Monday, October 29, 2012

Did you know?? - New Website

We are so excited for the updated RRH Website, online now at
However, please note, it is still under construction and evolving everyday! We hope to have it complete in the next couple of weeks. You may explore the new site or, for a more complete experience, you may also visit our previous site which is still available at

Remember, we are also available on Facebook, Twitter, Blogger and more!
We want to provide you with the best, informative, user-friendly website as possible when you research HBOT for your family, so we are very excited to have this project underway!

Thank you again for your patients.
Rapid Recovery Hyperbarics, LLC

Thursday, September 6, 2012

Winter Specials for HBOT at Rapid Recovery

Monday, September 3, 2012

Brain injury improves with Hyperbaric Oxygen Therapy

Brain injury improves with Hyperbaric Oxygen Therapy

Presented in Seattle at the Undersea and Hyperbaric Medical Society 1998 Annual Scientific Meeting
Patients with long-standing traumatic brain injury show a general improvement of speech, memory and attention after undergoing a series of hyperbaric oxygen therapy treatments. Hyperbaric oxygen therapy is a technique in which patients breathe pure oxygen in a chamber with a higher-than-normal atmospheric pressure. Hyperbaric oxygen therapy is commonly used to treat people suffering from carbon monoxide poisoning or divers with decompression sickness. Initially, five of the 11patients, at least 3 years post-brain injury had 80 sessions in a hyperbaric unit. After a 5-month rest period, those five patients underwent another 40 hyperbaric sessions. The remaining six patients, serving as controls, did not undergo hyperbaric oxygen therapy. There was no change in the blood flow of the six control patients during the study period. However, patients who did receive the Hyperbaric Oxygen Therapy showed increased blood flow in specific areas of the brain, as well as improvements in speech and memory functions. The improvements in these patients peaked at 80 hyperbaric oxygen sessions, and repeating the therapy every one to two weeks maintained improvement.
 The therapy sessions were also used to treat individuals with  Closed head injury, Autism stroke, cerebral palsy, anoxic and hypoxic brain injury, dementia, Alzheimer’s, and near-drowning and chronic carbon monoxide poisoning patients. Those patients were treated a year after the brain injury occurred. The patients had no other treatment options. Patients with the least loss of function following injury showed the greatest improvement with hyperbaric oxygen therapy. According to the researchers, it's not clear why hyperbaric oxygen therapy helped patients. "There is clinical and animal data to suggest that it might help, but the studies are not conclusive," said the president of the Undersea and Hyperbaric Medical Society. It's fertile ground for research.
Printed with Permission

Wednesday, June 27, 2012

HBOT after Blast Brain Injury, Study

Hyperbaric Oxygen Treatment after the Blast Injury of Rabbitbrain the Expression of AQP4 and PWI in the Study Phase

Hyperbaric Oxygen Treatment after the Blast Injury of Rabbit brain the Expression of AQP4 and PWI in the Study Phase
Objective:To establish explosive brain injury model in rabbits;To investigate the expression of aquaporin 4(AQP4) in model of explosive brain of rabbits injury,and perfusion changes in the expression, to explore the formation of brain edema after blast injury mechanism, and early hyperbaric oxygen treatment of traumatic brain edema formation and development of the role of early treatment for clinical hyperbaric oxygen provide the basis for traumatic brain edema.Method:30 New Zealand white rabbits, weighing 2.0 ~ 2.5kg, in accordance with the vertical distance between the detonators and the skull group, were randomly divided into groups 5.0cm, 6.5cm group, 8.0cm group, n = 10. 600mg TNT equivalent of paper detonators were used to explode respectively 5.0cm, 6.5cm, and 8.0cm vertical distance from the top of the rabbit head, observing animal survival after injury, and using magnetic resonance imaging methods to understand the pathology and brain damage in each group.150 New Zealand rabbits were randomly divided into non-treatment group, treatment group and control group, and 10 rabbits were in the latter. Explosive brain injury model was made by paper detonator. Injuryed rabbits were randomly divided into 1h6h12h24h72h7d14d ,14 groups according to a further killed time points after injury, and each group has 10 rabbits. Using dry weight to measure the content water in brain tissue, and using RT-PCR method and image analysis to detect the group at different time points aquaporin 4 (AQP4)mRNA expression, and Western blotting to measure the expression of AQP-4 in brain tissue. Using magnetic resonance perfusion imaging ( PWI) injury time points detected in brain tissue blood perfusion. Finally, it was used for statistical analysis.Results:5 rabbits died immediately after injury and 4 rabbits died within 3 days in group 5.0cm,and only one survived more than 7 days;The rabbit has appeared most extensive brain contusion, cortical surface vessel rupture occurs, and significant fragmentation in brain tissue, large subdural hematoma, and significant brain stem contusion. All rabbits in group 6.5cm survived more than 7 days,except that 1 rabbit died on the 4th day after injury because of inability eating. 4 rabbits occurred epilepsy and got paralysis of limbs; Pathology observed in the survival of the rabbits had cerebral cortex partial rupture of blood vessels, brain edema and obvious laceration and contusion lesions clear boundary with the surrounding brain tissue. All rabbits in group 8.0cm survived, but showed no significant changes in the brain.Blast injury after contusion brain 1h aquaporin 4 (AQP4) mRNA expression increased, and in turn increased, 72h peak (P <0.05), 7d pm down. Brain tissue aquaporin 4 (AQP4) began to express 1h after injury increases, and 72h reached its peak (P <0.05), it turned to down after 7d, but it still maintained on a high level. Brain tissue water content and water aquaporin 4 (AQP4) expression were the same. The correlation analysis, aquaporin 4 (AQP4) expression and brain tissue water content was positively correlated (r=0.8767,P<0.001). The hyperbaric oxygen treatment, aquaporin 4 (AQP4) expression at different time points are different degrees of decline, aquaporin 4 (AQP4) expression of injury group compared with control group at after 6h points were lower (P <0.05 ). Blast injury after contusion brain 1h AQP4 mRNA expression increased, and in turn increased, 72h peak (P <0.05), 7d pm down, but still maintain a high level. After intervention by hyperbaric oxygen, in 6h, AQP4 mRNA expression was significantly lower than the injury to 14d is still significantly lower (P <0.05). Post-traumatic cerebral contusion early peripheral blood perfusion decreased significantly to 6 hours after injury, blood perfusion decreased to the lowest (P <0.05), then gradually increased, and maintain a perfusion (close to the control group) for 2 weeks. The hyperbaric oxygen treatment group than in the early trauma group (1-6 hours after injury) perfusion decreased more significantly. 12 hours after infusion began to rise, and non-treatment group was essentially flat.Conclusion:Detonators and the vertical distance of the skull 6.5cm, can produce good stability, repeatability strong blast injury model of rabbit brain.The expression of post-traumatic brain aquaporin 4 (AQP4) in traumatic brain is closely related to the formation and development of injury and brain edema. Aquaporin 4 (AQP4) expression may be associated with brain ischemia and hypoxia in the Hyperbaric oxygen intervention aquaporin 4 (AQP4) expression was significantly reduced. Instead, the blood perfusion than the control group and non-treatment group decreased significantly, suggesting that brain tissue oxygen levels of early trauma and aquaporin 4 (AQP4) expression is closely related to early hyperbaric oxygen therapy on the relief plays an important role in traumatic brain edema. Early hyperbaric oxygen therapy can improve cerebral blood oxygen contusion, increased blood oxygen content, ease the secondary cerebral hypoxia caused by cerebral edema.

