Gait in relation to the level of lumbar disc herniation

On December 19, 2011, in Studies, by admin

Lumbar Disc Herniation Influences Gait

Lumbar Disc Herniation Influences Gait: Muscle weakness, reduced motor function, and change in walking capacity are potential complications resulting from an herniated disc. Other clinical symptoms include pain, sensory changes and impaired reflexes, although the specific effects of disc herniation on muscle function during gait have not been adequately documented in the literature.



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.


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.


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.


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.


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.


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.

Spinal decompression

On September 27, 2010, in , by admin

Spinal decompression: an effective treatment for herniated disc and chronic back pain.   Non-surgical spinal decompression therapy is: Noninvasive Conservative Painless Safe Supervised by a health professional who holds a doctorate degree Effective for a variety of back conditions (herniated disc, chronic pain, arthrosis, facet syndrome, etc.)   If you are visiting our website …It […]

Spinal decompression: an effective treatment for herniated disc and chronic back pain.


Non-surgical spinal decompression therapy is:

  • Noninvasive
  • Conservative
  • Painless
  • Safe
  • Supervised by a health professional who holds a doctorate degree
  • Effective for a variety of back conditions (herniated disc, chronic pain, arthrosis, facet syndrome, etc.)


If you are visiting our website …It is because you suffer from a condition described below!

This site was designed for those who suffer from chronic back pain, herniated disc or disc herniation, bulging of a disc, sciatica, leg pain, degenerative disc disease, tingling, numbness, pain in arms, neck pain, and for some patients with spinal stenosis and finally for those who underwent back surgery but still suffering from pain.


 What are your treatment options?


Types of Care


Acupuncture Unlikely
Heat & cryotherapy (cold) Unlikely
Electrotherapy (ultrasond, tens, etc.) Unlikely
Exercices Unlikely
Osteopathy Unlikely
Massage Therapy Unlikely
Surgery  likely
Spinal decompression  likely


Spinal decompression demystified


Spinal decompression reduces the pressure that builds up inside the discs. This technique consists of a mechanical disc decompression by suction causing decompression of the disc. The pain decreases because of resorption of the herniated disc, bulging disc or because of the reduced pressure on the nerves or spinal cord: that is to say that the disc returns to its original shape when the bulge or bulging disc disappears and the pressure on the spinal nerves is therefore eliminated.

Spinal decompression achieves this by creating a negative pressure inside the disc, known as negative intra-discal pressure. This essentially creates a vacuum to suck the bulging and herniated material inside the disc space by reducing the pressure.


The same phenomenon happens when you break the window of a pressurized airplane flying at high altitude: everything that is inside the airplane (positive pressure) is violently expelled to the outside (negative pressure).


When there is a bulging of the intervertebral disc and / or herniated disc, the ligaments that hold up the disk material has become stretched or torn. Spinal Decompression strengthens the ligament bands that hold the disc material in place, allowing healing and preventing a recurrence.


In most cases, the healing process requires only a few weeks of outpatient treatment.


Next Page – Herniated disc

Reduction of disc herniation

On September 27, 2010, in , by admin

Tags: disc herniation, non surgical spinal decompression, spinal decompression, spinal decompression therapy

Causes of low back pain

On September 27, 2010, in , by admin

Let’s have a look a the causes of low back pain and how it could be related to degenerative disc disease and herniated discs. common complaint among adults lifetime prevalence in working population up to 80% 60% experience functional limitation or disability second most common reason for work disability despite advances in imaging and surgical […]

Let’s have a look a the causes of low back pain and how it could be related to degenerative disc disease and herniated discs.

  • common complaint among adults
  • lifetime prevalence in working population up to 80%
  • 60% experience functional limitation or disability
  • second most common reason for work disability
  • despite advances in imaging and surgical techniques LBP prevalence and its cost are relatively unchanged
  • 90% people age >50 have Degenerative Disc Disease
  • Large disc herniation does NOT always need surgery
  • Neurologic loss is NOT an absolute indication for surgery
  • Small disc bulge is NOT always normal
  • Surgery does not have an 80% success rate
  • Conservative treatment is reversible. Surgery is not.


