Sunday, February 19, 2012

WHAT WE TREAT

The content and information provided within this site is for informational and educational purposes only. Consult a doctor before pursuing any form of therapy, including Hyperbaric Oxygen Therapy. The Information provided within this site is not to be considered Medical Advice. In Full Support of the F.D.A., Hyperbaric Oxygen Therapy is considered Investigational, Experimental, or Off Label. Please consult with your Treating Medical Physician

Who do we treat?
Rapid Recovery Hyperbarics treats all ages, infants to the elderly. Our clients have come from all over the world to be treated at our facility. We believe that everyone should have access to safe, Gentle, Private, and Productive Hyperbaric Oxygen Therapy.

What Conditions do we treat?
At Rapid Recovery Hyperbarics we treat many different types of health conditions. Any condition that benefits from increased circulation / oxygen can benefit from Hyperbaric Oxygen Therapy (HBOT). Many are listed below in alphabetical order. Please contact our office if you do not see your condition listed.
Studies indicate that following Conditions may greatly benefit include (but are not limited to):

Acute acoustic Trauma (Tinnitus)

Acute and Chronic Anemia

Anti-Aging

Aid to cardiac surgery and rehabilitation

Aid to prosthesis rehabilitative care

AIDS

Air or gas embolism

Autism

Autistic spectrum disorders

Auto- immune disorders ( SLE, Rheumatoid Arthritis

Anoxic and Hypoxic brain disorders

Aneurysms

ALS (Amyotrophic Lateral Sclerosis)

Alzheimer's Disease

Bell's Palsy (Facial Palsy)

Bone Grafts

Brain Injury / Closed Head Injury

Burns

Candida and fungal infections (yeast infections)

Carbon monoxide poisoning and CO poisoning complicated by cyanide poisoning.

Carbon monoxide poisoning and CO poisoning complicated by cyanide poisoning

Cerebral edema

Cerebral Palsy (CP)

Cerebral Palsy

Chemical Poisoning/ Pesticide

Chronic Fatigue Syndrome

Closed Head Injury

Clostridal myositis and myonecrosis, (gas gangrene)

Colitis

Crohn’s Disease

Crush injury, compartment syndrome, and other acute traumatic ischemias.

Decompression sickness

Diabetics disorders ( circulatory, nerve and wounds)

Degenerative Joint disease

Delayed radiation injury (soft tissue and bony necrosis)

Delayed radiation injury (soft tissue and bony necrosis)

Diabetes

Enhancement of healing in selected problem wounds

Epilepsy seizures

Exceptional blood loss (anemia)


Fractures (Non healing and non union)

Fibromyalgia

Flesh eating bacteria

Fracture repair, delayed and non-union

Gastric and Duodenal Ulcers

General Health

Guillain-Barre syndrome

Headaches, Cluster

Health Enhancement and Prevention

Heart attack, Myocardial ischemia

Hypoxic birth disorders

Inflammatory arthritis

Inflammatory Bowel Disease (IBS)

Intracranial abscess, actinomycosis

Liver disorders ( Hepatic)

Lupus

Lyme Disease and co-infections

Macular degeneration

Retinitis Pigmentosa *

Memory Loss

Mercury Poisoning

Migraine and Cluster headaches

Multiple Sclerosis (MS)

Multiple Sclerosis

Mycoplasma

Near drowning

Near hanging

Near-drown

Necrotizing soft tissue infections

Neurovascular compression

Non- healing post surgery, reconstruction and cosmetic surgery

Non-healing wounds

Neurological disorders

Optical And Eyesight Macular degeneration

Osteoporosis

Parkinson’s disease

Peripheral nerve injury and neuropathies, demyelization

Post surgical instability

Post surgical soft tissue infections

Pre and Post Surgery healing, reconstruction and cosmetic surgery

Radiation Necrosis ( soft tissue, brain or bone)

Reflex Sympathetic Dystrophy (RSD) CRPS Complex Pain Syndrome

Refractory osteomyelitis (Infected bone)

Retinitis Pigmentosa

Rheumatoid Arthritis

Ringing in the ears

Sacroiliac Syndrome

Scleroderma

Silicone induced disorders

Skin grafts and flaps (compromised)

Spider bite

Spinal Cord injury

Sports Injuries

Stem Cell Therapy

Stroke

Sudden Deafness tinnitus *

Thermal burns

TOS (Thoraxtic Outlet Syndrome *)

Vegetative coma

Wounds and Ulcers

And more!
Susan Rodriguez CHT
Dr Underwood, DO, MD, JD
Rapid Recovery Hyperbarics, LLC
9439 Archibald Ave. Suite 104
Rancho Cucamonga, CA 91730
909-477-4545

Danielle's Foundation is giving away a Nintendo Wii to a child with cerebral palsy or brain injury


Danielle's Foundation is giving away a Nintendo Wii to a child with cerebral palsy or brain injury. Many therapists have been using the Wii as a therapy tool for children with physical disabilities and motor coordination issues. Now one lucky child will have the chance to win a Wii for use at home. To receive an application, call 1-800-511-2283. We've just extended the deadline to March 1, 2012.


Hyperbaric oxygen therapy in the treatment of post cardiac surgical strokes--a case series and review of the literature.

Anaesth Intensive Care. 2010 Jan;38(1):175-84.
Hyperbaric oxygen therapy in the treatment of post cardiac surgical strokes--a case series and review of the literature.

Gibson AJ, Davis FM.

Hyperbaric Medicine Unit, Christchurch Hospital, Christchurch, New Zealand.

Strokes remain an uncommon but significant complication of cardiac surgery. Cerebral air embolism is the likely aetiology in the majority of cases. Hyperbaric oxygen therapy is the recognised treatment for cerebral air embolism associated with compressed air (SCUBA) diving accidents and is therefore also the standard of care for iatrogenic causes of air embolism. It follows that there is a logic in treating post-cardiac surgical stroke patients with hyperbaric oxygen. The aim of this retrospective review was to examine the outcomes of 12 such patients treated in the Christchurch Hospital hyperbaric unit and to appraise the evidence base for the use of hyperbaric oxygen therapy in this setting. Despite delays of up to 48 hours following surgery before the institution of hyperbaric oxygen therapy, 10 of the 12 patients made a full neurological recovery or were left with mild residual symptoms, with nine returning to their previous level of care. One patient remained hemiplegic and there was one early neurological death.

