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Thread: High-Pressure Chambers Could Prevent Paralysis After Spinal Cord Injury

  1. #1

    High-Pressure Chambers Could Prevent Paralysis After Spinal Cord Injury


    High-Pressure Chambers Could Prevent Paralysis After Spinal Cord Injury
    WASHINGTON D.C. -- High-pressure chambers used to treat deep sea divers for decompression sickness could play a key role in preventing permanent spinal cord damage and paralysis to many of the thousands of Americans who suffer spinal cord injuries every year, a doctor from Scotland reported May 10.
    Dr. Philip James of the University of Dundee reported at a conference here that putting patients under high pressure forces more cell-resuscitating oxygen into damaged spinal nerves than is possible at normal atmospheric pressure.

    "It may mean the difference between significant disability and no disability," James said.

    James made his remarks at a meeting of the Space and Underwater Research Group of the World Federation of Neurology. The meeting is being coordinated by the Stroke Research Center of the Wake Forest University Baptist Medical Center.

    James has been a consulting physician to North Sea diving operations for 25 years. Divers sometimes suffer from bubbles in their spinal cord, resulting in tissue damage that is similar to the bruising that spinal cords suffer from traumatic injury.

    Typically, nerve tissue in the spinal cord is starved of oxygen because the small capillaries that carry blood to the tissue are damaged. If adequate blood flow is not restored within hours, the nerve cells in the spinal cord die from lack of oxygen. This can result in complete or partial paralysis.

    Placing these divers in hyperbaric chambers and raising the pressure to 2.8 times the normal atmospheric pressure hastens their recovery, James said, because under high pressure the blood carries proportionally more oxygen. This raises the oxygen levels in the damaged nerve tissue toward normal levels to assist recovery. For spinal cord injury patients, raising the pressure to two times atmospheric pressure would be adequate, James said.

    An estimated 250,000 Americans have spinal cord injuries, according to the American Paralysis Association. On average, 11,000 new injuries are reported every year. The cost of treating and caring for these individuals can range from $600,000 to $1.3 million over a lifetime, depending on age and the degree of injury.

    James cautioned that hyperbaric oxygen therapy, as the high-pressure procedure is called, is useful only in cases where the spinal cord is bruised, but not in cases where it is physically severed.

    The National Spinal Cord Injury Statistical Center does not keep statistics on what proportion of spinal cord injuries are limited to bruising, but James said "the vast majority" fall into this category.

    A number of very positive animal studies on the use of hyperbaric oxygen therapy in treating spinal cord injury have been published, James said. On humans, it has been used on a number of spinal cord injured patients over the past 20 years in the United States, Germany and Australia but no large scale studies have been conducted.

    One impediment was that until recently, there was no way to tell whether the spinal cord was bruised or severed, James said.

    "If you go on the physical symptoms of the patient you can't tell," he said.

    Recent improvements in magnetic resonance imaging (MRI), however, now make it possible to determine which spinal cord casualties should be treated with hyperbaric oxygen therapy.

    Unfortunately, James said, "most trauma centers do not have hyperbaric chambers, which is a tragedy, and most physicians don't understand the need to increase the dissolved oxygen in the plasma of the blood. They stop at hemoglobin saturation."


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  2. #2
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    This is unbelievably good news! Now we have a clue why Dr. Kao uses HOT therapy after administration of his peripheral nerve graft....Dr. Young, what do you think, are the modes of action similar?

    How long has this been known about? This will be OUTSTANDING for people with acute injuries. The thing is, has it been tested in animals in conjunction with other treatments ? i.e. methylprednione? We need to pound very VERY hard on the FDA to get this treatment "from bench to bedside."

    Eric Texley

  3. #3


    I have a friend that was injured in the exactly as described in the article. He was injured during training wall scuba diving. He surfaced to quickly, resulting in bubbles going up his spinal cord and lodging in the C6 area. Because it was diving accident he was put in a high-pressure chamber.