Cause of low back pain

Causes of low back pain - Click to enlarge

Back pain causes:

  • Spasm
  • Sprain/strain
  • Biomechanical
  • Disc herniation
  • Disc bulge
  • Degenerative osteoarthritis
  • Facet syndrome
  • Spondylolithesis
  • Spinal stenosis
  • Osteoporosis
  • Inflammatory
  • Infection
  • Cancer


Disc Degeneration

Normal Vs Disc Degeneration - Clic to enlarge

Disc degeneration (arthrosis)

  • Changes in hydrostatic pressure
  • Lack of oxygen
  • Lack of glucose
  • Changes in pH levels
  • Death of proteoglycans

If the cells of the disc failed to get proper nutrients – such as oxygen, or glucose – or if the pH level of the disc drops (because waste is not being diffused out of the disc and it becomes anaerobic), disc cells would die and stop producing the vital proteoglycan aggregates. The disc loses its water content (dehydrates) and loses its hydrostatic pressure (osmotic pressure).

Symptoms of lumbar disc disease are the result of either herniation of the nucleus pulposus through a mechanically weak annulus fibrosis or from tearing of the annulus itself. This can lead to Radiculopathy from nerve root compression and/or Radiculitis – an inflammatory process affecting nerve roots or the spinal cord.  Herniation is thought to be the result of a defect in the annulus fibrosis, most likely the result of excessive stress applied to the disc.

Herniated disc

Three types of annular tears:

  1. Rim lesion – horizontal tearing of the very outer fibers of the disc near their attachments into the ring apophysis;
  2. Concentric tear – splitting apart of the lamellae of the annulus in a circumferential direction
  3. Radial tear – horizontal or obliquely horizontal tears

Next page – Causes

Spinal Decompression Studies

On September 27, 2010, in , by admin

Can Herniated Discs Reduce in Size or Resorb? by David BenEliyahu,DC,DACBSP,DAAPM In the past, it was believed that once a patient acquired a herniated disc, it was permanent. However, recent research with MRI and CT outcome studies has documented that this is fallacy. Herniated discs in the cervical and lumbar spine have been shown to […]

Can Herniated Discs Reduce in Size or Resorb?

by David BenEliyahu,DC,DACBSP,DAAPM

In the past, it was believed that once a patient acquired a herniated disc, it was permanent. However, recent research with MRI and CT outcome studies has documented that this is fallacy. Herniated discs in the cervical and lumbar spine have been shown to not only reduce in size after a period of conservative care, but in many cases regress and disappear upon reimaging.

Numerous medical studies and some chiropractic studies have been performed and published. In recent studies by Mochida et al., both cervical (CDH) and lumbar (LDH) disc herniations were studied in pre- and post-MR imaging conditions. In CDH cases, they demonstrated that in 40% of the time, there was a reduction in size or regression. In LDH cases, they demonstrated about a 60% reduction or regression in the size of the herniation. They also found that the larger the extrusion or sequestration, the better the rate of regression. They concluded that disc regression or resorption depended upon size, location and the phase of the injury. Discs tended to reduce in size early on after onset, and more so in the lateral or sequestered type of herniation than smaller or subligamentous herniations. It is interesting to note that most patients in Mochida’s study did well clinically with conservative care regardless of the MRI outcome.

In a different study, Mochida found that there is a large percentage of macrophages in excised herniated disc material, as well as evidence of neovascularization. As such, the reduction in size is most likely due to phagocytic or macrophagic digestion, since the body attacks the disc fragment as a foreign protein, much like any other antigen. Immunohistochemistry studies are being conducted at this time to elucidate the pathophysiology of disc herniation and regression.

