Abstract

STUDY DESIGN:

A comparison between gait in patients undergoing surgery for L4 and L5 lumbar disc herniations and that in an age- and weight-matched control group.

OBJECTIVES:

To study whether changes in the moments produced at the ankle and knee joints during walking reflect the neurologic level of a herniated nucleus pulposus.

SUMMARY OF BACKGROUND DATA:

Lumbar herniated discs often cause muscle weakness, reduced motor function, and change in walking capacity. The specific effects of a disc herniation on muscle function during gait is poorly documented.

METHODS:

Conventional physical examination and kinetic analysis of gait were performed on 16 patients who subsequently underwent surgery for herniated discs (eight with L4-L5 and eight with L5-S1 disc herniations) and 16 healthy control subjects. The three components of the external moment at the ankle and knee were computed. The peak magnitudes of specific components of the external moments were compared with those of the control group.

RESULTS:

Reduced external ankle plantar flexion moment, indicating a decreased function of the ankle dorsiflexors, was found in patients with herniated nucleus pulposus of both L4-L5 and L5-S1. Reduced external ankle dorsiflexion moment, indicating a decreased function of the ankle plantar flexors, was found only in patients with a lesion to the L5-S1 disc, but not in those with herniations at L4-L5.

CONCLUSIONS:

Preoperative gait analysis identified functional deficits of the muscles about the ankle and foot that relate to the level of the herniation. Kinetic measurements can assist in understanding the functional limitations associated with specific levels of a herniation.

Morag E, Hurwitz DE, Andriacchi TP, et al., Abnormalities in muscle function during gait in relation to the level of lumbar disc herniation, Spine, April 1, 2000:25(7), pp829-33.

It appears from a study by Vucetic and Svensson¹ that only three physical signs are of real diagnostic value in predicting whether there is a lumbar disc herniation and the degree or grade of herniation.

This study was a prospective rather than a retrospective study on 163 consecutive patients operated on for probable herniated discs. The three signs were the range of lumbar sagittal motion, the Lasegue sign, and the crossed Lasegue sign. They found that these tests were significant for the presence of a herniation and the degree of herniation, but not accurate for the level of herniation.

Neurologic signs, while important for distinguishing between radicular and referred pain, are not of great value in diagnosing the grade or level of a herniation.² One third of patients with an absent Achilles reflex had a hernia above L5-Sl and the diagnostic value of an absent Achilles reflex may decrease with age.³ The absence of an Achilles reflex is more reliable than a diminished reflex as a sign of disc herniation, and its diagnostic value increases markedly if correlated with diagnostic imaging.⁴ Although patellar areflexia is six to seven times more common in L3-L4 hernias than other levels, only one-quarter of the patients with this sign had L3-L4 hernias.¹

The strongest indicator for the grade of hernia was the range of sagittal lumbar motion. The range of lumbar motion decreased with increasing grades of herniation. The range was negligible for protruded hernia (generalized bulge with root involvement), and progressively decreased with an extruded disc hernia (posterior ligament still intact) and sequestrated (complete hernia beyond the posterior ligament). The crossed Lasegue sign, which was meaningful only if it was associated with the unilateral positive Laseque sign, was also proportionate to the grade of the hernia. Therefore the use of both the lumbar range-of-motion and crossed Lasegue sign predicted 74 percent of uncontained (sequestrated hernias), and 68 percent of contained hernias (protruded and extruded). In this study the Lasegue was only considered positive if pain radiated to the foot.

References

1. Vucetic N, Svensson O. Physical signs in lumbar disc hernia. Clinical Orthopaedics & Rel. Research. (333);192-201:1996.
2. Deburge A, Benoist M, Boyer D. The diagnosis of disc sequestration. Spine 9;496-499:1984. In: Vucetic N, Svensson O. Physical signs in lumbar disc hernia. Clinical Orthopaedics & Rel. Research. (333);192-201:1996.
3. Spangfort EV. The lumbar disc herniation. A computer-aided analysis of 2,504 operations. Acta Orthop Scand 142(Suppl):70-71, 1972; In: Vucetic N, Svensson O. Physical signs in lumbar disc hernia. Clinical Orthopaedics & Rel. Research. (333);192-201:1996.
4. Hakeliu A, Hindmarsh J. The significance of neurological signs and myelographic findings in the diagnosis of lumbar root compression. Acta Orthop Scand 43:239-24, 1972: In: Vucetic N, Svensson O. Physical signs in lumbar disc hernia. Clinical Orthopaedics & Rel. Research. (333);192-201:1996.