Tuesday, June 5, 2012

The Vitamin D Council: LINK? the autism epidemic and the vitamin D deficiency epidemic

The Vitamin D Council: LINK? the autism epidemic and the vitamin D deficiency epidemic
The Vitamin D Council’s free remote autism program is not only up and running, we now have some outcomes to report. First, as some readers may know, another paper appeared last month that recommended “urgent” research on the association of the autism epidemic with the vitamin D deficiency epidemic.
The senior author in the above review was Christopher Gillberg. I should say thee Christopher Gillberg, as he is famous as a prolific author, editor and the recipient of numerous awards. Dr. Gillberg is especially well known across the world for his autism research. When I saw his name, I knew it was just a matter of time before the entire theory was under the microscope, so to speak.
If you remember, we are offering a free autism program to help parents vigorously correct vitamin D deficiency in their children with autism. As long as the Council can afford it, everything is free for the families: the vitamin D blood tests, the vitamin D, the scales, and the help from me. Just email us at
The entire goal is to raise vitamin D levels from the very low levels that we find initially (5-20 ng/ml, if they’ve never supplemented), to high normal ranges (around 80 ng/ml). The “normal” range for most labs is 30-100 ng/ml, so all the parents are doing is raising their children’s levels to the same levels some lifeguards have at the end of summer. With our help, the parents use a combination of sunlight (when it is available) and supplements to do so.
The most common problem we have run into is parent’s unwillingness to give enough vitamin D to their child to obtain high normal levels. Too often, the child’s pediatrician tells the parents that the dose is too high – in spite of the normal blood levels – and the parents withdraw from the program. We never give advice contrary to the child’s doctor; in fact, we try to work with the doctor when possible.
If you remember, for more than 30 years, most of the infants in East Germany received 600,000 IU every 3 months. Many had a total dose of 3.6 million units by age 18 months, with transitory mild high blood calcium being the only side effect in one-third of the infants. The authors commented on how healthy the infants appeared. While the East German doctors gave way too much vitamin D, it demonstrates that even infants tolerate high doses of vitamin D with few serious side effects. Again, our kids are all older, receive much less vitamin D and are maintained in the normal range.
The second most common problem we have had is vitamin A. Vitamin A interferes with the action of vitamin D, probably at the receptor site. Unfortunately, some autistic children have taken 50,000 or 100,000 IU of vitamin A repeatedly or take cod liver oil. As vitamin A has no known catabolic (breakdown) pathway in the human body, these children may have subclinical vitamin A toxicity and in theory, vitamin D might not help. I try it anyway, but I have seen what I said; it does not help very much. The parents ask how long it takes to get the excess vitamin A out of the system, and I have no answer to their question.
However, in the children who obtain the high normal blood levels and who have not taken vitamin A, the response has been very satisfying. I believe the vitamin D’s mechanisms of action in these autistic children is through a combination of its antioxidant capabilities, glutathione and superoxide dismutase upregulation, increased Tregs (cells that help prevent autoimmunity), increased production of the proteins that repair DNA, and reduction of inflammation via multiple mechanisms. I have sometimes found that levels of 75 ng/ml work in most children while levels around 50 ng/ml do not. I can’t explain that and would welcome some theories why not?
Vitamin D appears to have beneficial effects in autism on meltdowns, tantrums and sleep (one mother, who works outside the home, was so thankful when her child no longer woke at 3 AM, wanting to play). Surprisingly, vitamin D also seems to benefit shyness, eye contact, speech and sometimes, compulsiveness. Several parents have commented on the neuromuscular improvements after vitamin D. Most of our children require around 5,000 IU/day to obtain a 25(OH)D of 80 ng/ml but all are different. We try to use D-Plus as studies show that many autistic children are deficient in magnesium as well as zinc.
Our autism program has been a great success, personally rewarding for all of us here at the Council, and is ongoing. So, if you have a child with autism and want to participate in it, contact us at As long as our money lasts, everything is free.

John J Cannell, MD
Executive Director

Office: (805) 439-1075

Wednesday, May 30, 2012

Parents with Purpose provides unique therapy options for children with disabilities!
 (Previously it had been posted as --- there is no "a").

Contact info is, office # is 214-502-2827

Monday, May 28, 2012

Definition: Hyperbaric Oxygen Therapy
By Mayo Clinic staff
Hyperbaric oxygen therapy involves breathing pure oxygen in a pressurized room. Hyperbaric oxygen therapy is a well-established treatment for decompression sickness, a hazard of scuba diving. Other conditions treated with hyperbaric oxygen therapy include serious infections, bubbles of air in your blood vessels, and wounds that won't heal as a result of diabetes or radiation injury. In a hyperbaric oxygen therapy room, the air pressure is raised up to three times higher than normal air pressure. Under these conditions, your lungs can gather up to three times more oxygen than would be possible breathing pure oxygen at normal air pressure.  
Your blood carries this oxygen throughout your body, stimulating the release of substances called growth factors and stem cells, which promote healing.

