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HyperMED - Spinal Cord Injury

 

 

HyperMED Australia

The final frontier in the treatment of complex spinal cord and neurovascular injury is focused on ‘repair and functional restoration’. This involves the use of growth factors to promote axonal sprouting, activation of idling and non-functional neurons whilst promoting neovascularization (new capillary formation) of damaged areas. Research efforts to bridge spinal cord and brain cell lesions are also underway experimentally, using transplanted tissues and bridging devices.

Developing biotechnology techniques and DNA restructuring show incredible promise, but the exquisite topographic organization of the ascending and descending nervous system pathways including the brain and spinal cord provide an extremely difficult hurdle still to be overcome. Success in these reconstructive efforts will undoubtedly overlap with the best outcome being the patient with capability to improve ‘neurovascular’ support into the damaged regions.

The extent of neurovascular deterioration can be significantly diminished with early and continued HBOT implementation. HBOT will provide a fertile neurovascular platform for emerging stem cell implant procedures and techniques using DNA restructuring. The dynamic impact of these and future procedures again, will be dependent upon the integrity of the underlying supporting neurovascular bed.

The objective HyperMED (Melbourne Hyperbaric and the Spinal Rehabilitation Group) is to raise the awareness of Hyperbaric Oxygenation promoting early usage and intervention in major hospitals and continued rehabilitation in day facilities for the long term injured. Our work demonstrates that even small gains can dynamically effect the quality of life for these patients.

Hyperbaric Medicine is not recommended as a 'cure' and is not the ‘missing link’ in spinal cord injury but certainly has a major role as part of the developing answer in the treatment of spinal cord and brain injury. HBOT with appropriate physical therapy and the emerging new frontier of biotechnology restorative medicine, will undoubtedly revolutionize the plight of those suffering from spinal injury and numerous other forms of crippling neurological and vascular disorders.

 

Case Study – C6/7 Quadriplegia

Peter a 39-year old quadriplegic male, suffered a C6/7 dislocation during a car accident in 1994. Surgical reduction and fixation of the dislocation immediately after the accident has observed limited return of function.

He has made partial recovery limited to his upper arms and partial hands enabling him to operate a wheel chair, but with difficulty.

MRI investigation before commencing treatment with Spinal Rehabilitation Group confirms severe spinal cord injury at the level of C6/7. A large atrophic T1 hypo and T2 hyperintense lesion in the cervical cord consistent with post traumatic ‘syrinx formation’ extending from the level of C6 to T1.

Accompanying medicolegal reports supplied by Peter identifies that ‘syrinx formation associated with post traumatic cord injury, is a common cause for further deterioration in the neurological status of a quadriplegic’. Continuing neurological deterioration warrants further invasive surgery.

Peter commenced daily HBOT and physical therapy. Change in Peter’s condition has been extremely slow, probably owing to the fact that his injury occurred during 1994 with fixed deficit for many years.

 

Peter states “ the first thing both my wife and I noticed was that my energy levels had gone up enormously. Before I started treatment I had extremely limited ability to get myself around in my wheel chair. I could only go so far and then needed a rest. I had always tried to push a little bit further, but I could never break through that barrier. Usually I would require at least three five-minute breaks to complete a 2 km block. This has now steadily improved and now I can cover the same distance in a shorter time and without even a break.

Also my skin has improved a lot, it doesn’t feel as dry and looks more natural. When I get my daily stretch exercises done I now know where my legs are with my eyes closed. Before treatment I had absolutely no idea where any part of my body was below the middle of my chest. You could place my foot up over my head and I wouldn’t even know! I can also now feel my muscles stretch and now have some sensation in my legs, stomach and back region. My back has become a lot stronger and I can now pull my stomach in and upwards towards my ribcage. I can also contract my buttocks now. I couldn’t even feel these areas let alone move before starting treatment. I can now sit and manage myself in my wheelchair and transfer a lot better because of improved pelvic and abdominal control.

During January 2000 my reflexes in my knees came back. This has been confirmed with a number of the insurance doctors evaluating my progress. About 18 months after of my accident I was required to be assessed by independent medical doctors for the insurance company. One of the tests during this insurance assessment identified which reflexes were present and which were completely gone. The reflexes in my knee were one of the groups that were completely absent. Now they have returned.

The other major improvement that I have had is that I can now tolerate the hot temperature a lot better. With my sort of injury there is difficulty in my body adjusting to temperature changes. In the summer of 98/99 I would have to go inside an air-conditioned room when the temperature got to about 25 degrees Celsius. This past summer in Melbourne with temperature up around 37 degrees, I have been able to cope without difficulty. This has given me a lot more quality of life because now I can go out with my family a lot more than before without having to worry about getting overheated.

The latest improvement is that I am getting some more feeling in my big toe and the lower part of my right leg. You can feel the muscle tighten in my right calf when I try to contract it. A lot of people comment that I look really well and healthy. I want to thank Dr Hooper for all he has done for me and I give God the glory for healing me.”

