HyperMED Spinal Cord Injury

‘HyperMED NeuroRecovery is committed to expanding the therapeutic window promoting worthwhile functional outcomes - gone are days of simply living and coping with disability!' Dr Mal Hooper _ HyperMED NeuroRecovery Australia

  • HyperMED/VNI HBO, Lokomat, Cerebrolysin Submission October 2009.pdf

  • HyperMED/TAC Funding Application Evidence Based Support.pdf

Information pertinent to HyperMED Protocols treating Spinal Cord Injury can be reviewed at the following link:

  • HyperMED/HyperMED Newsletter Spinal Cord Injury 2009.pdf

USA ARMY.MIL Retrain Injured War Veterans with Spinal Cord Injury Using Lokomat  - After the crash of his helicopter, Crew Chief Spc. Mark Lalli is learning to walk again with the aid of an advanced set of robotic legs, a team of doctors, nurses, specialists, and...his mother. www.army.mil ... army soldiers health technology lokomat robotic legs walk wounded warrior helicopter crash

The following is extracted from the HyperMED Newsletter Spinal Cord Injury

 

What Happens Following Spinal Cord Injury?

  • Spinal Injury may result in either complete or incomplete injury. Many patients informed they are 'complete' presume that their cord is severed. The term complete is defined by total or near-total loss of motor function and sensation below the area of injury. However, even in a complete injury, the spinal cord is almost never completely cut in half. Doctors use the term ‘complete’ to describe a large amount of damage to the spinal cord. It's a key distinction because many people with partial spinal cord injuries are able to experience significant recovery, while those with complete injuries are not. However many spinal patients classified as ‘complete’ may still re-gain some functional responses. This is evident with assertive therapeutic interventions designed to activate damaged nerve cells and re-train function

  • Folded Corner: ‘Christopher Reeve believed his improved function was the result of vigorous physical activity to re-train function and awaken dormant nerve pathways – the brain and spinal cord needs to reconnect!’ 
 
The scientific literature on spinal cord injury predicts that most recovery will occur in the first six months after injury and that it is generally complete within two years. However Christopher Reeve’s recovery commenced five to seven years after his injury - this defies these medical expectations and had a dramatic effect on his daily life. Why did he get better so long after his injury? Reeve believed his improved function was the result of vigorous physical activity to re-train function and awaken dormant nerve pathways – the brain and spinal cord needs to reconnect! [Source: American Association of Neurological Surgeons, Craig Hospital, Christopher and Dana Reeve Foundation, The National Institute of Neurological Disorders and Stroke]

  • Surgical strategies are primarily orthopedic focused with emphasis on reduction and stabilization of bony dislocation. All spinal patients require additional MRI within the following months to determine the integrity of the surgical procedure. Many spinal patients suffer additional complication due to scar formation, bony fragments and lack of plate and screw integrity. These additional factors not only inhibit recovery but often contribute to additional cord complications

  • Laceration, extensive bruising, and massive swelling results in extensive cord hypoxia (inadequate tissue oxygen) which fosters destructive cellular apoptosis (programmed degeneration). Hyperbaric Oxygenation impacts tissue hypoxia enhancing capacity to rescue damaged tissue and salvage back the destructive process. This is exactly how Hyperbaric Oxygenation works with a patient suffering a 'gangrene foot' that would otherwise without the benefit and impact of Hyperbaric Oxygenation require amputation! We often describe the impact of Hyperbaric Oxygenation is like 'getting more fizz into a flat can of coke'! The objective of Hyperbaric Oxygenation is to get more oxygen (fizz) into the hypoxic damaged cord accelerating recovery and preventing further destructive spread due to apoptosis

  • Hypoxic damage causes destructive Apoptotic cells from the immune system to migrate to the injury site causing further damage to some neurons and death to others that survived the initial trauma. Immediate strategies are must be implemented to minimize this cascade of programmed cellular destruction. Hyperbaric Oxygenation impacts tissue hypoxia minimizing the cascade effects of progressive damage

  • Within weeks of the initial spinal injury a fluid-filled cavity surrounded by glial scarring is left behind. Localized myelomalacia emerges (morbid softening at the injured site due to hypoxic necrosis of the spinal cord). Early HBOT intervention potentially has the greatest impact to the destructive spread of cord hypoxia

  • Continuing progression of spinal cord apoptosis due to hypoxia results in progressive hemorrhagic myelomalacia - spread of myelomalacia progresses above and below the injured site due to progressive intramedullary hemorrhage of the spinal cord. This can potentially lead to further loss of neurologic function and cord atrophy (wasting and thinning of the cord) severely inhibiting the capacity to regenerate and recover function. Comparison MRI post surgical stabilization is critical within the early months to evaluate this destructive process – functional changes an injured spinal patient may be getting does NOT rule out the potential cascade of secondary complications. Advanced Functional BOLD (Blood Oxygen Level Dependency) MRI measures progressive hypoxic damage and apoptosis spread. Functional BOLD MRI also measures the impact of Hyperbaric Oxygenation

  • Experiments conducted on spinalized cats demonstrate that spinal circuitry (reflex generators) below the level of injury remains active (even years after injury) and functional neuronal properties can respond to peripheral input from below the level of injury. Treadmill cats can be trained to walk

  • Lack of appropriate and 'accurate' stimulation induces functional incapacity called the ‘learning non-use’. Simply stated if you teach the remaining active spinal circuits to sit they will sit! Refer to the 'rat study'  Do Wheel Chairs Inhibit Recovery?