Oxygen, Genes, Inflammation and the Treatment of Multiple Sclerosis

Philip B James, MB ChB DIH PhD FFOM
Professor of Hyperbaric Medicine, Wolfson Hyperbaric Medicine Unit, University of Dundee.
A new centre will soon begin operating on the Isle of Mull, twenty three years after the first MS Therapy Centre began operations in an industrial unit in Peddie Street Dundee and it is time to take stock. The number of hyperbaric treatment sessions completed in MS National Therapy Centres will soon reach two million and we have full recognition of our centres by the Department of Health for the treatment of neurological conditions in the community, for example, for those with multiple sclerosis and cerebral pa1sy. Note that the term cerebral palsy is not exclusive to children; adults with a stroke have cerebral palsy. In England and Wales, but thankfully not in Scotland or Ireland, the centres come under the Private and Voluntary Healthcare Regulations. Note that hyperbaric treatment is recognized for use in the NHS by the Department of Health, under Specialist Services Definition Set No. 28, but most doctors are not aware of this and this will continue until hyperbaric medicine is taught in our medical schools.
Remember, the only way to access hyperbaric treatment is to ask for it. Although, of course, oxygen is widely prescribed, it is only at a low dosage and as a supplement, not as a treatment. It is understandable that doctors find it hard to accept that breathing a high level of oxygen for just one hour a week in a hyperbaric chamber can improve the course of a serious disease like multiple sclerosis, but this is set to change, not least because the concept of regular treatment is now firmly established for drugs. For example, the object of prescribing the beta interferons, which are injected either every other day, or once a week, is to reduce the rate of progression and note this is for life at £10,000 per year. Attitudes to oxygen in medicine are set to change because of the latest research which is at the cutting edge of science.
Oxygen in Control
Everyone knows that oxygen is needed to obtain energy from glucose, but the latest research has now shown that oxygen is also involved indirectly regulating our genes. 1 It controls the level of a family of proteins, known by the strange name Hypoxia-inducible Factor proteins, (HIF) which, translated, stands for Lack of Oxygen Inducible Factor. It is a paradox that the level of these proteins rises as oxygen levels fall. When oxygen levels are normal these HIF proteins, which are produced by every cell in the body, are actually destroyed by another protein, but the rate of this destruction is reduced as oxygen levels fall. The HIP proteins regulate the expression of many genes and over 36 have already been identified, including 12 involved in glucose metabolism. Others control the growth of new blood vessels. If the oxygen supply to a tissue reduces, the genes activate a factor to grow new capillaries. Oxygen is therefore the only agent which can act to correct a deficiency in its own level.
Oxygen also controls the behaviour of white blood cells in inflammation and this means that giving more oxygen is an anti inflammatory treatment. This astonishing information has been published in the most eminent scientific journals, but has not been publicized; oxygen is simply not of sufficient interest to warrant headlines and, as it cannot be patented, it will never be promoted. The research provides indisputable support for using high levels of oxygen as a continuing treatment for multiple sclerosis patients and is an immense endorsement of the tireless work of everyone involved in the MS Therapy Centres in the UK and Ireland over the last 23 years. To highlight the importance of these findings to patients with nervous system problems, especially those with multiple sclerosis, it must be put in context.
It has been known for some time that oxygen is involved in controlling blood flow because the effects on the diameter of blood vessels can actually be seen by looking into the eye. When more oxygen is breathed, the diameter of most blood vessels reduces and, conversely, when less oxygen is breathed, for example, by going to altitude, blood vessels enlarge, which increases blood flow. How oxygen achieves this has, until recently, remained a mystery but it is now known that oxygen controls the size of b1ood vesse1s by acting in concert with another gas, nitric oxide (NO) actually produced in the lining of blood vessels. Nitric oxide acts to increase blood vessel diameter by relaxing the muscle in the wall, but when oxygen levels are high, NO binds to oxyhaemoglobin thus neutralizing its effect. 2 Haemoglobin is, of course, the protein iron pigment which by binding oxygen is responsible for the redness of blood. Everyone knows that the brain and to a lesser extent the spinal cord require a large blood supply to meet their demand for oxygen, but many do not know that they contain some areas where the blood supply is relatively poor and these are the areas where the damage typical of multiple sclerosis is found.3
It comes as a surprise to many people that blood itself is toxic and must be kept within blood vessels, especially in the nervous system, so that the sensitive cells can be protected from many substances easily tolerated by other organs of the body. Five methods of brain imaging have confirmed beyond question that the disease causing multiple sclerosis or indeed single areas of sclerosis, mono sclerosis 4(both MS) is the result of internal damage to blood vessels 5 which means that the barrier protecting the brain, known as the blood-brain barrier fails.6 The leakage caused precedes the development of symptoms 7 and the effects can often be seen in the eye, as they may also affect the blood vessels of the retina where there is no myelin. 8 As there is an excellent blood supply to the retina and no myelin is present, little damage is caused.
Blood vessels, Inflammation and Current Theories in Multiple Sclerosis
The blood vessel changes in MS were first described by Rindfleisch in Zurich over a hundred and forty years ago 9 but, despite this, they are rarely mentioned in current textbooks and it is still fashionable to invoke a form of self destruction - auto immunity - to account for the disease. It is often suggested that this is in some way linked to a virus, but this has never actually been explained. Despite this and the billions spent on the research, much of it supported by the drug companies, there is actually no evidence that the activity of the immune system is actually causing harm. Studies of stroke patients have shown that they have just the same immune changes, even at the same levels, as MS patients. 10 As stroke patients tend to improve, this indicates that the immune changes are actually involved in recovery, that is repairing the damage; clearly a very necessary activity. The theory of auto immunity came from research into allergy before the Second World War and allergy involves inflammation. Inflammation is usually associated with infection, but MS is certainly not infectious and no virus has ever been found, despite some patients even being subjected to brain biopsy during attacks. However, in view of the proven loss of the protection afforded by the blood-brain barrier in the damaged areas of MS, it should be expected that blood-borne viruses will cause attacks in patients with established disease. Every MS patient should be told that relapses can be provoked simply by an excessively hot bath, because heat enlarges blood vessels, including those in the brain, causing blood leakage. 11 If this leakage goes unchecked then eventually scars, which are the lowest common denominator of healing in any tissue, begin to develop. As scars represent healing, looking for a cure in MS is looking for a cure for healing.
The Barrier Protecting the Brain -
