in transient experimental ischemia even when accounting
for delayed treatment onset of HBOT. http://www.ncbi.nlm.nih.gov/pubmed/17850964
Neural protection by inhibiting HIF-1a

(rat study) HBOT provides neuroprotection in cerebral ischemia in part due to its inhibition of
hypoxia-inducible factor-1a (that can increase inflammation) and the elevation of Bcl-2 that
reduces cell death. http://www.ncbi.nlm.nih.gov/pubmed/17462608
Time window in stroke for thrombolytic drugs

HBOT can extend the time window in acute ischemic stroke for tPA treatment.
Acupuncture combined with HBOT

72 patients with cerebral infarction were divided into two groups and either treated with a
combination of acupuncture and HBOT (experimental group) or routine medicine and HBOT
(control group). While balance was improved in both groups, the acupuncture and HBOT
combination showed greater improvement in motor function and balance.
HBOT combined with edaravone in embolic stroke

6 of 19 patients receiving HBOT and a free radical scavenger for 7 days had favorable outcomes
at a 90 day follow-up compared to 1 out of 19 in the control group who received conventional
treatment. Free article: http://www.ncbi.nlm.nih.gov/pubmed/16936457
Hyperbaric oxygen in neurological patients
The results of HBOT are promising and warrant further investigation.
Improvement in motor and cognitive impairment

Eighteen patients with cerebrovascular disease and lacunar infarcts received HBOT for 45
minues for 10 days and 8 patients received hyperbaric air (after the study, the control group was
also given the HBOT). Neurological improvement persisted in the majority of patients for up to
six months. Repetition of the protocol in patients with returning symptoms resulted in
improvement. http://www.ncbi.nlm.nih.gov/pubmed/16457083
A therapeutic window of 3-6 hours

HBOT within 3-6 hours of cerebral ischemia onset or repeated administration if delayed can
salvage injured neuronal tissues or promote functional recovery.
Here things liven up a bit…

The Hyperbaric Oxygen Therapy in Acute Ischemic Stroke Trial Pilot Study
Rusyniak and associates did a study with a flawed protocol and concluded that HBOT has no
benefit and can actually be harmful.
Criticism: Thirty-three subjects within 24 hours of stroke onset were divided into
two groups. One group received 100% oxygen at 1.14 ATA for 60 minutes (the
“sham” group) and the other group received 100% oxygen at 2.5 ATA for 60
minutes. The patients were then evaluated three months later on a battery of
stroke tests. The test scores were better for the sham group. The authors
concluded that HBO offers no benefit and may even be harmful in stroke. This
study provided heparin and standard medical practice. The study also omitted
hemorrhagic stroke patients. However, Rusyniak has been heavily criticized for
using 2.5 ATA for acute stroke patients, especially since Jain has been
recommending 1.5 ATA as safe for acute stroke patients for over twelve years.
The 1.5 ATA level avoids complications resulting from increased lipid
peroxidation and seizures. The 1.14 ATA was, in fact, closer to Jain’s
recommended pressures. 12 According to Jain, the design of the study invalidates
any conclusions.5 A 1.5 ATA group should have been included and the 2.5 ATA
changed to perhaps 2 ATA for the wellbeing of the patients.

Free article - Response by Dr. Hart -
Free article - Response by Dr. Jain -
Free article - Response from Dr. Zhang -
Neuroprotection from reducing elevated dopamine levels

(rat study) Dopamine levels in the striatum significantly increased at 30 minutes after cerebral
ischemia and continued to increase to peak levels at 60 minutes. Dopamine metabolites can
increase free radical damage so elevated levels of dopamine can indirectly produce more brain
damage. There was no increase in dopamine with HBOT treatment.
Lim’s HBOT case study with haemorrhagic stroke

A case study is presented of a patient with haemorrhagic stroke who was treated successfully
with HBOT. http://www.ncbi.nlm.nih.gov/pubmed/11513061
Dosage for Acute Stroke

According to Rogatsky, the rate of effect produced by an HBO treatment is dependent on the
oxygen pressure, the duration of the treatment (time) and the number of treatments (N). This
“dosage,” as an equation is DHBOT = pO2 x Ts x Nt. Rogatsky proceeded to calculate various
studies in terms of 2 ATA, treatment time (1 hour) and number of treatments. Rogatsky used
three studies, including Neubauer’s study of 2 ATA for one hour for an average of 16 sessions as
a parameter for 100% efficacy for acute stroke treatment within 4 hours of symptom onset.19
The authors conclude that any discussions of efficacy or non-efficacy of HBO should also
include these parameters that relate HBO dosage to efficacy. In addition, according to the
dosage to efficacy analysis, the benefit increased progressively as more treatments were given.
Rogatsky GG, Shifrin EG, Mayevsky SA. Optimal dosing as a necessary condition for the
efficacy of hyperbaric oxygen therapy in acute ischemic stroke: A critical review. Neurol Res
2003; 25: 95-98.
Dr. Steenblock’s Treatment Suggestions for Chronic Stroke Patients

