Home | Welcome | Vision 10 | Mission Statement | HyperMED NeuroRecovery Foundation | Gallery | BLOG | Testimonial | Video | Newsletter

 Patient Application | HBO Direct | Beyond Therapy | Conditions | Google News | Clinical Research | Stem Cells | Mild HBO Chambers

Hyperbaric Oxygenation | Adult & Pediatric Lokomat (Robotic Assisted) Walking | Vibration Training | Median Nerve Stimulation | Oxy Sports

Disc Prolapse, Chronic Pain, Tarlov Cyst, Failed Back Surgery | Spinal Cord Injury | Stroke | Multiple Sclerosis | Brain Injury | Crush Injury

Autism, Speech and Development Delay | Cerebral Palsy, Birth (Hypoxia), Near Drowning | Neurologic Illness | Chronic Fatigue Syndrome

 Non-Healing Wounds | Cosmetic Mishap | Cancer Survival | Radiation Necrosis | Heart Disease | Infertility | HIV AIDS | Burns | Mental Health

HyperMED Brain Injury - Aging, Dementia, Secondary damage

HyperMED Protocols are unique - we provide Hyperbaric Oxygenation combined with Lokomat (Gait Training) and other supportive modalities including Median Nerve Stimulation, Whole Body Vibration, immune stimulating supplements etc  - please review the following attachments.

 

 

Excellent podcast for all individuals and families affected by brain injury

 

 

Neuroprotective Effects of Hyperbaric Oxygen Treatment in Traumatic Brain Injury of Rat.

Wang G, Jiang Z. Institute of Nautical Medicine, Department of Neuropharmacology, Department of Neuropharmacology, Institute of Nautical Medicine, Nantong University, 19 Qixiu Road, Chongchuan District, Nantong, Jiangsu 226001, China, Nantong, China, 226001, 86-513-85051799, 86-513-85051796; wgh@ntu.edu.cn. J Neurotrauma. 2010 Jun 23. [Epub ahead of print]

Abstract: This study was designed to evaluate the potential benefits of hyperbaric oxygen (HBO) in the treatment of traumatic brain injury (TBI). The right cerebral cortex of rats was injured by the impact of a 20 g object dropped from a standard predetermined height. Rats received HBO treatment at 3 ATA for 60 min after TBI. Neurological behavior score, brain water content, morphological changes in the hippocampus, and cell apoptosis in brain tissue surrounding the primary injury were examined to reflect the brain damage severity. Three and six hours after TBI, HBO-treated rats displayed a significant reduction of brain damage. However, 12 h after TBI, the efficacy of HBO treatment was considerably attenuated. Furthermore, 24 h, 48 h and 72 h after TBI, the HBO treatment did not show notable effects. In contrast, multiple HBO treatments (3 or 5 times totally), even started from 48 h after TBI, remarkably reduced the neurology deficit score and the loss of neuronal number in the hippocampus. Although multiple treatments started from 48 h significantly improved the neurological behaviors and reduced the brain injury, the overall benefic effects were substantially weaker than the ones observed after single treatment from 6 h. These results suggest that: 1) HBO treatment could alleviate brain damage after TBI. 2) Single treatment of HBO has a time limitation of 12 h post-TBI. 3) Multiple HBO treatments have the possibility to extend the post-TBI delivery time-window. Therefore, our results clearly suggest the validity of HBO therapy for the treatment of TBI.

  • Hyperbaric Oxygen Chamber Advancements for Traumatic Brain Injury ...
    It is hoped that hyperbaric oxygen treatments will alleviate much of the long-term brain damage associated with roadside bomb blasts in Afghanistan and Iraq. Even though many veterans of both combat fronts had been injured multiple ...
    Spinal Cord Injury & Brain Injury... - http://www.brainandspinalcord.org/blog/

  • HBOT trial launches, seeking 1000 volunteers Special
    DigitalJournal.com The use of hyperbaric oxygen therapy for brain injuries started over eighty years ago for divers dealing with the bends. It worked at that time and now

  • Hyperbaric Oxygen Study Shows Potential Benefit for Patients With ...
    MINNEAPOLIS, Jan. 4 /PRNewswire-USNewswire/ -- A 5-year study of patients with severe traumatic brain injury conducted at Hennepin County Medical Center in ...

