HBOT for Traumatic Cervical Spinal Cord Injury

September 2000, Volume 38, Number 9, Pages 538-540

Article Hyperbaric oxygen (HBO) therapy for acute traumatic cervical spinal cord injury S Asamoto1, H Sugiyama1, H Doi1, M Iida1, T Nagao2 and K Matsumoto3 1Department of Neurosurgery, Tokyo Metropolitan Ebara Hospital, Tokyo, Japan 2Department of Neurology, Tokyo Metropolitan Ebara Hospital, Tokyo, Japan 3Department of Neurosurgery, Showa University, School of Medicine, Tokyo, Japan Correspondence to: S Asamoto, Department of Neurosurgery, Tokyo Metropolitan Ebara Hospital, 4-5-10 Higashi-Yukigaya, Ohta-Ku, Tokyo 145-0065, Japan Abstract Study design: A retrospective study of spinal cord injury (SCI) treated with and without hyperbaric oxygen (HBO) therapy. Objectives: To report on the use of HBO in spinal cord injury. Setting: Neurosurgical Unit, Tokyo, Japan. Methods: Thirty-four cases of hyperextension spinal cord injury without bone damage and previous history of surgical intervention were divided into two groups, with (HBO) or without (non-HBO) therapy. The neurological findings at admission and their outcomes were evaluated by means of Neurological Cervical Spine Scale (NCSS) and the average improvement rates in individual groups were compared. Results: The improvement rate ranged from 100% to 27.3% with the mean value of 75.2% in the HBO group, while these values were 100%, 25.0% and 65.1% respectively in the non HBO group. Conclusion: In the HBO group, the improvement rate indicated effectiveness in acute traumatic cervical spinal cord injury. Spinal Cord (2000) 38, 538-540.

Autism marked by Brain Inflammation. HBO reduces inflammation!

Autism Marked by Widespread Brain Inflammation

HBOT reduces the inflammation and restores circulation!

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NEW YORK (Reuters Health) Nov 18 - Brains obtained at autopsy from autism patients show widespread neuroglial activation and inflammation, according to a report in the November 15th online edition of Annals of Neurology.

Despite suggestions that immune dysfunction plays a role in the pathogenesis of autism, the authors explain, neuropathological studies have given little attention to immune and neuroglial activity in autism.

Dr. Carlos A. Pardo from Johns Hopkins University School of Medicine, Baltimore, and colleagues studied brain tissues obtained at autopsy from 11 autistic patients and cerebrospinal fluid from 6 living autistic patients.  Neuropathological examination of autistic brains revealed extensive neuroglial responses, along with patchy loss of neurons in the Purkinje cell layer and granular cell layer of the cerebellum.  "The marked neuroglial activity in the cerebellum is consistent with previous observations that the cerebellum is one focus of pathological abnormalities in morphological and neuroimaging studies of patients with autism," Dr. Pardo commented.  There was, however, no evidence of adaptive immune reactions in autistic brains, the authors report.

Brain tissues from autistic patients showed increased levels of proinflammatory cytokines, the results indicate, particularly in the region of the anterior cingulate gyrus. Cytokines originated principally from reactive astrocytes.

Cerebrospinal fluid from living autistic patients showed significant increases in MCP-1, IL-6, IFN-gamma, IL-8, MIP-1beta, and other proinflammatory cytokines and modulatory cytokines.

"These cytokines play important roles in immune mediated processes, and their presence in the CSF in autistic patients may reflect an ongoing stage of inflammatory reactions likely associated with neuroglial activation and/or neuronal injury," Dr. Pardo explained.  "At present, there is no indication for using anti-inflammatory medications in patients with autism," Dr. Pardo cautioned. "There are ongoing experimental studies to examine the effect of drugs that limit the activation of microglia and astrocytes, but their use in humans must await further evidence of their efficacy and safety."

Hyperbaric Oxygen Therapy is known for its ability to dramatically reduce inflammation!

Ann Neurol 2004.

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Study: Lyme Disease and HBOT

Research on Lyme Disease

Deer Tick

Effects of Hyperbaric Oxygen Therapy 

On Lyme Disease 

by William P. Fife, Ph. D.

29 January 1998

The purpose of this study was to determine if hyperbaric oxygen therapy affected Lyme disease caused by the spirochete, Borrelia burgdorferi.

The spirochete B. burgdorferi is a microaerophilic organism carried by the Deer tick (Ixodid) and transferred to humans and other mammals by its bite. Symptoms often begin by a bulls-eye rash and erythema migrans. Symptoms may include pain in joints and muscles, sore throat, fever, swollen glands, and mental " fogginess". If not diagnosed within the first one or two months, the disease may become a chronic infection. At that time it apparently becomes sequestered in fibroblasts and other cells which, in turn appear to protect it against effective treatment by all known antibiotics so far tested. The disease is difficult to diagnose without serological findings and requires the skill of a highly qualified physician, experienced in treating this disease.