In 1996, Dr. Steenblock’s research group evaluated 50 chronic stroke patients who underwent
HBOT (1.5 to 2 ATA), biofeedback and physical therapy in addition to standard medical care.
The average number of treatments was 55 and the results showed that about 97% of the patients
showed improvement in one or more of their lost or diminished functions. The study, “Improved
Therapy for Rehabilitation of Stroke” was presented in a Poster Session at the National Stroke
Association’s Ninth Annual Stroke Rehabilitation Conference in Boston, Massachusetts, October
16-17, 1997. According to Dr. Steenblock, about thirty to forty treatments are required for the
re-growth of the capillary beds. Additional treatments are then needed to strengthen the stability
of the capillaries. As more HBO treatments are done, more capillaries are strong enough to
penetrate deeper and deeper into the infarct zone. This re-growth results in more tissue repair
and/or replacement and better clinical outcome. For most chronic stroke patients, Dr. Steenblock
suggests a program of 60 HBO treatments and then if the patient is still making progress, another
20 treatments may be suggested.
Nighoghossian’s HBOT double-blind pilot study.

The Nighoghossian clinical trial divided 34 subjects with middle cerebral artery stroke into either
HBO or hyperbaric air within 24 hours of symptom onset. The treatments were administered
daily for ten days at 1.5 ATA for 40 minute sessions. While the HBO group performed
significantly better at one year on the Orgogozo and Trouillos tests (but not on the Rankin
scores), no difference was seen at six months or one year and pre- compared to post-treatment
scores on any scale. The authors concluded that HBO was safe in these patients and that there
was an outcome trend favoring HBO therapy.
Criticisms about this design include a small sample size and the inclusion of TBI subjects
where immediate HBOT treatment is imperative to outcome.
1) Ostrowski RP, Zhang JH. Chapter 4: Mechanisms of HBO for Neurological Disorders.
In Zhang, John (Ed), Hyperbaric Oxygen for Neurological Disorders, Best Publishing
Company, Flagstaff, AZ, 2008; pp 85-114.
2) Singhal AB, Lo EH. Chapter 5: Oxygen Therapy for Ischemic Stroke: Clinical Aspects.
In Zhang, John (Ed), Hyperbaric Oxygen for Neurological Disorders, Best Publishing
Company, Flagstaff, AZ, 2008; pp 115-134
Anderson’s pilot study of HBOT for acute stroke.

Also criticized for the study design.
Comment by Dr. Jain:

Anderson’s study in 1991 was randomized, using 39 acute stroke patients. One group was
given pressured air at 1.5 ATA and another group was given 100% oxygen at 1.5 ATA.
Both groups underwent 1 hour of treatment every 8 hours for 15 sessions. The results of
the two groups for post-treatment were compared four months after the treatments. The
group given pressured air also showed reduced infarct volumes, which reduced the
significance of the pressurized oxygen effects. The randomization process was also a
point of criticism. The control group (pressured air) also had less severe neurological
deficits and smaller infarcts. According to Jain, the results of this study neither prove or
disprove the usefulness of HBO in acute stroke and can be disregarded. (Jain, Textbook of
Hyperbaric Medicine, 2009)
Brain Imaging to identify hypometabolic areas in the brain

Neubauer concludes that HBOT in conjunction with physical and rehabilitative therapy may help
reactivate idling neurons to remain permanently active.
Kaasik’s HBOT study of stroke patients

HBOT significantly reduced metabolic acidosis in the cerebral venous blood compared to the
control group.
Neubauer’s study of generalized small-vessel stenosis in the brain

A case study is presented of a person suffering from mental confusion, memory loss, irrational
speech and occasional violence. HBOT resolved the symptoms and intermittent treatment
maintained the improvements for four years. When the patient had a stroke, HBOT again
improved his symptoms of disorientation and confusion.
Lebedev’s article on HBOT and ischemic stroke

Regression of the neurological defects was most evident in patients exposed to HBO. HBO
prevents the development of recurrent cerebral circulatory disorders in the acute stage of
ischemic stroke and reduces the incidence of some complications in this period (pneumonia,
pulmonary edema, thromboembolism.
Neubauer’s Lancet Letter reviewing HBOT benefits

