Advances in Therapy- May/June, 1999
The International Journal of Drug Device & Diagnostic Research

Spinal Disc Rehabilitation: A New Technology

By C.J. Goodman, D.C.
Chief of Staff, Goodman, Goodman & Goodman, Thousand Oaks, California

ABSTRACT
Low back pain and "computer neck" are frequent complaints during visits to a physician(1). Back and neck pain affects up to 60% of all employees at some time in their careers and is personally and financially devastating. Repetitive mechanical stress leads to disc degeneration, loss of disc height, and other abnormalities. The Vivatek, which is controlled and coordinated by on-board computer and fiberoptic feedback sensors, is the first biorobotic system that alleviates intradiscal pressure and myospasm.

INTRODUCTION
After the common cold, low back pain (LBP) is the most common reason for a visit to a physician. The leading cause of disability in people younger than 45, LBP is the second most prominent cause of industrial absenteeism, affecting up to 60% of all employees at some time in their careers (2). In 1990, costs associated with LBP were more than $50 billion in the United States alone. That year, workers' compensation costs for LBP exceeded $11 billion and have been rising steadily each year (3).

LBP can readily be called the health-care dilemma of the millennium, as our population ages and the incidence of spinal disc degeneration increases.

LBP is not the only cause of high health-care costs and vocational disability. Repetitive microtrauma to the neck ("computer neck" or microlesions of the spine) has been referred to as the curse of the information age. Eighty-eight percent of neck injuries do not resolve after 10 years.(4) Back and neck pain is financially and vocationally devastating, and the long-term prognosis is guarded.

CLINICAL COURSE
Disc degeneration, the most common producer of spinal pain, results from repetitive mechanical stress, altered nutrition to the disc, and ultimate annulus disruption with protrusions of the nucleus pulposus through the weakened area (5).

Disc degeneration and loss of disc height shift the weight-bearing stress posteriorly onto the articular facets, leading to unequal weight bearing of the facet joints and osteoarthritis of the joints.

The intervertebral disc acts as a hydraulic shock absorber that permits flexion, extension, rotation, and a combination of these motions. Essentially mucopolysaccharide gelatinous tissue, the disc comprises a central mass, the nucleus, which is contained within the annulus, an elastic structure. External pressure compresses the disc and increases intradiscal pressure, which causes deformity of the annulus and allows vertebral bodies to approximate. Release of the external pressure allows internal nuclear pressure to restore vertebral column length (by separating the vertebral endplates) and physiologic lordotic and kyphotic curvatures.

Migration of nuclear material and sequestra is influenced by compressive forces, shearing, and increased intradiscal pressure (6). Abnormal compressive loads on vertebral joints are responsible for a loss of disc volume and disruption of the normal triple-joint complex biomechanics of the spine. Small circumferential tears in an intervertebral disc set the stage for inflammatory reactions and neurotoxin formation.

Neuroischemia is a major feature of abnormal compressive loads. The anterior spinal artery, which supplies 65% to 70% of spinal cord tissues, is vulnerable to compression (7).

Neurotoxin accumulation and ischemia lead to back pain. The annulus of the disc and the zygapophyseal joints are richly innervated with nerves responsible for nociceptive and mechanoreceptive activities. Under normal intradisc pressures, the mechanoreceptive nerve fibers have a high mechanical threshold. During degenerative conditions, however, the mechanoreceptive fibers are activated at lower levels of loading (8). Peripheral nociceptive nerves become sensitized by tissue damage and degenerative change. This leads to persistent pain and increased muscular spasm (myospasm).

Electromyographic studies show that many patients with LBP have increased myospasm (9). Stimulation of low-threshold nerve endings in the disc and zygapophyseal joint activates the paraspinal musculature and demonstrates the reflex response of mechanoreceptors and nociceptors in adjacent musculature (10).

The medical practice of injecting anesthetics and corticosteroids into the zygapophyseal joint has resulted in varied and inconsistent outcomes. Physiologically, the injection leads to stretching of the joint capsule, which causes excitation of inhibitory interneurons that inhibit nociception through activation of mechanoreceptors. Saline injection effected an identical response, suggesting that a physiologic mechanism was responsible for reduction in pain and myospasm (11).