There is a paucity of prospective data in this area, but based on sound pathophysiological principles and clinical experience, we believe that patients suffering a stroke following open cardiac surgery should be considered for hyperbaric oxygen therapy.

Probiotic Effects in Infants Last Until 4 Years of Age

From Medscape Medical News

Probiotic Effects in Infants Last Until 4 Years of Age

Jennifer Garcia

Other Health Care Provider Rating: 0 stars ( 0 Votes )
Rate This Article:
0 stars

processing....

Like this article?
Read medical news in 32 specialty
areas with our Medscape App.
Choose the specialties you want
to follow.
Learn More

February 10, 2012 — Infants exposed to Lactobacillus rhamnosus through diet supplements from 35 weeks' gestation through 2 years of age had a significantly lower risk for eczema and rhinoconjunctivitis. The protective effect lasted until the children were at least 4 years of age, according to a study published online February 6 in Clinical and Experimental Allergy.

The researchers, led by Kristin Wickens, PhD, from the Wellington Asthma Research Group, Wellington School of Medicine and Health Sciences, University of Otago, New Zealand, and colleagues, followed 425 infants for 4 years after daily supplementation with L rhamnosus (HN001; 6 × 109 colony-forming units [cfu]/day), Bifidobacterium animalis subsp lactis (HN019; 9 × 109 cfu/day), or placebo. Mothers received supplements from 35 weeks' gestation until their child's birth, continuing to 6 months after birth if they were breast-feeding, and all infants received supplements from birth until age 2 years.

The cumulative prevalence of eczema by age 4 years was significantly reduced in the children taking HN001 (hazard ratio [HR], 0.57; 95% confidence interval [CI], 0.39 - 0.83) compared with in the children in the placebo group. The prevalence of rhinoconjunctivitis at age 4 years (relative risk, 0.38; 95% CI, 0.18 - 0.83) was also significantly reduced in the children in the HN001 group compared with in the children in the placebo group. HN019 did not affect the prevalence of any outcome relative to placebo.

"There have been a number of primary prevention studies investigating the effects of different species of probiotics taken by pregnant or breastfeeding mothers and/or their infants on the prevalence of eczema and sensitization by age 2 years. Reaching a consensus on the role of probiotics as primary preventers of allergic disease has been hampered by heterogeneity between studies in probiotic species and dose, duration and timing of intervention, and definitions of outcomes measured," the authors write.

The researchers previously published the initial results of their double-blind, randomized, placebo-controlled trial, in which they evaluated the effect of the probiotics on allergic disease and atopic sensitization in children in the first 2 years of life, in the October 2008 issue of the Journal of Allergy and Clinical Immunology (2008;122:788-794). That analysis demonstrated a 49% reduction in eczema prevalence in children receiving HN001 supplementation.

The current analysis demonstrates that the benefits of HN001 persist to age 4 years, despite cessation of therapy 2 years earlier, suggesting that this probiotic might be an appropriate preventative intervention for high-risk infants.

The researchers collected data regarding the presence (since the child turned 2 years old) of eczema and any history of asthma or hay fever. They assessed eczema severity using the Scoring Atopic Dermatitis (SCORAD) scale, with a cutoff of 10 or higher, and performed skin-prick tests on the child's forearm in accordance with the Australasian Society of Clinical Immunology and Allergy guidelines. They also evaluated the prevalence of current asthma symptoms, using standard International Study of Asthma and Allergies in Childhood questions.

In addition to significantly reducing the risk of eczema by 4 years of age, the use of the HN001 probiotic also provided some protection against SCORAD≥10, wheeze, and atopic sensitization by age 4 years. However, the protective effects did not reach statistical significance.

Fecal samples from a subset of children (n = 153) were analyzed using real-time polymerase chain reaction for the presence of L rhamnosus and B animalis. The researchers noted that HN019 was not detectable in the feces, but HN001 (or HN001-like strains) was detected in 33% of children.

The researchers had previously shown that there was no difference between study groups for sex, ethnicity, delivery, birth weight, length and head circumference, breast-feeding duration, smoking in pregnancy or in the household, pet ownership, family history of allergic disease, or antibiotic use before age 2 years.

Some of the children (24%) had received nonstudy commercially available probiotic supplements; however, exclusion of these children from the analysis did not alter relative risk estimates.

The authors acknowledge study limitations such as the unblinding of participants after 2 years of age, which may have biased responses to questions about eczema frequency and severity. The misclassification of infectious rhinitis as allergic rhinitis and asthma at 4 years of age may also have affected the results, but the authors report that this would not have had a significant effect on the study findings.

"Ours is the only study to separately evaluate two different probiotics, and show an effect for HN001 but not HN019. The different effects we found for each probiotic at age 2 years persisted to 4 years, highlighting the importance of the particular probiotic in allergic disease prevention. Another strength of our study is the high response rate (>86% of eligible infants in each group) and follow-up beyond infancy," Dr. Wickens and colleagues write.

"The precise pathways for effects [of probiotics] on allergic disease remain elusive and require more work, including the possibility that effects are mediated via epigenetic mechanisms," conclude the authors.

Support for this study was provided by Fonterra Cooperative Group, New Zealand. One coauthor is supported by Cure Kids. The other authors have disclosed no relevant financial relationships.

Clin Exp Allergy. Published online February 6, 2012. Abstract

DOGS can have a stroke too! and Dogs can have HBOT

Dogs Can Have Strokes, TooDOGS can have a stroke too!

and Dogs can have HBOT

Now that sophisticated diagnostic tests are routinely used at veterinary clinics, it’s increasingly clear that dogs can suffer from many of the same health problems as their owners.

