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Spinal cord injury

Spinal Cord Injury

Spinal Cord Injury (SCI) is an injury to the head and the spinal cord caused by trauma or destructive pathologies such as tumors that cause compression and deformity on spinal cord.  Left untreated this can lead to neurovascular deterioration, reduced blood supply and oxygen supply (ischemia and hypoxia), swelling and consequent degeneration of nerve cells (neurons) leading to Paraplegia and Quadriplegia.

“I was declared quadriplegic after my accident."
"Now, after hyperbaric I am driving my car.”  -  A.R. Parksville


Testimonial: Motor vehicle accident with SCI end result

Hello, my name is Ryan Clarkson and I am an incomplete paraplegic.
I went from a wheelchair to walking with a cane with a help of oxygen therapy
"
 -  Ryan C, Vancouver

 

Hyperbaric oxygen therapy can reverse neuronal damage by providing immediate high oxygen levels to injured nerve tissue. Sufficient oxygen can activate anatomically intact but dormant neurons in the penumbra zone, zone with diminished tissue oxygenation surrounding infarct (dead) cells.  Hyperbaric oxygen relieves ischemia of the grey matter of the spinal cord and reduces swelling of the white matter.  Increased oxygen levels in the cerebral spinal fluid correct biochemical disturbances at the immediate and distal sites of spinal cord injury including metabolic enzymatic disturbance, therefore reducing secondary spinal cord degeneration.

The key element in preventing neurovascular deterioration in spinal cord injury is early hyperbaric oxygen therapy implementation. Further hyperbaric oxygen therapy in later rehabilitation will speed up neuromuscular recovery.

Although SCI fits under “investigative condition” category and may not be covered by insurance, many hospitals around the world especially in Asia (ref Asamoto et al. 2000, Lee et al.  1989) are using hyperbaric oxygen as an initial treatment in acute patients and later as addition to rehabilitation in chronic patients.

Early oxygen therapy provides protection against progressive degeneration of post traumatic spinal cord injury.

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Spinal cord injury recovery 
by Ryan C, Vancouver
:

"I’ve already surpassed everyone’s expectations of what my limits are supposed to be, and I look forward to keep proving them wrong!!"

Spinal cord injury
A.R. - Parksville

"A picture tells a thousand words. Thanks!"

