Hyperbaric oxygen therapy and Brain Injury
Curt Allen, Jr. was a 17 year old man who was involved in a high speed motor vehicle accident in June, 2004, in which he sustained severe traumatic brain injury. Curt was in a coma at the scene of the accident. He was admitted to an acute care hospital, underwent brain surgery to relieve pressure and placed in the ICU in critical condition. After one month he was transferred to a highly regarded post-acute brain injury rehabilitation center in Southeast Louisiana where he remained for 3 months. During these three months he made such minimal progress that he was discharged as a failure of standard intensive traumatic brain injury therapy. The day before discharge from this center his mother attended a local church where she asked the priest to request that the congregation pray for her son’s recovery. After the priest fulfilled this request during Mass Mrs. Allen was approached by a physician patient of mine to whom I had delivered low-pressure HBOT years before for his stroke and subsequent traumatic brain injury. My patient referred Mrs. Allen to me and the following week Curt was evaluated at my clinic.
The video you will view records the astounding recovery that Curt made as he underwent a course of HBOT. The segments of the video were edited from the running VHS tape I recorded of Curt’s progress beginning 4 months after his severe traumatic brain injury through 89 HBOT’s. Since the voices on the tape are hard to discern in places and Curt is speaking in hushed tones the following narrative accompanies each segment on the tape...
New research on Hyperbaric Oxygen Therapy Treatment (HBOT) for traumatic brain injury (TBI) and Post Traumatic Stress Disorder (PTSD) was presented at the 8th World Congress on Brain Injury in Washington DC.
Study: Hyperbaric therapy treats brain injuries
Advocate staff writer
Published: Mar 16, 2010
Promising results from an LSU pilot study that treated veterans suffering traumatic brain injury with hyperbaric oxygen therapy have led to a national trial that will be launched in the coming weeks.
Dr. Paul Harch, a clinical associate professor with the LSU Interim Public Hospital in New Orleans, presented the cases of 15 military veterans during a meeting of the Eighth World Congress of the International Brain Injury Association in Washington, D.C. The cases all involved veterans who were helped by the treatments.
On Monday, Harch participated in a teleconference to explain the treatment process and trial results to journalists.
To date, Harch has treated nearly 40 veterans suffering from traumatic brain injury, usually as a result of explosions, with the hyperbaric oxygen therapy originally developed to help deep-sea divers suffering from brain decompression illness.
Tomorrow night (Mon. 8/3/09) on the CBS Evening News with Katie Couric there will be a special piece on a veteran that has been followed by 60 Minutes and CBS since his injury 5 years ago in Iraq. He is a double amputee with a brain injury who recently underwent HBOT in New Orleans at our clinic for his TBI. Because of the severity of his injury he was not treated under the current LSU pilot trial that I am conducting. Instead, he became one of my private patients, received the exact same protocol as the study patients, and benefited accordingly. He was so moved by his experience that he called CBS to report the latest chapter in his recovery. I have not seen the final edited segment, but believe that it highlights his plight in the military medical system. I hope it is positive.
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The Dosage of Hyperbaric Oxygen in Chronic Brain Injury
Paul G. Harch M.D.
The concept of dosage of hyperbaric oxygen therapy (HBOT) derives from the definition of HBOT as a drug. Using the broad definition of HBOT by Harch and Neubauer (1), HBOT is the use of greater than ambient pressure oxygen as a drug to treat basic pathophysiologic processes/states and their diseases. Drug dosage of HBOT, therefore, is a function of baseline or reference ambient pressure, depth of pressurization, duration, frequency, air breaks, surface interval, number of treatments, idiosyncratic genetic patient factors, and time to intervention in the disease process which determines the pathological targets. All of these factors cause HBOT to be a narrow-window drug in chronic brain injury similar to digoxin and coumadin: too litfie maybe ineffective and too much can be toxic. In addition, oxygen is a respiratory metabolite: ;too little has serious metabolic consequences and too much can cause metabolic fatigue. Determining the proper dosage in a given patient with a specific or multiple diseases can be difficult. Ultimately, one wants the best dosage that improves the patient while doing the least harm.
HBOT has both acute and chronic effects (2). This paper will address only the chronic effects. Chronic effects of HBOT include fibroblast stimulation, collagen deposition, anglogenesis, epithelialization, and bone remodeling. This is most evident in shallow perfusion gradient wounds such as the classic homogenous wound of external beam radiation. In this animal and human model, Marx (3) has shown that intermittent exposure to HBOT induces the aforementioned chronic trophic effects to cause wound healing. The final level of tissue oxygenation after HBOT is approximately 80% of normal tissue, but the effect is durable for years. The unproven mechanism of the effect is thought to be secondary to transient elevation of tissue oxygen levels that results in a steep oxygen gradient that causes anglogenesis. Since 1995 this effect has been better characterized as signal induction where the drug HBOT, by elevation of tissue oxygen pressures, alone or in combination with other factors, signals the DNA to begin transcription of various gene sequences to mRNA (4,5,6). The mRNA is translated to proteins which cause trophic tissue changes, i.e., wound healing. These mechanisms are thought to be responsible for the HBOT-induced wound healing that is seen in a large variety of chronic non-healing wounds, such as arterial insufficiency, venous insufficiency, diabetic, radiation, sickle cell, vasculitic, and other ulcers.
Cognitive & Cerebral Blood Flow Improvement in Chronic Stable Traumatic Brain Injury Induced by 1.5 ATA Hyperbaric Oxygen
Kevin Barrett, Paul Harch, Brent Masel, James Patterson, Kevan Corson, Jon Mader. The Transitional Learning Community at Galveston, 1528 Postoffice St., Galveston, TX 77550; and UTMB, Division Hyperbaric Medicine Galveston, TX
Background: Following severe traumatic brain injury, cognitive improvement is most dramatic the first six months following injury and largely static after 18 months. Anecdotal reports exist that attest to the efficacy of HBOT to improve posttraumatic neurologic deficits by increasing blood flow in the ischemic penumbra despite protocol differences, CBF, speech, neurological and cognitive testing have not been studied serially in patients undergoing HBOT for chronic stable TBI.
Low pressure hyperbaric oxygen therapy ( LPHBOT ) Induces cerebrovascular changes and improves cognitive function in a rat traumatic brain injury (TBI) model.
Paul G. Harch, CL Kriedt, MP Weisend, KW Van Meter, R.I Sutherland, Baromedical Research Institute & LSU School of Medicine, New Orleans, LA 70114, and University of New Mexico Depts. of Psychology and Physiology, Albuquerque, NM 87131
INTRODUCTION: In 1996 pilot data were reported on this project [UHM, 1996, 23: (Suppl); 48]. The present study ia a replication of the cognitive improvements and blood vessel changes in that experiment using a larger number of rats.
METHODS: 42 adult male Long-Evans hooded rats were subjected to the unilateral weight-drop focal cortical impact model of TBI. 49 days following TBI, the ram underwent LPHBOT in 2 groups: (1) 80 bid 13 ATA/90 HBOTs (n=l 9); (2) 80 bid sham air treatments (n=23). Motor function and spatial memory tasks were assessed before and after HBOT. Animals were sacrificed, brains sectioned, stained with T,T-diaminobenzidine, and vessel density analyzed via computer assisted densitometry.