    After arriving in the rehabilitation center he began to improve significantly. To make a long story short he can now walk on his own, sometimes with a little help from crutches. He has full control (almost) of bowel movements and urination. He doesn't walk all that well and doesn't have the feeling slice which makes it so much more difficult.

    After reading the article I began to wonder if these improvements have something to do with a high-pressure chamber. Just some food for thought.

    Are there any trials or studies in this area? If not maybe we should look at.

  4. #4
    Hyperbaric oxygenation therapy has been around for over 50 years and probably longer. There is little doubt that this therapy is useful if the problem is lack of oxygen. For example, it is beneficial for decubiti and other similar problems. There is also evidence that the treatment can increase healing rate and I believe that this is what Dr. Carl Kao is using it for. The evidence that hyperbaric oxygenation is useful and beneficial for chronic spinal cord injury, however, is still very limited.

    Please not that the use of hyperbaric oxygenation for the "bends" associated with diving is very different from its use as a means of oxygenating tissues. When divers suffer from "bends", they are having a problem with vascular occlusion due to the creation of nitrogen bubbles in their blood stream, resulting from the decompression of gas. The gas bubbles block blood flow and cause loss of oxygen. The use of high pressure oxygen not only eliminates the bubbles but also provides oxygen to the tissues. Therefore, it is the logical and effective therapy for decompressive sickness.

    A number of studies have attempted to show that hyperbaric oxygenation is beneficial for acute spinal cord injury. It is true that there is a decline of blood flow at the injury site during the hours that follow injury. The data that it is beneficial, however, is not yet convincing enough for the treatment to be used. It is expensive and introduce a number of logistic problems for the care of acute spinal cord injury. For example, it would be difficult to operate on somebody or to get MRI scans on people that are rushed into a chamber. This may delay diagnosis and other care that may be as important.

    In order to influence other American doctors to take the same approach, it would be important to collect rigorous data. At the present, there is a drive of "evidence-based" medicine and the lack of rigorous trial data indicating the benefit of an expensive and troublesome therapy would simply mean that the therapy will not be used.


  5. #5
    Advantages of Spinal Hyperbaric Therapy
    Approximately 20-30% of the body's consumption of oxygen occurs within 3-5% of the body mass - the brain and spinal cord structures (Teller/Jain 1995). These structures are extremely sensitive to oxygen deficiency, so the most dramatic results are produced from either deficiency or the benefits of Hyperbaric Medicine.

    Spinal injuries including acute spinal trauma and/or chronic degenerative compounding injury traumatize the supporting blood vessels, resulting in partial or complete destruction of the blood supply and capillary network systems required to maintain that region.

    Ischemia results in the normal delivery of oxygenated blood to the region being suppressed and ultimately becoming deficient. In spine and related disorders, this compromised condition usually begins with some form of direct trauma or impact, and deteriorates progressively over many years, often regardless of the treatment and/or surgery performed.

    When degenerative ischemia is severe and persistent, it may lead to an anaerobic form of tissue metabolism that may perpetuate the entire collapsing ischemic process. Opportunistic infections further complicate an already chronically impaired immune response (Nicolson 1998). Where degenerative ischemia is suspected, detailed DNA laboratory investigations are performed, followed by assertive medical management. Additional information is detailed in the section 'Chronic Illness'.

    The mechanisms of Spinal and Neurological Hyperbaric Medicine are based upon the fact that spinal and related structures are vascular dependent with the rate of degeneration, associated inflammatory pain and disability being greatly influenced by the 'ischemic model' (Jain 1995).

    Hyperbaric Oxygenation
    reduces inflammation and swelling of the supportive muscle, ligaments and connective tissue and reduces the swelling of the nerves and spinal cord vascular structures by improving metabolism
    improves blood supply to all essential structures: muscles, ligaments, bone, disc, spinal cord, nerves and cerebral spinal fluid
    accelerates immune function, increasing lymphocytes (WBCs) and promoting fibroblast replication and collagen production which are essential to repair disc and ligament structures. This enables the body to overcome infections and viral conditions which otherwise inhibit the repair process and or lead to further complication
    activates dormant and damaged nerve cells and stimulates new capillary blood supply (neovascularization)

