Distraction devices that apply either static or linear distraction forces have been found to increase the pressures of lumbar discs as noted by Dr. Tilaro in his review article. This is one of the reasons why such modalities have fallen into disrepute over the years. The concept of decompression was further expanded by an analysis carried out by Dr. Tilaro in collaboration with Dr. Miscovich of test results using the Current Perception Threshold (CPT) Neurometer. This is an objective means of assessing
the dysfunction of peripheral sensory nerves.

Their analysis demonstrated that sensory dysfunction showed a significant level of recovery after a course of VAX-D® treatments. In fact 64 % of the cases achieved complete remission. Their study demonstrated a recovery of neurological defect in a significant number of patients. This study was published in the Canadian Journal of Clinical Medicine. This study extends the clinical evidence on VAX-D® to include the conventional definition of decompression, that is the relief of the signs of neurocompression associated with discogenic dysfunction.

The following MRI films taken before and after VAX-D® treatments demonstrate reduction of a large extruded herniated disc that was impinging and displacing the S1 nerve root. (Figure 3 and Figure 4). We do not know what is the incidence of such findings and are trying to organize a study to examine this phenomenon.

 

Figure 3: MRI’s demonstrating the retraction of an extruded herniated nucleus pulposus after VAX-D® treatment.

Figure 4: MRI’s demonstrating the retraction of an extruded herniated nucleus pulposus after VAX-D® treatment.

Pre VAX-D® treatment MRI:
There are two axial MRI views of a large extruded herniated nucleus pulposus taken at two separate cuts through the same L4-L5 disc illustrating the size of the herniation and impingement on the cauda equina and retro-displacement of the nerve roots.

Post VAX-D® treatment MRI:
Post VAX-D® MRI views (comparable cuts) at the same L4-L5 level were repeated showing retraction of most of the extrusion. A small segment remains sequestered but no longer impinges on the cauda equina and/or displaces the nerve roots. The Radiologist that read and compared the before and after films commented that he was not aware of what "type of surgery" had been performed but that it was the most remarkable reduction of an extruded herniated disc that he had seen

Retraction of protruding segments has been observed in other cases and is an interesting phenomenon that intrigues the skeptics, however it has not been a consistent finding in all cases that have achieved complete remission. Therefore the significance and correlation is yet to be established.

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I want to first discuss the concepts relating to the class of herniated discs. The metabolism of the intervertebral discs, as in most tissues, deteriorates with age. This is exaggerated by the fact that the spinal column discs collectively represent the largest avascular structure in the body.

Studies show that during the waking hours, or two thirds of the day, the intradiscal pressures exceed the diastolic pressure in the capillary network of the vertebral endplates. During this period the metabolism of the disc is essentially anaerobic resulting in accumulation of metabolites of the glucose metabolic cycle such as CO2 and lactic acid. It is proposed that an anaerobic state also favors a shift of normal nuclear matrix to the more acidic compounds of chondroitin sulfates.

Aging augmented by gravity leads to loss of elasticity of the annulus. This is a precursor to the development of annular fissures exposing the annulus and thereby the disc integrity to stress trauma especially from asymmetric loading which leads to coalescence of annular fissures to form a radial extension leading to progressive intrusion of the nucleus pulposus and herniation.

The first genesis of low back discomfort is thought to occur when anaerobic nuclear contents, such as accumulated lactic acid and the more acidic forms of chondroitin sulfate reach the sinuvertebral nerve that innervates the outer one third of the annulus. Not infrequently patients will give a history of low back pain for a week or so prior to the onset of an acute episode.

Annular fissures develop in an environment that does not support tissue repair. Fibroblast and chondroblast cellular activity is suppressed in an anaerobic environment and is further dampened by the products of degradation. Fortunately when the body assumes a horizontal position at bed rest the intradiscal pressure normally lowers below that of the diastolic blood pressure permitting oxygen diffusion and reversal to an aerobic state. Cellular activity is enhanced and normal tissue repair can occur.