It may come as a surprise to many to learn that blood - so necessary for life - is toxic. The substances carried in our blood are changing all the time. For example, after a meal the amount of carbohydrate, protein and fat rises. The brain needs to have stable conditions to work properly and the contents of the fluid which surrounds the brain are very tightly controlled. The blood-brain barrier regulates the passage of substances into the brain, so we can think clearly all the time, although it is common to feel sleepy after a large meal! When leakage from damaged blood vessels occurs in an area of the brain or spinal cord containing myelinated nerve fibres there may be damage, either to individual sheaths, or to the parent cell which forms the sheaths, the oligodendrocyte. Note that myelin sheaths do not insulate nerve fibres; they increase the speed at which they transmit nerve impulses - often several hundred times. A single oligodendrocyte may form over 30 myelin segments and so loss of these cells results in significant loss of myelin. In a typical area in MS there is only relative preservation of the nerve fibres and in the spinal cord about 20% of the fibres may be lost in affected areas.12 Neurons may also be destroyed and it these two factors, rather than the loss of myelin, that are responsible for disability.
Magnetic Resonance Imaging- (M.R.I.) has shown that silent areas characteristic of those found in patients with multiple sclerosis are very common affecting at least 1 in 4 apparently normal people 13 and this is just a snapshot in time. It is likely that we all have small areas of damage from time to time, but without any symptoms and these areas heal naturally without any treatment, as long as there is sufficient oxygen available to the tissues. This natural healing has been shown in patients already labelled as MS who have been followed by M.R.I. over a six month period. The researchers injected a dye which transfers into the brain when the blood-brain barrier leaks. It was shown that new areas may form when other areas disappear. It therefore makes sense to help this healing naturally - by giving more oxygen on a regular basis and this is the reasoning behind the use of the interferons, which try to mimic the natural interferons produced by the body. It is likely that those people who develop symptoms have damage in certain critical areas where recovery is restricted by a poor blood supply. Recovery from nervous system damage, that is remission in MS, is now known to include new capillary formation and also stem cells from the bone marrow, which can form new nerves cells: bone marrow can make brain. 14 Fibres and myelin sheaths may also regrow but, of course, all of this requires oxygen.
Multiple Sclerosis, Inflammation and Oxygen
Although most attention has been given to the scarring process, it is universally accepted that the hallmark of MS is inflammation and it is associated with the activation of white blood cells with disruption of the blood-brain barrier. 'The behaviour of white blood cells has been a target for drugs designed to stop them sticking and migrating into the tissues. Unfortunately this approach has proved to be a poisoned chalice. Tysabri, produced by Biogen, which reduces white blood cell stickiness has just been withdrawn. 15 The drug had been fast tracked by the FDA and allowed to be marketed after one year instead of two, but now two patients have, predictably, developed fulminating infections of the brain. Ironically, oxygen actually controls white blood cell stickiness, again confirming the importance of hyperbaric oxygen treatment. Human studies have shown that inflammation may result in a profound lack of oxygen 16 because of the invasion of tissue by white blood cells when the water content of the tissue is increasing; simply, it is becoming swollen. The latest research has shown that as oxygen levels fall, the HIP proteins control inflammation by activating the genes which increase the permeability of blood vessels, white blood cell stickiness and their migration into the tissues, This is the normal response of the body to infection, but,
unfortunately, is inappropriately activated when there is lack of oxygen from any cause even an ascent to altitude! It is reasonable to question if lack of oxygen, that is hypoxia, has been found in MS patients. It has; a development of M.R.I. Magnetic Resonance Spectroscopy, has detected presence of lactic acid in acutely inflamed areas in MS patients. 17 Lactic acid, which is responsible fur the burning sensation in muscles on exercise, indicates lack of oxygen.
Hyperbaric Medicine: Oxygen as a Treatment
Lack of oxygen in a tissue can only be corrected by delivering more oxygen to the affected tissue. Unfortunately we cannot get more oxygen by breathing faster and so we need to breathe a higher concentration and this may need an increase in pressure; that is hyperbaric conditions. It is possible, however, that if pure (100%) oxygen was given as an emergency treatment for acute attacks it may be a successful treatment at normal atmospheric pressure. This given urgently, may prevent the tissue destruction which eventually leads to scar formation. In patients with established sclerosis, serial studies over several months using M.R.I. have shown that the blood vessel damage may become chronic and regular oxygen treatment by limiting inflammation may reduce the progression of the disease. The evidence from the MS National Therapy Centres, which have now been operating in the UK for 23 years, 18 based on Class 1 evidence from an excellent controlled trial 19 fully supports this contention. Those doctors who say there is no scientific evidence supporting the use of oxygen treatment for patients with multiple sclerosis need to be told the facts and just how important hyperbaric oxygen treatment is to the continued well being of multiple sclerosis treatment. Most of all we need to make every MS patient aware of our superb centres - we need the oxygen of publicity!
1. Nathan C Oxygen and the inflammatory cell. Nature 2003;422:675-676.
2. Stamler JS, Jia L, Eu JP, McMahon TJ, Demchenko IT, Bonaventura J, Gemert K, Piantooosi CA. Biood flow regulation by S-nitrosohemoglobin in the physiological oxygen gradient. Science 1997;276:2034-2037. .
3. Brownell B, Hughes JT. The distribution of plaques in the cerebrum in multiple sclerosis. J Neural Neurosurg Psychiatry 1962;25:315-320.
4. James PB. MRI mono sclerosis and multiple sclerosis. Lancet 2001 ;357:2052-53.
5. James PB. Multiple sclerosis or blood-brain barrier disease. Lancet 1989:i:46.
6. Compston A. Limiting and repairing the damage in multiple sclerosis. J Neural Neurasurg Psychiatry 1991 ;54:945-948.
7. Kermode AG, Thompson AJ, Tofts P, et al. Breakdo\VI1 of the blood-brain barrier precedes symptoms and other MR.I signs of new lesions in multiple sclerosis. Brain 1990;115:1477-89.
8. McDonald 1. The pathogenesis of optic neuritis. In; Hess RL, Plant M eds. Optic Neuritis. 1985.
9. Rindfleisch E. Histologisches detail zu der grauen degeneration von gehim und ruckenmark.
Arch Pathol Anat Physiol KlinMed 1863;26:474-483.
10. Wang WZ, Olsson T, Kostulas V, et al. Myelin antigen reactive T cells in cerebrovascular diseases. ClinExp ImmunoI1992;88:157-162.
11. Berger JR, Sheremata W A Persistent neurological deficit precipitated by hot bath test in multiple sclerosis. J AMA-r9K3; 249-:f75T=-5-3.
12. Putnam TJ, Alexander L. Loss of axis-cylinders in sclerotic plaques and similar lesions. Arch Neural Psychiatry 1947;57:661-672.
13. RinckPA, Svihus R, De Francisco P. J\1R imaging of the central nervous system in divers. J Mag Res Imaging 1991;1 :293-299.
14. Cogle CR,Yachnis AT, Laywell ED, Zander DS, et al. Bone marrow transdifferentiation in brain after transplantation. Lancet 2004;363:1432-1437.
15. Biotech companies pull MS drug Tysabri off market. Financial Times, Tuesday March 1st 2005.
16. Abbot NC, Beck JS, Camochan FMT, et al. Effect of hyperoxia at 1 and 2 ATA on hypoxia and hypercapnia in human skin during experimental inflammation. J Appl Physio11994;77:767773.
17. Miller DH, Austin SJ, Connelly A, et al. Proton magnetic resonance spectroscopy of an acute and chronic lesion in multiple sclerosis. Lancet 1991;1: 58-59.
18. Perrins DID, James PB. The treatment of multiple sclerosis with prolonged courses of hyperbaric oxygenation. Proceedings of the 1st European Consensus Conference on Hyperbaric Medicine, Lille 1998; 245-263. .
19. Fischer BH, Marks M, Reich T. Hyperbaric-oxygen treatment of multiple sclerosis: a randomized, placebo-controlled, double-blind study. N Engl J Med 1983;308:181-186.