MRI PHOTOS 

Comparison MRI studies of Peter were performed at different MRI facilities. MRI confirms traumatic cervical spinal cord involvement including mild atrophy of the mid and upper cervical cord, focal expansion spanning from C6 to T1 levels due to bilocular T1 hypo and T2 hyperintense lesion in keeping with hydromyelia. T2 hyperintense signal extends into the proximal thoracic cord centrally in keeping with myelomalacia/gliosis, down to the T2 level. Peter has undoubtedly continued to experience dynamic clinical changes however his medicolegal reports including comparison MRI reports indicate that his condition remains ‘stable’.

Peter continues with active treatment attending usually twice per week receiving 90-minute HBOT and appropriate physical therapy. Click here for more patient testimonials.

 

Case Study – C5/6 Quadriplegia

Another spinal cord injured patients attending for Hyperbaric therapy and spinal management is Ms. JK. Julie is a 20-year old female, with C5/6 dislocation resulting in quadriplegia. Julie’s injuries were the result of a severe motorcar accident that occurred in April 1998. She received intensive care for multiply injuries for an eight-week period. C5/6 spinal fusion was performed with an anterior spinal fusion supported by three screw-fixing device.

MRI investigation requested at the commencement of her treatment revealed realignment and fusion at the C5/6 level. However, screws placed in situ at the C5 and C6 are observed to be extending from the posterior aspect of the vertebral body into the central canal at both the levels resulting in significant central canal compromise causing obstruction of the cerebral spinal fluid with imposed cord rotation. The cord adjacent to the C5/6 fusion has deteriorated with T2 hyperintensity changes (compressive myelomalacia) of the normal cord signal.

Julie’s progress prior to commencing HBOT had been minimal since the accident and described with residual ‘fixed neurological deficit’. Julie has suffered significant sensory loss from the neck down with extremely limited and minimal motor ability of her upper arms and minimal response and movement to both her thumb and forefingers. Her legs suffered complete loss of motor function and normal sensory response. She complains of a burning sensation experienced across both hands, groin, upper posterior thighs and calf regions.

Treatment has included HBOT coupled with assertive physical therapy including high frequency electro-acupuncture directed to the injured site and distal affected areas including both upper and lower extremities.

Julie began to experience improvement with both bladder and bowel function within six chamber sessions. She reported movement of the toes in her right foot, and the reduction of a pressure sore that had been a concern for several months. After the 8th session Julie reported that she could feel her stomach muscles contracting and began experiencing sensation under her rib cage. She states that she is now able to ‘breathe more easily’. She has also recorded some improvement with movement of both her fingers and thumb.

By the 10th session Julie reports improved circulation to her legs and feet. She states that her skin is not as ‘blotchy’. Julie states that the wound has now begun to fade and disappear. She states that her pressure sore had previously required constant attention and dressing. 

By the 12th session she reports improvement her stomach muscles enabling her to breathe more easily. She reports that her pressure sore is now half the size it was before commencing treatment. She states that her legs and feet have not been as purple or as cold during the past several days.

By the 15th session, Julie reports continuing improvement of her stomach muscles, and noticing improvement in her bowel and bladder function. She reports that her breathing has improved considerably, with her ability to exert some force with a cough. She experienced continued improvement with extremity circulation, and her pressure sore had almost completely gone. Julie reports improved fine motor capability of her thumbs and forefinger, and improved ability to support herself with her upper arms. She states that spasms which were previously uncontrolled and uncoordinated now mimic movement. She reports that her foot would now move upwards with her leg following as if attempting to perform the movement voluntarily, where previously the spasms would result in her leg going straight and shaking violently.

By the 25th session Julie reports continuing improvement with extremity limb function. She could now slightly tense her left calf muscle, and contract her right thigh, calf and buttock muscles. She reports that she could feel her lower spine muscles contract slightly, and experienced improved sensations throughout her body. By the 29th sessions she states her ability to cough is ’10 times stronger’!

The following is extracted from Julie’s 1999/2000 diary :

 “….35th 90-minute chamber session. Back muscles feel stronger.  My stomach muscles and toes are showing slight improvements. Sensations are beginning to change. My legs feel the urge to move. When I was doing my bed transfer this morning, my leg felt as though it was ready to move. This doesn’t happen all the time.

37th 90-minute chamber session. I can begin to clinch a fist with my left hand. Movements in my little finger, thumb, pointer and middle fingers have improved slightly. People around me are beginning to notice changes. They are telling me I look healthier, and are beginning to notice the improvement in my hand function. I have more control. My wrists are stronger and movements are gradually coming back. My right leg is showing greater improvements than the left. The circulation has increased. The right leg tends to be warmer.

40th 90-minute chamber session. All my toes on my right foot moved. This is not consistent. My big toe and second toe move consistently. Thigh and calf muscle flicker consistently on my right leg. On my left leg my big toe and little toe are beginning to move more. I’ve been feeling tired when I come out of the chamber. I’ve noticed an increase in neurogenic pain, this mainly occurs in my feet at night- time. Foot rotations seem to help. Spasms have decreased. When I bypass the catheter the sensation beforehand is stronger.

