The outcomes of vertebral axial decompression

(DECOMPRESSION) therapy for patients with low back pain from

various causes are reported. Data was collected from twenty-two

medical centers for patients who received DECOMPRESSION

therapy for low back pain, which was sometimes accompanied by

referred leg pain. Only patients who received at least ten sessions

and had a diagnosis of herniated disc, degenerative disc, or facet

syndrome, which were confirmed by diagnostic imaging, were

included in this study; a total of 778 cases. The average time

between the initial onset of symptoms and the beginning of this

therapy was 40 months, and it was four months or more in 83% of

the cases. The data contained the patients' quantitative

assessments of their own pain, mobility, and ability to carry out the

usual 'activities of daily living'. The treatment was successful in

71% of the 778 cases, when success was defined as a reduction in

pain to 0 or 1, on a 0 to 5 scale. Improvements in mobility and

activities of daily living correlated strongly with pain reduction. The

causes of back pain and their relationship to this therapy are also

discussed. [Neurol Res 1998; 20: 186-190].

For most patients, the cause or causes of persistent low back pain remains

poorly understood. Although imaging procedures, including CT and MRI, are able

to accurately define structural pathology, the correlation of these anatomic

findings with physiology, back pain, and other clinical complaints is imprecise1.

Although surgical decompression, epidural blocks, and spinal instrumentation

can sometimes help patients suffering from back pain, these treatments do not

completely take the biomechanical function of the disc into account, and may

leave patients unrelieved of their suffering. In addressing the dysfunction of the

disc with discectomy or surgical instrumentation, the biomechanical and

physiological function of the disc is permanently disrupted.

Mechanical low back pain is usually aggravated by activities that increase axial

loading on the spine, such as sitting, standing, and lifting. Patients may describe

some relief with walking, but more particularly, by lying down, which unloads the

spine and reduces intradiscal pressure (2,3). The causes of mechanical low back

pain may include degenerative disc disease, degenerative spondylosis with

limitation of range of motion, facet arthropathy, relative lateral recess stenosis

from a combination of the above, microenvironment presure changes affecting

the thecal and epidural space from disc bulging, subligamentous and/or extruded

herniation, and segmental instability.

Pain generation from degenerative disc disease is probably multifactorial. A

number of potential mechanisms are specifically addressed by the lumbar

vertebral body separation achieved during therapy. With aging, disc desicction

occurs, disc height is lost, and this process is accelerated with activities which

produce high physical loading of the lumbar spine (4). Osteophytes develop

along the anterolateral and posterior border of the vertebral bodies, and facet

arthropathy increases as degenerative disc change advances (5). Normal

vertebral body separation is lost as the disc degenerates. Redundancy of the

posterior longitudinal ligament and ligamentum flavum combine with osteophyte

encroachment upon the neuroforamen or central canal, resulting in stenosis at

these sites, which is increased by axial loading of the spine.

The blood supply to the nerve roots of the cauda equina is sensitive to

compression. Even at pressures of only 5-10 mmHg, the flow in over 20% of the

venules was completely stopped (6). Flow in all the capillaries stopped at

pressures between 20 and 50 mmHg. A pressure of 30 mmHg is slightly less

than one pound per square inch, so solute transport is easily reduced. Even

vertebral distractions (increased separation) of 1 or 2 mm per disc would reduce

ligamental redundancy and help to restore canal/foraminal patency, reduce

venous congestion and increase axoplasmic flow. Furthermore, the effects of

lumbar spine lengthening may be sustained for a period of time after lumbar

distraction has been stopped.

Figure 1: Patient undergoing treatment on the DECOMPRESSION Therapy

Table

Twomey (7) placed lumbar vertebral columns removed from 23 male cadavers

under 9 Kg of sustained traction for 30 min and measured an average increase in

length of 9 mm. Thirty minutes after traction was removed, 13 of the 23

specimens had returned to baseline length, but the remaining 10 spines showed

residual elongations ranging from 0.3 mm to 4 mm. Additionally, the data

suggested that sustained traction had had a longer lasting effect on elderly

spines. The mechanism of this residual deformation was not elaborated upon by

the author, but disc rehydration may have been a factor since each column was

soaked in normal saline and remained saturated by periodic additions of saline to

a close fitting bag surrounding each column during the study.

That lumbar traction, if adequately applied, can effect physical change in patients

suffering from back pain is well described by Gupta and Ramarao (8). They used

water soluble contrast medium and epidurography to study 14 patients with

prolapsed intervertebral disc syndrome before and after 10 to 15 days of

continuous traction. Ten patients showed definite clinical improvement, with

reduction in back pain and sciatica. Nine of these patients showed complete

resolution of the defect on epidurogram and one of them showed partial

reduction. The authors concluded that disc protrusion may be safely treated by

traction. Mathews also demonstrated the effectiveness of lumbar traction in two

patients by epidurography. Disc protrusions were decreased and an average

vertebral distraction of 2 mm per disc space was shown in radiography (9).