News Story- 24 yr old Aimee Copeland's battle with Flesh-eating bacteria, HBOT helping!

Aimee Copeland shows improvement in palms after time in hyperbaric chamber, father says

(CBS/AP) Aimee Copeland looked at her hands ravaged by a flesh-eating bacterial infection and asked her father about the damage without tears, Andy Copeland said Wednesday.
"Her fingers are basically mummified. The flesh is dead," Andy said in a phone interview from Doctors Hospital in Augusta more than two weeks after a zip-lining accident left a gash in his daughter's leg that developed into the infection, necrotizing fasciitis.
What Aimee Copeland still doesn't know is that doctors plan to amputate her all of her fingers, just as they had to remove most of her left leg in order to save her life.
Copeland's father said she held one of her hands close to her face Wednesday and asked family members about it. He said they told her "your hands have been damaged...and we're trying to bring back as much of the life into the hands as possible."
"She was well accepting," Andy said. "No tears or anything."
The 24-year-old student from an Atlanta suburb remains in critical condition as she battles the infection. Doctors initially feared they might have to remove her remaining foot and both hands. But her father said she now faces losing only her fingers after two days of treatment using a hyperbaric chamber, in which patients breathe pure oxygen to boost white blood cells and accelerate healing. Flesh on her palms that had been purple was turning pink again, he said.
Andy Copeland said she was still unaware of plans to amputate her fingers, an emotional disclosure that will likely require a counselor's help.
"We don't know if she's aware of her (amputated) leg yet," he said. "We're in a don't ask, don't tell policy."
The flesh-eating bacteria, Aeromonas hydrophila, emit toxins that cut off blood flow to parts of the body, destryoing muscle, fat and skin tissue. The bacteria is found in warm and brackish waters.
Copeland contracted the infection days after she suffered the deep cut May 1 when the zip line snapped over rocks in the Little Tallapoosa River near the University of West Georgia, where she studies psychology.
Many people exposed to Aeromonas hydrophila won't get sick. When illnesses do occur, it's often diarrhea from swallowing bacteria in the water. Flesh-eating Aeromonas cases are so rare that only a handful of infections have been reported in medical journals in recent decades.
In addition to the damage to her extremities, Copeland is on a respirator and a dialysis machine as her lungs and kidneys recover. Doctors also had to remove much of the skin from her torso to keep the infection from spreading, her father said.
Though still heavily medicated, Copeland has become more alert and communicates with her parents and older sister despite the breathing tube in her throat. Her father said Wednesday doctors were removing that tube and inserting another directly into her trachea to make her more comfortable.
"If they take the tube out, I believe reading her lips is going to be a lot easier," he said. "And she might be able to actually cover the tube up and be able to talk."
Andy praised the doctors and nurses working with Aimee in a personal blog he's been updating on the University of West Georgia psychology department's student website.
"We have an amazing assortment of brilliant minds focusing on Aimee," he wrote in a post Tuesday evening.
Andy Copeland said his daughter has been asking for her cell phone, her laptop and a book to read, but is still in no condition to use any of those things. He said her sister, Paige, has been reading to her from a book on meditation.
An update on Thursday afternoon on the official website on the student blog that has been updating Aimee's condition says she continues to be in good spirits. It also states that two major medical developments happened that Andy Copeland will announce later today.
Also on Thursday, reports surfaced that a South Carolina woman living several hundred miles away, 36-year-old Lana Kuykendall, had been infected with necrotizing fasciitis following the birth of twins, HealthPop reported.
Dr. Jerry Gibson, an epidemiologist with the South Carolina Department of Health and Environmental Control, told Reuters on Thursday of recently reported cases of necrotizing fasciitis, "These cases don't cluster together except randomly."

Friday, May 25, 2012

The Buzz on Bees

Scientists may have solved the mystery of the honeybee disappearance
JANUARY 20, 2012
For several years, honeybees across the U.S. have been dying at high rates. The bees are flying away from their hives and never returning. Concerned scientists have been trying to figure out what is wrong. They thought a combination of problems might be causing entire beehives, or colonies, to disappear. They called it "colony collapse disorder." Now, researchers at San Francisco State University have found a new possible cause for the disorder: a parasitic fly.
"The parasite could be another stressor, enough to push the bee over a tipping point. Or it could play a primary role in causing the disease," says researcher John Hafernik.
The fly latches onto a honeybee, depositing eggs into the bee's abdomen. The eggs hatch into worms, which grow inside the bee. The bee begins to act strangely. It leaves the hive, flying in circles or blindly toward light. The bee soon dies.
Since 2006, 30% of colonies have been lost to colony collapse disorder. That is a problem for people as well as for bees. Bees are hardworking insects. They help us grow the food we eat. They fly from flower to flower, pollinating about a third of the U.S. food supply. Scientists are continuing to look for ways to help honeybees bounce back.
To access the digital edition of TIME For Kids, go to

Tuesday, May 15, 2012

Multiple Sclerosis and Hyperbaric Oxygen Therapy

Multiple Sclerosis and Hyperbaric Oxygen Therapy

HBOT is the only known treatment that alters the course of Multiple Sclerosis. Multiple sclerosis is the most common demyelinating disease of the central nervous system. It affects approximately half a million people in the United States today and about 2.5 million worldwide. Other physical manifestations noted are axon destruction, inflammation of the meninges (membranes that cover and protect the brain and spinal cord), peripheral nerve damage, changes in the retina, blood vessel changes outside areas of plaque formation, and rather curious pinpoint-sized red dots on the skin called skin petechiae, caused by the leakage from capillaries below the skin.
The lining of the bloods vessels where capillaries rejoin the veins is the weakest contact in the vascular system. Blood vessel permeability increases with increased capillary pressure, allowing migration of fluid (extravasation) and white blood cells (diapedesis) across the lining of the blood vessels (endothelium) into the surrounding tissues. These physical occurrences happen in response to inflammation and exposure to toxic substances. Endothelial cell receptors respond to inflammatory stimuli by increasing postcapillary venule permeability—inflammation makes the veins "leaky." Some medical researchers believe this vascular weakness may be the cause of multiple sclerosis.
Over the past twenty years, extensive international medical research has established hyperbaric oxygen therapy as part of an effective multiple sclerosis treatment program. In some European countries, it is not only the primary treatment, but also covered by insurance. For the past 30 years, an England charity has provided more than 1.5 million HBO treatments for MS in 100 MS dedicated centers.
In the United States, HBOT has a controversial history. Many reports have "proven" over and over again it is not effective. Today, it is not considered mainstream treatment, not covered by insurance, and often difficult to access. However, the discrepancy between how the U.S. perceives HBOT in the treatment of multiple sclerosis and how widely it is used in other countries is worth closer examination.
Research indicates the effectiveness of hyperbaric oxygen treatment depends on the total number of treatments, duration and pressure administered, the type of chambers, patients and type of MS treated, how the results are evaluated, and the use of booster/follow-up treatments. Controlled studies following patients who continue with HBOT show that initial improvements of MS can be maintained by regular treatment and in some cases the disease can be reversed.
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Monday, May 14, 2012

Hyperbaric Oxygen Therapy: Can It Turn Back the Clock?