Motor unit action potentials were recorded with the use of three sets of needle electrodes placed in the deepest fascicles of the multifidus, bilateral to the L4 and L5 spinous process, and into the center longissimus musculature, bilateral to the L4 spinous process. Stimulation of nerves within the posterior annulus elicited reactions in the multifidus and longissimus paraspinal musculature. Saline injection into the zygapophyseal joint resulted in immediate and constant reduction in the amplitude of the motor unit action potential, demonstrating a neuromuscular interaction among the intervertebral disc, zygapophyseal joint, and paraspinal muscles.

Stretching of the joint capsule is responsible for reducing muscular spasm. The focus of any treatment regimen is to restore and normalize reflexogenic neuronal activity.

Prolonged muscular spasm compounds ischemia, neurotoxin accumulation, and increased intradiscal pressure gradient. Intradiscal fluid and nutrient exchange is possible only when the intradiscal pressure gradient is lower than the diastolic vascular pressure. Intradiscal pressure that is greater than capillary pressure in the vertebral body impedes oxygen diffusion, which, in turn, impedes healing.

The intervertebral disc normally loses fluids while in a state of pressure gradient increase greater than diastolic pressure. This occurs during waking, working, and weight-bearing activities. During sleep and non-weight-bearing activities, intradiscal pressure drops below diastolic pressure, and intradiscal fluid reserves are replenished. Any activity, condition, or prolonged muscular spasm that disturbs intradiscal fluid reserve can produce pain and degenerative change, with possible catastrophic outcome. Increased and prolonged intradiscal pressure results in dehydration of the intervertebral disc and loss of disc height. At normal disc height, the angle of the annular fiber crisscross intersection is 120 degrees. As disc height decreases, the angle increases, forming a void conducive to annular tear and migration of nuclear material (12). Removal of extruded nuclear material by surgery or percutaneous or laser discectomy has short-term benefit as a result of degraded normalization of intradiscal fluid exchange, decreased disc height, and increased crisscross annular fiber intersection, leading to weakening of the annular wall.

Randomized studies by Revel et all (13) showed that percutaneous and laser discectomy procedures have little value. Normalization of postsurgical intradiscal fluid reserve promises the best long-term prognosis. In fact, normalizing fluid reserve before surgery promotes favorable long-term clinical outcome.

Studies of intradiscal pressures conducted by placing a cannula into the intervertebral disc have proved conclusively that negative intradiscal pressures (eg,-160 mm Hg) are not only possible but repeatable (14).

Negative intradiscal pressure gradients of this magnitude can draw nuclear material inward through the tear site into the nuclear cavity. Prolonged negative intradiscal pressure normalizes intradiscal fluid exchange and increases disc height, which, in turn, decreases the annular fiber crisscross angle, closes the tear site, and restores structural integrity. Therapeutic application of decreased intradiscal pressure gradient combined with treatment of the zygapophyseal joint capsule and alignment of the posterior articular facet results in myospasm reduction, neurotoxin evacuation, and peripheral nutrient exchange.

The PT machine by ITM (International Therapeutic Machines, Carson City, Nevada) provides the first and only fully integrated biorobotic system capable of simultaneous amelioration of all aspects. This is accomplished by simultaneous integrated applications of several therapies. Human studies at a local hospital and at the Division of Neurosurgery, Health Sciences Center, University of Texas, San Antonio, have revealed that significant negative intradiscal pressure gradients are possible.

Tests were conducted by placing a cannula connected to a pressure transducer into the L4-L5 intradiscal space. Intradiscal pressure demonstrated an inverse relationship to stresses applied to the vertebral segments (14). Pressures of minus 160 mm Hg were consistently shown. Intradiscal pressure at or below normal diastolic pressure of 70 mm Hg facilitates nutrient and fluid exchange across the vertebral endplates, replenishing fluid reserves.

As pressure approaches and exceeds negative values, subligamentous and extruded hernial retraction can be expected. Intradiscal nutrient infiltration stimulates fibroblast production, leading to repair of annular tears. Intradiscal pressure that is greater than capillary pressure in the vertebral body impedes oxygen diffusion to the disc, which in turn impedes healing (12). Reducing intradiscal pressure creates a diffusion gradient into the disc, allowing infusion of oxygen and nutrients.