In a similar study of LDH outcome by Bozzao et al., 63% of the patients treated nonsurgically with epidurals, medication, etc., demonstrated disc resorption upon repeat imaging. In a prospective study of patients with LDH, Ellenberg et al. documented that patients with CT evidence of herniated discs and EMG evidence of radiculopathy had a 78% rate of disc reduction. Matsubara found in a similar study that medical care involving medication, physiotherapy, traction and epidural steroid injections resulted in disc regression in 60% of the cases. In another prospective study, Bush et al. showed disc regression in 12 of the 13 cases studied. The period of care averaged six months, with a range of 2-12 months for good clinical and anatomical MRI outcome.

In one of the few chiropractic care MRI studies, I published a prospective case series of 27 patients with either CDH or LDH. I obtained pre- and post-chiropractic care MRIs and found that in 63% of the cases, there was either a reduction in size, or the disc herniation resorbed completely. I also found that 80% of the cases had good clinical outcomes, and 78% of the patients returned to their preinjury occupations. Chiropractic care was shown to be amenable to the clinical management of the disc herniation not only on a clinical level, but on an anatomical level as well. In a study by Cassidy et al. on the effects of side posture manipulation on CT-documented herniated discs, the authors found that 13 of 14 patients had good clinical results. Of those, about half had a decrease in the size of the herniation on repeat CT followups.

Case Report

In a recent case that I treated, a 48-year-old female patient presented with acute low back and associated leg/extremity pain into the foot. She had evidence of radiculopathy with diminished sensation at the L4/5 dermatomes, and positive root tension signs with a positive straight leg raise at 35 degrees on the left and 45 degrees on the right. DTRs were within normal limits, and there was no significant motor weakness. An MRI of the lumbar spine revealed a large focal disc herniation centrally and to the left.

The patient began treatment on a three times per week schedule and was treated with lumbar flexion/distraction, interferential current and microcurrent delivered by pads and probes. Microcurrent therapy was combined with regular interferential therapy and helped reduce pain and increase circulation to enhance the healing process. Microcurrent was then delivered to the LS spine and lower extremity by probes, stimulating the acupuncture points of the bladder meridian as well as stimulation along the affected dermatome.

The microcurrent therapy helped afford the patient pain management and reduced the healing period. The patient improved significantly with the above mode of care, and repeat MRI imaging showed a reduction in the size of the herniation.


  • BenEliyahu DJ. MRI and clinical followup study of 27 patients receiving chiropractic care for cervical and lumbar disc herniation. JMPT 1996;19(9):597-606.
  • Bush K. Pathomorphologic changes that accompany the resolution of cervical radiculopathy. Spine 1997;22(2):183-187.
  • Matsubara Y. Serial changes on MRI in lumbar disc herniations. Neuroradiology 1995;37:378-383.
  • Komori H. Natural history of herniated Nucleus pulposus with radiculopathy. Spine 1996;21(2):225-229.
  • Saal J. Nonoperative management of cervical herniated disc with radiculopathy. Spine 1996;21(16):1877-83.
  • Mochida K. Regression of cervical disc herniation observed on MRI. Spine 1998;23(9):990-997.
  • Ellenberg MR. Prospective evaluation of the course of disc herniations in patients with radiculopathy. Arch Phys Med Rehab 74; Jan 1993, p. 3.
  • Bozzao A. Lumbar disc herniation: MR imaging assessment of natural history in patients treated without surgery. Radiology 1992;185:135-141.
  • Maigne JY. CT followup study of 21 cases of nonoperatively treated cervical soft disc herniation. Spine 1994;19(2):189-191.

Next page – Spinal Decompression Outcome Study

Spinal decompression outcome of clinical study

On September 27, 2010, in Studies, by admin

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, CCICOrthopedic Technology Review, Vol. 5-6, Nov-Dec 2003. This clinical outcomes study was performed to evaluate the […]

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.


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.


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).


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.


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.


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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.

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