By Dr. Warren Hammer, MS, DC, DABCO

Published in: Dynamic Chiropractic – March 10, 1997, Vol. 15, Issue 06

The single randomized controlled trial of spinal decompression therapy compared the VAX-D® unit, which places the patient a prone rather than supine position, to transcutaneous electrical nerve stimulation (TENS) for the treatment of chronic low back pain. Subjects were recruited through advertisement and had chronic low back pain of greater than 3 months duration with associated leg pain. Disc protrusion or herniation confirmed by CT or MRI was also required. Average duration of pain in the study population was 7.3 years and average age was 42 years old. This study enrolled 44 patients and 40 completed the study. Patients were randomized in sequential order to their appropriate group. Outcome measures were the 10 centimeter visual analog pain scale (VAS) and a disability scale. The disability scale rated the subject’s ability to perform their most affected activity on a 0 to 4 scale, with 4 being “can do without limitation”. Treatments consisted of 30 minute sessions, five times per week for four weeks followed by weekly sessions for 4 weeks. The control group received TENS for 30 minutes daily for 20 days followed by weekly treatment for 4 weeks. Both groups were able to take anti-inflammatory and non-narcotic pain relievers as needed. Success of treatment was defined by 50% improvement in VAS and any improvement in disability. At the conclusion of the study 13 out of 19 (68.4%) of the treatment group showed improvement while 0 of 21 for the TENS group. At follow-up 7 of the original 19 subjects (36.8%) in the treatment group showed sustained improvement.

Sherry E, Kitchener P, Smart R. A prospective randomized controlled study of VAX-D and TENS for the treatment of chronic low back pain. Neurol Res 2001; 23(7):780-784.

C. Norman Shealy, MD, PhD, and Vera Borgmeyer, RN, MA. Decompression, Reduction, and Stabilization of the Lumbar Spine: A Cost-Effective Treatment for Lumbosacral Pain. American Journal of Pain Management Vol. 7 No. 2 April 1997

“Serial MRI of 20 patients treated with the decompression table shows in our study up to 90% reduction of subligamentous nucleus herniation in 10 of 14. Some rehydration occurs detected by T2 and proton density signal increase. Torn annulus repair is seen in all.”

Eyerman, Edward MD. Simple pelvic traction gives inconsistent relief to herniated lumbar disc sufferers. Journal of Neuroimaging. Paper presented to the American Society of Neuroimaging, Orlando, Florida 2-26-98.

“Results showed that 86% of the 219 patients who completed the therapy reported immediate resolution of symptoms, while 84% remained pain-free 90 days post-treatment. Physical examination findings showed improvement in 92% of the 219 patients, and remained intact in 89% of these patients 90 days after treatment.”

Gionis, Thomas MD; Groteke, Eric DC. Surgical Alternatives: Spinal Decompression. Orthopedic Technology Review. 2003; 6 (5).

“All but two of the patients in the study improved at least 30% or more in the first three weeks.” “Utilizing the outcome measures, this form of decompression reduces symptoms and improves activities of daily living.”

Bruce Gundersen, DC, FACO; Michael Henrie, MS II, Josh Christensen, DC. A Clinical Trial on Non-Surgical Spinal Decompression Using Vertebral Axial Distraction Delivered by a Computerized Traction Device. The Academy of Chiropractic Orthopedists, Quarterly Journal of ACO, June 2004

Wikipedia’s opinion about Spinal Decompression Therapy Effectiveness

In a small randomized study of 44 subjects, in which one author disclosed a proprietary interest in Vax-D, it was shown to have a clinical success rate of 68.4%. 11

A 2004 report by the State of Washington Department of Labor and Industries concluded “Published literature has not substantially shown whether powered traction devices are more effective than other forms of traction, other conservative treatments, or surgery.” 12 A 2005 review of VAX-D (including the Sherry study above) by the Workers’ Compensation Board of British Columbia concluded “To date there is no evidence that the VAX-D system is effective in treating chronic LBP associated with herniated disc, degenerative disc, posterior facet syndrome, sciatica or radiculopathy.” 13