"Hyperbaric oxygen (HBO) efficiently increases the diffusional driving force for oxygen,
thereby increasing tissue oxygen availability. This overcomes ischemia/hypoxia and so reduces
cerebral edema, restores integrity to the blood/brain barrier and cell membranes, neutralizes toxic
amines, promotes phagocytosis, scavenges free radicals, stimulates angiogenesis, and reactivates
idling neurons."
Neubauer, R. et al. "Stroke Treatment." (letter). THE LANCET, June 29, l991; 1601.
Neubauer’s Case Study of Chronic Stroke (15 years post-stroke onset)

In 1990, Neubauer and associates published a letter in the Lancet about treating a patient 15
years after her stroke with 60 HBO treatments. The results included reduced spasticity,
improved movement, improved speech and the cessation of drooling. There was also a sharp
increase in SPECT tracer uptake in areas previously showing hypometabolism.
Neubauer, R. et al. "Enhancing idling neurons." letter. THE LANCET, March 3, l990; 542.
No abstract: http://www.ncbi.nlm.nih.gov/pubmed/1968553
Neubauer’s review of 122 thrombotic stroke patients

Neubauer recommends that stroke patients be treated at 1.5 to 2 ATA.
Jain’s HBOT study on chronic stroke and spasticity

In 1989, Jain and associates published a study on HBO and its contributions to rehabilitative
medicine in 21 chronic stroke patients and a year later, 25 patients. The sessions were limited to
daily treatments for six weeks. All of the patients showed neurological improvement after the
treatment program. The degree of improvement varied according to the extent and duration of
the neurological deficit. The best results were achieved in those patients with a short disease
history and less spasticity and/or neurological deficit. The authors recommend that HBO therapy
be used as an adjunct in stroke management and whenever possible and have physical therapy
exercise carried out in the hyperbaric chamber. The authors also conclude that HBO is
considered an invaluable adjunct in stroke rehabilitation in patients with spastic hemiplegia. 2,3,4,5
Jain, K.K. Effect of hyperbaric Oxygenation on Spasticity in Stroke Patients. Journal of
Hyperbaric Medicine, 1989; 4(2): 55-61.
Marroni’s study on HBOT for chronic stroke patients
In 1987, Marroni and associates enlisted 80 stabilized stroke patients with stroke onset from two
to 172 months earlier. Thirty HBO sessions were given. Those undergoing hyperbaric oxygen
plus physical therapy showed the best results. The HBO alone and combined with physical
therapy produced improvements in neuromotor performance, especially at 2 ATA. The results
were still present at the third month after treatment.
Marroni, A. et al. "Hyperbaric Oxygen Therapy at 1.5 or 2.0 ATA as an Adjunct to the Rehab-
ilitation of Stabilized Stroke Patients. A Controlled Study." Proceedings of the 9th International
Congress on Hyperbaric Medicine, March 1-4, l987; Sydney, Australia, pp. 161-167.
Isakov’s article on ischemic stroke and respiratory disorders

HBOT had a normalizing effect on respiratory function in breathing disorders.
Holbach’s study of chronic stroke

This was one of the first studies in chronic stroke. Forty patients with stroke associated with
carotid artery occlusion participated.
Free Article: http://www.ncbi.nlm.nih.gov/pubmed/1273908
Sarno’s study on the mental and verbal improvements of stroke patients after HBOT.
Hart’s case study of stroke treated successfully with HBOT.

Dr. Hart was working at Long Beach Memorial Hospital with the Navy. They were involved in
helping divers who suffered from “the bends” recover with hyperbaric oxygen. One officer
suffered a stroke and Dr. Hart tried hyperbaric oxygen to see if it would help. It did. A series of
treatments were needed but the officer eventually returned to active duty.
The abstract: The treatment of a patient for three and one-half months, following occlusion of
the right middle cerebral artery with the associated neurological sequelae, with hyperbaric
oxygen combined with methyldopa and hydrochlorthazide is presented. Treatment scheduled
was two and one-half atmospheres absolute. The treatment was interrupted after 15 treatments to
rule out spontaneous remission for a period of 30 days, and no further improvement occurred
until treatments were reinstituted. The dramatic return to a near normal state during treatment
appears to indicate that he did benefit from therapy.
Hart, G.B. et al. "The Treatment of Cerebral Ischemia with Hyperbaric Oxygen (OHP)." Stroke,
l971; 2: 247-250. No online abstract: http://www.ncbi.nlm.nih.gov/pubmed/5165167
Hyperbaric Oxygen Therapy for Traumatic Brain Injury
Update Feb, 2011
HBOT neuroprotective effects in TBI

