Advantages Spinal HBO

 

Caveat

  • The following list provides a 'knowledge share base' working to collaborate and promote the benefits of Hyperbaric Oxygen Therapy.

  • Australia is not a leader in this field but lagging behind the rest of the world in relationship to the wider applications of modern Hyperbaric Oxygen Therapy using different 'pressure protocols for different conditions'. 

  • The information provided does not constitute a medical endorsement or recommendation. It is intended for informational purposes only, and no claims, either real or implied, are being made. 

  • 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.

  • 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.