Rationale

It was shown by Austin that the spirochete could not survive if transferred in air to another host, but would survive if transferred in a gas mixture of 4% oxygen. This demonstrated that the spirochete could not survive in an oxygen partial pressure of 160-mm Hg (the partial pressure of oxygen in air), but could survive in a partial pressure of 30-mm Hg (which is the partial pressure of 4% oxygen at 1 atmosphere, absolute (ground level pressure). Therefore, it seems clear that a lethal level of oxygen for the spirochete falls somewhere between 30 mm Hg, and 160 mm Hg.

It also is known that while the inspired partial pressure of oxygen is approximately 160 mm Hg, at the tissue level, the partial pressure of oxygen normally is approximately 30-35 mm Hg. Thus, it would not be expected that breathing air at ground level would cause any damage to the spirochete. However, if the patient were placed in a hyperbaric chamber and the pressure increased to 2. 36 atmospheres, absolute (ata), the total barometric pressure would be 1794 mm Hg. If the patient were then to breathe pure oxygen the inspired partial pressure of oxygen would be 1794 mm Hg. Inspired oxygen is diluted by carbon dioxide and water vapor in the alveoli, so that the arterial blood would be exposed to an oxygen partial pressure of approximately 1700-mm Hg, and the tissue oxygen would be between 200 and 300 mm Hg. This clearly would be above lethal oxygen levels for the spirochete since it is expected that oxygen normally would diffuse throughout all cells of the body.

This partial pressure of oxygen can be safely achieved in a hyperbaric chamber, and the patients can tolerate this level for 90 minutes or longer quite successfully.

Protocol

This study was approved by the University Institutional Review Board.

Subjects were selected from those referred by clinical physicians who were experienced in the treatment of Lyme disease. All subjects presented with a positive diagnosis of this disease according to the CDC criteria, including a positive Western blot serology of the proper bands. All had failed intravenous antibiotics, and many were continuing to deteriorate even though still on various antibiotics.

Subjects were given a briefing on the use of the hyperbaric chamber, including the risks, and signed a waiver and release in accordance with the Belmont Report. They were placed in the multiplace chamber and compressed to 2.36 ata, whereupon a plastic helmet was placed over the head and pure oxygen was administered. The oxygen flow pattern was such that the subject inspired 100% oxygen with each breath. Subjects were able to communicate with the attendant in the chamber as well as with each other.

Treatment duration was 60 minutes on oxygen, and in most instances the treatments were administered bid for 5 days followed by a two-day rest. Several different series were tried, ranging from 10 treatments to 30 treatments. One subject received 145 treatments over the course of 3 months.

Results

Ninety-one subjects completed a total of 1,995 hyperbaric oxygen treatments, although nine were eliminated later due to the presence of another medical problem not apparent during their treatments. These other medical problems were such things as babesiosis, ehrlichosis, hepatitis C, and previously unidentified neurological problems. Two subjects were eliminated due to the development of septicemia from IV catheters, and one because of recent breast cancer, although all three of them later showed an improvement of Lyme symptoms with hyperbaric oxygen administration.

Subject evaluation was carried out by an abbreviated questionnaire taken from a standard questionnaire used by several Lyme specialists as part of their evaluation. This questionnaire was designed so that zero reflected no symptoms, while ten reflected severe symptoms.

Although additional statistical evaluation still is being carried out, it appears that approximately 84.8% of those treated showed significant improvement by a decrease or elimination of symptoms. Only 12 subjects (13.1%) claimed no apparent benefit.

Before treatment, the subjects had an average score of 114.12 (of a possible 270), and after treatment they averaged 49.27. This reduction of 64.85 points was statistically significant in a paired t-test (p=0.000). The variability of the scores from patient-to-patient declined as well after the treatment series. The standard deviation of the scores was 56.00 before and 44.14 after treatment. The p-value of this reduction is 0.057 in a Fisher's F-test. Further, 58% of the respondents had score reduction of 41.86 points or more.

All except one of the 91 subjects developed severe Jarisch-Herxheimer reaction, usually appearing within the first 5 days of the beginning of hyperbaric oxygen treatment. In most cases, the Jarisch-Herxheimer reaction continued throughout the series of treatments, and in many instances continued for up to a month after the treatments were finished. Most subjects then began to show major improvement that in some instances has continued for 8 months.