(rat study) Three and six hours after the TBI, rats receiving the HBOT showed a significant
reduction in brain damage. The improvements subsided by 12 hours. In contrast, multiple HBO
treatments (3-5 sessions) even when started 48 hours after the TBI, significantly reduced
neurology deficit scores and neuronal loss in the hippocampus. Despite improvements in
behavior and reduced brain injury, the overall benefits were weaker than improvements at 6
hours after the TBI. The results suggest that HBOT can alleviate brain damage after a TBI and a
single HBO treatment has a time limitation of 12 hours and that multiple HBO treatments can
extend the post-TBI delivery time window. The results clearly suggest the validity of HBOT for
treating traumatic brain injuries. http://www.ncbi.nlm.nih.gov/pubmed/20568957
TBI treatment using a modified monoplace chamber

Twenty-seven patients with severe TBI were safely treated, monitored and managed in a
monoplace chamber. The compression used was pressurized air at 1.5 ATA. A total of 75
hyperbaric treatments were given. The patients also received 100% oxygen via mechanical
ventilation. The chambers were adapted to safely treat these critically ill patients. The patients
were monitored for cardiovascular, ventilatory, intracranial pressure, brain tissue oxygen levels,
brain temperature and cerebral microdialysis parameters.
Case report of treating mild TBI with hyperbaric oxygen

Six months after being injured in a roadside improvised explosive devise (IED) blast in Irqa, two
US Air Force airmen were treated with HBOT. They received 100% oxygen for one hour at 1.5
ATA. The treatment resulted in rapid improvements of their headaches, sleep disturbances and
other symptoms. These improvements were maintained for three months, with most measures
returning to pre-injury levels. These results were most likely due to the HBOT.
Severe TBI treated with HBOT or Normobaric hyperoxia

Sixty-nine patients with severe TBI’s (mean Glasgow Coma Scale Score 5.8) were randomized
into three groups, a control group, hyperbaric oxygen group and normobaric hyperoxia group.
Hyperbaric oxygen therapy was more robust in its increasing brain tissue oxygen levels. There
were also some improvements in the normobaric group as well. No signs of pulmonary or
cerebral oxygen toxicity were observed. http://www.ncbi.nlm.nih.gov/pubmed/19852540
Case Study of blast-induced chronic TBI

A 25 year old military veteran experienced an explosion in combat and lost consciousness.
Three years later, he still suffered from post concussion syndrome and post traumatic stress
disorder. The subject underwent 39 hyperbaric sessions of 1.5 ATA. There was permanent
marked improvement in his symptoms and the SPECT brain blood flow. He has since been
employed for eight consecutive months.
HBOT with Subacute TBI

Twenty-two stable TBI patients wee treated with HBOT and 22 patients were the control group.
The GCS of the HBOT group improved from 11.1 to 13.5 and the control group improved from
10.4 to 11.5. Those patients with GOS = 4 before HBOT maintained significant improvement
six months after HBOT. http://www.ncbi.nlm.nih.gov/pubmed/18642650
HBOT and spatial learning and memory in chronic TBI

(rat study) Rat models for TBI were divided into three groups – an untreated control group,
HBOT group and normobaric air group. The HBOT group received 80 sessions at 1.5 ATA for
90 minutes each. They were then retested in the Morris Water Task and sacrificed. HBOT
produced increased vascular density in the injured hippocampus that was associated with
improved spatial learning and cognitive function.
Case Study of HBOT for chronic brain injury

A 54 year old man sustained traumatic brain injuries that resulted in permanent neurological
symptoms. A year later, he underwent two series of HBOT, one year apart. The series consisted
of 20 and then 60 daily one hour sessions at 2 ATA using 100% oxygen. The first series resulted
in improvements in sensorimotor functions and enhanced P300l amplitude in the damaged
hemisphere. This first session was not long enough to achieve permanent benefits. However,
the improvements returned over a year later as a result of the second and longer series.
HBOT and neuropsychiatric disorders from TBI

Three hundred ten patients with neuropsychiatric disorders from TBI were treated twice with
HBOT and evaluated by pre- and post-SPECT as well as CT imaging. SPECT was more
sensitive in the degree of abnormal cerebral changed detected. After HBOT, 70.3% of the
SPECT scans showed no abnormalities and the patients showed clinical improvements. The
hyperbaric treatment also improved regional cerebral blood flow.
Review of HBOT for stroke, brain trauma and neurologic disease

The results of HBOT are promising and warrant further investigation.

