X Close Window
Spinal Decompression
By
Thomas A. Gionis, MD, JD, MBA, MHA, FICS, FRCS, and Eric Groteke, DC, CCIC
Orthopedic Technology Review, Vol. 5-6,
Nov-Dec 2003.
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.
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
1. Eyerman E. MRI evidence of mechanical
reduction and repair of the torn annulus disc. International Society of
Neuroradiologists; October 1998; Orlando.
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.
X Close Window |