These problems include stroke, which until recently was thought to be rare in dogs. In both humans and dogs, there are two types of stroke:

  • Ischemic stroke, which occurs when a blocked artery prevents blood from reaching the brain.
  • Hemorrhagic stroke, which occurs when blood vessels in the brain start to leak and blood pools around and in the brain.

Both types of stroke are medical emergencies and warrant an immediate call to your veterinarian. Although dog strokes can cause permanent disability or death, the good news is that they are usually not as serious as human strokes. With the right care and treatment, the odds are good that your dog will make a full recovery within a few weeks.

Causes of Dog Stroke

The main causes of ischemic strokes in dogs include:

  • Kidney, liver, heart or Cushing's disease.
  • Diabetes.
  • Parasites.
  • Tumors.
  • Obesity.
  • Dislodged spinal cartilage.
  • High blood pressure.
  • Over or under active of thyroid glands.

The main causes of hemorrhagic strokes in dogs include:

  • Diseases that lead to high blood pressure such as Cushing’s disease, and kidney, heart, and blood clothing diseases.
  • Head trauma.
  • Brain tumor.
  • Accidental consumption of rat poison.
  • Inflammation of the arteries (vasculitis).
  • Lung worm (angiostrongylosis).
  • Immune-mediated thrombocytopenia.
  • Abnormal blood vessel development in the brain.

Regardless of age, sex, or breed, any dog can suffer a stroke. But some reports suggest that stroke may be more likely to affect either very young dogs or very old dogs, and that greater precautions should be taken to avoid exposing such dogs to extreme temperatures.

Other reports suggest that stroke is more common in breeds with extremely thick coats, and in breeds with flat faces such as pugs and bulldogs which have unusually narrow airways for their size..

More than half of the time, a definite cause of dog stroke is never identified. These are known as idiopathic strokes. Regardless of the cause, it’s essential that you take your dog to a veterinarian or emergency clinic as soon as you notice any of the signs or symptoms of a stroke.

Symptoms of Dog Stroke

The signs of dog stroke are usually very different than the signs of human stroke. Only rarely do dogs show signs of human stroke such as a drooping face or total paralysis on one side of the body.

The most common signs of dog stroke include:

  • Head tilt.
  • Loss of balance, moving in circles and falling over.
  • Eating out of one side of food bowl.
  • Turning the wrong way when called.
  • Confusion.
  • Depression.
  • Loss of sight or blindness.
  • Lethargy.
  • Abrupt or drastic change in behavior.
  • Loss of bowel or bladder control.
  • Seizure.

Initially, such symptoms may not be particularly noticeable, especially if your dog is already likely to do such things as turn the wrong way when called or eat out of only one side of the bowl. But as the condition worsens, the symptoms will become more severe.

Diagnosis of Dog Stroke

A veterinarian may be able to identify a dog stroke from a physical examination. Because the clinical signs of dog stroke are similar to those of other diseases, however, tests may be necessary to make a positive diagnosis.

Such tests may include blood and urine tests as well as advanced imaging tests such as magnetic resonance imaging (MRI) and computed tomography (CT). Standard X-rays are not useful in the diagnosis of stroke.

Because the dog must be absolutely still during an MRI or CT scan, he or she must first be anesthetized. While the dog is unconscious, your veterinarian also may take a sample of spinal fluid (spinal fluid) to check for other conditions such as inflammation or infection that could be causing stroke-like symptoms.

Treatment of Dog Stroke

Once a dog stroke has occurred, there is no way to reverse or repair the brain damage. With proper care, however, dogs almost always survive a stroke and usually recover their motor functions and movement control within several weeks after even a severe stroke.

Sometimes, however, a stroke leads to permanent behavioral changes.

After your dog suffers a stroke, you may need to encourage him or her to eat, drink, and take regular bathroom breaks outside. Initially, all exercise – especially strenuous exercise –should be avoided.

After your dog has fully recovered from a stroke, the best way to prevent another stroke is to ensure that he or she has a healthy diet, and gets plenty of attention and exercise. It’s important to be vigilant for any signs of a new stroke.

It’s also important for your veterinarian to address the underlying cause or causes of the stroke. For example, a low-phosphorus diet may help control chronic kidney failure. A high-protein, high-fiber, and low-fat, low-carbohydrate diet may help control diabetes.

Dogs with diabetes also may require regular insulin treatments.

Your veterinarian will be able to prescribe the optimal regimen to keep your dog healthy and happy after a stroke. Don’t forget to schedule an annual checkup, which is important for all dogs.

Friday, February 3, 2012

Benefit for Miracle Maggie!

Benefit for Miracle Maggie

Written by Emily Luibrand

Text Box: 7 days old My almost two year old daughter calls out “Mama?” as I slip into my bedroom for a few moments of solitude. My heart melts as I hear those words, words I was told would never escape those precious lips. You see, my daughter didn’t come into this world with a furious cry that let my heart know that all was well. My daughter came into this world in complete silence, a silence that grew louder as the doctors worked hard to regain a heartbeat. After nineteen long minutes, God allowed my daughter to return to this world. I believe that Magdalaina Ilene Luibrand was truly born the moment her heart started beating again on March 15th 2010.

From that moment on, we have received many dire predictions for Maggie. We were never offered the one thing that we needed…hope. She was never supposed to make it home. We brought her home after 5 weeks in the NICU at Children’s Hospital in Minneapolis. We were told she would never have any “quality of life”. Maggie is one of the happiest kids I have ever seen, with the greatest giggle you have ever heard. She was never going to be capable of eating, talking, walking and all those activities that we take for granted everyday. She can eat and drink without her feeding tube now. She babbles endlessly now while inserting words like “more”, “hugs”, “luv you”, “good girl” “Mommy”, “Daddy” and “drink”. A lot of physical motor skills seem to be harder for her than most kids...but she is always improving, always trying...and those big blue eyes that know exactly what I'm saying never cease to amaze me! How I love to watch this bright, beautiful, bubbly little girl grow up! A little girl that laughs at her Daddy who makes some of the silliest noises!