A 2006 systematic review of studies of spinal decompression using motorized traction devices conducted between 1975 and October 2005 (including the two mentioned above) concluded that “…the efficacy of spinal decompression achieved with motorized traction for chronic discogenic low back pain [remained] unproved”, and called for “Scientifically more rigorous studies with better randomization, control groups, and standardized outcome measures … to overcome the limitations of past studies.” 14 A technology assessment conducted in 2007 by the Agency for Healthcare Research and Quality (for which the two studies cited above were included for analysis) said “Currently available evidence is too limited in quality and quantity to allow for the formulation of evidence-based conclusions regarding the efficacy of decompression therapy as a therapy for chronic back pain when compared with other non-surgical treatment options.” 15

A 2007 critique of research studies, including the two cited above, said:

There is very limited evidence in the scientific literature to support the effectiveness of non-surgical spinal decompression therapy. This intervention has never been compared to exercise, spinal manipulation, standard medical care or other less expensive conservative treatment options which have an ample body of research demonstrating efficacy. Considering the cost-benefit relationship, many better researched and less expensive treatment options are available to the clinician. 16

The truth about nonsurgical spinal decompression studies

More studies about spinal decompression

References

• Sherry, Eugene; Kitchener, Peter; Smart, Russell (October 2001). “A prospective randomized controlled study of VAX-D and TENS for the treatment of chronic low back pain”. Neurological Research 23 (7): 780–784. doi:10.1179/016164101101199180. PMID 11680522. One author disclosed a proprietary interest in Vax-D.


• Wang, Grace (2004-06-14). “Powered Traction Devices for Intervertebral Decompression” (PDF). Health Technology Asessment (sic) Update. Office of the Medical Director – Department of Labor and Industries – State of Washington. http://www.lni.wa.gov/ClaimsIns/Files/OMD/TractionTechAssessJun142004.pdf. Retrieved 2009-08-20.


• Martin, Craig W (February 2005). “Vertebral Axial Decompression For Low Back Pain” (PDF). WCB Evidence Based Practice Group – Program Design Division – Workers’ Compensation Board of British Columbia. http://www.worksafebc.com/health_care_providers/Assets/PDF/vertebral_axial_decompression_low_back_pain.pdf. Retrieved 2009-08-20.


• Macario, A; Pergolizzi, JV (September 2006). “Systematic literature review of spinal decompression via motorized traction for chronic discogenic low back pain”. Pain Practice 6 (3): 171–8. doi:10.1111/j.1533-2500.2006.00082.x. PMID 17147594.


• Jurecki-Tiller, Marie; Bruening, Wendy; Tregear, Stephen; Schoelles, Karen; Erinoff, Eileen; Coates, Vivian; ECRI Institute Evidence-based Practice Center (2007-04-26). “Decompression Therapy for the Treatment of Lumbosacral Pain” (PDF). Technology Assessments. Agency for Healthcare Research and Quality – United States Department of Health and Human Services. http://www.cms.hhs.gov/determinationprocess/downloads/id47TA.pdf. Retrieved 2009-08-20.


• Daniel, Dwain M (2007-05-18). “Non-surgical spinal decompression therapy: does the scientific literature support efficacy claims made in the advertising media?”. Chiropractic & Osteopathy 15 (7): 7. doi:10.1186/1746-1340-15-7. PMC 1887522. PMID 17511872.

In most industrialized countries, chronic low back pain is recognized as a widespreadcondition. However, a Special Report is now featured in the January issue of Pain Medicine News. The Special Report was first featured in the December 2007 issue of Anesthesiology News and was then presented on-line at: www.painmedicinenews.com in early January.

The article has since become the most read article on this website. The Special Report highlights exciting research on a medical device that offers patients a non-surgical treatment option in treating chronic low back pain. The authors of this Special Report are from the prestigious institutions of Duke University School of Medicine, Mayo Clinic, and Johns Hopkins University School of Medicine. They conclude their Special Report by stating, “computerized nonsurgical spinal decompression systems were designed to provide maximum patient benefits with the use of a noninvasive approach that may help minimize health care resources and offer a potentially optimal therapeutic approach to the treatment of LBP (low back pain).”