    prevents glycolysis and intracellular lactic acidosis (cellular toxic degeneration)

    maintains neurological metabolism in both the damaged and communicating areas

    reduces muscular, ligament and soft tissue splinting and spasticity

    improves joint synovial fluid dynamics and joint mobility

    improves muscular and motor power

    reduces the intensity and frequency of both acute episodes and injury recurrence

    increases physical and mental exercise capacity

    accelerates the effects of both physical therapies and prescribed medications

    Numerous text and journal references are available regarding the effects of Hyperbaric Medicine. Boyd 'Textbook of Pathology' (8th edition pg. 69), states that 'irritation of nerve roots with attending muscle spasm along the segmental distribution of the nerve root can create ischemic changes' that, if not corrected, can lead to chronic pain and permanent physical impairment.

    Jackson 'The Cervical Syndrome' (4th edition pg. 148), states that a major cause of 'musculoskeletal pain originates from ischemia, and compares with the pain experienced in angina'.

    Lewis 'Pain in muscular ischemia', Archives Internal Medicine 1932; 49(5): 713-27, asserts that 'many conditions of the central nervous system stem from vascular ischemia'.

    Hood 'Diseases of the central nervous system' British Medical Journal 1975; 3:398-400, identifies that 'ischemia has a depressant effect on nerve conduction', especially in the more sensitive afferent fibers.

    Magladery, et al 'Electrophysiological studies of nerve and reflex activity in normal man' Bulletin John Hopkins Hospital 1950; 86:291-312, reports that 'ischemic changes in nerve root microcirculation often leads to intraneural edema that aggravates and contributes to the underlying problem'.

    Rydevik and Brown 'Pathoanatomy and pathophysiology of nerve root compression' Spine 1984; 9 (1): 7-15, state that the 'recovery of nerve and other tissue depends on eliminating ischemia in the affected tissue'.

    Bentley and Schlapp 'Experiments on the blood supply of nerves' Journal Physiology, (London) 1943; 102:62-71, report that 'Hyperbaric Oxygenation has proven benefits in reversing the effects of ischemia'.

    Yeo 'A study of the effects of Hyperbaric Oxygenation on the experimental spinal cord injury' Medical Journal of Australia July 30, 1977pg.145-147.

    Eltorai 'Hyperbaric oxygen in the management of pressure sores in patients with injuries to the spinal cord' Journal Dermatological Surgical Oncology (7:9 Sept 1981; 737-739) and Sirsjö 'Hyperbaric Oxygen treatment enhances the recovery of blood flow and functional capillary density in post-ischemia striated muscle' Circulatory Shock, 1993 40:9-13, all describe the benefits of Hyperbaric Oxygenation.

    Davidkin (1977) used Hyperbaric Oxygenation in the comprehensive management of 134 orthopedic injury cases with a reported 72.2% improvement over conservative measures. Davidkin reports that HBOT combats hypoxia, both local and generalized.

    Tsybulyak (1973) used hypoxic states in cases of trauma as an indication for HBOT. Dekleva (1981) demonstrates HBOT to be an important auxiliary therapeutic measure in traumatology. Nylander (1985) demonstrated significant reduction of edema and facilitative aerobic metabolism in ischemic muscle structure as a result of HBOT.

    Nylander (1988) showed that HBOT dramatically reduced the phosphorylase activity, a sensitive marker for muscle cell damage. Sirsjo (1989) demonstrated that HBOT enhances the recovery of blood flow and functional capillary density in pressure induced post-ischemic muscle tissue.

    Some concerns have been raised regarding whether HBOT may result in free radical formation, aggravating reperfusion tissue injury. Nylander (1989) studied the effects of HBOT on the formation of free radicals in the tourniquet model of the rat hind limb, and used muscle biopsy with measurements of thiobarbituric acid reactive material, which included lipid peroxides and alkydes including malondialdehydes, a key intermediate in the formation of peroxides.