Nobody enjoys the little signs of aging we see when looking in the mirror each morning. We spend billions of dollars a year on products and surgeries to help us look and feel younger: hair re-growth products, dyes to hide the grey, anti-wrinkle face and eye creams, cosmetic injections, surgeries and more.
In today’s modern medicine, there is a therapy that is proven to offer anti-aging benefits through healing or regrowth of damaged cells: hyperbaric oxygen therapy (HBOT). In HBOT, patients breathe 100% pure oxygen while the pressure of the treatment chamber is slowly increased. Pressurized oxygen is delivered into the chamber, which increases the pressure of oxygen within a person’s body as much as 15 times normal tissue saturation. Each cell is literally saturated with 100% pure oxygen, accelerating the body’s natural healing processes.
Oxygen therapy can help to jump start the body’s antioxidant defenses, boost metabolism, and counteract low oxygen levels that lead to sluggish cell activity and oxidative stress. Research has shown that it can also help to improve the efficiency of hemoglobin in transporting oxygen around the body; improve blood flow by helping to keep cell membranes flexible; suppress inflammation; and detoxify and fight infection by destroying bacteria, viruses, parasites and fungi that thrive in low-oxygen environments.
HBOT is also commonly used in treating many age-related diseases and conditions such as stroke, rheumatoid Arthritis and cancer treatment recovery. We also treat Hypoxic brain injury, CP, Lyme disease, and austism, just to name a few.
In addition to its often lifesaving work in the medical industry, HBOT is gaining widespread recognition for its success in treating a breadth of cosmetic concerns. Regular treatment is widely thought to increase aging skin elasticity and to stimulate collagen production which, over time, can improve skin texture and reduce the appearance of fine lines, wrinkles, and scars. Plastic surgeons often prescribe the therapy to enhance recovery from reconstructive surgery.
Scientists have found that the chromosomes in our cells progressively shorten each time the cell divides. Eventually, the chromosomes can shorten no further and stop dividing. When this happens, the cells become senescent (sleepy) and die. In premature aging, the lifespan is shortened due to the effects of various stressors to the human body. The
most obvious, and often the most common, are alcohol, tobacco, and drugs. These substances have a tremendous aging effect on the human body and can cause progressive ‘wounding.’
In his book, The Oxygen Revolution, Dr. Paul G. Harch expresses that hyperbaric oxygen therapy will “likely become most appreciated by those Baby Boomers whose life spans have been compromised by years of drug experimentation in the 1960s and 1970s.” Wounds in the brain register as areas of low blood flow and low oxygenation, which cause decreased neurological function. Most commonly, this decreased neurological function leads to the premature aging diagnosis we call dementia.
Dr. Harch calls HBOT a “generic drug for repair of brain wounds.” The stereotypic chronic brain wound typically responds well to low pressures of hyperbaric oxygen treatments. What Drs. Neubauer, Harch, and others have shown in the past 30 years is that these premature aging wounds can be repaired for improvement neurologically, cognitively, behaviorally, and emotionally.
Repairing these chronic wounds is considered by many to be a reversal of premature aging by use of HBOT, aiding in prolonging longevity and an enhanced quality of life.
Considering that it delivers a natural substance which helps our body repair itself and has many significant medical benefits, including mending our DNA, it is easy to see why a growing population is utilizing hyperbaric oxygen as an anti-aging therapy.
For more information on hyperbaric oxygen therapy for anti-aging and other conditions,
Sources: 1) The Oxygen Revolution. Hyperbaric Oxygen Therapy: The Groundbreaking New Treatment. Paul G. Harch, MD. 2007. 2); 3)

STUDY: Hyperbaric Oxygen Therapy helped prevent or slow the progression of type 1 diabetes in mice

By Serena Gordon
HealthDay Reporter

FRIDAY, May 11 (HealthDay News) -- Treatment with hyperbaric oxygen therapy helped prevent or slow the progression of type 1 diabetes in mice, according to new research. It is too early to say if the results might apply to humans, however.
In mice, the treatment caused changes in the immune system's response to newly developing diabetes, and reduced the risk of diabetes between 20 and 40 percent. In the mice that still developed diabetes, the hyperbaric therapy delayed disease progression, the investigators found.
"Hyperbaric oxygen therapy is a relatively non-harmful way of enhancing oxygen delivery to the tissues," said the study's senior author, Dr. Antonello Pileggi, director of the preclinical cell processing and translational models program at the Diabetes Research Institute of the University of Miami Miller School of Medicine.
"We were able to suppress the transfer of the disease (in mice) before the onset of the disease. After diabetes had occurred, the efficacy [of hyperbaric therapy] was much less," said Pileggi. He said that combining hyperbaric therapy with medications might enhance the effectiveness of both treatments.
Results of this study, released online May 7, will be published in the July print issue of Diabetes.
In type 1 diabetes, the immune system mistakenly attacks healthy cells in the pancreas called beta cells. Beta cells produce the hormone insulin that allows your body to metabolize carbohydrates from food, providing fuel for energy. People with type 1 diabetes must replace the lost insulin through multiple daily injections or a pump.
Hyperbaric oxygen therapy -- commonly used to treat scuba divers who develop "the bends" from rising to the surface too quickly -- is delivered in a special pressurized chamber. The pressure inside the chamber is about two and half times greater than the normal pressure in the atmosphere, according to the U.S. National Library of Medicine. This puts more oxygen in your blood. Hyperbaric therapy can also be used to treat bone infections, burns, carbon monoxide poisoning, and wounds that aren't healing well, such as ulcers in people with diabetes. Currently, not very many hospitals offer hyperbaric oxygen therapy.
For the current research, Pileggi and his colleagues used two types of mice. One type develops diabetes spontaneously. It's not exactly the same as type 1 diabetes in humans, but it is very similar, and Pileggi said "it's a good surrogate of type 1." And, the second type doesn't develop diabetes on its own, but the researchers induced diabetes.
In the mice that spontaneously develop diabetes that received hyperbaric therapy, the risk of developing diabetes was reduced by 20 percent. In the mice with induced diabetes, the treatment reduced the risk of diabetes by 40 percent, according to the study. In the mice that still developed diabetes in both groups, treatment with hyperbaric therapy helped delay the onset or progression of the disease.
Pileggi said that the researchers aren't yet clear exactly how hyperbaric therapy prevents or slows the disease, but it's clear the therapy has positive effects on the immune system.
The researchers were also pleasantly surprised to see that the therapy caused a significant increase in creation of new beta cells. "If you can reeducate immune cells and enhance the beta cell mass, that's an ideal situation. But, it's not a silver bullet for diabetes. It could be an adjuvant to other therapies," said Pileggi.
Pileggi said the researchers will test combination treatments but added that it's too soon to guess when such a treatment might be tried in humans.
Another expert said any application to humans is years away.
"This is a novel idea from a good research group. But, while the mouse model is good to study, it doesn't mean that what is affected in mice will be affected in men," said Dr. Joel Zonszein, director of the clinical diabetes center at Montefiore Medical Center in New York City.
Also, it would be difficult to choose who would receive such a therapy, he said, because there isn't a reliable test to determine who will develop type 1 diabetes. There are tests for the antibodies present in type 1, but some people who never develop diabetes have those same antibodies.

Saturday, April 14, 2012

Health, Wellness & Safety Fair TODAY!

Come visit Rapid Recovery Hyperbarics at the 2012 Abundant Living Family Church Health, Wellness & Safety Fair, TODAY- Saturday April 14, 2012
10:00 AM- 1:00 PM!
Abundant Living Family Church
10900 Civic Center Dr.
, Rancho Cucamonga, CA, 91730

Ask questions, get answers and information about this amazing therapy!

Thursday, March 29, 2012


Audrey is 7 and loves Speak Smooth.She gladly takes it, and even requests it!If you want something that is totally kid friendly and you've tried everything to add oils to your child's diet, Speak Smooth from Speech Nutrients is a must have!
Say you saw it on the RRH blog!