Judovich found that a traction force of approximately 26% of the body weight was

needed just to overcome the resistance between the lower half of the patient and

a (nonsplit) table (10).

Intuitively, lumbar traction should be successful in alleviating many of the

conditions which cause low back pain and associated radiculopathy.

Unfortunately, studies of clinical efficacy have yielded equivocal results.

Previously, the successful application of lumbar traction has been limited by

patient tolerance and the design of mechanical devices. Patients had difficulty

tolerating the forces needed to relieve pain if delivered continuously.

Furthermore, the thoracic corsets worn by patients to prevent movement on the

table were uncomfortable, restrictred respiration, and can compromise venous

return to the heart. Technological advances have now led to the development of

equipment that has been found to achieve decompression of lumbar discs

without stimulating the reactive reflexes of the lumbar musculature that can

otherwise overcome efforts to effectively distract vertebral bodies.

The DECOMPRESSION therapy table is shown in Figure 1. The split table

design eliminates frictional resistance between the patient and the table and

allows controllable effective axial distraction tensions to be applied to the lumbar

vertebral column. The equipment applies distractive forces in a gradual,

progressive fashion, designed to achieve distraction of the vertebral bodies

without eliciting reactive reflex muscular resistance. A portion of a typical chart

recording of the tensile force applied to a patient's spine as a function of time is

shown in Figure 2. Each decompression phase, during which the tension is

increased, normally lasts for one minute. The force is increased more slowly in

the latter part of the decompression phase. The tension is then gradually

decreased, over a period of 30 sec, to about 20 pounds, which is maintained

during the rest phase. Another cycle then starts. The avoidance of paravertebral

muscle contraction, stimulated by homeostatic proprioceptor and axon reflex

mechanisms allows the distraction of the vertebral bodies necessary to achieve

decompression of the intervertebral disc. The therapy is administered via an

automated logic control mechanism which systematically applies distractive

tensions and rest periods in a cyclic fashion. The typical therapy session consists

of 15 cycles of tension and relaxation. This periodic process allows patients to

withstand stronger forces than can be tolerated when static techniques are used

and it promotes accommodation and relaxation during the therapy session. The

upper body is fixed by means of the patient grasping adjustable hand grips,

designed to eliminate the use of a thoracic corset. Consequently, there is no risk

of circulatory or respiratory compromise. The pelvis is secured with a specially

designed harness that adjusts snugly and applies forces primarily to the lateral

pelvic alae, thus minimizing anterior-posterior pressures and reactive muscle

spasm during the distractive period of each cycle.

DECOMPRESSION treatment has been shown (11) to decompress the nucleus

pulposus to pressures below - 100 mmHg. This creates a tremendous potential

diffusion gradient across the disc space, which is otherwise an avascular

structure. Glucose and oxygen enter the disc at the end plate region while

sulphate ions needed for the production of new glycosaminoglycans enter from

the annulus fibrosis (12). Thus therapy may augment nutrient flow into the disc,

facilitating structural restoration of the disc and promoting disc rehydration, since

proteoglycans bind water (13). These effects may be cumulative with repetitive

therapy sessions.

Figure 2: chart recording of tension versus time for five cycles of the typical 15-

cycle DECOMPRESSION Therapy session

Data was collected from twenty two medical centers in the USA for patients who

received DECOMPRESSION therapy for low back pain. Only patients who

received at least 10 treatments and had a diagnosis of herniated disc,

degenerated disc, or facet syndrome, which was confirmed by imaging studies,

were included in the study. The average number of treatments was 17 for facet

syndrome, 19 for degenerative disc disease, and 20 for other diagnoses. The

data contained the patients' assessment of their own pain, mobility, and ability to

walk and sit. The pain scale ran from no pain (0) to severe pain (3). The mobility

limitation scale was: No limitation (0), slightly limited (1), very limited (2), and

completely immobile (3). The activity limitation scale was: walks frequently (0),

walks occasionally (1), chairfast (2), and bedfast (3(). The treatment schedule,

including the use of other modalities, the duration and frequency of

DECOMPRESSION therapy, and medication was also recorded, as well as the

patient's history. The symptoms were recorded at the beginning, mid-point, and

end of the treatment schedule. The patients' satisfaction with the treatment was

quantified as: not satisfied (0), slightly satisfied (1), very satisfied (2), and

completely satisfied (3).

The data were divided into five groups:

1. The first group which contained 34 cases, included all patients with

extruded herniated discs, whether or not additional lesser problems were

present.

2. The second group contained 195 cases of multiple herniated discs,

without extrusion, with or without degenerative disc disease.

3. The third group consisted of 382 patients with a single herniated disc,

regardless of degenerative disease.