  • Motor cortex centers in the brain also show signs of functional loss due to spinal cord injury. Functional BOLD MRI demonstrate that the motor cortex and cerebellum parts of the brain 're-allocate functional capacity lost through spinal cord injury' – it is imperative to keep this ‘window open’

  • Body Weight Support Treadmill Training (BWSTT) and more recent studies on Lokomat (Robotic Gait Assisted Walking) demonstrate the potential of functional neuroplasticity - the ability to re-learn and re-organize function. Functional BOLD MRI measures the capacity to retrain function in both the brain and spinal cord neural pathways. The injured spinal cord has capacity to 'wake-up' - salvage back tissue damage, re-activate and re-train dormant neural pathways improving functionality

  • What happens with SCI?  Review Page 2 Spinal Research UK 2009 - HyperMED/spinalresearchUK.pdf

For additional information on Lokomat NeuroRecovery refer to

  • HyperMED Australia : Beyond Therapy - Treatment Program

  • HyperMED Australia : Lokomat NeuroRecovery

  • HyperMED/HyperMED Lokomat 2009.pdf

  • HyperMED/Lokomat - Australian Experience HyperMED NeuroRecovery.pdf

  • The economic cost of spinal cord injury and traumatic brain injury in Australia (1.31Mb)

Lokomat (Robotic Gait Assisted Walking) Gait Training

For the past 15-years bodyweight supported treadmill training (BWSTT) has become a prominent gait rehabilitation method in leading rehabilitation centers throughout the world.  

Experiments conducted on spinalized cats demonstrate that spinal circuitry (reflex generators) below the level of injury remains active and functional neuronal properties can respond to peripheral input from below the level of injury. Treadmill cats can be ‘trained to sit, stand and walk’

Lack of appropriate stimulation induces functional incapacity called the ‘learning non-use’. Simply stated if you teach the remaining active spinal circuits to sit they will sit! Motor cortex centers in the brain re-allocate functional capacity lost through spinal cord injury – it is imperative to keep this ‘window open’. Body Weight Support Treadmill Training (BWSTT) and more recent studies on Lokomat (Robotic Gait Assisted Walking) demonstrate the potential of functional neuroplasticity - the ability to re-learn and re-organize function.  

This type of locomotor training has many functional benefits but the labor costs are considerable. To reduce therapist effort, Robotically Gait Assisted BWSTT (Lokomat) has been shown to be more accurate and financially feasible, compared to the other BWSTT modalities. Currently 45+ Lokomat systems are in use in large Neurorehabilitation hospitals in the USA and approximately 150 Lokomat systems found in 31 Countries.

Internationally Lokomat (Robotic Gait Assisted Walking) and Body Weight Support Treadmill Training programs are payable under Third Party Insurance for spinal cord injury and a range of neurodegenerative and neurodevelopment gait disorders.

  • HyperMED/University of Michigan Spinal Cord Care.pdf

Lokomat (Robotic Gait Assisted Walking)  Gait Training

Patients receiving Lokomat (Robotic Gait Assisted Walking) are scheduled daily; initially 1-hour session and then as the patient builds we recommend up to 2-hours each day attending.

Lokomat is NOT passive involvement. The Lokomat is constantly adjusted to best assist the functional responses of the patient. Patients commence with passive assistance however as the patient compliancy builds the Lokomat settings and various programs are tailored to the patient performance and capabilities. Some patients have high level spasticity and others a complete loss of tone. Each patient's presentation is different - Lokomat provides excellent opportunity to 'best-fit' the patients specific capabilities and capacity to re-train function. And this is replicable on every separate training session!

In addition the support harness treadmill system are utilized independent of the Lokomat to promote functional changes. Functional changes being driven by 'man and machine' are then put to the test with the patient then able to implement strategies being focused on during each Lokomat session.

This combination effect is both unique and significant towards each neurologic patient developing a sense of supportive assistance whilst focusing on improving functional independence.

Walking requires a 'fluid like connection between spinal reflex generators and higher brain centers'. The combined approach is invaluable to promote functional changes - neuroplasticity (the ability to salvage back what has been damaged).

 


Please also take the time to watch the following National Geographic Documentary on Professor Ed Cooper pioneering work on Median Nerve Stimulation and its roll in spinal cord recovery.