The outcome of a clinical study evaluating the effect of nonsurgical intervention on symptoms of spine patients with herniated and degenerative disc disease is presented.

By Thomas A. Gionis, MD, JD, MBA, MHA, FICS, FRCS, and Eric Groteke, DC, CCIC
Orthopedic Technology Review, Vol. 5-6, Nov-Dec 2003.

This clinical outcomes study was performed to evaluate the effect of spinal decompression on symptoms and physical findings of patients with herniated and degenerative disc disease. Results showed that 86% of the 219 patients who completed the therapy reported immediate resolution of symptoms, while 84% remained pain-free 90 days post-treatment. Physical examination findings showed improvement in 92% of the 219 patients, and remained intact in 89% of these patients 90 days after treatment. This study shows that disc disease-the most common cause of back pain, which costs the American health care system more than $50 billion annually-can be cost-effectively treated using spinal decompression. The cost for successful non-surgical therapy is less than a tenth of that for surgery. These results show that biotechnological advances of spinal decompression reveal promising results for the future of effective management of patients with disc herniation and degenerative disc diseases. Long-term outcome studies are needed to determine if non-surgical treatment prevents later surgery, or merely delays it.

INTRODUCTION: ADVANCES IN BIOTECHNOLOGY

With the recent advances in biotechnology, spinal decompression has evolved into a cost-effective nonsurgical treatment for herniated and degenerative spinal disc disease, one of the major causes of back pain. This nonsurgical treatment for herniated and degenerative spinal disc disease works on the affected spinal segment by significantly reducing intradiscal pressures.1 Chronic low back pain disability is the most expensive benign condition that is medically treated in industrial countries. It is also the number one cause of disability in persons under age 45. After 45, it is the third leading cause of disability.2 Disc disease costs the health care system more than $50 billion a year.

The intervertebral disc is made up of sheets of fibers that form a fibrocartilaginous structure, which encapsulates the inner mucopolysaccharide gel nucleus. The outer wall and gel act hydrodynamically. The intrinsic pressure of the fluid within the semirigid enclosed outer wall allows hydrodynamic activity, making the intervertebral disc a mechanical structure.3 As a person utilizes various normal ranges of motion, spinal discs deform as a result of pressure changes within the disc.4 The disc deforms, causing nuclear migration and elongation of annular fibers. Osteophytes develop along the junction of vertebral bodies and discs, causing a disease known as spondylosis. This disc narrows from the alteration of the nucleus pulposus, which changes from a gelatinous consistency to a more fibrous nature as the aging process continues. The disc space thins with sclerosis of the cartilaginous end plates and new bone formation around the periphery of the contiguous vertebral surfaces. The altered mechanics place stress on the posterior diarthrodial joints, causing them to lose their normal nuclear fulcrum for movement. With the loss of disc space, the plane of articulation of the facet surface is no longer congruous. This stress results in degenerative arthritis of the articular surfaces.5

This is especially important in occupational repetitive injuries, which make up a majority of work-related injuries. When disc degeneration occurs, the layers of the annulus can separate in places and form circumferential tears. Several of these circumferential tears may unite and result in a radial tear where the material may herniate to produce disc herniation or prolapse. Even though a disc herniation may not occur, the annulus produces weakening, circumferential bulging, and loss of intervertebral disc height. As a result, discograms at this stage usually reveal reduced interdiscal pressure.

The early changes that have been identified in the nucleus pulposus and annulus fibrosis are probably biomechanical and relate to aging. Any additional trauma on these changes can speed up the process of degeneration. When there is a discogenic injury, physical displacement occurs, as well as tissue edema and muscle spasm, which increase the intradiscal pressures and restrict fluid migration.6 Additionally, compression injuries causing an endplate fracture can predispose the disc to degeneration in the future.