HBOT in TBI & Coma

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Thousands of Americans suffer brain damage as the result of near-hanging, near-drowning, near-choking, cardiac arrest, cyanide and carbon monoxide poisonings, and lightning strikes every year (150,000 Americans suffer severe head injuries just from trauma alone). This type of brain damage is known as an anoxic ischemic encephalopathy. It is both the size and the location of the irreparable damage (the umbra), as well as the reversibility of the damage within the surrounding brain tissue (the penumbra), that dictates the patient's prognosis.

Brain damage occurs after a head injury because, more often than not, the brain starts to swell, pressing delicate tissue against the unyielding skull. This swelling then cuts off the brain's blood supply, which leads the accumulation of toxic levels of normal cell wastes, which further aggravate the swelling. Such damage can lead to coma, a state of deep unconsciousness in which one does not respond to pain or sound, and cannot be awakened.

HBOT has the potential to break this cycle by constricting the brain's blood vessels, while delivering more oxygen. This seems like a paradox, but HBOT can increase oxygen levels because the increased pressure forces oxygen into the blood plasma, the liquid part of the blood that normally does not carry oxygen, and into the cerebrospinal fluid that surrounds the brain. The plasma and cerebrospinal fluid can then reach areas that the red blood cells, which normally carry oxygen, cannot penetrate. Giving a patient pure oxygen at normal pressure simply cannot put enough oxygen into either the bloodstream or the cerebrospinal fluid to overcome the oxygen deficit.

HBOT can also stabilize and repair what is called the blood-brain barrier, a protective layer of cells that keeps many toxins or noxious materials from reaching the brain. This barrier is often greatly disturbed when a head injury occurs.

In the immortal words of Dr. P.B. James, MB, ChB, DIH, PhD, FFOM, of the Wolfson Hyperbaric Medicine Unit, University of Dundee, "Those wanting to find out more about oxygen treatment will be disappointed that some professionals do not appear to be open minded. A head injury may close the mind, but hyperbaric oxygenation has been shown in a controlled trial to reduce the mortality of head injury by 50%. (Rockswold GL et al J Neurosurg see abstract below). Determine the knowledge of this therapy of a health professional by first asking if they know this paper. If they do not then move on. If they do then ask:"

 

Abstract

Results of a prospective randomized trial for treatment of severely brain-injured patients with hyperbaric oxygen

Authors: Rockswold GL , Ford SE , Anderson DC , Bergman TA , Sherman RE
Division of Neurosurgery, Hennepin County Medical Center, Minneapolis, Minnesota.
J Neurosurg 1992 Jun;76(6):929-34

Abstract: The authors enrolled 168 patients with closed-head trauma into a prospective trial to evaluate the effect of hyperbaric oxygen in the treatment of brain injury. Patients were included if they had a total Glasgow Coma Scale (GCS) score of 9 or less for at least 6 hours. After the GCS score was established and consent obtained, the patient was randomly assigned, stratified by GCS score and age, to either a treatment or a control group. Hyperbaric oxygen was administered to the treatment group in a monoplace chamber every 8 hours for 1 hour at 1.5 atm absolute; this treatment course continued for 2 weeks or until the patient was either brain dead or awake. An average of 21 treatments per patient was given. Outcome was assessed by blinded independent examiners. The entire group of 168 patients was followed for 12 months, with two patients lost to follow-up study. The mortality rate was 17% for the 84 hyperbaric oxygen-treated patients and 32% for the 82 control patients (chi-squared test, 1 df, p = 0.037). Among the 80 patients with an initial GCS score of 4, 5, or 6, the mortality rate was 17% for the hyperbaric oxygen-treated group and 42% for the controls (chi-squared test, 1 df, p = 0.04). Analysis of the 87 patients with peak intracranial pressures (ICP) greater than 20 mm Hg revealed a 21% mortality rate for the hyperbaric oxygen-treated patients, as opposed to 48% for the control group (chi-squared test, 1 df, p = 0.02). Myringotomy to reduce pain during hyperbaric oxygen treatment helped to reduce ICP. Analysis of the outcome of survivors reveals that hyperbaric oxygen treatment did not increase the number of patients in the favorable outcome categories (good recovery and moderate disability). The possibility that a different hyperbaric oxygen treatment paradigm or the addition of other agents, such as a 21-aminosteroid, may improve quality of survival is being explored.