41st 90-minute chamber session. Last night all my toes on my right foot moved, the muscle underneath moved also. It was a strong movement it happened consistently until I fell asleep. When they moved up I could feel an upward pull in my ankle and lower leg muscles. My toes on my left leg all moved, they had a strong movement. Bev woke Michael up she was excited.

43rd 90-minute chamber session. I can feel my pelvic floor muscles. I can squeeze them the tiniest bit. Stomach muscles are becoming stronger. Movement was consistent up until yesterday. My big toe and little toe move and the two toes next to my little toe twitch. I can control the twitch. On my right foot my big toe, second toe and little toe move. The third and fourth toes move also, not as much as the others. My right leg muscles tense consistently but the strength to which they tense varies. My left hand can squeeze more. The warmth in my legs is the significant change. Carers have noticed they aren’t as cold anymore. This shows an increase in circulation.

46th  90-minute session. This morning I went to the toilet myself! I took senokot and coloxyl last night the same as I do every night before a bowel morning. When I woke this morning I could feel I needed to go to the toilet. It’s being so long since I felt that sensation that I ignored it and still had my carer use a suppository. Five minutes later I felt a strong urge to go to the toilet. The suppository didn’t contribute to this; there wasn’t enough time for it to take effect. It came away separately. Wrist flexion has come back on my right hand. It has been getting stronger. After spasms in my feet, I can move my foot down slightly. This isn’t consistent, however it is happening more frequently.

47th 90-minute chamber session. Calf and thigh muscle still tense slightly. Spasms are now becoming a partial movement, this happens frequently. Mum noticed the tone in my legs, when she did my exercises. She noticed they are beginning to become firm and they have weight in them now. Pelvic floor muscles are still returning slightly. Stomach muscles have improved. I can breath in easier.

49th 90-minute chamber session. Circulation is continually improving. Finger movements on my right hand have improved, they all move except for my pointer finger, which the tip of it moves slightly, this is not consistent. The movements on my left hand are not as strong but I can begin to clinch a fist. I have noticed an improvement in stomach muscles. I am now able to do twenty sit- ups opposed to ten. Wrist flexion on my right hand is improving.

51st 90-minute chamber session. This morning I woke whilst I was still in bed, my bowel was ready to go off. This was about five six o’clock and everybody was still in bed asleep. I tried to wake Mum, but couldn’t. I was able to stop my bowel from going off. I don’t know how I was able to do this, I just was. I’m not sure if it was controlled or not. My pelvic floor muscles are very weak and not consistent.

54th 90-minute chamber session. My muscles are slowly returning e.g. stomach, calf and thigh muscles. My legs are gradually regaining tone and my right leg muscles are still tensing slightly. All in all I am noticing slow gradual changes. My toes move continuously on my right foot.  My skin has improved dramatically, it isn’t blotchy and I have not any problems with pressure sores. This is a significant indication that circulation is continually improving. Central abdominal muscle is returning slightly. Pelvic floor muscles are more noticeable in my buttocks.

55th 90-minute chamber session. . I have increased abdominal sensation. I have noticed more sensitivity. I can feel menstrual cramping. I felt as the sensation of needing to empty my bladder. This was strong and was not a spasm. Sensation is becoming stronger when I by-pass the catheter. The tone in my legs are beginning to become more defined. Right leg muscles are tensing slightly stronger and my legs have the urge to move they don’t feel as heavy. Wrist flexion in my right hand is consistent.

56th 90-minute chamber session. Spasm is more a movement and after the spasm I was able to move my foot twice. The spasm was a quick, swift movement. My foot lifted up followed by my ankle then calf, next my knee and then my thigh. The sensation in my left leg and right foot has changed to slight tingling.

60th 90-minute chamber session. Increased sensation in bowels, I can now feel a push. Tingles in my feet. I have had more of an appetite over the past few weeks. My legs have being feeling heavy and tired. Circulation is continually improving. There has been an increase in spasms. Hands have neurological pain through the fingers and wrists. Pelvic floor muscles are still slight. Hand function is continually improving. I am able to use more hands rather than the tendisis grip. I can pick objects up easier. My shoulder and upper arms move more easily.

63rd 90-minute chamber session. I have had the sensation that my bladder is full. This has happened twice. It is a strong sensation.

66th 90-minute chamber session. Sphincter muscles is becoming stronger. Bladder and bowel sensation is more sensitive. Calf muscle on my left leg has began to tense more firmly and when I tense this muscle I can feel the muscle at the base of my foot and ankle tense also. When I do this the top of my foot tenses. Tone in my legs is becoming more apparent. Circulation has improved and continues to improve. I have not had any problems with my skin, e.g. pressure sores and blotchiness.

67th 90-minute chamber session. I have noticed an increase in spasm. Spasm is particular in the morning and in my legs rather than my upper body. Toe movement continues to improve. My legs have a heavy sensation and my ankles have a burning sensation.  