  • Treating Brain Injuries
    Injured soliders benefit from Hyperbaric Oxygenation for brain injuires.
    Fogarty says the therapy works because the high pressure of a hyperbaric chamber forces oxygen into areas of the brain that, due to swelling, ...

  • Two Iraq War Veterans receive pro bono HBO treatments for brain ...
    Examiner.com ... RPT, President and CEO of Oxygen Rescue Care Centers of America, to receive a series of up to 80 pro bono sessions of “Hyperbaric Oxygen treatments”, ...

  • HyperMED/Hypoxic Induced Apoptosis - HyperMED.pdf

  • HyperMED Australia : Clinical Research - Hyperbaric Oxygenation

Please take the time to watch the following National Geographic Documentary on Professor Ed Cooper pioneering work on Median Nerve Stimulation .

  • National Geographic Documentary (VIDEO) - Professor Ed Cooper - Median Nerve Stimulation`

  • HyperMED Australia : Median Nerve Stimulation

The key message by Prof Cooper is the fact that  'awakening is the result of  accurate repetition many thousands of times that tells the brain and spinal cord  – wake-up, wake-up, wake- up, wake-up, wake-up ….’  

Median Nerve Stimulation (MNS) is an integral part of the HyperMED Protocol - application is recommend for all patients with neurologic disorders. The Brain Injured patient have vast regions of the brain that remain in a low metabolic state resulting in 'learned non-use'.

MNS provides a cost effective yet simple home application that enables patients to continue the benefits of HyperMED saturation and training. Equally Spinal Cord patients, victims of neurologic trauma and elderly patients suffering dementia related illness can also benefit from Median Nerve Stimulation. Science supports the fact that many disabled patients have intact but non-responding dormant neural pathways. These dormant pathways need to 'wake-up!'

  • HyperMED Australia : Do Wheel Chairs Inhibit Recovery?

Do Wheelchairs Hinder Brain Injured Recovery?

"Our data suggests that wheelchair restriction definitely impairs functional recovery in rats, and logically it would seem to apply also to humans," says David Magnuson of the Kentucky Spinal Cord Injury Research Center, University of Louisville; National Neurotrauma Society Symposium in Orlando, Florida 2008.

'Learned non-use' is a major contributor to progressive acquired disability. Median Nerve Stimulation can assist to 'keep the therapeutic window open - (alive)'. Mal Hooper_HyperMED

 

  • HyperMED Newsletter Brain Injury - Cerebral Palsy 2008.pdf

  • HyperMED Lokomat 2009

  • Therapy Information Lokomat Training for Traumatic Brain Injury

    Hocoma - How can Lokomat training help patients with traumatic brain injuries? ... What are the expected effects of the Lokomat system on patients with traumatic ...

  • HyperMED Newsletter Brain Injury - Cerebral Palsy 2008.pdf

  • Hypoxic Induced Apoptosis (programmed cellular degeneration)

  • Median Nerve Stimulation

  • Clinical study on effect of HBO plus electric stimulation on treatment for the vegetative state

  • Hyperbaric Oxygenation can repair and restore damaged brain -The Impact of Hyperbaric Medicine on Government Health Care, Disability and Education Expenditures Dr Paul Harch


In this section we will see how Hyperbaric Medicine is being used increasingly to assist patients with disabilities resulting from closed head injury and other related disabilities.

“There is no need of apology for tackling only a symptom rather than an etiology; the misery of these patients cannot wait” – Landau.

This section attempts to tackle a range of conditions that seldom receive attention and commitment other than ‘labeling’ the patient and recommending a supportive group program attempting to assist the sufferer with techniques of self awareness and how to ‘live and cope with disability’.

Our objective is to shed some light on the subject of Closed Head Brain Involvement, and add a degree of inspired outcome for those suffering head and related neurological disability. We are not offering a ‘cure’, but rather a sound medical approach to improving the neurovascular structure directly affecting brain metabolism and function.

 

The importance of Oxygen to the Brain

Of all the chemical elements, oxygen is the most vital to the human body. We would survive for only minutes without oxygen. Oxygen is a life giving, life-sustaining element which creates approximately 90% of the body’s energy. Nearly all of the body’s activities, from brain function to the process of elimination, are regulated by oxygen. The ability to think, feel and act is derived from the energy supplied by oxygen.