Friday, March 16, 2012

HBOT & Blast-induced Traumatic Brain Injury and PTSD, military

Journal List > Cases J > v.2; 2009 Formats: Abstract | Full Text | PDF (360K)
Cases J. 2009; 2: 6538. Published online 2009 June 9. doi: 10.1186/1757-1626-0002-0000006538 PMCID: PMC2740054 Copyright ©2009 licensee BioMed Central Ltd.

Low pressure hyperbaric oxygen therapy and SPECT brain imaging in the treatment of blast-induced chronic traumatic brain injury (post-concussion syndrome) and post traumatic stress disorder: a case report Paul G Harch,1 Edward F Fogarty,2 Paul K Staab,1 and Keith Van Meter1 1Section of Emergency Medicine, Department of Medicine, Louisiana State University Health Sciences Center, 2021 Perdido St, Room W535, New Orleans, Louisiana, 70112, USA 2Department of Radiology, University of North Dakota School of Medicine and Health Sciences, Post Office Box 1975, 515 ½ East Broadway Avenue, Suite 106, Bismarck, North Dakota, 58502, USA Corresponding author. Paul G Harch:; Edward F Fogarty:; Paul K; Keith Van Meter: Received March 12, 2009; Accepted April 4, 2009. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. This article has been cited by other articles in PMC. Other Sections▼

Abstract A 25-year-old male military veteran presented with diagnoses of post concussion syndrome and post traumatic stress disorder three years after loss of consciousness from an explosion in combat. The patient underwent single photon emission computed tomography brain blood flow imaging before and after a block of thirty-nine 1.5 atmospheres absolute hyperbaric oxygen treatments. The patient experienced a permanent marked improvement in his post-concussive symptoms, physical exam findings, and brain blood flow. In addition, he experienced a complete resolution of post-traumatic stress disorder symptoms. After treatment he became and has remained employed for eight consecutive months. This case suggests a novel treatment for the combined diagnoses of blast-induced post-concussion syndrome and post-traumatic stress disorder.

Other Sections▼ Introduction By January, 2008 it was estimated that as many as 300,000 servicemen and women from the current Iraq and Afghanistan Wars have PTSD or major depression, 320,000 have experienced a TBI, and 82,000 have all three diagnoses [1]. Treatment is available for PTSD and depression, but there is no proven therapy for the dual diagnoses of PTSD and the residual effects of TBI, the PCS [2]. HBOT is the use of greater than atmospheric pressure oxygen in an enclosed chamber to treat basic disease processes [3]. HBOT has been traditionally applied to certain emergent conditions and chronic wound conditions, but not to blast-induced TBI/PCS or PTSD. This case report is the first application of the authors' low pressure HBOT protocol for chronic brain injury to blast-induced TBI/PCS and PTSD. An early version of this protocol was recently reported in an animal model of chronic TBI that duplicated the human experience [4].

Other Sections▼ Case presentation A 25-year-old retired Caucasian male U.S. Marine presented with headaches, tinnitus, and sleep disturbance. Three years before evaluation the patient sustained LOC (a few minutes) from an IED explosion with anterograde memory loss and confusion (one hour), and persistent right ear tinnitus, headaches, imbalance, and sleep disturbance. He developed PTSD symptoms within 3 months and experienced six more explosions with near LOC within 15 months. After medical evaluation diagnoses were TBI/PCS, PTSD, depression, hearing loss, and tinnitus. Prioritized Symptom List: 1) Constant headaches with intermittent confusion, irritability, tunnel vision, and dizziness, 2) Bilateral tinnitus, 3) Sleep disruption, 4) Left eye blurred vision, 5) Irritability, 6) Depression, social withdrawal; Additional Symptoms: 7) Fatigue, 8) Decreased hearing, 9) Imbalance, 10) Cognitive problems-memory, attention, decreased speed of thinking, 11) Back pain, 12) Bilateral knee pain, 13) PTSD symptoms: intrusive thoughts, combat thoughts, nightmares, tachycardia.
Med-Surg, Medications: None. FH, ROS, and PHIS: non-contributory or negative.PSH: Engaged, no children, lives with parents, 3 years college education, no tobacco or drugs, one to two beers/week. Neuro PEx Abnormalities: Slight deviation of right eye laterally, bilateral: decreased hearing to softly rubbing fingers at one foot, noxious response to 512 Hz tuning fork, decreased finger tapping speed, unstable: rotation exam, tandem gait, and Romberg. Treatment and testing: MRI brain-normal. SPECT brain imaging pre-HBOT and 72 h after the 39th HBOT.

The patient underwent 39 HBOT's in 26 calendar days at 1.5 ATA/60 minutes total dive time, twice/day, five days/week in a monoplace chamber with 100% oxygen. Outcome: Headache permanently gone after the 1st HBOT. After 12 HBOT's symptoms 3, 6, and 7 improved. At 25th HBOT absence of PTSD symptoms. Re-evaluation after 37 HBOT's: 1) 4/6 primary problems improved (#'s 1, 3, 5, 6), 2/6 no change, 2) 4/7 additional symptoms improved (7, 9, 10, 13), 3/7 no change, 3) 6/6 abnormal exam findings retested improved, 1 finding not retested (right eye deviation). SPECT: heterogeneous with bilateral frontal and temporal defects-all improved post HBOT. (See Additional file 1, Figures Figures11 and and2.2. (Figure (Figure1):1): Pre-HBOT SPECT brain scan three dimensional surface reconstruction and processed transverse images. Pre-HBOT scan was rendered in three dimensional surface reconstruction format by PJT based on the method developed and taught by Picker International using Picker software. In this method brain blood flow is computer indexed to frontal lobe blood flow. A frontal lobe surface defect was identified on a selected transverse slice. Processed/filtered transverse slices were then featured with a 100% window such that all pixels render a white image. Counts were slowly subtracted by decreasing the window threshold until the defect was visible as a full thickness black defect in the contour of the cortex. As the defect emerged and was registered in proper anatomic proportion to the rest of frontal cortical blood flow the numerical window level was taken as the determination threshold. Three separate determinations were made for each scan and the final threshold taken as an average of the three determinations. The technologist was blind to the final image reconstruction due to software restrictions that only allow threshold determination. The surface reconstruction image at this threshold is featured in the image above. Color is aesthetic. Note bilateral orbital frontal and temporal lobe defects, areas typically injured in traumatic brain injury, consistent with processed transverse images in the right hand columns. Processed images also show an abnormal diffuse heterogeneous pattern of
blood flow. Description of processing is in (SD1). (Figure (Figure2):2):