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

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

Median Nerve Stimulation (MNS) is an integral part of the HyperMED Protocol - application is recommend for all patients with neurologic disorders. The Cerebral Palsy and Brain Injured child have vast regions of the brain that remain underdeveloped and immature causing inadequate metabolic and signal responses resulting in 'learned non-use'.

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

 

Do Wheelchairs Hinder Spinal-Cord Recovery? Acquired Non-Use!

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

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

 

 

  • HyperMED Australia : Do Wheel Chairs Inhibit Recovery?

  • Typical HyperMED Email Inquiry and Response - Spinal Cord Injury

  • International NeuroRehabilitation Symposium Feb 12, 2009 - The Use of the Lokomat System in Clinical Research

  • HyperMED/Comprehensive evaluation of spinal cord function accompanying Lokomat.pdf - Spinal Injury Abstracts Sept 2008

  • HyperMED/Specific locomotor versus unspecific weight training and their effects on gait.pdf - Spinal Injury Abstracts Sept 2008

MEDIA file University Hospital of Balgrist

 

 

 

 

 

 

 

 

 

HyperMED UPDATE T6 Incomplete - Mexico

 

HyperMED UPDATE Dion McCafferty - T6 Incomplete - South Africa

HyperMED UPDATE Isabel Martin

 

HyperMED UPDATE Channel 7 News - Spinal Injury Break-Through

HyperMED UPDATE Peter Roefs - C5/6 Complete

 

HyperMED UPDATE Chronic Spinal Cord Injury: Quadriplegic - C5/6

Hyperbaric Oxygenation ONLY

 

 

 

 

 

HyperMED Australia

  • HyperMED Treatment Protocols

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.

 

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.

 

Historical HBOT 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


  • HyperMED Lokomat NeuroRecovery - Robotic Gait Assisted Walking

  • Hyperbaric Oxygen Therapy Increases Stem Cells By Eight-Fold

  • Review: mesenchymal stem cells: cell-based reconstructive therapy in orthopedics

  • Mesenchymal stem cells for bone repair: preclinical studies and potential
    orthopedic applications

  • Mesenchymal stem cells as potential source cartilage repair

  • Mesenchymal stem cells: clinical applications and biological characterization

  • Human mesenchymal stem cells differentiate into neuron-like cells and show SMN protein expression

  • Sulfur in human nutrition and applications in medicine

  • Rapid recovery of segmental neurological function in a tetraplegic patient following transplantation of fetal olfactory bulb-derived cells

  • Autologous olfactory ensheathing cell transplantation in human spinal cord injury

  • Obtaining olfactory ensheathing cells from extra-cranial sources a step closer to clinical transplants

  • Hyperbaric Oxygenation improves altered T2 signal intensities in brain and spinal cord and cerebrospinal disturbances

  • Administering stem cells leads to a reduction of myocardial infarcts

  • Meningococcal Conjugate Vaccine May be Linked to Cases of Guillain-Barre Syndrome

  • Stem cells aid spinal cord injured-mice

  • Prevention of wound edge necrosis by local application of dimethylsulfoxide

  • cAMP and Schwann cells promote axonal growth and functional recovery after spinal cord injury

  • Effects of hyperbaric oxygen on GDNF expression and apoptosis in spinal cord injury

  • The role of multiple hyperbaric oxygenation in expanding therapeutic windows after acute spinal cord injury in rats

  • Neuroprotection by minocycline facilitates significant recovery from spinal cord injury in mice

  • Magnetic resonance imaging of hyperbaric oxygen treated rats with spinal cord injury: preliminary studies

  • Therapeutic use of hyperbaric oxygenation in lesions of the spinal cord

  • Beneficial effects of acupuncture treatment following experimental spinal cord injury: a behavioral, morphological, and biochemical study

  • Robot helps paralyzed patients learn to walk - LOKOMAT

  • Stem-Cell Transplantation Improves Locomotion After Spinal Injury in Rats

  • Cytomegalovirus, Epstein Barr virus and Other Herpesvirus Infections after Stem Cell Transplantation

  • Hyperbaric Oxygenation protects against Mitochondrial Dysfunction and significantly delays the onset of Neurological deficits in Mice study

  • Preconditioning with hyperbaric oxygen and hyperoxia induces tolerance against spinal cord ischemia in rabbits.

  • Spinal Cord stimulation helps man walk again

  • Scar Tissue Blocks Spinal Cord Neurons From Linking

  • Adult Bone Marrow Stem Cells Can Become Blood Vessels

  • Wrapping Rats' Severed Spines in Tube Shows Promise

  • Bone Marrow Stem Cells turn into Brain Cells in Study

  • Stem Cell Transplantation Abrogates Inflammatory Phase of MS

  • Scientists isolate, grow Brain cells from Corpses