This Oxygen energy cycle has become critically important today, more than at any time in human history, because of the sudden unnatural decrease in atmospheric oxygen. It is estimated that the air breathed by our distant ancestors contained approximately 50% oxygen. Reports suggest that in excess of two hundred years ago, the air was composed of 35% oxygen and 1% carbon dioxide. Oxygen levels measured by Swiss scientists during 1946 were reported to be 22%. Most recent report measurements have fallen to 19% with more than 25% carbon dioxide. In major industrial cities, records have indicated oxygen levels to be considerably lower, so it is understandable that respiratory and asthma related illnesses have been on the increase over the past decade.

Oxidation is the term used to describe the complex process of combining oxygen with various elements in the body to reduce or ‘burn’ them for various purposes. Oxidation is the essential factor in healthy metabolic function, better circulation, assimilation, digestion and elimination. The oxidation process is responsible for purifying the blood, keeping it free from toxic cellular waste accumulation. Adequate oxygen levels allow the body to recuperate during sleep, strengthening the immune system. Oxygen calms and renews the nervous system. A lack of this vital ingredient leads to a multitude of biochemical reactions becoming dysfunctional.

Closed Head Injury  covers an ever widening range of direct trauma and indirect neurodegenerative disorders. Conditions range from acute brain trauma due to impact and related injuries to complex motor neuron disorders. Conditions that have been previously thought to be beyond hope are now achieving clinical improvement through the application of Hyperbaric Medicine.

 

Mechanism of Closed Head injury

Since hypoxia (reduced oxygen) and ischemia (reduced blood flow) are involved in the pathophysiology of many disorders of the nervous system, Hyperbaric Oxygenation has an important role in their management. To understand the role of HBOT in neurological disorders, a basic knowledge of cerebral (brain) metabolism, blood flow and neurophysiology is essential.

Cerebral hypoxia is defined as oxygen deprivation to the brain and its structures. Oxygen is vital and oxygen deficiency, regardless of the cause, starts a vicious cycle of destructive pathological changes in the brain tissue. This cycle, unless interrupted, continues with disabling consequences.

  • Primary brain damage results in tissue hypoxia causing edema (swelling)  which results in further aggravation of hypoxia causing  secondary brain damage and complex residual disability

Cerebral edema is a frequent finding in many disorders of the CNS (Central Nervous System including brain and spinal cord structures). Cerebral edema can be directly influenced by numerous factors including heart related conditions and obstructive circulatory conditions including thrombosis and atherosclerosis. Other conditions to influence cerebral edema include infectious processes, vitamin deficiency, and trauma due to direct impact head and neck injury.

Generalized brain edema is life threatening due to the rise in intracranial pressure associated with it. Edema aggravates the neurological deficits of numerous conditions resulting from focal vascular and demyelinating lesions.

SPECT (Single Photon Emission Computed Tomography) scanning has ushered in a new age of neurological investigation with patients who have developed disorders of the brain and related function. SPECT has the ability to image the pathophysiological blood flow throughout the brain.

SPECT scans together with initial hyperbaric chamber sessions are being used with numerous forms of neurological deficits. HBOT and repeat SPECT scans help identify viable non-functional brain tissue, which have the potential to respond to the stimulatory and reparative effects of repetitive HBOT. This potential is realized with actual increased brain blood flow on the final SPECT scans and reduction of hyperintensity changes on MRI.

The motor and cognitive improvements of a patient can be correlated with recovery of specific previously hypometabolic brain areas. This data also supports the fact that traumatic, vascular and anoxic brain injuries and long-standing ischemic hypoxia have a common pathophysiology, including recoverable idling neurons in a penumbra zone surrounding infarct regions.

SPECT/MRI and effective HBOT have been investigated with significant improvement in the following conditions including 'multiple sclerosis, supra nuclear palsy, near drowning, chronic carbon monoxide poisoning, cerebral palsy and numerous neuropathies, motor neuron disorders and ischemic degenerative processes including Parkinson’s, Alzheimer’s, dementia and toxic disorders' (Jain 1999).