Post-HBOT SPECT brain scan three dimensional surface reconstruction and processed transverse images. Three dimensional surface image was prepared in identical fashion to the image in Figure Figure1.1. Note relative improvement in brain blood flow to bilateral focal frontal and temporal defects, consistent with processed transverse images in the right hand columns. Transverse slices also show normalization of the blood flow to a more homogeneous pattern.
Figure 1 Pre-HBOT SPECT brain scan three dimensional surface reconstruction and processed transverse images. Note bilateral orbital frontal and temporal lobe defects and diffuse heterogeneous pattern of blood flow.
Figure 2 Post-HBOT SPECT brain scan three dimensional surface reconstruction and processed transverse images. Note relative improvement in brain blood flow to bilateral focal frontal and temporal defects and overall normalization of blood flow to a more homogeneous (more ...) Discussion The present case is the first application of the author's HBOT protocol to blast-induced TBI/PCS and PTSD. The patient's symptomatic, physical exam, and SPECT improvements are similar to ours [3,5,6,9] and others' [7,8] previous cases/case series of non-blast TBI suggesting common pathophysiology. The unexpected result was the complete resolution of PTSD. With the overlap of symptoms, pathophysiology, and anatomy in TBI/PCS and PTSD [10] HBOT is likely impacting common shared targets in this case. Conclusion Thirty-nine low pressure HBOT's caused a reduction in symptoms and signs of chronic mild-moderate blast-induced TBI/PCS and PTSD.
The resolution of symptoms and signs of TBI/PCS and PTSD were reflected in global and focal improvements in brain blood flow imaging, suggesting a novel treatment for these combined diagnoses. Patient's perspective Patient has declined to submit his perspective due to privacy concerns.
List of abbreviations ATA: Atmospheres absolute; ECD: Ethyl cysteinate dimer; FH: Family history; HBOT: Hyperbaric oxygen therapy; HPI: History of present illness; IED: Improvised explosive device; LOC: Loss of consciousness; MRI: Magnetic resonance imaging; PCS: Post-concussion syndrome; PEx: Physical exam; PHIS: Prior head injury history; PMH: Past medical history; PSH: Personal and Social history; PTSD: post-traumatic stress disorder; ROS: Review of systems; SPECT: Single photon emission computed tomography; TBI: Traumatic brain injury. Consent Written informed consent was obtained from the patient for publication of this case report and accompanying images. A copy of the written consent is available for review by the Editor-in-Chief of this journal. In addition, this case was approved by the LSU School of Medicine's Institutional Review Board as a case report. Competing interests The authors declare competing interests. The primary author has a small corporation, Harch Hyperbarics, Inc. that does hyperbaric consulting. Author KVM has a corporation that leases hyperbaric oxygen chambers and a corporation that contracts to provide hyperbaric oxygen and woundcare services. None of the authors have personal or financial relationships with people or organizations that would influence the interpretation of data in this report. Authors' contributions PGH evaluated the patient, ordered the treatment and imaging, and wrote the draft of the manuscript. EFF analyzed and presented the SPECT imaging and assisted in writing the manuscript. PKS assisted in the treatment of the patient and assisted in writing the manuscript. KVM assisted in development of the hyperbaric protocol and writing the manuscript. All authors read and approved the final manuscript. Other Sections▼ Supplementary Material
Additional file 1 Side by side Pre and Post HBOT processed transverse SPECT brain blood flow images. Pre-HBOT scan is on the left and post-HBOT on the right. Click on either image to initialize movie. Images were obtained on a Picker Prism 3000 triple-head gamma camera. Both scans were processed by technologist PJT: 25 mCi of ECD was prepared with the standard manufacturer's kit and injected in a peripheral vein in a low noise low light area while the patient was quiet and motionless. One hour after injection acquisition proceeded with a 360 degree rotation and 40 stops, 20 seconds/stop on a 128 x 128 matrix, using low energy high resolution fan beam collimators. Motion correction was used for minor movement. Raw data was processed by transverse reconstruction using 360 degree filtered back projection and a ramp filter, followed by a LoPass filter, order 2.2. Cutoff was taken at the intersection of the best fit LoPass filter and noise on the power spectrum graph. Per file attenuation correction and best fit ellipse were applied. Images were oblique reformatted with slice thickness at 4 mm (2 pixels), aligned, and off-center zoom applied (20 cm2 area). Images were presented in all 3 orthogonal planes. Transverse processed images were analyzed with Osirix Open-source software (version 3.3.2) and windowed at a level of 1000 with a window width of 2000. They were subsequently rendered in QuickTime movie format starting from vertex and proceeding through the base of the brain. Images are in standard SPECT format and orientation. Color map is red, yellow, green, blue, and violet from highest brain blood flow to lowest. Note the marked generalized increase in perfusion on the post-HBOT scan Click here for file(3.2M, mov) Acknowledgements The authors are indebted to nuclear technologist Philip J. Tranchina for expert processing and three dimensional thresholding of the SPECT brain imaging.

Other Sections▼ References 1. Tanielian TJaycox LH, editor. Invisible Wounds of War: Psychological and Cognitive Injuries, Their Consequences, and Services to Assist Recovery. Center for Military Health Policy Research, the Rand Corporation; 2008. 2. King NS. PTSD and traumatic brain injury: Folklore and fact? Brain Injury. 2008;22:1–5. doi: 10.1080/02699050701829696. [PubMed] [Cross Ref] 3. Harch PG, Neubauer RA. In: The Textbook of Hyperbaric Medicine. 3. Jain KK, editor. Hogrefe and Huber; 1999. pp. 318–349. 4. Harch PG, Kriedt C, Van Meter KW, Sutherland RJ. Hyperbaric oxygen therapy improves spatial learning and memory in a rat model of chronic traumatic brain injury. Brain Res.2007;1174:120–129. doi: 10.1016/j.brainres.2007.06.105. [PubMed] [Cross Ref] 5. Harch PG, Van Meter KW, Neubauer RA, Gottlieb SF. In: The Textbook of Hyperbaric Medicine. 2. Jain KK, editor. Hogrefe and Huber; 1996. pp. 480–491. 6. Harch PG, Neubauer RA. In: The Textbook of Hyperbaric Medicine. 4. Jain KK, editor. Hogrefe & Huber; 2004. Hyperbaric oxygen therapy in global cerebral ischemia/anoxia and coma; pp. 223–262. 7. Neubauer RA, Gottlieb SF, Pevsner NH. Hyperbaric oxygen treatment of closed head injury.South Med J. 1994;87:933–936. [PubMed] 8. Golden ZL, Neubauer RA, Golden CJ. Improvement in cerebral metabol-ism in chronic brain injury after hyperbaric oxygen therapy. Int J Neurosci. 2002;112:119–131. doi: 10.1080/00207450212027. [PubMed] [Cross Ref] 9. Harch PG, Gottlieb SF, Van Meter KW, Staab P. HMPAO SPECT brain imaging and low pressure HBOT in the diagnosis and treatment of chronic traumatic, ischemic, hypoxic and anoxic encephalopathies. Undersea & Hyperbaric Medicine. 1994;21:30. 10. Kennedy JE, Jaffee MS, Leskin GA. Posttraumatic stress disorder and posttraumatic stress disorder-like symptoms and mild traumatic brain injury. J Rehab Res Devel. 2007;44:895–920. doi: 10.1682/JRRD.2006.12.0166. [PubMed] [Cross Ref]