4. The fourth group contained 147 cases of degenerative disc disease,

without herniation.

5. The fifth group contained 19 cases with facet syndrome. Five cases of

facet syndrome which had a pain reduction to 0 or 1 before 10 treatments,

and one that had a reduction to 2, received less than 10 total reatments,

so they were not included in the data base.

If treatment success is defined as a reduction in pain to 0 or 1 on a 0 to 5 scale,

the treatment was successful in 71% of the 778 cases. The success rate varied

from 53% for the patients with extruded herniated discs, to 73% for patients with

a single herniated disc. It was 72% for people with multiple herniated discs and

68% for facet syndrome. On a pain scale of 0 to 5, the people with extruded

herniated discs had an average pain of 4.16 at the beginning of treatment and an

average of 1.82 after treatment, a reduction of 56%. The cases of multiple

herniated discs went from 4.13 to 1.18, a reduction of 71%. The patients with a

single herniation had a reduction from 4.16 to 1.09, or 71%. The degenerative

fisc cases reduced from 3.93 to 1.17, a 70% reduction. The patients with facet

syndrome had a reduction of 4.00 to 1.13, a 72% reduction in pain. Overall, 71%

of the patients experienced a reduction in pain to 0 or 1. The reduction in the

average pain score was also 71%. One percent of the patients reported

increased pain, 7% had no change, 92% improved by 1 unit or more, 87%

improved by 2 units or more, and 70% improved by 3 units or more. A summary

of these findings is shown in Table 1.

Table 2 shows how the average pain, mobility, and activity scores for the entire

group of 778 patients improved during treatment. Although 51% of the pain

reduction occurred during the first half of the course of treatment, 56% of the

mobility improvement and 55% of the activity improvement occurred during the

last half.

On a rating scale of 0 to 3, increases in spine mobility of one grade or more was

seen in 77% of the patients with mobility limitations. Functional increases of 1 or

more grades in the activity score was recorded in 78% of the patients who,

before treatment were either unable to walk or capable of only limited walking.

The coefficient of linear correlation14 between mobility and pain scores was

0.72. Between pain and activity the correlation was 0.60, and between activity

and mobility it was 0.59. On a scale of 0 to 3, the average satisfaction with

treatment was 2.4, which lies between 'very satisfied' and 'completely satisfied'.

In this study, 31 patients had previous lumbar disc surgery. MRI scans showed

scar tissue that could potentially entrap nerve roots. Despite this, 84% of this

group's pain scores and 71% of their mobility scores and 61% of their activity

scores improved by one unit or more with therapy, and 65% of their pain scores

were reduced to 0 or 1. Vertebral axial decompression was well tolerated.

Table 1: Pain outcomes for venous diagnoses

Extruded herniation 34 4.16 1.82 56 53

Multiple herniation 195 4.13 1.18 71 72

Single herniation 382 4.16 1.09 71 73

Degenerative disc

disease 147 3.93 1.17 70 72

Facet syndrome 19 4.00 1.13 72 68

Average over 778 cases: > 4.10 1.21 71 71

Table 2: Variation of average pain, mobility, and activity scores during treatment,

and final outcome measures for the entire group

Before therapy 4.10 1.81 1.24

At midpoint 2.62 1.30 0.80

After therapy 1.21 0.64 0.27

Overall improvement 71% 65% 78%

Improved by 1 unit or more 92% 77% 63%

W

e consider DECOMPRESSION therapy to be a primary treatment modality for

low back pain associated with lumbar disc herniation at single or multiple levels,

degenerative disc disease, facet arthropathy, and decreased spine mobility.

Physiology (pain and mobility) and pathology correlate imprecisely. We believe

that post-surgical patients with persistent pain or "Failed Back Syndrome' should

not be considered candidates for further surgery until a reasonable trial of

vertebral axial decompression has been tried.

Low back mobility increased subsequent to therapy and correlated well with pain

reduction. Both of these factors are important in areas such as Workers

Compensation and personal injury. Estimates of permanent partial impairment

rely heavily on mobility aspects, as seen in the AMA Guides to the Evaluation of

Permanent Impairment, 4th edition. Although allowance for pain is made in the

percentage of impairment, the determination of impairment is made by

determination of spine mobility using the range of motion model. By definition no

patient can be assigned any impairment rating until maximum medical

improvement (MMI) is reached. We submit that patients can usually be brought

to a higher level of MMI by this therapy because of the anticipated improvements

in mobility.

In summary, the pain, activity, and mobility scores were all greatly improved after

therapy. DECOMPRESSION by its unique design may more precisely address

the physiology of persistent low back pain than other conventional therapies. We

consider it to be a front line treatment for degenerative spondylosis, facet

syndrome, disc disease and nonsurgical lumbar radiculopathy.

1. Heldeman S. North America Spine Society: Failure of the pathology model

to predict low back pain. Spine 1990; 15:718-724.