Text Box: Kisses for MamaA little girl that wakes up cuddly and gives her Mama so many kisses that I honestly lose count! A little girl that puts her arms up to help us get her shirt on and then she grins and giggles when we tell what a big helper she is! A little girl that looks for her Daddy and says “Da da?” My heart gets so overwhelmed with happiness and thanksgiving when I see her “quality of life” that our God has given her!

Maggie’s journey has been a tough one. At only five hours old, she started Cold Therapy to help stop further brain damage from occurring. Maggie’s first EEG showed no brain activity, her second EEG at 5 weeks old showed very little brain activity and what activity they did see was incredibly abnormal. Maggie also developed a very rare condition called Subcutaneous Fat Necrosis were 80% of her fat mass died. When this happened, the areas on Maggie’s body that were affected became hard like concrete causing Maggie to be in pain every time she was moved. Subsequently, she developed

Hypercalcemia. This condition could cause Maggie’s calcium levels to skyrocket and if they got too high it would cause her heart to stop. We were constantly monitoring her levels as they seemed to always remain just below the danger point. During this time, we were looking into Hyperbaric Oxygen Therapy treatments. We were hearing some amazing stories of how it has helped children and adults with brain injuries.

“Hyperbaric Oxygen Therapy or HBOT is a method of administering pure oxygen at greater than atmospheric pressure to a patient in order to improve or correct conditions. By providing pure oxygen in a pressurized chamber we are able to deliver 10-15 times more oxygen then if delivered at sea level or at normal atmospheric levels….“Nature has dictated that healing cannot take place without appropriate oxygen levels in the body’s tissues. In many cases, such as those involving circulatory problems, Strokes, anoxic brain injury, and near drowning just to name a few, adequate oxygen cannot reach the damaged area and therefore the body’s natural healing process fails to function properly.”

“Oxygen given with increased pressure can correct many serious health problems. To provide this increased pressure one must be within a pressurized room, a Hyperbaric Oxygen Chamber. Oxygen, given at normal atmospheric pressure is insufficient to raise tissue oxygen levels. The answer is to deliver oxygen with a slight increase in pressure with a chamber to raise the oxygen tension above the normal red blood cell saturation.”

“Blood is made up of three main components: white cells that fight infection, red blood cells that carry oxygen, and plasma, the fluid that carries both kinds of cells throughout the body. Under normal circumstances, only the red blood cells carry oxygen. However, because HBOT forces oxygen into the body under pressure, Oxygen dissolves into all of the body’s fluids, including the plasma, the Lymph, the cerebrospinal fluids surrounding the brain and spinal cord. These fluids can carry the extra oxygen even to areas where circulation is poor or blocked, either by trickling past the blockages or by seeping into the affected area. This extra oxygen helps in the healing process and enhances the white blood cells’ ability to fight infection. It can promote the development of New Capillaries, the tiny blood vessels that connect arteries to veins. It also helps the body build new connective tissue. In addition, HBOT helps the organs function in a normal manner.” Reprinted with permission from www.hbot4u.com

Text Box:  HBOT treatments So when Maggie was just nine weeks old we made the long drive to San Bernardino California to start her first round of HBOT treatments. I was amazed at the results! After just one treatment Maggie stopped throwing up at every feeding. After the second treatment, her tremors stopped. After the third treatment, she drank 3.5 oz from a bottle for the first time! She only needed the feeding tube now for supplemental feedings at night. We stayed for 16 treatments. When we got home Maggie continued to show progress in all areas except for the fact that her skull size never changed. We were told that the reason that Maggie’s skull wasn’t growing was due to the fact that her brain wasn’t growing. This can be a problem that occurs after a serious brain injury in young children. We were told that there is no treatment for this problem. So naturally, after having seen the amazing results with HBOT, I called the founder of Rapid Recovery Hyperbarics to find out if she knew of any treatments for this particular problem. We decided that we would once again head for California, this time for 39 treatments, this time in hopes that Maggie’s brain would grow and increase the size of her tiny skull.

We still have concerns about her brain being stunted due to the brain injury at birth. Her skull size has changed very little since we left California over a year ago and this means that her brain has not grown enough either. Our main concern is that if her skull starts to permanently fuse and her brain continues its slow growth but eventually reaches its limit of space in the small skull. The consequences would be more brain damage as the brain will not stop growing and it will eventually start to compress itself causing further brain damage. So the only thing we can do to help her now is to do more HBOT treatments and pray that her skull and brain would grow while her skull is still able to grow. HBOT treatments can help with developmental problems as well. In combination with Maggie’s HBOT treatments we are also doing Craniosacral Massage therapy twice a week at Active Life Massage in Grand Forks along with Physical, Occupational, and Speech Therapies at Little Miracles two to three times a week to help her catch up developmentally. What truly makes even the most difficult experiences with Maggie bearable is faith that God has an intention for her life. He gave her strengths, and I am able to see those now amid and beyond the challenges with which she was born. She has a purpose, and I cling to it knowing that she was intended for greatness and a higher calling. This is what enables me to see her future as bright and beautiful. I can’t wait to see what she will be able to accomplish some day. Maggie’s limitations are not larger than His plan for her life!

We are asking for the help of our community, friends, and family. We have had to pay for all of these HBOT treatments out of pocket since they are not covered by insurance. We are trying to raise enough funds so that Maggie can get one more much needed round of HBOT treatments before she turns two. A fundraiser is being held at the Cavalier Community Center on March 11th, 2012 from 11am - 2 pm. There will be a baked potato bar, salads and desserts. There will also be a bake sale and auction. All proceeds will go directly to pay for medical bills and HBOT treatments. Donations can be made for auction items by calling Janine Moris at 701- 886-7647. Monetary donations can be made out to the Cavalier Baptist Deacons Fund and sent to the Cavalier Baptist Church, 201 Division Avenue South Cavalier, ND 58220

Text Box: Playing with DaddyPlease come join use for an afternoon of fun! And thank you to all who have already supported us! We have been so humbled by your generosity!