The alteration of normal kinetics is the most prevalent cause of lower back pain and disc disruption and thus it is vital to maintain homeostasis in and around the spinal disc; Yong-Hing and Kirkaldy-Willis7 have correlated this degeneration to clinical symptoms. The three clinical stages of spinal degeneration include:

1. Stage of Dysfunction. There is little pathology and symptoms are subtle or absent. The diagnosis of Lumbalgia and rotatory strain are commonly used.


2. Stage of Instability. Abnormal movement of the motion segment of instability exists and the patient complains of moderate symptoms with objective findings. Conservative care is used and sometimes surgery is indicated.


3. Stage of Stabilization. The third phase where there are severe degenerative changes of the disc and facets reduce motion with likely stenosis.

Spinal decompression has been shown to decompress the disc space, and in the clinical picture of low back pain is distinguishable from conventional spinal traction.8,9 According to the literature, traditional traction has proven to be less effective and biomechanically inadequate to produce optimal therapeutic results.8-11 In fact, one study by Mangion et al concluded that any benefit derived from continuous traction devices was due to enforced immobilization rather than actual traction.10 In another study, Weber compared patients treated with traction to a control group that had simulated traction and demonstrated no significant differences.11 Research confirms that traditional traction does not produce spinal decompression. Instead, decompression, that is, unloading due to distraction and positioning of the intervertebral discs and facet joints of the lumbar spine, has been proven an effective treatment for herniated and degenerative disc disease, by producing and sustaining negative intradiscal pressure in the disc space. In agreement with Nachemon’s findings and Yong-Hing and Kirkaldy-Willis,1 spinal decompression treatment for low back pain intervenes in the natural history of spinal degeneration.7,12 Matthews13 used epidurography to study patients thought to have lumbar disc protrusion. With applied forces of 120 pounds x 20 minutes, he was able to demonstrate that the contrast material was drawn into the disc spaces by osmotic changes. Goldfish14 speculates that the degenerated disc may benefit by lowering intradiscal pressure, affecting the nutritional state of the nucleus pulposus. Ramos and Martin8 showed by precisely directed distraction forces, intradiscal pressure could dramatically drop into a negative range. A study by Onel et al15 reported the positive effects of distraction on the disc with contour changes by computed tomography imaging. High intradiscal pressures associated with both herniated and degenerated discs interfere with the restoration of homeostasis and repair of injured tissue.

Biotechnological advances have fostered the design of Food and Drug Administration-approved ergonomic devices that decompress the intervertebral discs. The biomechanics of these decompression/reduction machines work by decompression at the specific disc level that is diagnosed from finding on a comprehensive physical examination and the appropriate diagnostic imaging studies. The angle of decompression to the affected level causes a negative pressure intradiscally that creates an osmotic pressure gradient for nutrients, water, and blood to flow into the degenerated and/or herniated disc thereby allowing the phases of healing to take place.

This clinical outcomes study, which was performed to evaluate the effect of spinal decompression on symptoms of patients with herniated and degenerative disc disease, showed that 86% of the 219 patients who completed therapy reported immediate resolution of symptoms, and 84% of those remained pain-free 90 days post-treatment. Physical examination findings revealed improvement in 92% of the 219 patients who completed the therapy.

METHODS

The study group included 229 people, randomly chosen from 500 patients who had symptoms associated with herniated and degenerative disc disease that had been ongoing for at least 4 weeks. Inclusion criteria included pain due to herniated and bulging lumbar discs that is more than 4 weeks old, or persistent pain from degenerated discs not responding to 4 weeks of conservative therapy. All patients had to be available for 4 weeks of treatment protocol, be at least 18 years of age, and have an MRI within 6 months. Those patients who had previous back surgery were excluded. Of note, 73 of the patients had experienced one to three epidural injections prior to this episode of back pain and 22 of those patients had epidurals for their current condition. Measurements were taken before the treatments began and again at week two, four, six, and 90 days post treatment. At each testing point a questionnaire and physical examination were performed without prior documentation present in order to avoid bias. Testing included the Oswetry questionnaire, which was utilized to quantify information related to measurement of symptoms and functional status. Ten categories of questions about everyday activities were asked prior to the first session and again after treatment and 30 days following the last treatment.