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Brain injury improves with Hyperbaric Oxygen Therapy

Brain injury improves with Hyperbaric Oxygen Therapy

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Presented in Seattle at the Undersea and Hyperbaric Medical Society 1998 Annual Scientific Meeting

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

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

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

23. June 2012 · Comments Off · Categories: Surgery · Tags: aquaporin-4, brain injury, hyperbaric oxygen treatment, magnetic resonance perfusion imaging, Rabbit

Title

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

Abstract

Objective:To establish explosive brain injury model in rabbits;To investigate the expression of aquaporin 4(AQP4) in model of explosive brain of rabbits injury,and perfusion changes in the expression, to explore the formation of brain edema after blast injury mechanism, and early hyperbaric oxygen treatment of traumatic brain edema formation and development of the role of early treatment for clinical hyperbaric oxygen provide the basis for traumatic brain edema.Method:①30 New Zealand white rabbits, weighing 2.0 ~ 2.5kg, in accordance with the vertical distance between the detonators and the skull group, were randomly divided into groups 5.0cm, 6.5cm group, 8.0cm group, n = 10. 600mg TNT equivalent of paper detonators were used to explode respectively 5.0cm, 6.5cm, and 8.0cm vertical distance from the top of the rabbit head, observing animal survival after injury, and using magnetic resonance imaging methods to understand the pathology and brain damage in each group.②150 New Zealand rabbits were randomly divided into non-treatment group, treatment group and control group, and 10 rabbits were in the latter. Explosive brain injury model was made by paper detonator. Injuryed rabbits were randomly divided into 1h、6h、12h、24h、72h、7d、14d ,14 groups according to a further killed time points after injury, and each group has 10 rabbits. Using dry weight to measure the content water in brain tissue, and using RT-PCR method and image analysis to detect the group at different time points aquaporin 4 (AQP4)mRNA expression, and Western blotting to measure the expression of AQP-4 in brain tissue. Using magnetic resonance perfusion imaging ( PWI) injury time points detected in brain tissue blood perfusion. Finally, it was used for statistical analysis.Results:①5 rabbits died immediately after injury and 4 rabbits died within 3 days in group 5.0cm,and only one survived more than 7 days;The rabbit has appeared most extensive brain contusion, cortical surface vessel rupture occurs, and significant fragmentation in brain tissue, large subdural hematoma, and significant brain stem contusion. All rabbits in group 6.5cm survived more than 7 days,except that 1 rabbit died on the 4th day after injury because of inability eating. 4 rabbits occurred epilepsy and got paralysis of limbs; Pathology observed in the survival of the rabbits had cerebral cortex partial rupture of blood vessels, brain edema and obvious laceration and contusion lesions clear boundary with the surrounding brain tissue. All rabbits in group 8.0cm survived, but showed no significant changes in the brain.②Blast injury after contusion brain 1h aquaporin 4 (AQP4) mRNA expression increased, and in turn increased, 72h peak (P <0.05), 7d pm down. Brain tissue aquaporin 4 (AQP4) began to express 1h after injury increases, and 72h reached its peak (P <0.05), it turned to down after 7d, but it still maintained on a high level. Brain tissue water content and water aquaporin 4 (AQP4) expression were the same. The correlation analysis, aquaporin 4 (AQP4) expression and brain tissue water content was positively correlated (r=0.8767,P<0.001). The hyperbaric oxygen treatment, aquaporin 4 (AQP4) expression at different time points are different degrees of decline, aquaporin 4 (AQP4) expression of injury group compared with control group at after 6h points were lower (P <0.05 ). Blast injury after contusion brain 1h AQP4 mRNA expression increased, and in turn increased, 72h peak (P <0.05), 7d pm down, but still maintain a high level. After intervention by hyperbaric oxygen, in 6h, AQP4 mRNA expression was significantly lower than the injury to 14d is still significantly lower (P <0.05). Post-traumatic cerebral contusion early peripheral blood perfusion decreased significantly to 6 hours after injury, blood perfusion decreased to the lowest (P <0.05), then gradually increased, and maintain a perfusion (close to the control group) for 2 weeks. The hyperbaric oxygen treatment group than in the early trauma group (1-6 hours after injury) perfusion decreased more significantly. 12 hours after infusion began to rise, and non-treatment group was essentially flat.Conclusion:①Detonators and the vertical distance of the skull 6.5cm, can produce good stability, repeatability strong blast injury model of rabbit brain.②The expression of post-traumatic brain aquaporin 4 (AQP4) in traumatic brain is closely related to the formation and development of injury and brain edema. Aquaporin 4 (AQP4) expression may be associated with brain ischemia and hypoxia in the Hyperbaric oxygen intervention aquaporin 4 (AQP4) expression was significantly reduced. Instead, the blood perfusion than the control group and non-treatment group decreased significantly, suggesting that brain tissue oxygen levels of early trauma and aquaporin 4 (AQP4) expression is closely related to early hyperbaric oxygen therapy on the relief plays an important role in traumatic brain edema. Early hyperbaric oxygen therapy can improve cerebral blood oxygen contusion, increased blood oxygen content, ease the secondary cerebral hypoxia caused by cerebral edema.