70th 90-minute chamber session. I can control spasms at night more easily. My legs are starting to become restless. Bladder and bowel continue to improve. My hands have still being getting neurogenic pain in them. Finger movement on my right hand is consistent and gradually becoming stronger. I am able to tense my calf muscle in my left leg slightly more. I have not noticed a dramatic difference. My abdominal muscles are slightly noticeable, they are gradually becoming stronger. I am not noticing new improvements however I are noticing the improvements are becoming consistent and stronger….”

This young lady continues in the early stages of treatment program. The promising changes experienced to date have continued including the ability to ‘hold a pen and sign her name’. Julie also now reports ‘sensation to hot and cold water on her lower extremities’. Small but consistent changes continue to alter and improve the quality of her life. It is reasonable to expect that with continuing treatments, further gains may be accomplished.

 

Hyperbaric Oxygenation and SCI

The application of Hyperbaric Oxygenation in spinal cord injury is similar to the role of HBOT that has been identified in closed head injury including brain injuries. Hyperbaric Medicine has gained considerable acceptance and respect in the management of brain and related injuries. 

The ability of HBOT to reduce edema and correct cellular ischemia are the key factors in the application HBOT in treatment of spinal cord injury. Neurosurgeon Prof. K. K. Jain in his book Text in Hyperbaric Medicine (1996 and 1999) reports numerous publications supporting the effectiveness of Hyperbaric Oxygenation in traumatic spinal cord function.

Spinal cord injury (SCI) can vary from partial cord compression to complete severance of the cord, partial obstruction of the supporting neurovascular mechanisms to complete neurovascular compression. 'Traumatic myelopathies (abnormalities of cord function) are characterized by ischemia and edema, which may lead to a cascade of degenerative effects (Jain 1996). Vasoparalysis of the cord means abnormality with constriction of the blood vessels supplying vital blood flow through the cord'.

'Compromise of the microvasculature of the cord results in decreased blood flow and oxygen supply to the grey matter (deeper structure) of the cord, with surrounding hyperemia (increased blood flow) of the white matter, and associated swelling and edema' (Jain 1996).

Jain reports that the best application of HBOT is within 2-4 hours and no more than 12 hours after direct injury for the most dramatic effects. Jain refers to this period as the ‘Golden Hour’. This is the period that relates to the transitory phase in the progression of the pathophysiological sequence of events in spinal cord injury resulting in permanent anatomical disruption. Jain states that Hyperbaric Oxygenation within this initial period, even before surgical fixation, will have a significant impact on both the short and long term outcome for the injured patient. Traction of the spine to maintain proper alignment is essential whilst HBOT is administered.

 

There are two major effects of SCI:

  • anatomical disruption of the cord with immediate secondary vascular compromise following venous stasis, edema and hypoxia (oxygen starvation), resulting in a cascade of inflammatory degenerative effects, which occur at the site of the lesion and usually spread down the cord from the site of disruption

  • functional loss and paralysis below the level of the cord injury

Surgery is usually performed in an attempt to reduce the displaced vertebral segment. Often, with severe impact trauma, the vertebral body may fracture with bone fragments displacing into the spinal cord canal and contributing to compressive changes of the cord. Most surgery involves reduction of the displacement followed by fixing and/or fusing the bone structure using bone grafts, screws, rods and other metallic fixing devices.

Surgical stabilization is generally performed within hours of the trauma. CT Scan and more recently MRI (Magnetic Resonance Imaging) investigations are performed as a post-operative measure to ensure reduction of the displaced segment. However the essential requirement of surgical reduction may in fact contribute to long term compressive effects of the already damaged cord.

This statement may ‘rock the boat’ of the conservatives. When many spinal cord injured patients, including para and quadriplegics, are reassessed with additional MRI investigations, high percentage of patients have contributory cord compression due to the fixing devices. Screws that have been inappropriately placed, or have moved over time, can project through the vertebral bone, causing further canal compromise and stenosis resulting in laceration, cavitation and other cystic changes of the cord.

Bone grafts, used as a fixing measure, are often placed within the central canal may reduce displacement of the offending vertebra, but may also contribute to compression of the cord and exiting nerve root structures. Forced removal of displaced screws may cause further spinal cord rupture as the screw is removed because cord material may be extracted along with the screw.

Spinal cord neurovascular compression differs from actual and total severance, in that many cellular structures remain intact but are non-functional. The degree of cellular damage varies within the damaged zone however, many neuronal cells do survive. This evidence is reinforced by the progressive return of certain functions of SCI patients. Many patients state that they felt as though their spine was completely disconnected but that with time there is some element of sensory and functional return.

Progressive improvement of the patient is probably due to the fact that ‘idling or inactivated’ nerve cells eventually respond as the degree of cord edema and ischemia resolves. Many patients are not so fortunate, and spinal cord degenerative changes actually progress, with further deterioration. This usually results in atrophy of the limbs, cold extremities, and the predisposition to multi level circulatory problems including ulcers, and local and systemic infections.

  

Clinical studies

Maeda (1965) published the first documented effects of Hyperbaric Oxygenation with SCI in animal experiments. Maeda suggested that tissue ischemia resulted in hypoxia due to spinal cord injury induced in dogs. HBOT at 2 ATA resulted in dramatic increases in spinal cord tissue oxygen (pO2) levels (Maeda 1965).