TREATMENT
The PT machine provides intervertebral-segment separation pressures sufficient to produce significant negative intradiscal pressures. These pressures are superimposed by an integrated subsonic 10Hz pulse, which maximizes the efficacy of volumetric nutrient exchange. This pulse also maximizes vertebral segment separation, which simultaneously decreases the annular fiber crisscross angle, closing annular tears and stretching the zygapophyseal joint capsule. The result is excitation of inhibitory interneurons that inhibit nociception and mechanoreception, thereby reducing myospasms. This integrated and simultaneous therapeutic application is controlled and coordinated by on-board computer and fiberoptic feedback sensors.

NON-INVASIVE DISC REHABILITATION
This combination of simultaneous therapeutic applications is called noninvasive disc rehabilitation (NDR). NDR combines the effects of intradiscal pressure reduction to negative values, resulting in hernial retraction, nutrient and toxin exchange at the intervertebral endplate, replenished intradiscal fluid reserves, vertebral segment separation (which decreases the annular fiber crisscross angle and closes annular tears), and fibroblast activation and stimulation, which promotes annular repair.

Zygapophyseal joint capsule stretch results in reflexogenic neuronal activity, with reduced pain and myospasm and increased range of joint motion. Neurotoxin evacuation is facilitated, and ischemia in and around the primary and secondary supporting structures is reduced.

Back pain has a large psychological component. Issues must be addressed to alleviate stress-related syndromes and ensure compliance with treatment until symptoms resolve. A video monitor records stressful events, which the patient can view during treatment. Explanations of the cause of the condition and visualization of the healing process are injury-preventive measures.

SUMMARY
There is no single cause of neck and back pain. For the first time, however, the multifaceted and complicated clinical resolution of this ubiquitous condition may be addressed by means of an integrated therapeutic application.

 

REFERENCES

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2. Krause N, Rangland D. Occupational disability due to low back pain: a new interdisciplinary classification based on a phase model of desirability. Spine. 1994;19:1011-1020.

3. Frymoyer JW. Predicting disability from low back pain. Clin Orthop. 1992;279:101-109.

4. Gargon M, Bannister G. Long term prognosis of soft tissue injuries of the neck. J Bone Joint Surg. 1990;72B:901-903.

5. MacNab L: The classic: disc degeneration and low back pain. Clin Orthop. 1986;208:3-14.

6. McKenzie RA. The Lumbar Spine: Mechanical Diagnosis and Therapy. Waikane, New Zealand: Spinal Publications; 1981.

7. Bernhardt M et al. Current concepts review: cervical spondylitic myelopathy. J Bone Joint Surg. 1991;75A:119-126.

8. Auramov Al, Cavanaugh JM, Ozaktay CA, Getchell TV, King AI. The effects of controlled mechanical loading on group II, III, IV afferent units from the lumbar facet joint and surrounding tissue: an in vitro study. J Bone Joint Surg. 1992;74A:1464-1471.

9. Indahl A, Kaigle AM, Reiker USO, Holm SH. Interaction between the porcine lumbar intervertebral disc, zygapophyseal joints, and paraspinal muscles. Spine. 1997;22:2834-2840.

10. Cavanaugh JM, El-Bohy AA, Hardy WH, Getchell TV, Getchell ML, King AI. Sensory innervation of soft tissues of the lumbar spine in the rat. J Orthop Res. 1989;7:389-397.

11. Lilius G, Laasonen EM, Myllynen P, Harilainen A, Grinlund G. Lumbar facet joint syndrome. A randomized clinical trial. J Bone Joint Surg. 1989;71:681-684.

12. Frymoyer JW. The Adult Spine. Principles and Practice. New York: Raven Press; 1991.

13. Revel M, Payan C, Vallee C, et al. Automated percutaneous discectomy versus chemonucleolysis in the treatment of sciatica. A randomized multicenter trial. Spine. 1993:18:1-7.

14. Ramos G, Martin W. Effects of vertebral axial decompression on intradiscal pressure. J Neurosurg. 1994;81:350-353.

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