Testing also consisted of a modified physical examination, including evaluation of reflexes (normal, sluggish, or absent), gait evaluation, the presence of kyphosis, and a straight leg raising test (radiating pain into the lower back and leg was categorized when raising the leg over 30 degrees or less is considered positive, but if pain remained isolated in the lower back, it was considered negative). Lumbar range of motion was measured with an ergonometer. Limitations ranging from normal to over 15 degrees in flexion and over 10 degrees in rotation and extension were positive findings. The investigator used pinprick and soft touch to determine the presence of gross sensory deficit in the lower extremities.

Of the 229 patients selected, only 10 patients did not complete the treatment protocol. Reasons for noncompletion included transportation issues, family emergencies, scheduling conflicts, lack of motivation, and transient discomfort. The patient protocol provided for 20 treatments of spinal decompression over a 6-week course of therapy. Each session consisted of a 45-minute treatment on the equipment followed by 15 minutes of ice and interferential frequency therapy to consolidate the lumbar paravertebral muscles. The patient regimen included 2 weeks of daily spinal decompression treatment (5 days per week), followed by three sessions per week for 2 weeks, concluding with two sessions per week for the remaining 2 weeks of therapy.

On the first day of treatment, the applied pressure was measured as one half of the person’s body weight minus 10 pounds, followed on the second day with one half of the person’s body weight. The pressure placed for the remainder of the 18 sessions was equivalent to one half of the patient’s body weight plus an additional 10 pounds. The angle of treatment was set according to manufacturer’s protocol after identifying a specific lumbar disc correlated with MRI findings. A session would begin with the patient being fitted with a customized lower and upper harness to fit their specific body frame. The patient would step onto a platform located at the base of the equipment, which simultaneously calculated body weight and determined proper treatment pressure. The patient was then lowered into the supine position, where the investigator would align the split of table with the top of the patient’s iliac crest. A pneumatic air pump was used to automatically increase lordosis of the lumbar spine for patient comfort. The patient’s chest harness was attached and tightened to the table. An automatic shoulder support system tightened and affixed the patient’s upper body. A knee pillow was placed to maintain slight flexion of the knees. With use of the previously calculated treatment pressures, spinal decompression was then applied. After treatment, the patient received 15 minutes of interferential frequency (80 to 120 Hz) therapy and cold packs to consolidate paravertebral muscles.

During the initial 2 weeks of treatment, the patients were instructed to wear lumbar support belts and limit activities, and were placed on light duty at work. In addition, they were prescribed a nonsteroidal, to be taken 1 hour before therapy and at bedtime during the first 2 weeks of treatment. After the second week of treatment, medication was decreased and moderate activity was permitted.

Data was collected from 219 patients treated during this clinical study. Study demographics consisted of 79 female and 140 male patients. The patients treated ranged from 24 to 74 years of age (see Table 1). The average weight of the females was 146 pounds and the average weight of the men was 195 pounds. According to the Oswestry Pain Scale, patients reported their symptoms ranging from no pain (0) to severe pain (5).

RESULTS

According to the self-rated Oswestry Pain Scale, treatment was successful in 86% of the 219 patients included in this study. Treatment success was defined by a reduction in pain to 0 or 1 on the pain scale. The perception of pain was none 0 to occasional 1 without any further need for medication or treatment in 188 patients. These patients reported complete resolution of pain, lumbar range of motion was normalized, and there was recovery of any sensory or motor loss. The remaining 31 patients reported significant pain and disability, despite some improvement in their overall pain and disability score.

In this study, only patients diagnosed with herniated and degenerative discs with at least a 4-week onset were eligible. Each patient’s diagnosis was confirmed by MRI findings. All selected patients reported 3 to 5 on the pain scale with radiating neuritis into the lower extremities. By the second week of treatment, 77% of patients had a greater than 50% resolution of low back pain. Subsequent orthopedic examinations demonstrated that an increase in spinal range of motion directly correlated with an improvement in straight leg raises and reflex response. Table 2 shows a summary of the subjective findings obtained during this study by category and total results post treatment. After 90 days, only five patients (2%) were found to have relapsed from the initial treatment program.