    The results showed that HBOT at 2.5 ATA or less for 45 minutes had a favourable effect on the muscle tissue and did not cause increased lipid peroxidation in the skeletal muscle of rats. The current recommendation for spinal HBOT is at 2 ATA for periods extending for 45 to 60 minutes duration.

    Strauss (1983) demonstrated that HBOT reduces muscle damage significantly in experimentally produced compartment syndromes. In 1987, he reported a prospective study with results including resolution of neuropathies, arrest of tissue necrosis and absence of secondary infections.

    HBOT as an adjunct to peripheral nerve repair has also been explored. Zhao (1991) obtained good results in 89.2% of 54 patients, with 65 nerve injuries repaired using HBOT as a supplementary treatment. HBOT has also been documented as improving ischemic limb pain.

    HBOT is reported to be effective as adjunctive therapy for the management of fractures. Bassett and Hermann (1961) demonstrated multi-potential precursors of fibroblastic origin form bone when exposed to increased oxygen tensions and compressive forces.

    From: SPINAL
    ***-the first facility within Australia to offer comprehensive Hyperbaric Medicine as an adjunctive measure in the management and treatment of degenerative spinal neurological and vascular related disorders'

  6. #6

    If hyperbaric oxygenation significantly reduced progressive damage in acute traumatic spinal cord injury, there would be a lot more data supporting its use by now. Itt has been available for over 30 years and people have been speculating about its potential beneficial effects on acute spinal cord injury for decades. I am not saying that the treatment may not be beneficial when used after surgery, like Dr. Kao is, to improve healing and possibly even increase oxygenation of the spinal cord. However, there is simply no convincing data that hyperbaric oxygen therapy really does anything for acute traumatic spinal cord injury.

    It is in appropriate for these scientists to be claiming or implying that it does based on the limited evidence cited. I would be very happy to reconsider my opinion but the statement that hyperbaric oxygen therapy is good for acute spinal cord is sort of like saying the growth factors much be good for the spinal cord and therefore it will regenerate the spinal cord if we give it.

    In my opinion, It is inappropriate to make these types of claims without data, especially since the claims are not novel and have not been substantiated in the past 20-30 years that the therapy has been available. If people believe that hyperbaric oxygenation therapy improves recovery in acute or chronic spinal cord injury, they have an obligation to show that it does so before making the claim, either in animal or human studies.


  7. #7 Dr. Young I did not write this , nor do I think it is all true, I just thought that it was something worth posting for everyone...the link above is where it is from....Thanks

  8. #8
    Senior Member DA's Avatar
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    If hyperbaric oxygenation significantly reduced progressive damage in acute traumatic spinal cord injury, it would have still been in animal testing 30 years after the original breakthrough.

    deja vu

  9. #9
    Sorry, BirdeR, I hope that you did not get the impression that I was criticizing you for posting the information. That was not my intention at all and I want to thank you posting the information.

    I just wanted to balance what I consider the over-exuberant listing of the benefits of hyberbaric oxygenation therapy for acute or chronic spinal cord injury when there is little evidence for ischemia (loss of blood flow) as the cause of injury or disability.

    Every couple of weeks, I get an email for somebody asking me if they should get hyberbaric oxygen therapy, thinking that they would benefit from the treatment. Over the past several decades, many people with chronic spinal cord injury have been treated with hyperbaric oxygenation.

    Below are some abstracts of articles relating to HBO. I am writing a more detailed article on the subject which I shall post in a day or so.


    • Akman MN, Loubser PG, Fife CE and Donovan WH (1994). Hyperbaric oxygen therapy: implications for spinal cord injury patients with intrathecal baclofen infusion pumps. Case report. Paraplegia. 32 (4): 281-4. Summary: A patient with a cervical spinal cord injury receiving intrathecal baclofen for spasticity control underwent a 7 week course of hyperbaric oxygen therapy to induce healing of an ischial decubitus ulcer. After completion of this treatment and during a routine baclofen infusion pump refill, the actual pump reservoir volume exceeded computer measurements obtained with telemetry. Examination of the physiology of hyperbaric oxygen therapy in relation to infusion pump function revealed that the intraspinal pressures attained during hyperbaric oxygen therapy produced retrograde leakage of cerebrospinal fluid into the infusion pump reservoir. <> Department of Physical Medicine and Rehabilitation, Inuonu University Medical School, Malatya, Turkey.