This is probably one of the beneficial effects of bed rest in the management of discogenic dysfunction. Unfortunately the effects of the positive diffusion gradient that occurs in the horizontal position is limited by the fact that imbibation of fluid into the disc gradually raises the intradiscal pressure reducing the diffusion gradient. This is estimated to reach equilibrium within a few hours.

Due to the normal anatomical configuration of the capillary network in the end plate, when a diffusion gradient favors inflow to the disc, oxygen transport has a steep concentration gradient across the disc with the peripheral diffusion some 20-30 times that of the center of the disc. Negative pressures in the decompression phase facilitate migration and equilibration of oxygen throughout the disc. Because this structure is avascular, there is no concentration gradient effect in reverse. Therefore oxygen tends to be retained and utilization by cellular elements continues beyond the end of the decompression phase. Thus aerobic metabolism is thought to persist during the relaxation phase of a VAX-D® cycle and even for a period of time after a treatment session.

In addition to the Therapeutic Curve – cyclic periodicity is an essential component of VAX-D®. Retraction and relaxation phases must be controlled to achieve an optimum effectiveness. Furthermore the length of the cycles is fairly critical. Decompression and relaxation phases of two minutes duration are not as effective as the current protocol. Although the controls permit setting varied time duration for the decompression phase and the relaxation phase the optimum is still sixty seconds and sixty seconds. Shortening either phase appears only to increase throughput slightly at the possible sacrifice of efficacy.

It is interesting that certain repetitive exercises perfected by the McKenzie technique may reduce the extent of protrusion of a bulging disc. If performed properly, these programs can prove complimentary to the aerobic metabolism and nutrient transport created through VAX-D® therapy. When static distraction forces are applied, the hydraulic equilibrium that normally develops in a few hours at bed rest, tends to be reached in a much shorter period of time. This phenomenon is also thought to be a contributing factor to the increase in intradiscal pressure that has been observed when devices apply distraction forces in a linear fashion. This would be counterproductive in the management of discogenic dysfunction.

Internal Disc Disruption (IDD) is a condition marked by alterations in the internal structure and metabolic functions of one or more discs. It is a common cause of low back pain in a substantial number of young, otherwise healthy adults. Crock described this painful entity and reported annular fissures that distort the internal architecture of the disc. A pathological marker has been described as the High Intensity Zone (HIZ) viewed on MRI scans using spin echo gradient T2 imaging (Figure 5). Discography studies have demonstrated a significant correlation with the presence of HIZ in patients with symptomatic grade three annular fissures.

Figure 5: MRI of HIZ

The high intensity of the zone differentiates the material entrapped from that of herniated nuclear matrix, and is believed to indicate that the HIZ reflects the presence of inflammatory fluid. These observations indicate that inflammation could play a significant role in the development of localized irritation associated with some discogenic disorders. Dr. Tilaro points out in the Journal of Clinical Medicine, that experience using anti-inflammatory drugs in the management of patients with discogenic dysfunction has in the past been disappointing. However in combination with VAX-D®, certain non-steroidal anti-inflammatory compounds have been found to exert definite benefits for some patients. While there have not been research studies to identify the contributing properties, the more

