Tuesday, February 28, 2012

DTP Vaccine and Mortality

Early diphtheria-tetanus-pertussis vaccination associated with higher female mortality and no difference in male mortality in a cohort of low birthweight children: an observational study within a randomised trial
(13 Feb 2012)
Arch Dis Child doi:10.1136/archdischild-2011-300646

open access

Background: Studies from low-income countries have suggested that diphtheria-tetanus-pertussis (DTP) vaccine provided after Bacille Calmette-Guerin (BCG) vaccination may have a negative effect on female survival. The authors examined the effect of DTP in a cohort of low birthweight (LBW) infants.

Methods: 2320 LBW newborns were visited at 2, 6 and 12 months of age to assess nutritional and vaccination status. The authors examined survival until the 6-month visit for children who were DTP vaccinated and DTP unvaccinated at the 2-month visit.

Results: Two-thirds of the children had received DTP at 2 months and 50 deaths occurred between the 2-month and 6-month visits. DTP vaccinated children had a better anthropometric status for all indices than DTP unvaccinated children. Small mid-upper arm circumference (MUAC) was the strongest predictor of mortality. The death rate ratio (DRR) for DTP vaccinated versus DTP unvaccinated children differed significantly for girls (DRR 2.45; 95% CI 0.93 to 6.45) and boys (DRR 0.53; 95% CI 0.23 to 1.20) (p=0.018, homogeneity test). Adjusting for MUAC, the overall effect for DTP vaccinated children was 2.62 (95% CI 1.34 to 5.09); DRR was 5.68 (95% CI 1.83 to 17.7) for girls and 1.29 (95% CI 0.56 to 2.97) for boys (p=0.023, homogeneity test). While anthropometric indices were a strong predictor of mortality among boys, there was little or no association for girls.

Conclusion: Surprisingly, even though the children with the best nutritional status were vaccinated early, early DTP vaccination was associated with increased mortality for girls.

Wednesday, February 22, 2012

HBOT and Breast Cancer

James Slaby, MD, discusses hyperbaric oxygen therapy's (HBO's) effect on breast cancer cells.

Photo: James Slaby, MD

The total metastatic load in the lung is reduced after HBO --— that’s one of the most significant new findings from a 2007 study. Despite the misconception that HBO could actually have cancer-enhancing effect, HBO is frequently administered to cancer patients.

In the 2007 study, Haroon, Patel, and Al-Mehdi decided to evaluate the growth of murine breast cancer cells in the lung after hyperbaric oxygen treatment in an experimental metastasis assay. To do this, young nu/nu mice were injected intravenously with 3x 10(3) 4T1-GFP tumor cells per g body weight followed by lung isolation, perfusion, and intact organ epifluorescence microscopy 1 to 37 days after injection. A group of animals (n=32) was exposed once daily for five days a week to 45 minutes of 2.8 ATA hyperbaric oxygen in a research animal chamber.

Control animals (n=31) were not subjected to HBO, but received similar intravenous administration of 3x 10(3) 4T 1- GFP tumor cells. Single tumor cells and colonies were counted in the subpleural vessels in areas of about 0.5 cm2 of lung surface [Haroon et al]. What Haroon et al found was that HBO treatment did not lead to an increase in the number of the large colonies or small colonies in the lungs. Instead, there was a significant reduction in the number of the large colonies when observed at varying periods of the time after hyperbaric treatment.

Most importantly, there was a significant decrease in large colony size in the HBO group during all periods of observation. The results indicate that HBO is not prometastatic for breast cancer cells, but, instead restricts the growth of large tumor cell colonies [Haroon et al]. One of the most significant new findings from the study was that the total metastic load (the combined mass of large colonies, small colonies, and the single cell colonies in the target organ) in the lung is reduced after HBO. What’s more, HBO treatment did not lead to an increase in the combined number of metastic foci in the lung. The load reduction was accomplished because the size of the colonies was limited states Haroon et al.

Studies reveal that there is no adverse effect of HBO on tumor growth. In fact, the research suggests that HBO may have an anti-cancer effect with breast cancer cells. Use of HBO in human breast cancer patients did not have any adverse effects in a recent long-term follow up study and is even considered for treating lymphedema associated with breast cancer surgery.

These findings represent good news for patients that have cancer and other issues that would benefit from HBO therapy. In the past we were hesitant to use HBO on patients with cancer for fear of encouraging tumor growth. Now, for example, a patient with breast cancer that needed radiation therapy and developed soft tissues radiation neurosis would benefit from HBO therapy. As a result, her healing ability after breast reconstruction would improve.

Dr. James Slaby is a plastic surgeon specializing in wound care and a panel physician at the Wound Healing & Hyperbaric Oxygen Center at Wooster Community Hospital.