    • Asamoto S, Sugiyama H, Doi H, Iida M, Nagao T and Matsumoto K (2000). Hyperbaric oxygen (HBO) therapy for acute traumatic cervical spinal cord injury. Spinal Cord. 38 (9): 538-40. Summary: 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)1 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. <> Department of Neurosurgery, Tokyo Metropolitan Ebara Hospital, Tokyo, Japan.

    • Bedbrook G (1978). Spinal injuries and hyperbaric oxygen. Med J Aust. 2 (14): 618-9. Summary: <>

    • De Jesus-Greenberg DA (1980). Acute spinal cord injury and hyperbaric oxygen therapy: a new adjunct in management. J Neurosurg Nurs. 12 (3): 155-60. Summary: <>

    • Gamache FW, Jr., Myers RA, Ducker TB and Cowley RA (1981). The clinical application of hyperbaric oxygen therapy in spinal cord injury: a preliminary report. Surg Neurol. 15 (2): 85-7. Summary: While reports of the beneficial effects of hyperbaric oxygen therapy in experimental use appear in the literature, there have been no reports of clinical trials with hyperbaric oxygen therapy of acute spinal cord injury. A series of treatment protocols have thus been designed for treatment of acute spinal cord injury utilizing hyperbaric oxygen. The study has been in progress for the last two years and involved more than 50 patients; results from the therapy trial in 25 patients over the last 18 months will be presented in this preliminary report. Hyperbaric oxygen therapy was generally initiated approximately 7 1/2 hours following injury. Pretreatment and posttreatment motor scores were compared with those of patients given conventional therapy for acute spinal cord injury. Under these circumstances, patients receiving hyperbaric oxygen therapy appeared to recover more quickly, although their final motor scores were about the same as those of patients receiving conventional therapy. Thus, alter the time course of recovery, perhaps without altering the final neurological outcome. <>

    • Gelderd JB, Fife WP, Bowers DE, Deschner SH and Welch DW (1983). Spinal cord transection in rats: the therapeutic effects of dimethyl sulfoxide and hyperbaric oxygen. Ann N Y Acad Sci. 411: 218-33. Summary: <>

    • Gelderd JB, Welch DW, Fife WP and Bowers DE (1980). Therapeutic effects of hyperbaric oxygen and dimethyl sulfoxide following spinal cord transections in rats. Undersea Biomed Res. 7 (4): 305-20. Summary: Thirty adult, male, Long-Evans hooded rats underwent spinal cord transections at the T5 vertebral level. Following surgery, animals were separated into three groups: Group I received only normal postoperative care; Group II received daily hyperbaric oxygen (HBO) treatments for 47- 54 consecutive days; Group III received the same HBO treatment as Group II in addition to subcutaneous injections of dimethyl sulfoxide (DMSO) for 10 consecutive days. All animals were killed 60-70 days postlesion. The lesioned area of spinal cord was removed and prepared for light and electron microscopy. Group I animals showed typical scar reduction of cavitations, increased scarring, and more nerve fibers within the lesion. Three animals in this group exhibited coordinated hindlimb movement, with one animal showing weight-bearing ability. The lesion sit in group III animals revealed a reduction in collagen formation and a further increase in the number of nerve fibers. Six animals in Group III showed coordinated hindlimb movements; among these two displayed weight-bearing ability and sensory return. <>