active products appear to share anti-prostaglandin and COX-II inhibition properties, and only non-albumin bound molecules in the serum would be free to diffuse into the disc space under a magnified diffusion gradient. NSAID's that freely dissociate from the protein bound state are reflected generally by certain pharmacological parameters. Such as whether a particular compound passes the blood-brain barrier and the percentage excreted intact in the urine. Drugs that are highly conjugated with albumin tend not to transfer into the cerebral spinal fluid and also do not pass through the glomeruli into the urine. These may be common characteristics of compounds that fail to diffuse into the HNP under positive diffusion gradients. Dr. Ramos, the neurosurgeon whose research demonstrated in-vivo negative intradiscal pressures, carried out a prospective clinical evaluation of the effect of administering half the number of sessions recommended in the VAX-D® protocol. This clinical trial is typical of two-dose relationship commonly used in pharmaceutical research where placebos are not applicable. Because the level of success was governed by a dose response relationship, among other interesting aspects, this study indicates that a biological mechanism of action is involved in addition to the biomechanical retraction of a prolapsed disc. While retraction of a prolapse is believed to contribute to the reduction in low back pain and radiculopathy, remission of symptoms and disability does occur without visible change in the MRI picture. The MRI may not disclose closure of the radial fissure that interrupts the integrity of the annulus and restores the function of the intervertebral disc. A large-scale clinical study showed a success rate for degenerative disc disease comparable to that achieved in cases with subligamentous herniation. It is interesting that apparently none of the 147 cases of degenerative disc disease were diagnosed as suffering from IDD. It is possible that since the average chronicity was reported to be 42 months it could be that there were no cases of IDD because such cases either ended up on the surgical table or converted over time to classic degenerative disc disease with loss of disc height and configuration. One of the problems in this regard is that radiology reports of MRI films generally do not distinguish IDD from degenerated disc disease. Although T2 weighted imaging displays a loss of signal intensity similar to degenerative disc disease. A loss in disc height on an MRI scan is not prevalent in IDD as with degenerative disc disease. Maintenance of the disc height in IDD presents a problem in relying on normal radiological views in the confirmation of the clinical symptoms. IDD is described, as a condition marked by alterations in the internal structure and metabolic functions of the disc usually following significant trauma. What happens if after major trauma, edema or inflammation results in a sustained elevation of intradiscal pressure and the benefit of the normal diurnal physiological variation in oxygen uptake is insufficient to reverse degradation? A persistent anaerobic state might predispose the nuclear matrix to a type of necrotizing discopathy. The release of protein and cellular degradation that permeate into the peripheral venous plexus is believed to give rise to the systemic complications. Unlike herniation of the nucleus pulposus IDD is not in itself associated with annular fissures and the escape of nuclear contents from the confines of the disc space. The etiology of both localized and radicular pain is thought to be principally from chemical irritation. This shifts the emphasis of treatment from mechanical origins of nerve root compression to more complex aspects of a biochemical nature. IDD presents localized and peripheral symptomatology similar to that of herniated discs, however, the pain is more diffuse in nature and it is more likely to involve generalized systemic symptoms such as fatigue, malaise and loss of weight. Neurological deficits are not commonly associated with IDD. Typically a patient with IDD does not find relief from bed rest as is the case with disc prolapse, and physical exercises tend to exacerbate localized and radicular symptoms (if present). Local steroid injections, as well as the routine use of non-steroidal anti-inflammatory drugs have been disappointing as a pharmacological adjunct in the treatment of IDD. However in combination with VAX-D®, anti-inflammatory products should be routinely employed in the treatment of IDD to reduce the chemical irritation from catabolites. Experience indicates, in some patients the combination appears to be synergistic. Neurological sensitivity is heightened to chemical irritation by even minor changes in blood flow or hypoxia therefore the application of tight pelvic belts can cause discomfort. Patients on VAX-D® that experience an increase or shift in their pain syndrome in the initial stages of VAX-D® treatments, may be due to the tight harness affecting venous congestion which could increase the sensitivity to chemically irritant catabolites. This could be one of the reasons for non-compliance especially when the therapist or patient become discouraged and discontinue treatment prematurely. If the treatment succeeds in improving the catabolic state this complication should subside as treatment progresses. Experience and further clinical trials aimed at addressing this particular problem will hopefully provide further guidelines in managing these difficult cases. Patients with IDD that have lost intrinsic cellular viability could be expected to be refractory to VAX-D® treatments and likely will not be able to be helped until we succeed in developing the science of bio-transplant. In the future, destructive surgery causing iatrogenic stenosis should be replaced by reconstructive surgery that combines nucleus pulposus transplant procedures facilitated by specially designed VAX-D® tables that will be adapted to the surgical operatory. The viability of such transplants will require follow up VAX-D® to provide the aerobic environment necessary for transplant tissue survival and healing.