SPECT imaging to assess HBOT in TBI patients
320 patients with TBI were divided into two groups – one with HBOT and the other as the
control group. The HBOT was superior to medication treatment alone in the recovery of clinical
symptoms, control of epilepsy and resolution of hydrocephalus. HBOT has specific curative
effects on patients with postbrain injury neural status and SPECT can be used to monitor the
effects. The results of HBOT are promising and warrant further investigation.
Improved cerebral metabolism in chronic brain injury after HBOT

This study compared 25 older and 25 younger subjects on SPECT scans before, during and after
HBOT treatment for chronic TBI. There was improvement in blood flow from the beginning of
treatment to the end of the study. An age effect was found on only two measures. The younger
group had higher blood flows but not more improvement. HBOT can be an effective part of the
treatment for chronic TBI patients. http://www.ncbi.nlm.nih.gov/pubmed/12325401
Benefits of HBOT in severe brain injury

Fifty-five patients with severe TBI were divided into an HBOT group and a medication control
group. They were evaluated with the Glasgow Coma Scale, brain electric activity mapping
(BEAM) prognosis and Glasgow Outcome Scale before and after HBOT. In the hyperbaric
group, GCS, BEAM and GOS were significantly improved after 3 courses of treatment. HBOT
effectively reduced the mortality and morbidity of the patients. The authors conclude that HBOT
is an effective method of treating severe TBI patients.
Shorter, more frequent HBOT sessions for TBI

HBOT, using 100% oxygen at 1.5 ATA was given to 37 patients for 60 minutes each day for 7
treatments. The HBOT increased cerebral metabolic rate of oxygen (CMRO2) and decreased
ventricular cerebrospinal fluid lactate, suggesting that the treatments can improve aerobic
metabolism in severely brain injured patients. Dr. Sukoff suggests that shorter, more frequent
exposure to HBOT may optimize treatment.
HBOT in closed head injury

This 1994 article by Neubauer and associates presents a case study of a patients with a closed
head injury that was successfully treated with intensive HBOT and evaluated with SPECT
imaging. http://www.ncbi.nlm.nih.gov/pubmed/8091261
Mental disorders from TBI

20 patients with severe brain damage were treated with HBOT, resulting in a more rapid
restitution of consciousness and shortened comatose episode. In cases of delirious states HBOT

resulted in a disappearance of psychotic disturbances after the first session. This study by
Tishchenko was published in 1976. http://www.ncbi.nlm.nih.gov/pubmed/1266492
Hyperbaric Oxygen Therapy for Other Conditions

2010 Articles
Overview
HBOT is suggested as an additional option in conditions that include problem wounds, spinal
cord injury and cerebral ischemic injury. http://www.ncbi.nlm.nih.gov/pubmed/20636981
Anastomosis (surgical resection and reconnection of tissue, generally after irradiation)
Colonic anastomosis
(rat study) HBOT reduced interstitial edema and increased hydroxyproline at the anastomotic
site, resulting in greater healing of anastomotic ischemia.
Tracheal anastomosis
(rat study) Animals treated with HBOT showed excellent healing at the anastomosis.
Anti-Aging
Aging is associated with impaired wound healing and reduced blood vessel growth to ischemic
tissue. Gene expression was analyzed before and after hyperbaric oxygen. There was an
upregulation of genes for antioxidant production and an increased resistance to lethal oxidative
stress in endothelial cells. HBOT is suggested as a treatment to help promote healthy aging.
Bone/Skeletal Conditions
Cervical spondylotic amyotrophy
Beneficial in cervical spondylotic amyotrophy - http://www.ncbi.nlm.nih.gov/pubmed/21243002
Disc degeneration
(lab study) Inflammatory changes in intervertebral disc degeneration may be due to interleukin
1B and p38 MAPK signal pathways. HBOT improved tissue balance and is suggested for
slowing the course of disc degeneration. http://www.ncbi.nlm.nih.gov/pubmed/20661932
Femoral head necrosis

Nine patients with Ficat stage II femoral head necrosis were treated with 30 sessions of HBOT.
There were significant improvements in pain threshold after twenty treatments. Range of motion
improvements were observed between 20 and 30 treatments. In a seven year follow-up, all
patients reported being pain free, none of the patients required hip surgery and 7 of the 9 hips
showed substantial healing of the osteonecrosis.
Osteonecrosis
Bisphosphonates are used for metabolic or malignant bone diseases but also promote
osteonecrosis of the jaw bone. Moderate osteonecrosis of the upper jaw was treated with
platelet-rich plasma, HBOT and the cessation of bisphosphonates.
Paraspinal compartment syndrome (from acute exertion)

A football was weight-lifting and developed myonecrosis. He was successfully treated with
forced diuresis and six session of HBOT. http://www.ncbi.nlm.nih.gov/pubmed/21045996
Spinal Cord Injury

There were reduces risk of secondary spinal cord injury by early decompression and high
pressure oxygen after operation. http://www.ncbi.nlm.nih.gov/pubmed/21254684
(rat study) The combination of hypothermia and HBOT can be effective in reducing secondary
damage in spinal cord tissue.
Bronchitis (ischemic)
Beneficial in postoperative ischemic bronchitis after lung cancer treatment in 82% of the cases.
Cancer
(laboratory study) The combination of HBOT and artemisinin is suggested as an anticancer
chemotherapy strategy. http://www.ncbi.nlm.nih.gov/pubmed/21115894
Liver Cancer
HBOT after liver resection reduced complications in patients who experienced major bleeding or
showed severe hepatic hypoxia during surgery. Improved immune function and long term
survival were additional benefits.
Nasopharyngeal carcinoma
(lab study) The combination of HBOT and 5-fluorouracil was effective in inhibiting metastasis.
Ovarian cancer