Symptoms Rational for HBOT Cost vs benefits
In acute, early SCI neurovascular damage of the spinal cord results in decreased blood flow (ischemia) and reduced oxygen supply (hypoxia) causing swelling and inflammation that further reduce blood supply. This vicious circle causes further progressive neuronal damage. Early oxygen therapy provides protection against progressive degeneration of post traumatic spinal cord injury Shorter hospital stay and faster rehabilitation
Inability to exercise due to excess concentrations of lactate, pyruvate and ammonia cause spasticity andfatigue Improves metabolic circulatory function which reduces muscle spasm and increases muscle strength. Increases capacity for exercise and reduces fatigue Improved neuromuscular function and faster recovery
Headaches Improves CSF (cerebral spinal fluid) dynamics, reduces intracranial pressure (ICP) and neurovascular deterioration. This would reduce migraine and cluster headache attacks and pains Improved quality of life
Immobility can cause pressure sores (decubitus ulcer) – open wound caused by pressure on the skin. Speeds up wound healing by promoting micro circulation and fibroblastic function of collagen synthesis A few sessions of HBO can turn a hypoxic/ischemic non-healing wound into a healing wound. Cost of wound dressing alone can reach $4000-$5000 per year
Inflammation – caused by reduced blood flow, leads to accumulation of toxic substances (ammonia and lactate). Consequent swelling further impairs blood supply causing pain. Improved blood supply reduces inflammation and swelling which cause pain. Improved quality of life
Bacterial infection promotes ischemia and hypoxic development which interferes with local perfusion. Hypoxia limits antibiotics therapeutic function. Prevents and treats infection by: having direct bacteriostatic effect (kills most bacteria), improving function of white blood cells (phagocytosis), improves function of antibiotics. Improved circulation in the wound bed allows for successful skin grafting.
Deep bone infection – osteomyelitis Improves removal of necrotic (dead) bone, facilitates formation of a new bone tissue(osteogenesis) and strengthens the existing bone structure If not responding to antibiotics osteomyelitis can cause death. (Christopher Reeves)
Muscle weakness and pain Relives pain by removing excess of ammonia, lactate and pyruvate. Reduces muscle spasm and increases muscle strength. Increases exercise capacity and range of movement, reduces weakness and fatigue Faster recovery. Effect magnified when combined with physiotherapy and electrical stimulation.
Peripheral nerve damage Facilitates nerve regenerationImproves sensitivity and decreases parasthesia “pins and needles” sensation Faster recovery. Results even better when combined with functional electrical stimulation.
Central nerve damage – loss of control, inability to make a movement Improved brain oxygenation and circulation. Improved permeability of blood brain barrier (BBB). Activation of the unaffected (dormant) neurons in the penumbra zone. Faster recovery due to improved control of movement combined with improved neuromuscular function.
Bowel problems such as constipation, diarrhea and impaction that can lead to perineal fissure, fistulas and other complication. Soiled skin can be source of infection. Regulates motility.Enhances closure of perineal fistulas and fissures. Prevents infections by improving skin microcirculation and strengthening immune system. Reduced/avoided hospital stay.
Bladder dysfunction (incontinence) – susceptibility to infection is due to retention of urine and frequent need for catheterization (causing bacteria that are normally on the skin to be pushed into the bladder) Reduces bladder spasticity (muscle tension). Increases bladder capacity and improves bladder control of emptying. Urinary urgency and frequency is reduced. Prevents infections. Reduced possibility of infections and open wounds (pressure sores).
Respiratory problem – reduced vital capacity, impaired cough reflex (aspiration pneumonia) Increases vital capacity. Prevents respiratory tract infections. Improved quality of life.
Further reading:
  1. Asamoto S, Sugiyama H, Doi H, Iida M, Nagao T, Matsumoto K. Hyperbaric oxygen (HBO) therapy for acute traumatic cervical spinal cord injury.Spinal Cord. 2000 Sep;38(9):538-40.
  2. Jain,KK: Textbook of hyperbaric medicine: Ch 14:Hyperbaric Oxygen Therapy in Wound Healing, Plastic Surgery, and Dermatology, Hogrefe& Huber Publishers, Inc., 3rd Ed.14: 213–241, 1999
  3. Jain,KK: Textbook of hyperbaric medicine: Ch 13: Hyperbaric Oxygen Therapy in Infections, Hogrefe& Huber Publishers, Inc., 3rd Ed.13: 189 –211, 1999
  4. Kindwall, Eric P., MD: Hyperbaric Medicine Practice: Ch 17:Wound Management: Best Chronic Wound Care Practices for The Hyperbaric Practitioners, Best Publishing Company, 2nd Ed: Ch 17:395-429,1999
  5. Kindwall, Eric P.,MD: Hyperbaric Medicine Practice: Ch 33:Enhancement of Healing in Selected Problem Wounds, Best Publishing Company, 2nd Ed: Ch 33:813-850,1999
  6. Kindwal, Eric P.,MD “The use of Hyperbaric Oxygen in Treatment of Osteomyelitis” Hyperbaric Medical Practice 1999; 23:604 –613
  7. Park TS, Owen JH. Surgical management of spastic diplegia in cerebral palsy. The New England Journal of Medicine 1999 326:745-749.
  8. Neubauer RA, et al. Cerebral oxygenation and the recoverable brain. Neurol Res, 20 Suppl 1: S33-6, 1998
  9. Tompach PC, Lew D, Stoll JL.Cell response to hyperbaric oxygen treatment.Int J Oral Maxillofac Surg. 1997 Apr;26(2):82-6
  10. Yeo (1977) A study of the effects of hyperbaric oxygen on the experimental spinal cord
  11. Stempien LM. Gaebler-Spira D. Rehabilitation of children and adults with cerebral palsy. In: Physical Medicine and Rehabilitation. Braddon. RL, Buschbacher. R, Dumitra, D, Johnson. EW. Matthews, D, Sinaki, M.eds., Saunders, 1996, pp.1113-1132.