Monday, February 20, 2012

Horses and HBOT

Equine Vet J. 2012 Feb 15. doi: 10.1111/j.2042-3306.2011.00536.x. [Epub ahead of print]

(photo from http://www.sanctuaryequinerehab.com)

Equine peripheral blood-derived mesenchymal stem cells: Isolation, identification, trilineage differentiation and effect of hyperbaric oxygen treatment.

Dhar M, Neilsen N, Beatty K, Eaker S, Adair H, Geiser D.


Departments of Large Animal Clinical Sciences Pathobiology, College of Veterinary Medicine, University of Tennessee, Knoxville, USA GE Healthcare Cell Therapy Division, Piscataway, New Jersey, USA.

Reasons for performing study: Two studies report variability in proliferation and limited adipocyte differentiation of equine peripheral blood-derived adult mesenchymal stem cells, thus casting doubt on their adipogenic potential. Peripheral blood can be a valuable source of adult mesenchymal stem cells if cell culture conditions permissive for their adherence, proliferation and differentiation are defined. Hyperbaric oxygen treatment has been reported to mobilise haematopoietic progenitor stem cells into the peripheral blood in humans and mice, but similar experiments have not been done in horses. Objectives: To optimise cell culture conditions for isolation, propagation and differentiation of adult stem cells from peripheral blood and to assess the effect of hyperbaric oxygen treatment on adult stem cell concentrations. Methods: Peripheral blood was collected from the jugular vein of 6 research mares, and mononuclear cells were isolated. They were subjected to cell culture conditions that promote the adherence and proliferation of adult stem cells. The cells were characterised by their adherence, expression of cellular antigen markers, and trans-differentiation. Each horse was subjected to 3 hyperbaric oxygen treatments, and stem cells were compared before and after treatments. Stem cells derived from adipose tissue were used as controls. Results: One-third of the horses yielded viable stem cells from peripheral blood, positive for CD51, CD90 and CD105, and demonstrated osteocyte, chondrocyte and adipocyte differentiation. Hyperbaric oxygen treatment resulted in a significant increase in CD90-positive cells. Horses that did not yield any cells pretreatment did so only after 3 hyperbaric oxygen treatments. Conclusions and potential relevance: Peripheral blood can be a valuable source of adult stem cells, if one can identify reliable equine-specific markers, provide methods to increase the number of circulating progenitor cells and optimise cell culture conditions for growth and viability. Our findings are important for further studies towards technological advances in basic and clinical equine regenerative medicine.

Sunday, February 19, 2012

Wounded Troops and HBOT, news articles

Wounded Troops and HBOT, news articles




December 15, 2011

By Becky Murphy

It was recently announced that returning Veterans will no longer need to document the specific event which traumatized them, and caused them to experience symptoms of PTSD. This is definitely a start in the right direction to helping returning troops in adjusting to returning Stateside. Eliminating some of the red tape they have to deal with will be a welcome relief; and will enable veterans to focus on their health, and their families. It will hopefully enable them to quickly access whatever help they need to recover from their injuries. Trauma induced injuries are a natural response to traumatic experiences; which can have a devastating impact on a person’s overall health long-term, if not swiftly and effectively treated. PTSD is a never a sign of weakness; it is simply evidence of one’s humanity—like bleeding when cut open.

I have had a link to the International Hyperbaric Medical Association for quite some time in the Veterans section here on Involuntary Transformation, this type of treatment is known to assist in the recovery from PTSD and TBI which are extremely devastating injuries and more unfortunately, common injuries inflicted upon soldiers serving in Afghanistan and Iraq. I urge you to check out this site; on the main page there is a link to send and email to your State Senator and State Representatives asking that they support this legislation. I pray you will find this cause worthy of your support. Let’s give our returning Veterans a fighting chance for a full recovery from the invisible injuries of TBI and PTSD! These injuries are devastating and can prevent their successful return to civilian life; or a continued career serving in the United States Military.


an excerpt:

“Hyperbaric oxygen therapy has been requested for veterans by Commanders and Veterans Service organizations alike. General Conway, when Commandant of the Marine Corps, reported to the House Armed Services Committee about sending some of his most injured Marines to Dr. Harch in New Orleans to receive Hyperbaric treatment. General Chandler, as Vice Chief of Staff of the Air Force requested Chairman Levin provide hyperbaric treatments to his Airmen in the SASC hearing on Suicide in 2010, and Chairman Levin agreed. The American Legion asked for this treatment in their Senate testimony last year. The TBI Treatment Act is the only provision in the Senate Armed Services bill that will permit the Chairman to keep his pledge to General Chandler, and does so in real time.”

via Alliance for Natural Health:

New Study Reaffirms: Hyperbaric Oxygen Therapy Should Be Standard Treatment for Veterans

December 6, 2011 Research from health pioneer (and former ANH-USA board member) Dr. Paul G. Harch published in the Journal of Neurotrauma indicates that hyperbaric oxygen therapy, or HBOT, is able to dramatically help veterans with post-concussion syndrome (a form of traumatic brain injury) and post-traumatic stress disorder (PTSD). Dr. Harch is an associate clinical professor of medicine at Louisiana State University in New Orleans. Since January 2007, ANH-USA has been bringing attention to a project to have veterans treated with HBOT.