Hartzog (1969) demonstrated reversal of cord injured baboons with 100% O2 at 3 ATA absolute within 24 hours of injury. Locke (1971) found that lactic acid accumulates with SCI, as a direct result of restrictive tissue blood flow. Lactic acid leads to tissue hypoxia (oxygen starvation).

Yeo (1976) observed significant improvement of acute SCI induced in sheep. HBOT was performed at 3 ATA absolute within several hours of induced injury. Improved motor recovery was observed over the following eight weeks.

Yeo (1977) further demonstrated the benefits of improved blood supply with HBOT evidenced by significant reduction of cystic cord tissue necrosis and degeneration of the surrounding white matter (myelopathy) when compared to the control study group. In summary, Yeo demonstrated improved motor function and reduction of secondary cord degeneration.

Higgins (1981) studied spinal cord electro-potentials in subjects with cord damage due to impact injuries. The HBOT treated group demonstrated beneficial effects on long tract neuronal function. Higgins concluded that HBOT might afford protection against progressive degeneration of post traumatic spinal cord injury if early treatments were applied.

Sukoff (1982) studied the impact of HBOT on experimental compressive spinal cord injury. 17 cats were treated immediately after injury with 100% O2 at various pressures. No animals treated with HBOT remained paralysed, whereas six of the 13 controls remained paralysed. Five treated animals recovered fully, and all but one could walk. Only one of the control animals could walk.

De la Torre (1981) initially summarized the effects of HBOT with SCI. Further, Drs Sukoff, Professor of Neurosurgery at the University of California and Jain, Neurosurgeon (1996) assert that HBOT :

  • can reverse neuronal damage that is due to bruising rather than laceration

  • activates recoverable idling and dormant neurons in the penumbra zone (where there is diminished tissue oxygenation) surrounding infarct cells

  • relieves ischemia of the grey matter of the spinal cord

  • reduces edema of the white matter

  • increases pO2 levels in the cerebral spinal fluid dynamics

  • corrects biochemical disturbances at the immediate and distal sites of spinal cord injury including metabolic enzymatic disturbance

  • stabilizes the negative impact of metabolic disturbances. This includes the production of free radicals capable of causing vasodilatation and vascular wall damage. Hypoxia (oxygen starvation) causes a shift in glycolysis with the production of lactic acid and lowered pH levels. An imbalance of energy demand and availability results in further ischemic like state with loss of ATP available to the neurons and surrounding tissue. In addition to oxidative free radicals, excitatory amino acids are released as a consequence of vascular injury. The loss of cellular integrity and edema, combined with continuing biochemical toxic effects results in further ischemia, swelling and compression

  • can minimize and even reverse secondary cascade degenerative spinal cord effects

SCI and DMSO (Dimethyl sulfoxide)

Geldert (1983) performed spinal cord transection in animal studies. Animals were then exposed to HBOT and treated topically with DMSO (Dimethyl sulfoxide). The animals were then examined at autopsy 60-120 days after treatments, with investigations including transmission electron microscopy. Geldert demonstrated that the treated group had ‘significantly less degeneration and post lesion naked axon’s. Normally the growth of axons is completely retarded within several days of being severed. Geldert reported ‘benefits of DMSO and HBOT, as evidenced by markedly less cavitation and degeneration of the cord when compared to the control group’. 

Our treatment protocol at Spinal Rehab Group includes the use of topical application of Rehab Gel which includes DMSO applied at both the injured site as well as the myotomes and dermatomes of all spinal and degenerative neurologic patients.

Geldert identified that ‘reduction of microcirculation leads to decreased oxygen and cellular ATP levels resulting with massive platelet aggregation within the microvasculature which further compromises the blood supply to adjacent neural tissue and causes eventual cell death’. Geldert demonstrated that the inclusion of HBOT performed on the acute groups of animals sectioned all showed improved return of function.

Geldert demonstrated that the inclusion of 'DMSO protected axons and their myelin sheaths, reduced edema, increased blood flow, and accelerated return of function'. Spinal animals treated with HBOT/DMSO showed reduced cavitation and scar formation and enhanced return of function.

As free radicals are produced by all aerobic tissue and highly toxic to living cells they are rapidly eliminated by normal enzymatic activity. Following SCI, altered metabolic activity may increase free radical production resulting in cell death and release of lysosomal enzymes. DMSO has been shown to stabilize lysosomal membranes and scavenge free radicals, it may function in these capacities to reduce neural tissue destruction following injury.

Studies indicate a positive synergistic effect in combined HBO/DMSO treatments. De La Torre's results were not as favourable as he used different procedures. But Gelderd's study demonstrated a 60% effectiveness of acute transected animal spinal studies.