  12. Mader JT, Adams KR, Wallace WR, Calhoun JH:Hyperbaric oxygen as adjunctive therapy for osteomyelitis.Infect Dis Clin North Am. 1990 Sep;4(3):433-40. Review
  13. Boykin JV Jr, Crossland MC, Cole LM.Wound healing management: enhancing patient outcomes and reducing costs.J Healthc Resour Manag. 1997 May;15(4):22, 24-6.
  14. Marmo M, Contaldi G, Luongo C, Imperatore F, Tufano MA, Catalanotti P, Baroni A, Mangoni G, Stefano S, Rossi F[Effects of hyperbaric oxygenation in skin and pulmonary infections caused by Pseudomonas aeruginosa].Minerva Anestesiol. 1996 Sep;62(9):281-7
  15. Brown RB, Sands M. Infectious disease indications for hyperbaric oxygen therapy.Compr Ther. 1995 Nov;21(11):663-7. Review
  16. Biether JK, Cummins 5K, Nelson KB. The California cerebral palsy project Pediatric Perinatology and Epidemiology 1993; 6:339-351.
  17. Krageloh-Mann, Hagberg G, Meisner C, Schelp B, Haas G, Eeg-Olofsson KE, Hagberg B, Michaelis R. Bilateral spastic cerebral palsy – A comparative study between southwest Germany and western Sweden. I Clinical patterns and disabilities. Developmental Medicine and Child Neurology 1993; 35:1031-1047.
  18. Halm M, Zearley C.:Assessment and follow-up of problem wounds in the hyperbaric oxygen setting.Ostomy Wound Manage. 1991 Nov-Dec;37:51-9
  19. Mayo N,. The effect of physical therapy for children with motor delay and cerebral palsy: A randomized clinical trial. American Journal of Physical Medicine and Rehabilitation 1991; 70-258-267.
  20. Peacock WJ, Staudt LA. Spasticity in cerebral palsy and the selective dorsal rhizotomy procedure. Journal of Child Neurology 1990; 5:179-185.
  21. Katz RT, Rymer WZ. Spastic hypertonia: Mechanisms and measurement. Archives of Physical Medicine and Rehabilitation 1989; 70:144-155.Lee HC, Niu KC, Chen SH, Chang LP, Lee AJ.Hyperbaric oxygen therapy in clinical application. A report of a 12-year experience. Zhonghua Yi Xue Za Zhi (Taipei). 1989 May;43(5):307-16
  22. Bozynski MEA, Nelson MN, Genaze D, Rosati-Skertich, C, Matalon. TAS. Vasan, U, Naughton, PM. Cranial ultrasonographyand the prediction of cerebral palsy in infants weighing < 1200 grams at birth. Developmental Medicine and Child Neurology 1988; 30:342-348.
  23. Palmer FB, Shapiro BK, Wachtel RC, Allen, MC, Hiller JE. Harryman SE. Mosher BS. – Meinert CL, Capute AJ. The effects of physical therapy on cerebral palsy. A controlled trial in infants with spastic diplegia. The New England Journal Medicine 1988: 318:803-808
  24. Kieper NR (1987) the use of Hyperbaric Oxygen Therapy in the rehabilitation of spinal cord injured patients due to decompression sickness. In Kindwall EP (ed) Proceedings of the 8th international congress on hyperbaric medicine. Best, San Pedro, Ca
  25. Herndon WA, Troup P, Yngve DA, et al. Effects of neurodevelopmental treatment on movement patterns of children with cerebral palsy. Journal of Pediatric Orthopedics 1987; 7:395-400.
  26. Kudrjavcev T, Schoenberg BS, Kurland LT, Groover RV. Cerebral palsy: Survival rates, associated handicaps, and distribution by clinical subtype. Rochester, MN 1950 – 1976. Neurology 1985; 35:900-903.
  27. Molnar GE. Cerebral palsy. In Molnar GE (ed): Pediatric Rehabilitation, Baltimore. Williams & Wilkins. 1985,481-533.
  28. Eltorai I, Hart GB, Strauss MB.Osteomyelitis in the spinal cord injured: a review and a preliminary report on the use of hyperbaric oxygen therapy.Paraplegia. 1984 Feb;22(1):17-24
  29. Hart GB, Strauss MB (1984) Vital capacity of quadriplegia patients treated with hyperbaric oxygen therapy. J Am Paraplegia Soc: 113-114.
  30. Yeo JD.The use of hyperbaric oxygen to modify the effects of recent contusion injury to
    the spinal cord.Cent Nerv Syst Trauma. 1984 Winter;1(2):161-5
  31. Geldert JB, Fife WP, Bowers DE, Deschner SH, Welch DW (1983) Spinal cord transection in rats: the therapeutic effects of dimethyl sulfoxide and hyperbaric oxygen therapy. Ann NY Acad Sci 911: 218-233
  32. Kudrjavcev T. Schoenberg BS,  Kurland LT. Groover, RV. Cerebral Palsy: Trends in incidence and changes in concurrent neonatal mortality: Rochester. Mn, 1985 – 1970. Neurology 1983; 33:1433-1438.
  33. Sukoff MH (1982) Use of hyperbaric oxygen therapy for spinal cord injury. Neurochirurgia 24:19.
  34. Lance JW. Symposium Synopsis. In: Feldman RG, Young RR, Koella WP Spasticitv:Disordered Motor Control. (Eds).Chicago: Yearbook Publishers: 1980. p. 485-494.
  35. Higgins AC, Pearlstein RD, Mullen JB (1981) Effect of hyperbaric therapy on long tract neuronal conduction in acute phase of spinal cord injury. J Neurosurg 55:501-510
  36. Tator, C.,MD, Current concepts in the immediate management of Spinal Cord Injury; December 1979 [PDF]
  37. Yeo (1977) A Study of the effects of hyperbaric oxygen on the experimental spinal cord injury. July 30, 1977 Medical Journal of Australia pg.145-147.
  38. Yeo JD (1976) Treatment of paraplegic sheep with hyperbaric oxygenation. Med J Austr 1:538-540.
  39. Tator, C., MD, Review Article; Acute Spinal Cord Injury: A review of recent studies on treatment and pathophysiology; CMA Journal, 1972 [PDF]
  40. Locke GE, Yashon D, Feldmann RA (1971) Ischemia in primate spinal cord injury. J Neurosurg 34:614
  41. Hartzog JI, Fischer RG, Snow C (1969) Spinal cord trauma: effects of hyperbaric oxygenation. Proc Ann Clin Spinal Cord Injury Conf 17:70-71
  42. Machado JJ. Reduction of spasticity, clinicallv observed in patients with neurological diseases, submitted .to hyperbaric oxygen-therapy specially children with cerebral palsis. Transcripts from the annual meeting of the Undersea and Hyperbaric Medicine conference, 1969
  43. Maeda N (1965) Experimental studies on the effect of decompression procedures and hyperbaric oxygenation for the treatment of spinal cord injury. J Natl Med Assoc 16:429-447

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