(mice study) Hypoxia, a common characteristic of solid tumors, compromises the effectiveness
of chemotherapy and radiation. Hypoxia also promotes tumor progression and drug resistance
by signal transducer and activator transcription 3 (STAT3). HBOT reduced tumor volume and
inhibited STAT3 activation. The combination of HBOT and cisplatin also reduced the tumor
volume but also drastically reduced body weight.
Carbon Monoxide Poisoning

Carbon monoxide poisoning causes neurological damage from programmed cell death
(apoptosis) in neurons. HBOT, especially between 3 and 5 hours after the poisoning, has a
protective effect on the neurons. http://www.ncbi.nlm.nih.gov/pubmed/20843278
Cardiovascular Disease
Vascular Degeneration
Matrix metalloproteinase-9 (MMP-9) is an enzyme involved in extracellular matrix degradation.
It helps with matrix remodeling but excessive amounts are detrimental to the tissue. MMP-9
over-expression is associated with stroke, cell death, non-healing wounds, TBI, aneurysms and
blood vessel leakage in atherosclerosis. This is a case report of a patient’s MMP-9 levels
dramatically increasing after surgery and hyperbaric oxygen significantly reduced the MMP-9
expression. http://www.ncbi.nlm.nih.gov/pubmed/20824409
Hypertension
(rat study) Normotensive rats (WKY) and genetic rat models for hypertension (SHR) were
subjected to hyperbaric oxygen. The hypertensive rats showed reduced systolic blood pressure
after three weeks and lower diastolic blood pressure after seven weeks of treatment compared to
a normobaric rat group. Both the normotensive and hypertensive rats who received HBOT
showed lower levels of reactive oxygen metabolites than the control group and the hypertensive
rats receiving HBOT showed higher antioxidant levels than the control SHR rats. The results
suggest that HBOT may be effective in reducing genetically-induced hypertension.
Peripheral Artery Disease

Patients with chronic occlusive arteries in the lower legs showed significant improvements in
muscle perfusion with HBOT. http://www.ncbi.nlm.nih.gov/pubmed/20465155
Cerebral ischemia (stroke) and hemorrhage

See first section on Stroke and TBI.
Dementia (Vascular)

(rat study) Neurogenesis in the piriform cortex of the brain is closely related to cognitive
function. Hyperbaric oxygen increased the brain blood supply and neurogenesis in this area in
rat models of vascular dementia. http://www.ncbi.nlm.nih.gov/pubmed/20715898
Diabetes
Atherosclerosis and glycemic control
Twenty-eight diabetic patients undergoing HBOT for foot ulcers received improvements in their
fasting blood glucose, hemoglobin A1c, insulin resistance (HOMA-IR), C-reactive protein (hs-
CRP), uric acid mean platelet volume, complete blood count and lipid profile.
Hyperlipidemia
(mice study) Six weeks of hyperbaric air (21% oxygen) significantly reduced free fatty acids
and triglycerides in diabetic mice. The results suggest that hyperbaric air treatments can improve
lipid metabolism in type 2 diabetes patients.
Foot Ulcer
Hyperbaric oxygen improves ulcer healing and consequently patient quality of life
HBOT is suggested for foot ulcer cases that are resistant to antibiotics.
Baseline transcutaneous oximetry correlated more with healing from HBOT than toe blood
pressure or ankle-brachial index. http://www.ncbi.nlm.nih.gov/pubmed/20957342
HBOT for infected diabetic feet can improve healing and reduce the amputation rate in diabetic
patients. http://www.ncbi.nlm.nih.gov/pubmed/20483142
Ears/Hearing
Ear and HBOT Side Effects
Middle-ear barotrauma can be a side effect of hyperbaric oxygen. In 130 patients receiving
HBOT, barotraumas occurred in 13.6% of the patients.
Acute Noise Damage

(guinea pig study) Guinea pigs were exposed to acute acoustic trauma and suffered damaged to
the outer hair cells in the cochlea. One exposure to HBOT was not improve the brainstem
auditory evoked potential but did reduce the number of injured cochlear outer hair cells and their
function.
Sudden hearing loss