2. Wheeler A.D. Diagnosis and management of low back pain and sciatica.

Am Family Physician 1995; 52:1333-1341.

3. Scientific approach to the assessment and management of activit-related

spinal disorders. A monograph for clinicians. Report of the Quebec Task

Force on spinal disorders. Spine 1987; 12(Suppl 7):1-59.

4. Videman T, Saina S, Crites Battle M, Koskinen S, Gill K, Paanaman H.

The long term effects of physical loading and exercise lifestyles on backrelated

symptoms, disability, and spinal pathology among men. Spine

1995; 20:699-709.

5. Anderson GBJ, McNeill TW. Lumbar Spine Syndromes Evaluation and

Treatment. New York: Springer-Veriag Wien, 1989: pp.1-215.

6. Olmarker K, Rydeuik B, Holm S, et al. Effects of experimental graded

compression on blood-flow in spinal nerve roots. J Orthop Res 1989;

7:817-823.

7. Twomey LT. Sustained lumbar traction: An experimental study of long

spine segments. Spine 1985; 10:146-149.

8. Gupta RC, Romarao SV. Epidurography in reduction of lumbar disc

prolapse by traction. Arch Phys Med Rehabilitation 1978; 59:322-327.

9. Mathews JA. Dynamic discography: A study of lumbar traction. Ann Phys

Med 1968; IV:275-279.

10. Judovich BC. Lumbar traction therapy-elimination of physical factors that

prevent lumbar stretch. JAMA 1955; 159:549-550.

11. Ramos G, Martin W. Effects of vertebral axial decompression on

intradiscal pressure. J Neurosurg 1994; 81:350-353.

12. Nachemson AL. The lumbar spine: An orthopaedic challenge. Spine 1975;

1:59-71.

13. Ballard WT, Weinstein JN. Biochemistry of the intervertebral disc. In:

Kirkaldy-Willis WH, Burton CV, eds. Managing Low Back Pain, New York:

Churchill Livingston, 1992: pp.39-48.

14. Gose EE, Johnsonbaugh R, Jost S. Pattern Recognition and Image

Analysis, Upper Saddle River, NJ: Prentice-Hall PTR, 1996: pp.1-484.

15. This article is reprinted with the permission of the authors from The

Canadian Journal Of Clinical Medicine, Volume 5, Number 1.

Low back pain is a growing epidemic among industrialized societies. In the

United States it is the most common work related disorder. The cost to industry is

staggering, with estimates running 20 billion dollars or more annually. (4,42)

Total payments for a single Workman's Compensation claim may be as high as

$100,000.

Abenhain and Suissa studied the 1-yearincidence of work related low back pain

in the province of Quebec for the year 1981. (1) Work absence due to back pain

has an incidence of 1.4%. Seventy-four percent of work related injuries return to

work within 1 month. 7.4% were out of work for more than 6 months. 75% of the

direct total cost was borne by 10% of the absentees. Recurrence rates were 20%

at 1 year and 36% after 3 years. Men had higher recurrence rates than women;

drivers and nurses had higher recurrence rates than other occupations.

The recovery rate of the Quebec workers is similar to other countries. After 1

year 4.3% remained absent from work. Incidence rates of compensated back

injuries by industrial sector showed that foresters and miners are at the top with

4.9% and 3.3% respectively.

Effective diagnosis and therapy requires thorough knowledge of spinal

model but unfortunately the model frequently fails to comply with the

clinical picture. The Quebec Task Force Report stated: "There is so much

variability in making a diagnosis that this initial step (i.e. clinical assessment)

routinely introduces inaccuracies which are then further confounded with each

succeeding step in care."(43) Adding to the confusion is the belief by too many

physicians, patients and insurers that high tech imaging is the standard for

establishing a diagnosis. However, the high rates of false positive and false

negative findings point to the inadequacies of these studies in identifying the pain

generating lesions (8,19,20,48,49). Nachemson states: "A confirmatory imaging

study is indicated only if surgery is contemplated. Clinical symptoms and findings

remain the most important basis for diagnosis."(28)

The natural history of low back pain with and without radiculopathy has been

described.(10,37,47) Spontaneous regression takes place in 80% to 90% of

patients with low back pain by 6 weeks and a significant percentage of patients

with sciatica report a satisfactory response to conservative medical management.

Studies on disc surgery emphasize inappropriate patient selection as the cause

for surgical failure. (11,16,30,44) In Kramer's address to the International Spine

Society he emphasized that the surgical failed back syndrome is the worst

possible scenario a spine surgeon faces. (22) In North America the incidence for

this iatrogenic disease is about 15%, compared to 5% with most European

countries.(28) Comparisons between the United States and Europe indicate that

the frequency of surgery in the U.S. is four times greater.(11) Statistics from the

Back Pain Outcome Assessment Team compiled from 1979 to 1987 indicate a

rapidly growing number of disc excision and fusion operations performed each

year, further escalating the cost. (11,44)

Studies of the various surgical procedures largely lack validity and controlled

prospective studies are rare .(7) A randomized study by Revel demonstrated

percutaneous discectomy has little value (32) and the same is true for laser

discectomy.