Ninety-two percent of patients with abnormal physical findings improved post-treatment. Ninety days later only 3% of these patients had abnormal findings. Table 3 summarizes the percentage of patients that showed improvement in physician examination findings testing both motor and sensory system function after treatment. Gait improved in 96% of the individuals who started with an abnormal gait, while 96% of those with sluggish reflexes normalized. Sensory perception improved in 93% of the patients, motor limitation diminished in 86%, 89% had a normal straight leg raise test who initially tested abnormal, and 90% showed improvement in their spinal range of motion.

SUMMARY

In conclusion, nonsurgical spinal decompression provides a method for physicians to properly apply and direct the decompressive force necessary to effectively treat discogenic disease. With the biotechnological advances of spinal decompression, symptoms were restored by subjective report in 86% of patients previously thought to be surgical candidates and mechanical function was restored in 92% using objective data. Ninety days after treatment only 2% reported pain and 3% relapsed, by physical examination exhibiting motor limitations and decreased spinal range of motion. Our results indicate that in treating 219 patients with MRI-documented disc herniation and degenerative disc diseases, treatment was successful as defined by: pain reduction; reduction in use of pain medications; normalization of range of motion, reflex, and gait; and recovery of sensory or motor loss. Biotechnological advances of spinal decompression indeed reveal promising results for the future of effective management of patients with disc herniation and degenerative disc diseases. The cost for successful nonsurgical therapy is less than a tenth of that for surgery. Long-term outcome studies are needed to determine if nonsurgical treatment prevents later surgery or merely delays it.

Thomas A. Gionis, MD, JD, MBA, MHA, FICS, FRCS, is chairman of the American Board of Healthcare Law and Medicine, Chicago; a diplomate professor of surgery, American Academy of Neurological and Orthopaedic Surgeons; and a fellow of the International College of Surgeons and the Royal College of Surgeons.

Eric Groteke, DC, CCIC, is a chiropractor and is certified in manipulation under anesthesia. He is also a chiropractic insurance consultant, a certified independent chiropractic examiner, and a certified chiropractic insurance consultant. Groteke maintains chiropractic centers in northeastern Pennsylvania, in Stroudsburg, Scranton, and Wilkes-Barre.

REFERENCES

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2. Narayan P, Morris IM. A preliminary audit of the management of acute low back pain in the Kettering District. Br J Rheumatol. 1995;34:693-694.


3. McDevitt C. Proteoglycans of the intervertebral disc. In: Gosh, P, ed. The Biology of the Intervertebral Disc. Boca Raton, Fla: CRC Press; 1988:151-170.


4. Bogduk N, Twomey L. Clinical Anatomy of the Lumbar Spine. New York: Churchill Livingstone; 1991.


5. Cox JM. Low Back Pain: Mechanism, Diagnosis, and Treatment. 5th ed. Baltimore: Williams & Wilkins; 1990:69-70, 144.


6. Cyriax JH. Textbook of Orthopaedic Medicine: Diagnosis of Soft Tissue Lesions. Vol 1. 8th ed. London: Balliere Tindall; 1982.


7. Nachemson AL. The lumbar spine, an orthopaedic challenge. Spine. 1976;1(1):59-69.


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


9. Shealy CN, Leroy P. New concepts in back pain management: decompression, reduction, and stabilization. In: Weiner R, ed. Pain Management: A Practical Guide for Clinicians. Boca Raton, Fla: St Lucie Press; 1998:239-257.


10. Pal B, Mangion P, Hossain MA, et al. A controlled trial of continuous lumbar traction in back pain and sciatica. Br J Rheumatol. 1986;25:181-183.


11. Weber H. Traction therapy in sciatica due to disc prolapse. J Oslo City Hosp. 1973;23(10):167-176.


12. Yong-Hing K, Kirkaldy-Willis WH. The pathophysiology of degenerative disease of the lumbar spine. Orthop Clin North Am. 1983;14:501-503.


13. Matthews J. The effects of spinal traction. Physiotherapy. 1972;58:64-66.


14. Goldfish G. Lumbar traction. In: Tollison CD, Kriegel M, eds. Inter-


15. disciplinary Rehabilitation of Low Back Pain. Baltimore: Williams & Wilkins; 1989.


16. Onel D, Tuzlaci M, Sari H, Demir K. Computed tomographic investigation of the effect of traction on lumbar disc herniations. Spine. 1989; 14(1):82-90.