Geldert summary:

  • In order for axons to grow through an injured area they must be provided with a compatible biological environment such as that found in viable neuropil

  • Cavitation formation seems to be a result of the destruction of microcirculation, which results in ischemia, hypoxia, and eventual cell death with subsequent release and or production of substances that accelerate the demise of surrounding neural tissue in the spinal cord

Recent advances in the continuing treatment of SCI

Omentum transposition is one the many new advances giving doctors additional measures to close the gap between incomplete and partial recovery of spinal cord injury. In the abdominal cavity there is a membrane, called the omentum, which hangs in front of the abdominal organs and acts as a protective buffer. The omentum is extremely rich in the 'supply of neurotransmitters', the chemicals that carry nerve impulses between nerve cells. The omentum is also rich in the supply of neurovascular factors that foster both blood vessel and nerve growth.

Surgeons have developed techniques that tailor this membrane so that it can be laid directly over the damaged cord structure while still attached in the abdomen. The benefit of this procedure is that blood vessels from the omentum will grow directly into the spinal cord, supplying a potentially rich source of neurotransmitters and growth factors. This bridging technique is also being adapted with embryonic stem cell transfers for stroke and brain injured and degenerative upper motor neuron patients.

Hyperbaric Oxygenation is currently being piloted together with omentum transposition. In fact Neubauer (1998) states that HBOT provides an excellent screening technique, since those patients who improve after receiving HBOT are likely to improve after this and related cell transplant surgical procedures. We are currently investigating the availability of both this surgical and related procedures in Australia.

 

Embryonic foetal cells

Another current advancement includes the technique of grafting embryonic foetal cells into the region of damaged regions of the spinal cord and brain in injured patients. Florida scientist Dr Douglas Anderson and his colleagues at the University of Florida, repaired damaged spinal cords in cats by implanting neurons from cat foetuses in 1992. In 40% of the cases the graft recipients regained some walking ability. Anderson states that this technique, still undergoing vigorous research may some day replace ‘screw and plate’ grafting techniques.

Anderson reports that the cats that received grafting within a short period after the spinal cord injury responded the most favourably. Anderson states that the 'implanted cells may be restoring essential myelin insulation around the axons and providing essential neurochemical growth factors to assist with reproduction and growth'.

Reier, also from the University of Florida asserts that many spinal cord injured patients suffer cord trauma but unless the injury is extremely severe, many fibers are spared. Reier states that it is possible to gain many ‘little victories’ with new techniques. “If you can restore bladder or bowel function, relieve spasticity, restore sex,” he says, “those gains can bring huge improvements in the quality of life.”

Although the human spinal cord has an estimated 20-million axons, only a tiny fraction of them are necessary to restore significant function. Wise Young New York University neuroscientist states that surgeons sometimes “remove a tumour from the spinal cord that destroyed 90% of the axons, and the patient walks out of the hospital.” Anderson states that smaller functional improvements are realistic rather than dramatic ‘rising from the wheel chair’ recoveries. “Human embryo cell transplantation will happen,” states Reier and “it will occur sooner than you think.”  

 

Stem Cell Transplant

Recent studies involving laboratory rats injected with embryonic stem cells as a treatment for spinal cord injuries show better lower extremity function than control animals, according to data presented at the recent 68th annual meeting of the American Association of Neurological Surgeons in San Francisco, California.

Dr. Todd J. Stewart, from Washington University School of Medicine in St. Louis, Missouri, reported that he and colleagues delivered controlled contusion injuries to the spinal cords of 40 rats, causing complete initial flaccidity followed by some recovery at 3 weeks.

The researchers randomised the injured rats to receive either approximately 1 million embryonic stem cells by injection into the spinal cord at 9 days post-injury or no treatment. The St. Louis team compared the expected return of function in the control group with that seen in the treated rats.

At 2 weeks post-transplant, 'the treatment group showed improvement in lower extremity function', Dr. Stewart told Reuters Health in an interview during the meeting. 'This improvement continued, and at 6 weeks the rats were able to walk but displayed much spasticity. Conversely, functional improvement in the control group maximized at 3 weeks post-injury and did not improve beyond expectations for this type of spinal injury', Dr. Stewart said.

Additional analysis of the treatment group indicated that the embryonic stem cells differentiated into oligodendrocytes that wrap axons in the spinal cord.  According to Dr. Stewart, this caused myelination, which may be a partial cause of improvement.  'We are in the infancy of this research,' he noted. He and colleagues are now researching the underlying mechanisms that may have caused the functional improvements in the treated rats.  

 

What are the expectations of treatment with Hyperbaric Oxygenation?

The rationale and clinical usage of Hyperbaric Oxygenation has been detailed previously. HBOT used in the early stages of SCI are a proven rehabilitative measure, minimizing edema and the progressive ischemic changes associated with contusion. Currently Australian hospitals do not offer this vital service in acute spinal injury. Specialist neurosurgical facilities and hospitals in the United States of America and throughout Europe offer Hyperbaric Oxygenation as an initial front line measure in the treatment of acute spinal cord injury.

Before embarking on a course of HBOT it is essential to establish the exact position and integrity of the spinal cord and surrounding structures. This usually means that current MRIs and possibly CT Scan investigation are performed to determine the structural relationship between the surgical fixing devises and the cord. Enhanced MRI also enables an accurate determination of secondary myelopathy degenerative changes of the cord.