 

Case Study : 23 year old female with Impact Closed Head Injury

As previously mentioned in the section titled Stroke, Professor Jain (1996) reports on a 23-year-old female with Chronic Brain Contusion. The patient suffers mutism, left sided paresis, lack of coordination, balance problems, daily mood swings and temperamental behaviour. Five and half years before HBOT she suffered a severe motor car accident and sustained severe left sided frontal temporal closed head injury. She was in a coma and required full respiratory support for three weeks and eventually made a partial recovery. The patient entered multiple rehabilitative programs, consulted numerous doctors and received multiple medical and non-medical forms of therapy, even making a religious pilgrimage to a religious site in Yugoslavia.

Baseline SPECT scans revealed significant regions of reduced and near absent right sided blood brain barrier activity and marked right cerebellar hypoperfusion and widening of the interhemispheric fissure. One initial HBOT session was performed, followed by an additional SPECT, which revealed recoverable tissue due to tracer uptake in both the right temporal and right cerebellar regions. The case continued with an additional 40 HBOT sessions followed by further SPECT studies, and then an additional 40 HBOT (total 80 HBOT sessions) with SPECT.

Overall conclusive and measurable improvements were recorded with significant increased blood brain blood flow (demonstrated by SPECT) and clinical improvement – mood swings, gait, balance, bladder control, cognitive and general behaviour.

 

The effects of Hyperbaric Medicine on Closed Head Injury

Meyer (1968) provided evidence for a Pasteur effect (inhibition of glycolysis by oxygen) with hyperoxia (increased oxygen supply) in the case of carbohydrate metabolism in cerebrovascular disease. Inhalation of 100% pure oxygen significantly decreased the cerebral metabolic rate for lactate and pyruvate. Since cerebral blood flow decreased and the cerebral pressure of oxygen increased, total glycolysis was decreased.

Pierce and Jacobson (1977) reviewed the role of HBOT in cerebral edema and concluded: “This therapy directly decreases vasogenic brain edema and due to improvement of the oxygen delivery to hypoxic tissue acts on cytotoxic brain edema as well. The mechanism underlying the potentially beneficial action of HBOT appears clear and is well supported by both animal and clinical studies. HBOT should be considered an adjunct for patients who are not sufficiently responsive to standard methods”.

Sukoff and Ragatz (1982) concluded that ‘HBOT relieves cerebral edema by reducing cerebral blood flow but continues to maintain the levels of cerebral oxygenation. This mechanism reduces further damage due to plasma and vascular leakage, which precipitates localized edema and swelling resulting in localized ischemia that further inhibits essential nutritional support leading to cellular dysfunction’.

Studies performed by Kohshi (1991) demonstrated the effectiveness of Hyperbaric Oxygenation in reducing the raised intracranial pressure of patients suffering brain tumours and cerebrovascular disease. This demonstrates that reduced intracranial pressure is initially due to direct vasoconstriction caused by hyperoxia (increased oxygen delivery).

Hyperbaric Medicine lowers the raised intracranial pressure in traumatic cerebral edema. The effects of Hyperbaric Oxygenation can persist after conclusion of a chamber session and there are no reported negative effects. If the intracranial pressure remains elevated this factor alone will precipitate further cerebral damage.

Studies have shown that the injured brain is susceptible to oxygen toxicity if excessively high pressures are used. This is not a problem as the pressures used with Hyperbaric Medicine seldom exceed 2 ATA, in fact 1.5 ATA are used with most neurological patients (Jain 1995).

In acute and semi-acute neurologic conditions, HBOT has been demonstrated to promote beneficial effects including :

  • significantly increased oxygen in the cerebrospinal fluid (in excess of 20-fold increase)

  • reduces cerebral edema

  • reduces intracranial pressure

  • elevates diffusional driving force for oxygen increasing tissue oxygen availability into damaged areas

  • restores the integrity of the blood-brain barrier and cell membranes

  • neutralises toxic amines

  • increases neovascularisation (over time)

  • acts as a scavenger of free radicals

  • promotes phagocytosis (thereby internal debridement)

  • stimulates angiogenesis (over time)

  • reactivates idling neurons

  • inhibits anaerobic glycolysis

  • promotes epithelization

  • de-agglutination of platelets

  • makes available molecular oxygen for immediate use without energy transfer

  • reduces lactate peak in hypoxia

Selected summary of published papers regarding Hyperbaric Oxygenation for Anoxic Encephalopathy and Coma

  • Neubauer RA, 'The effect of hyperbaric oxygen in prolonged coma. Possible identification of marginally functioning brain zones'. Medicina Subacquea ed Iperbarica. 1985: (3) 75-79. 17 cases of vegetative coma for 1-22 months. 40 - 120 exposures over 20 - 90 days. Glasgow Coma Scale improved in all. Complete recovery of 5.

