Vertebral Axial Decompression Therapy for pain associated with herniated or degenerated discs or facet syndrome: An outcome study
Journal of Neurological Research Vol. 20, No3, April 1988
Earl E Gose, William K. Naguszewski* and Robert K. Naguszewski*
Department of Bioengineering, University of Illinois at Chicago, Chicago, Il. USA
*Coosa Medical Group, Rome Georgia, USA
The outcomes of vertebral axial decompression (VAX-D) therapy for patients with low back pain from various causes are reported. Data was collected from twenty-two medical centers for patients who received VAX-D therapy for low back pain, which was sometimes accompanied by referred leg pain. Only patients who received at least ten sessions and had a diagnosis of herniated disc, degenerative disc or facet syndrome which were confirmed by diagnostic imaging, were included in this study; a total of 778 cases. The average time between the initial onset of symptoms and the beginning of this therapy was 40 months, and it was four months or more in 83% of the cases.
The data contained the patients' quantitative assessments of their own pain, mobility, and ability to carry out the usual 'activities of daily living'. The treatment was successful in 71% of the 778 cases, when success was defined as a reduction in pain to 0 or 1, on a 0 to 5 scale. Improvements in mobility and activities of daily living correlated strongly with pain reduction. The causes of back pain and their relationship to this therapy are also discussed.
Introduction
For most patients, the cause or causes of persistent low back pain remains poorly understood. Although imaging procedures, including CT and MRI, are able to accurately define structural pathology, the correlation of these anatomic findings with physiology, back pain, and other clinical complaints is imprecise1. Although surgical decompression, epidural blocks, and spinal instrumentation can sometimes help patients suffering from back pain, these treatments do not completely take the biomechanical function of the disc into account, and may leave patients unrelieved of their suffering. In addressing the dysfunction of the disc with discectomy or surgical instrumentation, the biomechanical and physiological function of the disc is permanently disrupted.
Mechanical low back pain is usually aggravated by activities that increase axial loading on the spine, such as sitting, standing, and lifting. Patients may describe some relief with walking, but more particularly, by lying down, which unloads the spine and reduces intradiscal pressure (2,3). The causes of mechanical low back pain may include degenerative disc disease, degenerative spondylosis with limitation of range of motion, facet arthropathy, relative lateral recess stenosis from a combination of the above, microenvironment presure changes affecting the thecal and epidural space from disc bulging, subligamentous and/or extruded herniation, and segmental instability.
Pain generation from degenerative disc disease is probably multifactorial. A number of potential mechanisms are specifically addressed by the lumbar vertebral body separation achieved during therapy. With aging, disc desicction occurs, disc height is lost, and this process is accelerated with activities which produce high physical loading of the lumbar spine (4). Osteophytes develop along the anterolateral and posterior border of the vertebral bodies, and facet arthropathy increases as degenerative disc change advances (5). Normal vertebral body separation is lost as the disc degenerates. Redundancy of the posterior longitudinal ligament and ligamentum flavum combine with osteophyte encroachment upon the neuroforamen or central canal, resulting in stenosis at these sites, which is increased by axial loading of the spine.
The blood supply to the nerve roots of the cauda equina is sensitive to compression. Even at pressures of only 5-10 mmHg, the flow in over 20% of the venules was completely stopped (6). Flow in all the capillaries stopped at pressures between 20 and 50 mmHg. A pressure of 30 mmHg is slightly less than one pound per square inch, so solute transport is easily reduced. Even vertebral distractions (increased separation) of 1 or 2 mm per disc would reduce ligamental redundancy and help to restore canal/foraminal patency, reduce venous congestion and increase axoplasmic flow. Furthermore, the effects of lumbar spine lengthening may be sustained for a period of time after lumbar distraction has been stopped.
Twomey (7) placed lumbar vertebral columns removed from 23 male cadavers under 9 Kg of sustained traction for 30 min and measured an average increase in length of 9 mm. Thirty minutes after traction was removed, 13 of the 23 specimens had returned to baseline length, but the remaining 10 spines showed residual elongations ranging from 0.3 mm to 4 mm. Additionally, the data suggested that sustained traction had had a longer lasting effect on elderly spines. The mechanism of this residual deformation was not elaborated upon by the author, but disc rehydration may have been a factor since each column was soaked in normal saline and remained saturated by periodic additions of saline to a close fitting bag surrounding each column during the study.
That lumbar traction, if adequately applied, can effect physical change in patients suffering from back pain is well described by Gupta and Ramarao (8).
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