'Continuing compressive changes of the cord results in cord cavitation and a range of significant degenerative effects (myelomalacia) due to progressive ischemic effects and swelling. Deformity of the cord above the lesion can lead to upper spinal cord pressure, resulting in headaches and upper motor neuron signs due to obstructive CSF (cerebral spinal fluid) dynamics. CSF obstruction at the lesion site can occur due to the nature of the injury, and in fact be as a direct consequence of poor surgical fixation'.

The immediate benefit of HBOT in the long term injured patient is an increased capacity for exercise. Established spinal cord injured patients suffer significant biochemical limitations including excess concentrations of lactate, pyruvate and ammonia that prohibit exercise and promote fatigue. Metabolic complications associated with vascular insufficiency of the extremities lead to progressive degenerative problems, further complicating the long term prognosis of the SCI patient.

Quadriplegics and many paraplegics have a reduced vital lung capacity. Hart and Strauss (1984) tested the effects on 22 quadriplegics with an average vital capacity of 2.38 litres, as compared to the normal 5.10 litres for the same age group of able bodied people. HBOT improves vital lung capacity whilst improving tissue oxygenation.

Spasticity is also a major problem for the SCI patient, diminishing the impact of physical therapy and exercise capability. HBOT has been demonstrated to reduce extremity spasticity by improving metabolic circulatory function (Kieper 1987).

 

Teaching the Spinal Cord to walk

Another exciting development in working with SCI is the recent work performed by neurophysiologist Anton Wernig at the University of Bonn located near Karlsruhe, Germany (Science Magazine vol. 279, pp16, 1998). Spinal cord injured patients entering the Wernig rehabilitation program are rigorously evaluated, with suitable candidates undergoing an intensive program designed to encourage a ‘walking response’.

Wernig’s program revolves around the idea that the injured spinal cord can be reprogrammed with a limited ability to walk. Initial experiments conducted on cats demonstrated that cats with severed and injured spinal cords could be trained to support their weight and walk. This concept has considerable interest because evidence now indicates that the adult mammalian spinal cord can perform activities on its own, largely independently of the brain, including the functions necessary to walk.

Recent data also shows that neural circuits governing locomotion in the spinal cord can ‘learn’ by altering connections, in a way that may assist walking (Wernig 1995). Sten Grillner, neurophysiologist at the Karolinska Institute in Stockholm, Sweden states that the ability to retrain is unlikely to produce useful results in patients whose cords are so badly damaged that no connections survive between their brains and the region below the injury. Grillner states that these patients would have enormous trouble voluntarily keeping control when their legs started or stopped walking. In addition, Grillner states that locomotion training does not restore balance. As a result, quadriplegics like actor Christopher Reeve, who cannot use their arms to hold onto walkers and other devices for stability, could not learn to walk without being held upright.

Today, doctors generally leave spinal cord injured patients alone, except for therapy to strengthen muscles or maintain some degree of flexibility. J. Thomas Mortimer, biomedical engineer at Case Western Reserve University in Cleveland states that this new work is clearly stating to the injured patient that this ‘may not be your lot’. Mortimer concedes that ‘training will not restore normal walking’, but states that ‘merely being able to walk a few paces and climb a few stairs could vastly improve such a person’s life, enabling him to enter a friend’s home, movie theatre, or a narrow bathroom that would otherwise be out of limits to him or her’.

In 1967, Anders Lundberg and colleagues at the University of Goteborg Sweden, isolated the spinal cord in adult cats by cutting its link to the brain and also paralysing all the muscles to deprive the cord of movement related sensory cues. The researchers then activated the animal’s spinal neurons with an injection of L-dopa, a precursor for one of the cord’s main neurotransmitters, noradrenaline. They recorded that the neurons that flex the legs and those that extend the legs fired in alternating patterns.

Lundberg concluded that the spinal cord holds a ‘rhythm generator’ for locomotion that beats like a heart and is independent of both sensory cues and the brain. During the 1970s, Grillner and Peter Zangger further demonstrated that the cord not only produces a rhythm generator but also a more detailed electrical pattern in which different neural signals are sent to different leg muscles. Grillner showed that cats with severed spinal cords walked well if they were given certain drugs immediately after their cord had been cut. The older the animal, the more difficult it was to walk after injury.

Edgerton and Rossignol of the University of California Los Angeles (UCLA) showed that cats with severed cords, ‘spinal cats’, were able to relearn the locomotion pattern of a normal cat. Rossignol and Barbeau (1987) demonstrated dramatic improvements in the walking abilities of three spinal cats after 2-3 sessions a week, during which they were retrained to walk with their hind-limbs on a treadmill. At first, the animals had to be held up by their tails, but eventually became able to support their own hindquarters while they walked. They also learned to place their paws sole first on the treadmill and to take longer and more natural steps. In addition, the cats’ leg muscles also began to exhibit more normal patterns of electrical activity.