Chemonucleolysis is superior to saline injection but inferior to surgical

discectomy. While chemonucleolysis had its followers for a period of time, it has

fallen into disrepute because of the serious side effects including anaphylaxis

and myelitis and should no longer be considered an option. There are not any

studies demonstrating the superiority of one particular surgical intervention and

there is no support for adding a fusion to a routine discectomy. (11,27,28)

The DECOMPRESSION therapeutic table (Vertebral Axial Decompression)

addresses the functional and mechanical aspects of discogenic pain and

disease. The table was invented by Dr. Allan Dyer, former Deputy Minister of

Health from Ontario and a pioneer in the development of the external cardiac

defibrillator.

The table is designed to apply distraction tension to the patients lumbar spine

without eliciting reflex paravertebral muscle contractions. The patient lies in a

prone position, the upper body is over the stationary portion of the table, and the

body is restrained by the patient holding on to adjustable handgrips which can be

released at anytime for safety.

The table is a split table design, whereby distraction tensions are applied to the

patient through a pelvic harness attached to a tensionometer and by separation

of the movable part of the table. The distraction-relaxation cycles are automated

or variably timed.

Distraction tensions and rates are continuously monitored and measured by the

tensionometer and the output is shown on a digital gauge and captured on a penwrite

printout. The table exerts its effects through decompression of the

intervertebral discs.

Dr.'s G. Ramos and W. Martin of the Departments of Neurosurgery and

Radiology at the HCA Rio Grande Regional Hospital, McAllen, Texas studied

intradiscal pressure during DECOMPRESSION therapy.(30)

The patient population was comprised of individuals with unresolved low back

pain who were referred for neurosurgical consultation. Previous management

programs included conventional bedrest, medications, physical therapy, and or

chiropractic treatments.

Depending on the diagnosis and findings of the examinations, patients were

assigned to one of the following study groups: Intradiscal Pressure Study and

Clinical Outcome Assessment Study. Patients with a subligamentous herniation

at L4-5 who were candidates for percutaneous discectomy were included in a

study of intradiscal pressure manometry. The pressure measurements were

recorded by two different methods; an Ohmeda pressure transducer connected

to a Hewlett Packer pressure monitor via a saline bridge and a Camino fiberoptic

intracranial transducer adapted for intradiscal measurements. Both transducers

were recalibrated after each procedure utilizing a Pneumatic Calibration

Analyzer.

The transducers were placed in the L4-5 disc under A-P and lateral fluoroscopy.

With the catheter in place the patient was placed prone on the

DECOMPRESSION table. Various decompression tensions from 50 to 100

pounds were applied. The distraction tensions and the resulting changes in

intradiscal pressure were observed on digital readout and recorded on a graph

tracing produced by the chart recorder.

Intradiscal pressures were significantly reduced to minus 150-160 mm Hg. It was

observed that a threshold distraction tension was necessary to develop negative

pressures in the disc. The extent of decompression measured in mmHg follows

an inverse relationship to the tensions applied.

The significance of this study cannot be overemphasized. The reduction of

intradiscal pressure to negative levels has far reaching therapeutic implications.

Prior to the introduction of DECOMPRESSION, a non surgical method for disc

decompression was unavailable. In numerous studies, conventional traction has

never demonstrated a reduction of intradiscal pressure to negative ranges, on

the contrary many traction devices actually increased intradiscal pressure most

likely secondary to reflex muscle spasm .(5)

DECOMPRESSION is indicated for patients with low back pain that has been

unresponsive to conventional therapy for 6-8 weeks. Patients with

radiculopathies are also candidates. The presence of a neurological deficit does

not affect patient eligibility since studies have revealed the outcome in patients

with neurological deficits was not affected by surgical or medical

management.(15) The presence of a rapidly progressive neurological deficit is an

indication for surgery. Patients presenting with a fusion and the post surgical

failed back syndrome may also be candidates.

Contraindications for DECOMPRESSION therapy include infection, neoplasm,

osteoporosis, bilateral pars defect or Grade 2 spondylolysthesis if unstable,

fractures, the presence of surgical hardware in the spine, and the cauda equina

syndrome. Patients with lateral stenosis and central stenosis may respond if

severe secondary changes are not present in the vertebra. The patient should be

evaluated by a therapist or physician prior to initiating therapy and routine spine

films are necessary to rule out any contraindications. A CT scan or MRI is not

necessarily a prerequisite before therapy.

The daily therapy sessions are administered by a trained DECOMPRESSION

technician. All DECOMPRESSION technicians are encouraged to complete a

certification exam. Treatments are administered on a daily basis for

approximately twenty sessions and are routinely given Monday through Friday.