Thursday, February 2, 2012

Football head injuries: Testimony

1
Written Testimony
Ann C. McKee, M.D.
Associate Professor of Neurology and Pathology
Boston University School of Medicine
Director of the VISN-1 Neuropathology Laboratory for the New England Veterans
Administration Medical Centers
Director of the Brain Banks for the Boston University Alzheimer’s Disease Center,
Framingham Heart Study, and Centenarian Study
Co-Director, Center for the Study of Traumatic Encephalopathy
Hearing before the House Judiciary Committee
Legal Issues Relating to Football Head Injuries
October 28, 2009
2
3
Mr. Chairman and Members of the Committee:
Thank you for the invitation to testify today on legal issues relating to football head
injuries. My name is Dr. Ann McKee. I am an associate professor of Neurology and
Pathology at Boston University School of Medicine, and I am the Director of the
Neuropathology Laboratory for the New England Veterans Administration Medical
Centers at the Bedford VA Medical Center, the Director of the Brain Banks for the
Boston University Alzheimer’s Disease Center, the Framingham Heart Study, and the
Centenarian Study, and I am a co-director for the Center for the Study of Traumatic
Encephalopathy at Boston University.
I received my medical degree in 1979, and I am board certified in both Neurology and
Neuropathology. I have extensive experience in neuropathology of neurological disease
and have written extensively on the neuropathology of many neurodegenerative
diseases, including Alzheimer’s disease, Parkinson’s disease, and Frontotemporal
Dementia, as well as normal aging. For the past 23 years, I have been studying the
brains of individuals after death and correlating the pathological findings to the patient’s
clinical symptoms during life. I have examined thousands of brains, brains from people in
all walks of life including brains from individuals who have lived to be well over the age of
100. In addition, for most of my professional career, I have been focused on tau protein,
a protein that becomes toxic when abnormally phosphorylated and builds up in the
brains of patients with some neurodegenerative diseases, including Alzheimer’s disease,
but is found only in very limited quantities in the brains of normally functioning people.
In January of 2003, as part of my work with the Boston University Alzheimer’s Disease
Center and the Bedford VA, I examined the brain of a man who died at the age of 72
after 15 years of severe dementia requiring institutionalization. The man had been a
4
world champion boxer and had been clinically diagnosed with Alzheimer’s disease
beginning at the age of 58. However, when I looked at his brain on post-mortem
examination, I found that there was absolutely no evidence of Alzheimer’s disease;
there was no evidence of beta amyloid, a protein that accumulates in the brain in people
with Alzheimer’s disease and is thought by many to be the cause of Alzheimer’s disease.
Instead, the brain of this world champion boxer showed a massive build-up of the toxic
form of tau protein as neurofibrillary tangles (NFTs) and glial tangles throughout his
brain. The neurofibrillary and glial tangles were also distributed in a unique pattern, a
pattern not found in any neurodegenerative condition except Chronic Traumatic
Encephalopathy, or CTE. In CTE, tau protein builds up in individual nerve cells and
prevents them from making normal connections with other nerve cells, eventually killing
the cells. In this man’s brain, there were massive numbers of NFTs and glial tangles, so
many in fact that you could see the abnormalities on the glass slides without the use of a
microscope, as you can see in the right panels of Figure 1. There is tremendous
accumulation of tau protein that appears as a brown pigment. All the brown pigment you
see is abnormal, please compare what you see on the right to the brain of a normal 65
year old man on the left, all the slides are prepared and stained in exactly the same way,
and there is absolutely no brown pigment visible in the normal individual. When you look
at the brain microscopically as in the lower panels, you can see that many individual
nerve cells of the boxer contain NFTs – they are found in nearly every nerve cell and
there are almost no normal appearing cells. This individual, a former professional boxer,
was clinically diagnosed with Alzheimer’s disease during life, but the disease that
actually caused his tragic 15 year decline in intellect and eventually killed him, was CTE,
a disorder that would have been entirely prevented if he hadn’t suffered repeated head
injury in his younger years as a boxer.
5
My second case of CTE came in 2004, again when I was examining the brain of a man
who had been clinically diagnosed with Alzheimer’s disease when he was alive. When I
looked at the slides, I immediately realized that the changes found in this individual were
nearly identical to those that I had found in the world champion boxer, but in this case,
the medical records did not indicate that he had ever had any head injury. So I called the
patient’s daughter, and sure enough, it turned out that the man had been a professional
boxer during his twenties. Again, his post-mortem examination indicated that his
functional deterioration, dementia and placement in a nursing home were not due to
Alzheimer’s disease, but instead due to CTE, a disorder that could have been entirely
prevented. Over the ensuing years, I examined several other cases of CTE in
professional boxers, all with a similar appearance and pattern of abnormalities.
I met Chris Nowinski in the summer of 2007 and through Chris’s efforts in early 2008, I
had my first opportunity to examine the brain of a retired professional football player. It
was the brain of John Grimsley, a former linebacker for the Houston Oilers who had died
of an accidental gunshot wound while cleaning his gun at the age of 45. According to his
wife, he was concussed 3 times during his college football years, and at least 8 times
during his NFL career, however, only one "cerebral concussion" was medically
confirmed. He was never formally diagnosed with post-concussion syndrome and never
sought medical attention for residual cognitive and behavioral difficulties. There was no
history of ever losing consciousness for more than a few seconds and he never required
being carried off the field or hospitalization. He never took any performance-enhancing
drugs or used illicit drugs. He was a nonsmoker and there was no known family history
of dementia.
6
According to his wife and close friends, he began showing changes in his behavior and
cognitive decline at age 40. He developed difficulties in short-term memory, attention,
concentration, organization, planning, problem-solving, judgment, and the ability to
juggle more than one task at a time. For example, he would ask the same questions
repeatedly over the course of the day and he would ask to rent a movie that he had
already seen. He had difficulty assembling his tax records, shopping alone, and
understanding television. His symptoms gradually progressed and became quite severe
by the end of his life. He also developed a “shorter and shorter fuse” and would become
angry and verbally aggressive over seemingly trivial issues.
When I first looked at his brain (it had been previously dissected by the coroner), I didn’t
see any gross changes. Yet when the microscopic slides were prepared, they showed
the exact same pattern of changes that I had found in the brains of the boxers with CTE.
There were large numbers of tau containing neurofibrillary tangles throughout all parts of
the brain and there was absolutely no evidence of beta amyloid protein or Alzheimer’s
disease. The brain of this 45 year old husband and father, at the prime of his life,
showed profound neurofibrillary degeneration, changes of CTE that were identical in
nature to the changes I found in the brains of the boxers, but were now in a football
linebacker some 30 years younger. In John Grimsley’s brain, there were striking
changes in regions of the brain controlling personality and behavior, such as the frontal
lobes, profound changes in the areas controlling impulsivity and rage behavior such as
the amygdala, and severe changes in anatomic structures that are responsible for
memory, such as the hippocampus, mammillary bodies and thalamus. In Figure 1, the
brain of John Grimsley is seen in the middle; in the top middle panel, you can see severe
tau deposition in the frontal lobe and microscopically; in the bottom middle panel, you
can see numerous nerve cells containing tau and NFTs.
7
Figure 1
In a normal 45 year old, absolutely none of these changes would be found. Indeed these