Edgerton (1990) compared the walking abilities of three groups of spinal cats: untrained animals, those trained to step and another group trained to stand only. The team showed that the step-trained cats could, after 5 months walk more naturally and rapidly than the untrained cats. By contrast, the cats that had only practiced standing could hardly step at all. Edgerton concludes,

“… Not only can the injured spinal cord learn, but also what it learns depends on the exact sensory input it receives. If you teach a cat to step, it learns to step, if you teach it to stand, it learns to stand, but cannot step”.

Barbeau (1989), performed a pilot study involving 10 patients, using a harness that could support up to 40% of their body weight. After 6 weeks of training, the researchers observed significant improvements – both on the treadmill and on the ground. Wernig (1990) in Bonn also had results with 12 patients showing that treadmill training had positive effects.

Volker Dietz (1995) at the University Hospital Balgist in Zurich induced stepping in 10 paraplegics whose spinal cords were completely disconnected from their brains by placing them on moving treadmills with each patient supported in a harness. They reported that the patterns of leg-muscle activity in these patients were similar to those in healthy subjects during treadmill walking.

Wernig (1995) published in the European Journal of Neuroscience a comparison study comparing results with partially paralysed patients trained on a treadmill program for three to twenty weeks, compared with matched controls treated with conventional exercise programs. Of the 36 patients with recent spinal cord injury who were wheelchair bound at the start of the study, 33 learned to walk independently, at least with the aid of walkers or canes, after treadmill training. By comparison, only 12 of the 24 wheelchair bound controls became independent walkers with conventional therapy. Further, 25 of another 33 patients with older injuries who had been wheelchair bound learned to walk independently with Wernig’s program, compared to just 14 of the controls.

Keir Pearson (1995 and 1997), neurobiologist at the University of Alberta in Canada and colleagues Whelan and Hiebert demonstrated that the influence of sensory nerves in the spinal locomotion system could adapt to compensate for injury. Pearson and his team made a significant discovery whilst studying sensations from a walking cat. In 1994, they cut sensory nerves in the cat’s calf muscle observing outcomes. Significant trials observed that the neuronal circuitry changes to compensate for an injury deficit.

Harkema, Dobkin and Edgerton (1997) in the Journal of Neurophysiology reported detailed evidence from the human spinal cord that explains how a program of exercise assists spinal cord injured patients to walk. Electrical activity responses the instant load bearing was sustained with each leg. The researchers found that the spinal cord’s output, as measured by muscle activity, depended greatly upon the load on the legs. The greater the load, the higher the activity. Furthermore, the activity was timed to the phase of the step cycle, so that it rose just when appropriate to facilitate stepping. Edgerton reported that the human spinal cord relies on complex sensory information, including load, to orchestrate walking.

Edgerton maintains that this new approach to spinal cord injury still requires extensive study and evaluation. “A lot more of these studies need to be done to show that training makes a significant difference” notes Edgerton. “We’re confident that it does, but we need to be careful, because that’s an important conclusion”. Recently, Rossignol in the Journal of Neurophysiology showed that the drug clonidine could speed the recovery of cats with spinal cord transection when combined with locomotion training. “Within a week”  Rossignol says, “the cats are walking with their hind-limbs” without requiring more drugs. Edgerton and Rossignol state that future treatments will require both a medication and walking program of locomotion retraining.  

 

Wernig Clinic : Spinal Cord Walking Program – Case Study

Sauer (a 27 year-old paraplegic) took his first step in 6 years since being confined to a wheelchair after a motorcycle accident, which left him almost completely paralysed from the ribs down in 1989. Sauer received an intensive-walking program at the Wernig’s clinic and now walks with a wheeled walker around his apartment. With help, Sauer can climb a few stairs. “The human body is not built for sitting”, Sauer declares. “Sometimes it should walk”.

 

What factors ultimately influence improvement?

  • immediate intervention with HBOT, optimally before surgical reduction: ‘the earlier the better’

  • an intact spinal cord as opposed to complete severance

  • the extent of initial compressive changes of the cord

  • the stability of surgical fixation and whether it is contributing to cord and or spinal canal compromise

  • the extent of secondary myelopathy (degenerative changes) of the spinal cord

  • the degree of obstruction to the CSF (cerebral spinal fluid)

  • involvement and extent of secondary infections and systemic disorders including ‘opportunistic bacterial and viral’ infestation requiring specific antibiotic treatments and immune stimulation

  • whether or not the patient smokes, as smoking reduces small vessels in the cord, contributing to further constriction and cord ischemia

Comment: Hyperbaric Oxygenation has received virtually no attention in Australia in the management of spinal cord injury. It is not featured on the ‘accepted’ hospital listing for Medicare reimbursement: subsequently there is no funding allocation towards continued clinical research. It is apparent that the advances in this vital area of rehabilitative medicine will require private organizations committed to promotion of this treatment that has such potential for the alleviation of suffering.

Undoubtedly, spinal cord injury and numerous other forms of crippling and disabling conditions including stroke, motor neuron disorders etc, may find greater hope in the near future.