  • Eltorai I, Montroy R, 'Hyperbaric Oxygen Therapy leading to recovery of a 6-week comatose patient afflicted by anoxic encephalopathy and post-traumatic edema'. J. Hyperbaric Medicine 1991: (3) 189-198. 90 mins HBO2 bd. After 24 sessions, started talking and ate meals. Gradually mobilized to a wheelchair.

  • Harch PG, et al. 'SPECT brain imaging and low pressure HBO2 in the diagnosis and treatment of chronic traumatic, ischaemic, hypoxic and anoxic encephalopathies'. Undersea and Hyperbaric Med. 1994 (Supp) 4/5 showed improvement in focal cortical & deep grey matter deficits.

  • Shn-rong Z, 'Hyperbaric Oxygen Therapy for Coma - report of 336 Cases'. In Proc XI Intnl Cong Hyperbaric Med. Best, Flagstaff. 1995; 279-285 HBO2 is effective in acute brain hypoxia and oedema and can hasten recovery of consciousness, including prolonged coma.

  • Neubauer RA, Gottlieb SF, Pevsner NH, 'Long-anoxic ischaemic encephalopathy: predictability of recovery'. In Proc XII Intnl Cong Hyperbaric Med. Best, Flagstaff. 1996. (In press). 8 long-term patients with severe anoxic ischaemic encephalopathy between 3 months and 12 years. Improvement in all cases, both clinically and on SPECT scans. Until the introduction of SPECT scanning there has been no diagnostic technique providing evidence that any treatment would be effective.

  • Quinly C, Shaoji Y, 'Nursing of Brain-Stem injury with HBO2'. Ibid. 39 patients treated with HBO2. Decreased mortality and increased awake rate.

  • Zhi Y, et al. 'Assessment of the efficacy of HBO2 in patients with a persistent vegetative state'. Ibid. 8 patients in coma, longest 281 days prior to HBO2. 20 - 86 daily sessions. All resumed consciousness.

Conclusions

  • all patients with closed head involvement and suffering neurological deficits due to hypometabolism, confirmed with pre/post SPECT/MRI HBOT studies are recommended to commence Hyperbaric Oxygenation at 1.5 – 2.0 ATA (Jain 1995)

  • the response of HBOT requires an initial intensive oxygen saturation effect. Usually 40-60 and even up to 80 HBOT sessions are considered as an introduction. HBOT should be maintained whilst demonstrable improvements are noted by both patient and physician. Sessions are held daily.

  • the benefits of HBOT are dependent upon the size of the penumbra zone (recoverable neurons) and the extent of initial neuronal damage done during the original insult/trauma

  • spasticity was reduced, mobility and ambulation improved, speech and cognitive behaviour improved in most cases with Hyperbaric Oxygenation. Improvement directly relates to the revascularization of ischemic zones and the reactivation of idling neurons (Jain 1995)

  • HBOT should be instituted early in the rehabilitative process. Those treated with HBOT within the initial 3-6 months after impact head injury had greater chances of recovery

  • HBOT at 1.5-2.0 ATA is safe and well tolerated by impaired neurological patients

  • response to HBOT is not observed in the initial sessions. Oxygen saturation effects vary from patient to patient. Some case studies report in excess of 100-200 chamber sessions before impact of the oxygenation process was observed clinically

  • fixed neurological deficits persisting for years after closed head injury are not contraindications to HBOT management. Neubauer and End (1980) and Holbach (1977) have demonstrated improvement with stroke patients more than five years after initial stroke onset. Neubauer (1996) and Steenblock recorded significant improvement with patients who suffered closed head injury including stroke, more than 15 years from injury

  • SPECT and MRI investigations are essential measures to identify potentially viable neuronal cells and regions of the brain that can be influenced with HBOT.  HBOT programs cannot be instigated without this current information