The Effects of Vertebral Axial Decompression On Sensory Nerve Dysfunction
in Patients with Low back Pain and Radiculopathy:
Frank Tilaro, M.D. Dennis Miskovich, M.D.
Canadian Journal of Clinical Medicine Vol 6, No 1, January 1999
(page four of five)

DISCUSSION

The data from this study demonstrate that the VAX-D therapeutic table is capable of affecting spinal sensory nerve dysfunction in abnormal nerves secondary to a compressive radiculopathy. 16/22 nerves showed abnormalities in the large myelinated fibers, 13/22 demonstrated abnormalities in the small myelinated fibers and 8/22 demonstrated abnormalities in the small unmyelinated fibers. These fibers are the major subpopulation of sensory nerve fibers that provide innervation to the test sites that were measured in this study.

The mechanism responsible for the signs and symptoms of sciatica are complex and not fully elucidated. Although compression of the nerve or nerve root is a consistent finding in sciatica, compression by itself does not explain all the observed symptomatology (11,24).

Many of the studies that have yielded data regarding the effects of compression come from studies on peripheral nerves. There are anatomical differences between peripheral nerves and the spinal nerve roots that render the spinal nerve roots more vulnerable to compression. The spinal nerve has both an intrathecal and extrathecal portion. The intrathecal portion is bathed by the CSF which offers some protection from compression. The extrathecal portion has very little collagen supporting tissue, which renders the fibers susceptible to the effects of compression. By comparison, the peripheral nerve fibers have a generous amount of supporting collagen tissue that afford it some protection from compression (11).

Compression of a peripheral nerve does not cause pain unless the nerve has been previously irritated (17,38). Compression of the dorsal root ganglion (DRG) can result in pain. Rydevik compared the dorsal root ganglion to a closed compartment syndrome when mechanically deformed. The DRG has a rich vascular supply and a tight capsule. Compression leads to edema and hemorrhage in the endoneurial space with subsequent elevation of interstitial tissue fluid pressure and reduced blood supply to the sensory nerve cells in the DRG (36). The DRG has the capability to act as a neuromodulator of pain through release of substance P, calcitonin gene related peptide and possibly other chemical mediators (44).

The compressive force and rapidity of onset are both important factors leading to nerve dysfunction (26-30). Olmarker reported that a rapid onset of compression induced a more pronounced effect than a slower onset both in terms of intraneural edema formation and impairment of the nutritional supply to the nerve roots. The compressive forces exerted by a herniated disc can be as high as 400mmHg.

Vascular compromise has been an attractive theory to explain the effects of compression. Rydevik has shown that with slow nerve compression there is compromise first of the venules, then capillaries, and finally the arterioles. In the animal model this occurred at 30mmHg. Compression studies performed on the pig cauda equina have shown that electrophysiologic changes occur at 30 mmHg., the same pressure that causes vascular compromise (35).

If the compressive force is great enough and or occurs rapidly, compression can cause significant nutritional compromise in the nerve root and peripheral nerves (8,29,32,34,42). The primary nutritional support is through the arterial tree and the secondary nutritional support is through the cerebrospinal fluid. Compromise of the arterial tree can be partially negated by continued nutrition via the cerebrospinal fluid. If compression affects the spinal nerve root proximal to the dorsal root ganglion both support systems are compromised and diffusion of metabolites and nutritional support mechanisms are markedly reduced.

The mechanism through which the VAX-D table accomplishes decompression is related to reduction of intradiscal pressure. Both a direct mechanical effect and biochemical effect may be responsible. Reduction of intradiscal pressure could allow for retraction of the herniation. A possible shearing affect that interrupts the connection of the herniation to the central nucleus, given the arrangement of the annular fibers is a possibility with extruded hernias. This study indicates that the distraction of vertebral structures by VAX-D also reduces compression of spinal nerve roots.

Inflammation and the inflammatory response very likely play an important role in producing some symptoms associated with sciatica. The nucleus pulposus has demonstrated inflammatogenic properties and is capable of inducing an immune reaction (21,24,25,40). Saal has documented elevated levels of phospholipase A2 in herniated disc tissue (37). Phospholipase A2 is a precursor for arachidonic acid responsible for production of the inflammatory Prostaglandins and Leukotrines. Alterations in disc metabolism may be partly responsible for inflammation. The central portion of the disc is oxygen starved, there is a steep oxygen concentration gradient across the disc, concentrations being 20 to 30 times greater in the periphery (1O). High levels of lactate have been measured within the central nucleus (1O). The high levels of lactate may be responsible for activating destructive proteolytic enzymes and initiating the inflammatory cascade.

Since elevated intradiscal pressure adversely affects the diffusion gradient, nutrient and oxygen diffusion to the disc is impaired and anaerobic metabolism prevails. Anaerobic metabolism negatively affects the capabilities for healing and repair of all tissues. By significantly reducing intradiscal pressure the VAX-D therapeutic table creates a diffusion gradient enhancing the delivery of nutrients and oxygen to an oxygen starved disc, creating an aerobic environment, enhancing repair, and possibly interrupting the inflammatory cycle.

CONCLUSIONS

Fourteen of twenty-two peripheral nerves (64%) showing abnormal dysfunction secondary to a compressive radiculopathy returned to normal function after a therapeutic course of VAX-D therapy. The data from this study implies that VAX-D therapy is capable of influencing sensory nerve dysfunction associated with a compressive radiculopathy. Motor dysfunction returns before sensory dysfunction in compressive radiculopathies so it is rather striking that we observed total remission in 64% of the cases with sensory dysfunction (2). It is possible that reduction of intradiscal pressure by VAX-D significantly alters the biomechanics and biochemistry of the disc and nerve root.

The author realizes there are shortcomings with nonrandomized retrospective analysis such as this study. In attempts to minimize selection bias, the patients reported on in this study were uniform regarding duration of therapy, physical findings, symptomatology, and imaging results. Also, the final outcome was an objective measure which could not be influenced by subjective or other external factors.

The objective of this study was to make any observations on sensory nerve dysfunction attributed to VAX-D therapy. Patient outcomes were not measured although the majority of patients reported subjective relief of pain. Further studies investigating the effects of VAX-D therapy on sensory and motor dysfunction are encouraged.

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