An occasional patient may require a short maintenance period where 2 to 3

treatments a week are given for 2 to 4 weeks post therapy. The average patient

has required 20-25 sessions. Each session is comprised of 15 cycles, each cycle

being 1 minute in distraction and 1 minute in relaxation.

The table is designed to be operator friendly. With the patient standing, a

specially made pelvic harness is fitted and tightened on the patient. The patient:

lies prone on the table with the lower portion of the belt placed at the level of the

table separation point. The adjustable handgrips are positioned such that the

elbows remain straight. Repositioning and tightening of the pelvic harness is

completed at this point. The harness is attached to a movable pretension housing

that maintains a baseline tension of 20 lbs. throughout the rest phase. Once the

pretension is set the treatment cycles may begin. The Ramos study indicated

that 50 lbs. of tension was the threshold tension necessary to develop negative

intradiscal pressures. The p.s.i. is slowly increased until tensions of 60-80 lbs.

are developed, this may take 3 to 4 days of therapy. Some patients have

required 90-100 lbs. of tension for a full therapeutic effect.

Pain distribution frequently changes during or immediately after therapy. A

phenomenon called centralization first observed by McKenzie (24) has been

noticed during a course of DECOMPRESSION therapy. Centralization is the

process by which the pain pattern migrates from a peripheral distribution to a

more central or proximal location and is an indication of a favorable clinical

outcome. Centralization of pain patterns may be associated with increased

central back pain, but this should be interpreted as a positive sign and is likely

secondary to stretching of the posterior longitudinal ligament as the lateral

distortion of the disc retracts to a more concentric position. Centralization is a

predictable prognostic indicator for symptomatic discs and anular competence

(12) The observed occurrence of centralization during DECOMPRESSION

therapy in a patient who initially could not centralize their pain pattern implies

healing of the anulus as a result of DECOMPRESSION therapy.

As higher distraction tensions are reached few patients may report an increase in

pain of a different quality. Overstretching of the soft tissues in the back likely

represents the cause of this pain and the patient should be treated by decreased

distraction tensions, so as not to traumatize the soft tissues.

The development of a sharp, burning, radiating pain during therapy could

represent the stretching of an entrapped nerve. Since the breakdown of scar

tissue is an objective, the patient should continue but distraction tensions should

be reduced such that any pain elicited does not last more than 15-20 minutes

post therapy. Distraction forces are then slowly increased over the ensuing days.

No serious side effects have been reported with DECOMPRESSION therapy. A

limiting factor affecting the patient's tolerance to therapy is stress to the shoulder

girdle and rotator cuff. This may be mitigated by placing a roll under the axilla of

the affected side. Should a patient have discomfort from any cause, they may

release the handgrips at any time. This adds an important safety factor to the

treatment.

An understanding of spinal biomechanics is necessary to appreciate

DECOMPRESSION's mechanism of action, to effectively treat and diagnose

spinal disorders, and to objectively review old and new therapies.

The literature is replete with biomechanical data. Vogel and Stahl have carried

out in vitro experiments on intradiscal movements with symmetrical and

asymmetrical loading. (21) With symmetrical loading the nucleus expands and is

retained by the anulus. By contrast, if the disc is subjected to an asymmetrical

load, the nucleus migrates to the area of least load or resistance.(38) With

removal of the load the nucleus moves from an eccentric to a more concentric

position within the disc. Relocation can be accelerated by compression in the

opposite direction or by distraction. (21) The anulus of a normal disc can restrain

the nuclear movement, but when the elastic properties of the anulus are

compromised the structures become susceptible to injury. Fissures and ruptures

develop which allow the nucleus to migrate.

Fissures are normally present by 30-35 years of age and increase with

advancing age. Fragment sequestra appear as a result of age and trauma.

These fragments can move independently and result in protrusions and disc

prolapses. Migration of nuclear material and sequestra is influenced by

compressive forces, shearing, and increased intradiscal pressure. (24)

Epidemiological data and scientific data have demonstrated that prolonged or

repetitive flexion loads stress the posterior anulus resulting in discogenic pain

and in some patients disc herniation.(3,25) Adams and Hutton carried out

experiments with gradual loading of the disc and concluded that disc prolapses

can occur with a sustained flexion load.(2) Hickey and Hukins performed

experiments with bending and torsion and demonstrated that the anulus failed

posteriorly. (17) Shirtzi-Adl demonstrated that disc fiber layers are most loaded in

flexion and least in extension. (40) Nachemson's research on intradiscal

pressures showed pressures were highest with flexion. (26) The outer third of the

anulus is innervated by the sinuvertebral nerve. Any asymmetrical load

associated with elevated intradiscal pressure can result in overstretching and

fatigue of the anulus, thereby stimulating the mechanoreceptors in the outer third

of the annular wall. Eventually fissure's will develop in the anulus which can lead

to herniation of the central mass of the nucleus. By reducing intradiscal pressure

with DECOMPRESSION therapy, a therapeutic and prophylactic effect can be

realized.