    • Higgins AC, Pearlstein RD, Mullen JB and Nashold BS, Jr. (1981). Effects of hyperbaric oxygen therapy on long-tract neuronal conduction in the acute phase of spinal cord injury. J Neurosurg. 55 (4): 501-10. Summary: To study the acute effects of hyperbaric oxygen ventilation (HBO) on long-tract function following spinal cord trauma, the authors employed a technique for monitoring spinal cord evoked potentials (SCEP) as an objective measure of translesion neuronal conduction in cats subjected to transdural impact injuries of the spinal cord. Control animals subjected to injuries of a magnitude of 400 or 500 gm-cm occasionally demonstrated spontaneous return of translesion SCEP within 2 hours of injury when maintained by pentobarbital anesthesia and by ventilation with ambient room air at 1 atmosphere absolute pressure (1 ATA). Animals sustaining corresponding injuries but receiving immediate treatment with HBO at 2 ATA for a period of 3 hours following impact demonstrated variable responses to this treatment modality. Animals sustaining injuries of 400 gm-cm magnitude showed recovery of translesion SCEP in four of five cases, while animals sustaining injuries of 500 gm-cm magnitude responded to HBO treatment by recovery of SCEP no more frequently than did control animals. When the onset of HBO therapy was delayed by 2 hours following impact, there appeared to be no demonstrable protective effect on long-tract neuronal conduction mediated by HBO alone. The observations suggest that HBO treatments can mediate preservation of marginally injured neuronal elements of the spinal cord long tracts during the early phases of traumatic spinal cord injury. These protective effects may be based upon the reversal of focal tissue hypoxia, or by reduction of tissue edema. HBO treatment markedly diminished the protective effects of HBO on long-tract neuronal conduction following traumatic spinal cord injury. <>

    • Ishihara H, Matsui H, Kitagawa H, Yonezawa T and Tsuji H (1997). Prediction of the surgical outcome for the treatment of cervical myelopathy by using hyperbaric oxygen therapy. Spinal Cord. 35 (11): 763-7. Summary: The effectiveness of hyperbaric oxygen therapy (HBO) in predicting the recovery after surgery in patients with cervical compression myelopathy was evaluated. HBO has been used to treat brain and spinal cord diseases, but the effect is generally temporary. This is the first paper to utilize HBO as a diagnostic tool to evaluate the functional integrity of the spinal cord. The study group consisted of 41 cervical myelopathy patients aged 32-78 years. Before surgery, the effect of HBO was evaluated and was categorized as four grades. The severity of the myelopathy and the recovery after surgery were evaluated by the score proposed by the Japanese Orthopaedic Association (JOA score). The correlation between many clinical parameters including the HBO effect and the recovery rate of JOA score was evaluated. The recovery rate of JOA score was found to be 75.2 +/- 20.8% in the excellent group, 78.1 +/- 17.0% in the good group, 66.7 +/- 21.9% in the fair group and 31.7 +/- 16.4% in the poor group. There was a statistically significant correlation between the HBO effect and the recovery rate of the JOA score after surgery (r = 0.641, P < 0.0001). The effect of HBO showed a high correlation with the recovery rate after surgery as compared to the other investigated parameters. HBO can be employed to assess the chance of recovery of spinal cord function after surgical decompression. <> Department of Orthopaedic Surgery, Toyama Medical and Pharmaceutical University, Japan.

    • James PB (1993). Dysbarism: the medical problems from high and low atmospheric pressure. J R Coll Physicians Lond. 27 (4): 367-74. Summary: The most serious problems resulting from a change in ambient pressure are pulmonary barotrauma with air embolism and decompression sickness. The small differential pressures used in ventilators at atmospheric pressure may tear lung tissue and, in diving, deaths have occurred from the expansion of pulmonary gas on an ascent of less than two metres. The bubbles of respired gas that enter the systemic circulation often occlude cerebral arteries and may cause infarction. In decompression sickness, bubbles form in the tissues from supersaturation of the nitrogen or helium absorbed under pressure. Joint pain--the 'bends'--is associated with gas in particular connective tissue. Serious decompression sickness results from the entry of microbubbles into the systemic veins. Large numbers of bubbles trapped in the lung cause an acute respiratory syndrome known as 'chokes'. If the lung filter is overwhelmed, or microbubbles pass into the systemic arteries through an atrial septal defect, they may open the blood-brain barrier, affecting brain and spinal cord function. Untreated, demyelination with relative preservation of axons may occur, the pathological hallmarks of multiple sclerosis. Gas bubble disease requires urgent compression in a hyperbaric chamber and the use of high partial pressures of oxygen. <> Wolfson Hyperbaric Medicine Unit, Ninewells Hospital, Medical School, Dundee.