174 patients with idiopathic sudden sensorineural hearing loss were treated with tapering doses
of hydrocortisone sodium succinate and hyperbaric oxygen. There were significant correlations

between hearing improvement rate and age, duration, initial hearing level and vertigo.
HBOT improved idiopathic sudden sensorineural hearing loss in a retrospective review of 97

cases. The average hearing gain in all cases after HBOT was 29.5 dB. Significant
improvements were found in cases that received HBOT early after the symptoms appeared, in
cases that had a higher number of HBOT sessions, those who also received steroids, those with
low frequency-ascending and total audiogram configuration and those with profound hearing
loss. High frequency-descending audiogram configurations showed significantly lower
improvement. http://www.ncbi.nlm.nih.gov/pubmed/20628751
Severe Deafness
HBOT combined with drug treatment can be effective in moderate and severe cases of deafness.
Otitis (infection)
Beneficial in fungal malignant external otitis (can result from prolonged antibiotoic treatment)
Embolism
Risks in divers, compressed air workers, aviators, astronauts, patients with cardiac shunts, etc.)
Beneficial in arterial gas embolism and decompression sickness
Systemic Gas Embolism from surgery

Anti-thrombotic prevention and hyperbaric oxygen was rapidly administered to a patient who
suffered from sudden hypotension and gas embolism during surgery. A left fronto-parietal blood
clot was subsequently found. This case study suggests anticoagulant therapy should not be used
in the early stages of gas embolism. http://www.ncbi.nlm.nih.gov/pubmed/20462140
Encephalitis
With acute lymphoblastic leukemia
Granulomatous amebic encephalitis is usually fatal. A child with brain abscesses from the
Acanthamoeba
Received antimicrobial chemotherapy and HBOT and had complete resolution of symptoms.
Eyes/Vision
Age-related macular degeneration
Fourteen patients with advanced AMD underwent a one hour session of HBOT at either 1.5 or
1.75 ATA that resulted in significant improvements in visual acuity and/or visual field and daily
living vision.

Radiation-induced macular ischemia
A 62 year old patient was treated with radiation for brain glioma and subsequently experienced a
visual acuity of 20/400 in his right eye. Focal laser and intravitreal triamcinolione improved the
vision to 20/100. HBOT further improved his vision to 20/50 and resulted in improvement in
macular perfusion. Free article: http://www.ncbi.nlm.nih.gov/pubmed/20505835
Retinal artery occlusion

Five patients with retinal artery occlusion were treated with HBOT and all patients improved.
Gangrene
Beneficial in ulcerative pyoderma gangrenosum -
Gastrointestinal toxicity
Hyperbaric oxygen is a suggested option for cancer treatments that include radiation, surgery
and/or chemotherapy. http://www.ncbi.nlm.nih.gov/pubmed/20709653
Heatstroke
(mice study) Hyperbaric oxygen protected against heatstroke-induced ischemia and neuronal
damage to the hypothalamus and its temperature regulation function.
Helium vapor-induced frostbite

A case report of a patient is presented who suffered frostbite injury on his hand from exposure to
helium vapor. The treatment program included hyperbaric oxygen. At an 8 month follow up, he
demonstrated a good range of hand movement and healing of the injury.
Full article: http://www.ncbi.nlm.nih.gov/pubmed/20514135
Iron Overdose (acute)

(rat study) Iron overdose, that causes free radicals and lipid peroxidation, is one of the leading
causes of injury and death in children. Animals with acute iron toxicity who were given HBOT
showed a significant reduction in death. http://www.ncbi.nlm.nih.gov/pubmed/20374236
Kidney disease
Renal cyst infections
A patient with polycystic kidney disease experienced a severe infection after surgery. A large
abscess had developed. There was no improvement with antibiotics. After 26 HBOT sessions,
the inflammation was gone and has not returned.

Lung Injury (acute)
(rat study) Hyperbaric oxygen inhibited inflammation and improved arterial blood gases and
lung water transport in rat models of acute lung injury.
Pancreatitis (acute)
(rat study) Seven days of HBOT improved immune function, balanced the T lymphocyte profile
and significantly reduced the pathology associated with acute pancreatitis.
(rat study) The combination of HBOT and ulinastatin was more effective in treating acute
necrotizing pancreatitis than either treatment by itself. Full article:
Periodontal disease
Twenty patients with severe generalized chronic periodontitis underwent scaling and root
planning. Ten patients also underwent five HBOT sessions. The combination treatment
program was more effective for up to three months. Five sessions of HBOT has a short-term
benefit in pocket reduction and bacterial elimination in chronic periodontitis.
Post-traumatic stress disorder

HBOT is beneficial in motor vehicle accident with crush injury resulting in pelvic fractures and
severe pain; the patient who had experienced unconsciousness, showed complete cognitive and
psychiatric recovery after seven sessions. Full article:
Systemic lupus erythematosus