Numerous studies utilizing discography have helped us to understand the role of

the disc as a pain generator. Provocational discography is the standard test for

discogenic pain.(41) Its reliability has been questioned and opponents generally

refer to the work of Holt, but his study has been refuted on methodological

grounds.(9,18,41)

Recently a pathological marker of symptomatic disc disruption called the high

intensity zone (HIZ) was demonstrated on MRI using spin echo gradient heavy

T2 imaging. (6,38) An HIZ is evident in the posterolateral view on the sagittal

section, which on provocation discography corresponded to a Grade 3 radial

tear. The high signal intensity represents fluid within the fissure that may be

causing pain either by chemical irritation or mechanical traction of the

sinuvertebral nerve. By its cyclic action and ability to reduce intranegative

pressure, DECOMPRESSION therapy could displace the fluid to the internal

portion of the nucleus thereby ameliorating pain and enhancing healing of the

anulus.

Donelson demonstrated it is possible to predict anular competence with the

McKenzie mechanical assessment protocol.(12) In his study patients were

separated into centralizer's and non centralizer's. Discography was performed in

both groups. Centralizer's tended to have an intact anulus or Grade 1-2 tears.

Non centralizer's had a disrupted anulus , that is fissures to the outer third of the

anular wall or Grade 3 tear. This is very exciting news for those who appreciate

the centralization phenomenon because it allows us to clinically assess the

competency of the anulus. Patients who centralize on initial evaluation may be

treated with specific exercise. Patients who do not centralize on initial

examination are excellent candidates for DECOMPRESSION therapy. With such

an approach, the patients disposition regarding effective therapy is known

immediately, which arguably translates to reduced disability and reduced cost.

DECOMPRESSION therapy has been shown to convert non centralizer's to

centralizer's during or after successful DECOMPRESSION therapy. This implies

DECOMPRESSION is condusive to anular healing.

Asymmetrical loading of the disc and increased intradiscal pressure is partly

responsible for internal derangement, discdegeneration and herniation. Changes

in intradiscal pressure also play a prominent role in affecting nourishment of the

disc since the disc is an avascular structure and receives its nourishment

primarily by diffusion.

Intradiscal pressure that is greater than capillary pressure in the vertebral body

impedes oxygen diffusion to the disc which in turn impedes healing.(13)

Reducing intradiscal pressure with DECOMPRESSION creates a diffusion

gradient into the disc allowing nourishment to proceed. Solutes such as oxygen

have a steep concentration gradient across the disc, with the peripheral

concentration 20-30 times more than the concentration at the center of the

nucleus. The availability of oxygen may be inadequate to meet the metabolic

requirements required to heal a damaged anulus, and higher concentrations of

lactate have been measured within the central portion of the disc, By reducing

intradiscal pressure, DECOMPRESSION therapy creates a diffusion gradient

thereby enhancing solute transfer. High levels of lactate could facilitate

chondrocyte cell death as well as increase the activity of degradative enzymes

further promoting the loss of the proteoglycan cell matrix. A vicious cycle is

produced, accelerating disc degeneration.

The mechanical effects of fluid loss during a compressive load are followed by a

slow rate of disc deformation termed creep. The rate of creep is faster in a

damaged or degenerated disc than a normal disc. Both vibration (overstress) and

inactivity (understress) affect the rate of creep and disc degeneration. Pigs who

were subjected to vibratory creep had lower levels of oxygen and sulfate

transport, and higher levels of lactate within the disc. (13)

Somewhere between the overstress of vibration and the understress resulting

from inactivity is an optimum mechanical environment. Through its action,

DECOMPRESSION may be capable of restoring that environment, enhancing

healing of the disc and retarding degeneration.

The pathophysiology of nerve root compression has been described by Rydevik.

(33,34,35) The nerve root ganglion has an extensive venous plexus, which if

obstructed, results in venous hypertension and endoneural edema, leading to

hypoxia, ischemia and pain. External decompression with DECOMPRESSION

therapy can be expected to relieve venous hypertension and reverse the

pathognomonic process.

By significantly reducing intradiscal pressure, DECOMPRESSION promotes

retraction of the herniation into the disc. DECOMPRESSION therapy could

possibly shear a herniation from its connection to the central nucleus, creating a

severed fragment within the spinal canal. This sequestered disc is susceptible to

small vessel invasion and digestion as a result of contact with the epidural space.