changes would not be found in a normal 65 year old, 85 year old or 110 year old.
8
The next football player’s brain that I examined was that of Tom McHale, a 45 year old
retired offensive lineman for the Tampa Bay Buccaneers. He was a husband and father
of 3 young boys. After a 3 year decline in his ability to make sound business decisions,
increasing apathy, depression, and memory loss, he died as a result of substance
abuse. His wife did not know of any reported formal concussions during his year as a
lineman. His brain too showed profound tau immunoreactive neurofibrillary
degeneration in areas controlling memory, impulsivity, organization and problem solving
(as you can see in Figure 2) and again with no evidence of any other disorder other than
CTE.
Figure 2
The third brain of a professional football player I examined was that of Wally Hilgenberg,
a 66 year old former linebacker who died from complications related to Amyotrophic
Lateral sclerosis or Lou Gehrigs disease. He played 16 seasons with the Minnesota
Vikings and had at least 10 concussions, including losing consciousness on 1 or 2
occasions. He began showing slow and steady cognitive decline at the age of 56. His
cognitive difficulties were manifest mainly by “not understanding things at a deeper level”
and he had difficulties with executive functioning, including worsening organization and
9
planning skills. His cognitive decline progressed with worsening memory and language
functions. In his last year, he stopped being able to read and was completely unable to
learn how to operate an assistive communication device, even using the simplest level of
commands. Inspection of his brain showed damage to the frontal cortex in a pattern that
suggested it had been used as a battering ram, and the interior spinal fluid spaces were
enlarged suggesting that the volume of the brain had declined. Microscopically the brain
was densely riddled by tau containing NFTs and glial tangles throughout the cerebral
cortex, basal ganglia, thalamus, and brainstem in the unique pattern that defines CTE,
and again, in the complete absence of Alzheimer’s disease and beta amyloid.
Furthermore, the damage found in his brain was far greater in density and the damage
was much more widespread than anything that I have ever found in Alzheimer’s disease
or any of the other common neurodegenerative disorders.
Figure 3
10
The fourth, fifth and sixth brains from former NFL football players that I examined,
including one individual who took his own life, all showed the same distinctive,
characteristic changes of CTE. The seventh brain of a former NFL player I analyzed was
that of Louis Creekmur, a former offensive lineman for the Detroit Lions and an eighttime
Pro Bowler. Louis Creekmur played ten seasons for the Lions, and was famous for
suffering at least thirteen broken noses and 16 concussions. Beginning at the age of 58,
he began to show increasing cognitive and behavioral difficulties including memory loss,
problems with attention and organization, and outbursts of anger and aggression. He
died from complications of dementia at the age of 82. The brain of Mr. Creekmur showed
extensive damage including marked shrinkage of medial temporal lobe structures that
control memory, shrinkage of the frontal and temporal lobes, and marked dilation of the
spinal fluid cavities that line the brain’s interior. There was widespread and severe tau
deposition as NFTs throughout the frontal and temporal lobes, amygdala, hippocampus,
thalamus and brainstem in the unique pattern that is only found in CTE. In Mr.
Creekmur’s case, the abnormalities were profound, they were severe, and they
paralleled the changes found in the world champion professional boxer. Mr. Creekmur
was also a member the NFL’s Plan 88. Yet again, there was absolutely no evidence of
Alzheimer’s disease or any other neurodegenerative disorder, and the findings indicated
that if Mr. Creekmur had not sustained repetitive head trauma during the play of football,
he would be alive and well and enjoying his family and grandchildren today.
11
Figure 4
I have also examined the brain of a former college football player, Mike Borich, a former
wide receiver for Snow College and Western Illinois University who died at the age of 42
after a several-year period of increasing irritability, aggressive and violent outbursts, and
drug and alcohol abuse. His brain, too, showed CTE affecting widespread parts of his
cerebral cortex and deep brain nuclei. Brains from 3 other college football players
showed similar changes.
Lastly, I have had the opportunity to examine the brain of a high school football player
who died at the age of 18. He had played football and other sports for 4 years and
suffered several concussions. The brain of an 18 year old should be pristine, there
should be no abnormalities anywhere, no abnormalities whatsoever. But in the brain of
this young man, a brain that should be entirely normal, there were spots of undeniable
pathology. They were 4 areas of damage in the frontal lobe that you could see even
looking at the slides with your naked eye (Figure 5). In those areas, there were hundreds
of degenerating nerve cells containing tau neurofibrillary tangles and disordered nerve
12
cell processes. Even in this 18 year old high school student, with only a few years
experience playing football, there were signs of the earliest stages of CTE. Had he lived
longer, this 18 year old would have almost certainly developed the same full blown CTE
that we found in the other college and professional football players.
Figure 5
I have now examined the brains of 7 former NFL players, and 4 college layers, and all 11
have shown profound and widespread changes of CTE. I have also found CTE in a
college level player and the earliest signs of CTE in a high school football player. I
realize that this is just a handful of cases, so – so what? -what can you say from just 11
cases? Well, I can say that for the past 23 years, I have looked at thousands of brains,
from individuals from all walks of life, of all ages, and during the past 20 years, I have
primarily focused on abnormalities of tau protein. But I have only seen this unique
13
pattern of changes, in this severity, in individuals with a history of repetitive head trauma,
including boxers and football players. These changes are dramatically not normal -there
is no way these pathological changes represent a variation in normal that we find under
a bell shaped curve. We have found these changes in every professional football
players’ brain that has come into my laboratory at the BU Center for the Study of
Traumatic Encephalopathy and I have never seen this in 20 plus years of examining
brains. I have had colleagues of mine from other institutions – leading neuropathologists
from Harvard and Mt. Sinai—independently examine these brains, and they have come
up with the same diagnosis as I had, CTE. I know that the argument is often made that
there are hundreds of thousands of former football players, including former professional
football players, with no signs of any cognitive decline or memory loss or personality
change, but what I don’t understand is why are we expecting that this exposure to
repetitive head trauma will have 100% penetrance into the population and cause disease
in every football player? Do we expect 100% of cigarette smokers will develop lung
cancer? Do we expect 100% of children who play with matches or even chain saws will
get hurt? No. Even if the percentage of affected players is 20%, or 10%, there are still
thousands of kids and adults out there, right now, playing football at all levels -who will
eventually come down with this devastating and debilitating disorder. And as a doctor
and as a mother, I think this calls for immediate action. We need to take radical steps to
change the way football is played and we need to make those changes today.
14
B.U. Center for the Study of Traumatic Encephalopathy Grant Support
Title: Development of Pathology Diagnostic Criteria for Chronic Traumatic
Encephalopathy
Co-Principal Investigators: Ann McKee and Robert Stern
Type of Grant: Supplement to P30 Center Grant (N. Kowell, P.I); P30-AG13846
Funding Agency: National Institute on Aging
Years Funded: 2009-2010
Total Direct Costs: $83,287
Title: Neuropathologic Examination of Traumatic Encephalopathy in Athletes with
Histories of Repetitive Concussion
Co-Principal Investigators: Ann McKee and Robert Stern
Type of Grant: Supplement to P30 Center Grant (N. Kowell, P.I); P30-AG13846
Funding Agency: National Institute on Aging
Years Funded: 2008-2009
Total Direct Costs: $100,000