In HBOT, the patient is put in a hyperbaric oxygen chamber, which saturates the tissues with twelve times more oxygen than can be absorbed by breathing. This greatly enhances the body’s own healing process. Under normal circumstances, oxygen is transported throughout the body only by red blood cells. With HBOT, oxygen is dissolved into all of the body’s fluids, the plasma, the central nervous system fluids, the lymph, and the bone, and can be carried to areas where circulation is diminished or blocked.

In this way, extra oxygen can reach all of the damaged tissues and the body can support its own healing process. The increased oxygen greatly enhances the ability of white blood cells to kill bacteria, reduces swelling, and allows new blood vessels to grow more rapidly into the affected areas. It is a simple, non-invasive, and painless treatment. According to Dr. Harch’s new study, even three years after the vets sustained brain injury, one month of HBOT was able to induce improvements in brain blood flow, cognition, symptoms, and quality of life, while the veterans experienced fewer suicidal thoughts. Specifically, improvements were seen in 92% of vets experiencing short-term memory problems, 87% of those complaining of headaches, 93% of those with cognitive deficits, 75% with sleep disruption, and 93% with depression.

There were also improvements in irritability, mood swings, impulsivity, balance, motor function, IQ, and blood flow in the brain, as well as the reduction in PTSD symptoms and suicidal thoughts. And there was a reduction in—or complete elimination of—psychoactive and narcotic prescription medication usage in 64% of those previously prescribed the medication. One major problem is that the HBOT treatment is currently “off-label.”

In other words, it is an FDA-approved treatment for some conditions—but not for traumatic brain injury (TBI) or PTSD. Because of this, the Department of Defense does not allow HBOT to be prescribed for its veterans—they say they don’t prescribe off-label medications and treatments for these diagnoses, and claim that they can only use HBOT after it has been approved by the FDA for this use. This is a completely false and misleading statement! The Department of Defense often uses off-label antipsychotic drugs for treatment of TBI and PTSD. This should not surprise us.

The FDA receives a large proportion of its budget from pharmaceutical manufacturers. And the government turns to drugs, often very inappropriate and damaging drugs, to treat damaged veterans without even considering alternatives. Nearly 280,000 individuals received antipsychotic medication in 2007. Yet over 60% of them had no record of a diagnosis for which these drugs are approved. Antipsychotic drugs were prescribed off-label for PTSD (42% of the patients), minor depression (40%), major depression (23%), and anxiety disorder (20%)—with about 20% having more than one condition.

About 20% of veterans diagnosed with PTSD—or nearly 87,000 patients—are prescribed an antipsychotic each year even though it is an off-label use. TBI and PTSD severely and disproportionally affect military who have served in Iraq and Afghanistan—approximately 546,000 have TBI, post-concussion syndrome (PCS), and PTSD, and yet their treatment options are limited. HBOT is an effective and economical treatment for PCS and PTSD, without the very dangerous and negative side effects of antipsychotic medication. The off-label use of HBOT is a huge freedom of choice issue in medicine. But even more important, if we really want to support our troops rather than just pay lip service, don’t we need to give them the safest, most economical, and most effective treatment for their traumatic brain injuries and PTSD? photo credit


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


Aid to cardiac surgery and rehabilitation

Aid to prosthesis rehabilitative care


Air or gas embolism


Autistic spectrum disorders

Auto- immune disorders ( SLE, Rheumatoid Arthritis

Anoxic and Hypoxic brain disorders


ALS (Amyotrophic Lateral Sclerosis)

Alzheimer's Disease

Bell's Palsy (Facial Palsy)

Bone Grafts

Brain Injury / Closed Head Injury


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)


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)


Enhancement of healing in selected problem wounds

Epilepsy seizures

Exceptional blood loss (anemia)

Fractures (Non healing and non union)


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)


Lyme Disease and co-infections

Macular degeneration

Retinitis Pigmentosa *

Memory Loss

Mercury Poisoning

Migraine and Cluster headaches

Multiple Sclerosis (MS)

Multiple Sclerosis


Near drowning

Near hanging


Necrotizing soft tissue infections

Neurovascular compression

Non- healing post surgery, reconstruction and cosmetic surgery

Non-healing wounds

Neurological disorders

Optical And Eyesight Macular degeneration


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


Silicone induced disorders

Skin grafts and flaps (compromised)

Spider bite

Spinal Cord injury

Sports Injuries

Stem Cell Therapy


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

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

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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

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
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
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.
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.
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.
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.
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
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
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
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.
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
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
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.
B.U. Center for the Study of Traumatic Encephalopathy Grant Support
Title: Development of Pathology Diagnostic Criteria for Chronic Traumatic
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