An Overview of Vertebral Axial Decompression
Canadian Journal of Clinical Medicine Vol. 5, No. 1, January 1998
Dr. Frank Tilaro, M.D.
(page four of six)

Asymmetrical loading of the disc and increased intradiscal pressure is partly responsible for internal derangement, disc degeneration and herniation. Changes in intradiscal pressure also play a prominent role in affecting nourishment of the disc since the disc is an avascular structure and receives its nourishment primarily by diffusion. Intradiscal pressure that is greater than capillary pressure in the vertebral body impedes oxygen diffusion to the disc which in turn impedes healing.(13) Reducing intradiscal pressure with VAX-D creates a diffusion gradient into the disc allowing nourishment to proceed. Solutes such as oxygen have a steep concentration gradient across the disc, with the peripheral concentration 20-30 times more than the concentration at the center of the nucleus.

The availability of oxygen may be inadequate to meet the metabolic requirements required to heal a damaged annulus, and higher concentrations of lactate have been measured within the central portion of the disc. By reducing intradiscal pressure, VAX-D therapy creates a diffusion gradient thereby enhancing solute transfer. High levels of lactate could facilitate chondrocyte cell death as well as increase the activity of degradative enzymes further promoting the loss of the proteoglycan cell matrix. A vicious cycle is produced, accelerating disc degeneration. The mechanical effects of fluid loss during a compressive load are followed by a slow rate of disc deformation termed creep. The rate of creep is faster in a damaged or degenerated disc than a normal disc. Both vibration (overstress) and inactivity (understress) affect the rate of creep and disc degeneration. Pigs who were subjected to vibratory creep had lower levels of oxygen and sulfate transport, and higher levels of lactate within the disc.(13)

Somewhere between the overstress of vibration and the understress resulting from inactivity is an optimum mechanical environment.

Through its action, VAX-D may be capable of restoring that environment, enhancing healing of the disc and retarding degeneration. The pathophysiology of nerve root compression has been described by Rydevik.(33,34,35) The nerve root ganglion has an extensive venous plexus, which if obstructed, results in venous hypertension and endoneural edema, leading to hypoxia, ischemia and pain. External decompression with VAX-D therapy can be expected to relieve venous hypertension and reverse the pathognomonic process.

By significantly reducing intradiscal pressure, VAX-D promotes retraction of the herniation into the disc. VAX-D therapy could possibly shear a herniation from its connection to the central nucleus, creating a severed fragment within the spinal canal. This sequestered disc is susceptible to small vessel invasion and digestion as a result of contact with the epidural space. Reinforcing this theme is the study by Modic et al who studied the natural history of disc herniation by MRI in patients with acute radiculopathy and discovered that large (6mm) sequestered hernias were the first to undergo spontaneous resolution.(23)

I have studied sensory nerve dysfunction measured before and after VAX-D therapy, in order to determine the effect of VAX-D on nerve root compression. The results from this study are very significant and the data will be published in the future. Inflammation very likely plays a role in disc pathology and herniation, but the response to anti-inflammatories is rather disappointing. Saal found high levels of Phospholipase A2 in human disc samples removed at surgery in patients with radiculopathy.(36) As the enzyme responsible for liberation of arachidonic acid from cell membranes, Phospholipase A2 is the rate limiting step in the production of prostaglandins and leukotrienes. Controlled studies have shown that anti-inflammatories are not useful for acute sciatica,(46) but since solute transfer to the disc may be enhanced by VAX-D therapy, the administration of anti-inflammatories during VAX-D therapy may result in higher concentrations of the drug within the disc, neutralizing inflammatory mediators responsible for nerve root inflammation and some forms of discogenic pain. As previously mentioned, the fluid within the HIZ is thought to be an inflammatory fluid and VAX-D may be able to effectively pump this fluid into the central nucleus where it is not possible for it to exert an inflammatory effect. The fissure may be able to approximate its borders and heal once the fluid is pumped out.

VAX-D VS. TRACTION

The VAX-D table is an external decompression device and this separates it from conventional traction. Studies verifying decompression of the disc and nerve root are now available for VAX-D. I reviewed the literature and I could not find any available data that conventional traction reduced intradiscal pressure to the negative range nor are there any studies on conventional traction showing beneficial effects in nerve root compression and conditions associated with discogenic dysfunction.

Many patients who receive VAX-D therapy have had chronic back pain and failed numerous modalities including traction. Their positive response to VAX-D therapy, after having failed conventional therapy and traction confirms VAX-D's assertion that it is not conventional traction.

CLINICAL STUDIES

The Acute Low Back Distress Study was conducted by the John P. Robarts Research Institute, London Ontario. The efficacy of VAX-D therapy was established with this study. The parameters measured were severity and duration of pain and disability, including analgesic requirements, and the presence and degree of neurological involve-ment. One hundred and ten patients were entered into the study.

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