    • Jones RF, Unsworth IP and Marosszeky JE (1978). Hyperbaric oxygen and acute spinal cord injuries in humans. Med J Aust. 2 (12): 573-5. Summary: Clinical assessment of a regime of hyperbaric oxygen within 12 hours of acute spinal injury in humans suggests that further study of this method of treatment is indicated. For statistical proof of the efficacy of this form of treatment study of a large number of patients is necessary and an Australia-wide study is suggested. A recommendation is made for early referral to the spinal unit. <>

    • Kochanek PM, Jenkins LW, Edward Dixon C and Clark RS (2001). HBO: It's not ready for prime time for the treatment of acute central nervous system trauma. Crit Care Med. 29 (4): 906-8. Summary: <>

    • McVicar JP and Luce JM (1986). Management of spinal cord injury in the critical care setting. Crit Care Clin. 2 (4): 747-58. Summary: Approximately 12,000 Americans suffer traumatic spinal cord injuries each year. This article discusses the management of their neurologic, respiratory, cardiovascular, gastroenterologic, and genitourinary complications in the critical care setting. <> University of California, San Francisco, School of Medicine.

    • Narayana PA, Kudrle WA, Liu SJ, Charnov JH, Butler BD and Harris JH, Jr. (1991). Magnetic resonance imaging of hyperbaric oxygen treated rats with spinal cord injury: preliminary studies. Magn Reson Imaging. 9 (3): 423-8. Summary: Magnetic resonance imaging (MRI) has been performed to assess the efficacy of hyperbaric oxygen (HBO) treatment on experimental spinal cord injury in a rat animal model. A moderately severe injury, similar to Type III injury seen in humans (Kulkarni et al. Radiology 164:837;1987) has been chosen for these studies. An improvement in the neurologic recovery (based on Tarlov scale) has been observed following HBO treatment over a period of 72 hr. Based on MRI, HBO treatment appears to arrest the spread of hemorrhage and resolve edema. <> Department of Radiology, University of Texas Medical School, Houston 77030.

    • Puttaswamy V, Bennett M and Frawley JE (1999). Hyperbaric oxygenation treatment of acute paraplegia after resection of a thoracoabdominal aortic aneurysm. J Vasc Surg. 30 (6): 1158-61. Summary: Acute spinal cord ischemic injury after resection of thoracoabdominal aneurysm remains a relatively common and potentially devastating complication. The complete resolution of postoperative paraplegia after resection of a type II thoracoabdominal aneurysm, after treatment with hyperbaric oxygenation, is reported. <> Department of Vascular and Transplantation Surgery, Prince of Wales Hospital, University of New South Wales, Sydney, Australia.

    • Yeo JD, Lowry C and McKenzie B (1978). Preliminary report on ten patients with spinal cord injuries treated with hyperbaric oxygen. Med J Aust. 2 (12): 572-3. Summary: A preliminary report is presented on 10 patients with spinal cord injuries who were treated with hyperbaric oxygen. The results suggest that by supporting injured spinal cord tissue with oxygen under pressure, improvement in nerve function may occur. No deterioration of motor power or sensation was evident during or after hyperbaric oxygen treatment in any of these patients. The possible contribution of ischaemia to the pathology of spinal cord injury should encourage further experimental research and clinical trials with hyperbaric oxygen. <>

  10. #10

    hyperbaric treatment in 1834

    For an historical perspective on hyperbaric treatment of spinal cord injuries, I just happened to come across a reference that states the first use of a hyperbaric chanber occurred in 1834 by Junod. (

    My first impression was that in spite of the fact that Junod reported favorable results, that in the past 167 years since his study that there's been plenty of time to hash things out and fully investigate his results.

    As an aside, there is also some interesting reading in this article about nerve cells that were reported to continue to regenerate after death.

    David Berg

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