Skin ulcers
Skin ulcers can be a complication of vasculitis. A patient with digital ulcer that was resistant to
conventional therapy showed benefit with HBOT.
Snake bite
Beneficial for preventing infection and enhancing healing –
Suggested for venomous snake bite - http://www.ncbi.nlm.nih.gov/pubmed/21226389
Testosterone Levels

Testosterone reduces inflammation and improves healing. 14 male patients and 6 healthy male
volunteers underwent HBOT sessions with pre- and post- evaluation of testosterone levels. Both
patients and controls showed significant increases in blood testosterone after a series of
hyperbaric oxygen sessions. http://www.ncbi.nlm.nih.gov/pubmed/20890859
Urology
Beneficial in necrotizing fasciitis, radiation-induced cystitis and urgency and frequency
syndrome.
Cystitis (non-bacterial)
HBOT is beneficial for cystitis http://www.ncbi.nlm.nih.gov/pubmed/21082515
In 62 patients, the combined treatment of anti-inflammatory therapy and 7-10 HBOT sessions,
there were improvements in microcirculation and long-term remission from interstitial cystitis.
Erectile dysfunction after surgery for urethral stricture

HBOT shows benefit in recovery of erectile function after posterior urethral reconstruction.
Wound healing
Overview
Oxygen promotes blood vessel growth, collagen, renewal of the epithelial lining, kills bacteria
and reduces infections. http://www.ncbi.nlm.nih.gov/pubmed/20216492
Appears effective in acute, difficult to heal wounds, that include crush wounds and burn wounds.
Wound healing and smoking

Chronic smoking undergoing HBOT show slower wound healing due to chronically injured
endothelial cells (composing the blood vessels) from carbon monoxide, hydrogen cyanide and
other smoke toxins rather from transient elevations in nicotine.
For more research on HBOT, go to http://www.ncbi.nlm.nih.gov

and type in hyperbaric oxygen therapy


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David A. Steenblock, D.O.

Hyperbaric Oxygen Research

Dr. David A. Steenblock

Back to the Future!

In 2009, a paper on HBOT from the Department of Neurosurgery, University Hospital of

Where in the world is HBOT now?

Stroke is a brain attack

What are the benefits of HBOT for stroke?

Hyperbaric oxygen provides the following neuroprotective benefits:

3. Improves tissue metabolism

4. Reduces excitotoxic effects.

5. Reduces risk of infection.

6. Reduces oxidative stress.

8. Decreases size of the cerebral infarction

9. Reduces edema (swelling)

10. Reduces intracranial pressure.

11. Reduces breakdown of the blood-brain barrier

12. Reduced programmed cell death (apoptosis).

13. Promotes the development of new blood vessels

14. Promotes peripheral nerve regeneration

16. Promotes bone marrow stem cell mobilization.

17. Promotes axonal growth.

18. Promotes new neurons

19. The sooner the better for Stroke and TBI.

20.. Oxidative Stress can result from higher pressures.

Hyperbaric Oxygen Therapy for Stroke

Stroke after cardiac surgery

Stroke and secondary damage

Integrative medicine program for stroke

Delayed hyperbaric oxygenation compared to normobaric hyperoxia

Neural protection by inhibiting HIF-1a

Time window in stroke for thrombolytic drugs

Acupuncture combined with HBOT

HBOT combined with edaravone in embolic stroke

Improvement in motor and cognitive impairment

A therapeutic window of 3-6 hours

Here things liven up a bit…

David A Steenblock, D.O. 8

Neuroprotection from reducing elevated dopamine levels

Lim’s HBOT case study with haemorrhagic stroke

Dosage for Acute Stroke

Dr. Steenblock’s Treatment Suggestions for Chronic Stroke Patients

Nighoghossian’s HBOT double-blind pilot study.

Anderson’s pilot study of HBOT for acute stroke.

Comment by Dr. Jain:

Brain Imaging to identify hypometabolic areas in the brain

Kaasik’s HBOT study of stroke patients

Neubauer’s study of generalized small-vessel stenosis in the brain

Lebedev’s article on HBOT and ischemic stroke

Neubauer’s Lancet Letter reviewing HBOT benefits

Neubauer’s Case Study of Chronic Stroke (15 years post-stroke onset)

Neubauer’s review of 122 thrombotic stroke patients

Jain’s HBOT study on chronic stroke and spasticity

Isakov’s article on ischemic stroke and respiratory disorders

Holbach’s study of chronic stroke

Hart’s case study of stroke treated successfully with HBOT.

HBOT neuroprotective effects in TBI

TBI treatment using a modified monoplace chamber

Case report of treating mild TBI with hyperbaric oxygen

Severe TBI treated with HBOT or Normobaric hyperoxia

Case Study of blast-induced chronic TBI

HBOT with Subacute TBI

HBOT and spatial learning and memory in chronic TBI