Low pressure hyperbaric oxygen therapy and SPECT brain imaging

Case report
Open Access
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 Harch1*, Edward F Fogarty2, Paul K Staab1 and Keith Van Meter1
Addresses: 1Section of Emergency Medicine, Department of Medicine, Louisiana State University Health Sciences Center, 2021 Perdido St, Room
W535, New Orleans, Louisiana, 70112, USA and 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
Email: PGH* - paulharchmd@aol.com; EFF - efogarty@medicine.nodak.edu; PKS - pstaab@wjmc.org; KVM - kvanmeter@aol.com
* Corresponding author
Published: 5 June 2009 Received: 12 March 2009
Accepted: 4 April 2009
Cases Journal 2009, 2:6538 doi: 10.4076/1757-1626-2-6538
This article is available from: http://casesjournal.com/casesjournal/article/view/6538
© 2009 Harch et al; licensee Cases Network Ltd.
This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0),
which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
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 blastinduced
post-concussion syndrome and post-traumatic stress disorder.
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].
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
Page 1 of 4
(page number not for citation purposes)
(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 problemsmemory,
attention, decreased speed of thinking, 11) Back
pain, 12) Bilateral knee pain, 13) PTSDsymptoms: intrusive
thoughts, combat thoughts, nightmares, tachycardia.
Med-Surg, Medications: None. FH, ROS, and PHIS: noncontributory
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:
Movie 1, Figures 1 and 2. (Movie 1): Side by side Pre and
Post HBOT processed transverse SPECT brain blood flow
images-movie. File Format: Quicktime Video. Description
of Data: 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
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 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.
Page 2 of 4
(page number not for citation purposes)
Cases Journal 2009, 2:6538 http://casesjournal.com/casesjournal/article/view/6538
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. (Figure 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 (Movie 1). (Figure 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 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.
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 blastinduced
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
Page 3 of 4
(page number not for citation purposes)
Cases Journal 2009, 2:6538 http://casesjournal.com/casesjournal/article/view/6538
assisted in development of the hyperbaric protocol and
writing the manuscript. All authors read and approved the
final manuscript.
Acknowledgements
The authors are indebted to nuclear technologist Philip J.
Tranchina for expert processing and three dimensional
thresholding of the SPECT brain imaging.
References
1. Tanielian T, Jaycox LH, Eds: Invisible Wounds of War: Psychological
and Cognitive Injuries, Their Consequences, and
Services to Assist Recovery. Center for Military Health Policy
Research, the Rand Corporation, Arlington, VA, 2008.
2. King NS: PTSD and traumatic brain injury: Folklore and fact?
Brain Injury 2008, 22:1-5.
3. Harch PG, Neubauer RA: Hyperbaric oxygen therapy in global
cerebral ischemia, anoxia, and coma. In The Textbook of
Hyperbaric Medicine, Chapter 18, 3rd Edition. Edited by Jain KK. Seattle,
Washington, Hogrefe and Huber; 1999:318-349.
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.
5. Harch PG, Van Meter KW, Neubauer RA, Gottlieb SF: Use of
HMPAO SPECT for assessment of response to HBO in
ischemic/hypoxic encephalopathies. In The Textbook of Hyperbaric
Medicine. Chapter 35, Appendix 2. 2nd Edition. Edited by Jain KK.
Seattle, Washington, Hogrefe and Huber; 1996:480-491.
6. Harch PG, Neubauer RA: Hyperbaric oxygen therapy in global
cerebral ischemia/anoxia and coma. In The Textbook of Hyperbaric
Medicine. Chapter 18, 4th Revised Edition. Edited by Jain KK. Seattle,
Washington, Hogrefe & Huber; 2004:223-262.
7. Neubauer RA, Gottlieb SF, Pevsner NH: Hyperbaric oxygen
treatment of closed head injury. South Med J 1994, 87:933-936.
8. Golden ZL, Neubauer RA, Golden CJ et al.: Improvement in
cerebral metabol-ism in chronic brain injury after hyperbaric
oxygen therapy. Int J Neurosci 2002, 112:119-131.
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 et al.: Posttraumatic stress
disorder and posttraumatic stress disorder-like symptoms
and mild traumatic brain injury. J Rehab Res Devel 2007,
44:895-920.
Movie 1. Side by side Pre and Post HBOT processed
transverse SPECT brain blood flow images-movie. Click on
this link to activate the video: http://casesjournal.com/
casesjournal/article/downloadFile/6538/303311
Page 4 of 4
(page number not for citation purposes)
Cases Journal 2009, 2:6538 http://casesjournal.com/casesjournal/article/view/6538
Do you have a case to share?
Submit your case report today
• Rapid peer review
• Fast publication
• PubMed indexing
• Inclusion in Cases Database
Any patient, any case, can teach us
something
www.casesnetwork.com