Reinforcing this theme is the study by Modic et al who studied the natural history

of disc herniation by MRI in patients with acute radiculopathy and discovered that

large (6 mm ) sequestered hernias were the first undergo spontaneous

resolution.(23)

I have studied sensory nerve dysfunction measured before and after

DECOMPRESSION therapy, in order to determine the effect of

DECOMPRESSION on nerve root compression. The results from this study are

very significant and the data will be published in the future.

Inflammation very likely plays a role in disc pathology and herniation but the

response to anti-inflammatories is rather disappointing. Saal found high levels of

Phospholipase A2 in human disc samples removed at surgery in patients with

radiculopathy.(36) As the enzyme responsible for liberation of arachidonic acid

from cell membranes, Phospholipase A2 is the rate limiting step in the production

of prostaglandin's and leukotrienes. Controlled studies have shown that antiinflammatories

are not useful for acute sciatica,(46) but since solute transfer to

the disc may be enhanced by DECOMPRESSION therapy, the administration of

anti-inflammatories during DECOMPRESSION therapy may result in higher

concentrations of the drug within the disc, neutralizing inflammatory mediators

responsible for nerve root inflammation and some forms of discogenic pain. As

previously mentioned the fluid within the HIZ is thought to be an inflammatory

fluid and DECOMPRESSION may be able to effectively pump this fluid into the

central nucleus where it is not possible for it to exert an inflammatory effect. The

fissure may be able to approximate its borders and heal once the fluid is pumped

out.

The DECOMPRESSION table is an external decompression device and this

separates it from conventional traction. Studies verifying decompression of the

disc and nerve root are now available for DECOMPRESSION. I reviewed the

literature and I could not find any available data that conventional traction

reduced intradiscal pressure to the negative range nor are there any studies on

conventional traction showing beneficial effects in nerve root compression and

conditions associated with discogenic dysfunction.

Many patients who receive DECOMPRESSION therapy have had chronic back

pain and failed numerous modalities including traction. Their positive response to

DECOMPRESSION therapy, after having failed conventional therapy and traction

confirms DECOMPRESSION's assertion that it is not conventional traction.

The Acute Low Back Distress Study was conducted by the John P. Robarts

Research Institute, London Ontario. The efficacy of DECOMPRESSION therapy

was established with this study. The parameters measured were severity and

duration of pain and disability, including analgesic requirements, and the

presence and degree of neurological involvement. One hundred and ten patients

were entered into the study.

The treatment was considered a success if the baseline aggregate score for pain

and disability was reduced by 50% after 10 treatments of DECOMPRESSION

therapy. Sixty-six percent of the patients achieved success according to the

study protocol. Prior to therapy the aggregate score for pain and disability was

5.1 and after 10 treatment sessions in the successful group it was 1.2.

The Clinical Outcome Assessment Study was conducted at McAllen HCA

Hospital by Dr. G Ramos.(31) Fifty-two patients completed DECOMPRESSION

therapy as the primary modality. Thirty-eight patients (73%) achieved a positive

outcome with remission of their low back pain symptoms and a return to

functional levels of activity. Ninety percent of the recovered group were suffering

from disc herniations, the majority (89%) being subligamentous while 11% had

extruded herniations. Neurological deficits did not compromise the response to

therapy.

Review of the patients clinical findings for those who achieved remission showed

that 33% exhibited neurological deficits and 73% had sciatic pain prior to therapy

with DECOMPRESSION.

Dr. E. Gose, Dr. W Naguszewski, and Dr. R Naguszewski have completed an

outcome study of DECOMPRESSION therapy from over twenty medical centers

that included over 700 patients. Patients with back pain, with or without leg pain

were included in the study as well as the failed surgical back patient. All patients

had a diagnosis of a herniated disc, degenerative disc or facet syndrome. The

authors are very enthusiastic about the outcome and have prepared a detailed

report of their findings which been accepted for publication in another respected

medical journal.

An outcome study at Columbia hospital, Tulsa OK. is currently being conducted

that shows a level of success consistent with the above study.

DECOMPRESSION therapy addresses the biomechanical aspects of discogenic

disease and achieves its objective through decompression. It should be utilized

in patients with low back pain, with or without radiculopathy who have failed

conventional therapy (physiotherapy and chiropractic), and should be utilized

prior to addressing surgery. By addressing the altered biomechanics responsible

for disc disease, the DECOMPRESSION therapeutic table not only alleviates

pain but has been shown to exert a beneficial effect on a major determinant in

the equation responsible for discogenic disease, that is elevated intradiscal

pressure.

Further analysis of future and unpublished research should be considered to

further validate the therapeutic benefit of DECOMPRESSION therapy, however,

these clinical studies have shown it to be effective in back pain syndromes with

or without radiculopathy including herniated discs and internal disc disruption.

The chronic back pain patients and surgical patients are very costly to society.

Since many of these patients are responsive to DECOMPRESSION therapy, this

unique non-obtrusive means of managing the common forms of debilitating low

back pain associated with discogenic disease could represent a considerable

savings.

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