Vitamins & Healthy Fats Promote Mental Acuity

Vitamins & Healthy Fats Promote Mental Acuity

Posted on 2012-01-16 06:00:01 in Alzheimer's Disease | Brain and Mental Performance | Diet |Vitamins |

Vitamins & Healthy Fats Promote Mental AcuityA diet rich in key vitamins and healthy fats may help older men and women to stay cognitively sharp, as well as reduce brain shrinkage associated with Alzheimer’s Disease. Conversely, a “junk food” diet (characterized by high trans fat intake) predicts lower cognitive scores, as well as reduced total cerebral brain volume. G.L. Bowman, from Oregon Health and Science University (or guide, USA), and colleagues completed a study that specifically measured a wide range of blood nutrient levels and correlated them to performance on mental acuity tests. The researchers enrolled 104 people, average age 87 years, none of whom experienced special risk factors for memory or mental acuity. The team tested 30 different nutrient biomarkers in their blood, and 42 participants also had MRI scans to measure their brain volume. The most favorable cognitive outcomes and brain size measurements were associated with two dietary patterns – high levels of marine fatty acids, and high levels of vitamins B, C, D and E. In contrast, consistently worse cognitive performance was associated with a higher intake of the type of trans-fats found in baked and fried foods, margarine, fast food and other less-healthy dietary choices. The researchers conclude that: "Distinct nutrient biomarker patterns detected in plasma are interwpretable and account for a significant degree of variance in both cognitive function and brain volume.”

Diet, nutrient levels linked to cognitive ability, brain shrinkage

CORVALLIS, Ore. – New research has found that elderly people with higher levels of several vitamins and omega 3 fatty acids in their blood had better performance on mental acuity tests and less of the brain shrinkage typical of Alzheimer's disease – while "junk food" diets produced just the opposite result.

The study was among the first of its type to specifically measure a wide range of blood nutrient levels instead of basing findings on less precise data such as food questionnaires, and found positive effects of high levels of vitamins B, C, D, E and the healthy oils most commonly found in fish.

The research was done by scientists from the Oregon Health and Science University in Portland, Ore., and the Linus Pauling Institute at Oregon State University. It was published today in Neurology, the medical journal of the American Academy of Neurology.

"This approach clearly shows the biological and neurological activity that's associated with actual nutrient levels, both good and bad," said Maret Traber, a principal investigator with the Linus Pauling Institute and co-author on the study.

"The vitamins and nutrients you get from eating a wide range of fruits, vegetables and fish can be measured in blood biomarkers," Traber said. "I'm a firm believer these nutrients have strong potential to protect your brain and make it work better."

The study was done with 104 people, at an average age of 87, with no special risk factors for memory or mental acuity. It tested 30 different nutrient biomarkers in their blood, and 42 participants also had MRI scans to measure their brain volume.

"These findings are based on average people eating average American diets," Traber said. "If anyone right now is considering a New Year's resolution to improve their diet, this would certainly give them another reason to eat more fruits and vegetables."

Among the findings and observations:

  • The most favorable cognitive outcomes and brain size measurements were associated with two dietary patterns – high levels of marine fatty acids, and high levels of vitamins B, C, D and E.
  • Consistently worse cognitive performance was associated with a higher intake of the type of trans-fats found in baked and fried foods, margarine, fast food and other less-healthy dietary choices.
  • The range of demographic and lifestyle habits examined included age, gender, education, smoking, drinking, blood pressure, body mass index and many others.
  • The use of blood analysis helped to eliminate issues such as people's flawed recollection of what they ate, and personal variability in nutrients absorbed.
  • Much of the variation in mental performance depended on factors such as age or education, but nutrient status accounted for 17 percent of thinking and memory scores and 37 percent of the variation in brain size.
  • Cognitive changes related to different diets may be due both to impacts on brain size and cardiovascular function.

The epidemiology of Alzheimer's disease has suggested a role for nutrition, the researchers said in their study, but previous research using conventional analysis, and looking in isolation at single nutrients or small groups, have been disappointing. The study of 30 different blood nutrient levels done in this research reflects a wider range of nutrients and adds specificity to the findings.

The study needs to be confirmed with further research and other variables tested, the scientists said

This work was supported by the National Institutes of Health.