discogenic low back pain: a retrospective cohort study

chronic low back pain (LBP) due to disc degeneration (discogenic low back pain) and disc herniation, it has accordingly

been hypothesized that the reduction of pressure on affected discs will facilitate their regeneration. The goal of this

study was to determine if changes in LBP, as measured on a verbal rating scale, before and after a 6-week treatment

period with non-surgical spinal decompression, correlate with changes in lumbar disc height, as measured on

computed tomography (CT) scans.

who underwent a 6-week treatment protocol of motorized non-surgical spinal decompression via the DRX9000 with

CT scans before and after treatment. The main outcomes were changes in pain as measured on a verbal rating scale

from 0 to 10 during a flexion-extension range of motion evaluation and changes in disc height as measured on CT

scans. Paired t-test or linear regression was used as appropriate with p < 0.05 considered to be statistically significant.

decreased from 6.2 (SD 2.2) to 1.6 (2.3, p < 0.001) and disc height increased from 7.5 (1.7) mm to 8.8 (1.7) mm (p <

0.001). Increase in disc height and reduction in pain were significantly correlated (r = 0.36, p = 0.044).

height. The correlation of these variables suggests that pain reduction may be mediated, at least in part, through a

restoration of disc height. A randomized controlled trial is needed to confirm these promising results.

An estimated 80% of the population will suffer from low

back pain (LBP) at some point of their lives[1]. Low back

pain is the number one factor limiting activity in patients

less that 45 years old, the second most frequent reason for

doctor's visits, and the third most common cause for surgical

procedures[2]. In addition to imposing upon

patients' quality of life, LBP is of significant socioeconomic

relevance because it may lead to a temporary loss

of productivity, enormous medical and indirect costs, or

even permanent disability[3].

While the management of persistent low back pain

remains hotly debated, the traditional approach has been

non-surgical treatment with analgesia supplemented by

physiotherapy. Given the limited efficacy of these modalities,

there are also a number of alternative interventions

such as massage, spinal manipulation, exercises, acu-

* Correspondence: apfel@ponv.org

Perioperative Care, University of California San Francisco, San Francisco,

California, USA

Full list of author information is available at the end of the article

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Page 2 of 6

puncture, back school and cognitive behavioral therapy[

4]. The two most common diseases involving chronic

LBP are discogenic low back pain, responsible for 39% of

cases, and disc herniation, accounting for just less than

30% of LBP incidence. These incidence frequencies are

supported by the current data that most closely link the

clinical pathology of discogenic low back pain and disc

herniation to the anatomical structure of the intervertebral

disc. Thus, another treatment option is motorized

decompression, a technique designed to lessen pressure

on the discs, vertically expand the intervertebral space,

and restore disc height[5-7]. However, systematic reviews

to date were unable to find sufficient evidence in the literature

to support the use of this modality[8,9]. A subsequent

chart review of 94 patients suggests that motorized

non-surgical spinal decompression may be effective in

reducing chronic low back pain[10]. Furthermore, preliminary

data from a prospective cohort study in patients

with chronic low back pain reported a median pain score

reduction from 7 to 0 (on a 11-point verbal rating scale)

following a 6-week non-surgical spinal decompression

treatment protocol[11].

The goal of this study was therefore to determine if

changes in LBP, as measured on a verbal rating scale,

before and after a 6-week treatment period with motorized

non-surgical spinal decompression, correlate with

changes in lumbar disc height, as measured on computed

tomography scans.

Study design

This is a retrospective cohort study of patients who

underwent a 6-week treatment protocol of non-surgical

spinal decompression via the DRX9000. A HIPAA

(Health Insurance Portability and Accountability Act)

waiver was obtained through Quorum IRB. This waiver

permitted a review of medical records and access to CT

scans ordered as part of standard of care.

Clinical Trial Registration Number: NCT00828880

Inclusion and exclusion criteria

Patients and their medical records were eligible for inclusion

if the patient was at least 18 years of age, consented

for the 6-week treatment protocol, and presented with

chronic LBP of at least 3 out of 10 on a verbal rating scale

and was due to either discogenic LBP or disc herniation

according to a radiological diagnosis using standard medical

definitions. Discogenic LBP is most succinctly

defined as a loss of lower back function with pain due to

disc degeneration. Degenerative disc diseases often

emerge when abnormal stresses cause the nucleus gelatinosus

to unevenly distribute weight, the annular fibrosis

and end plate incur structural damage, and a destructive

inflammatory response is triggered to accelerate and perpetuate

the degeneration of the disc. A herniated disc

(synonymous with a protruding or bulging disc) arises

when the intervertebral disc degenerates and is weakened

to such an extent that cartilage is pushed into the space

containing the spinal cord or a nerve root and causes

pain[1].

All patients were treated at the Upper Valley Interventional

Radiology facility (McAllen, Texas). Patient symptoms

were evaluated by medical history review, physical

examination, and a current CT scan (not older than 2

months prior to the start of treatment) to support a diagnosis

of chronic discogenic LBP due to bulging, protruding

or herniated intervertebral discs that may have been

brought on by degenerative disc disease. Patients were

only included if pre- and post-treatment CT scans were

performed on the same device, measurements taken by

the same investigator (WM), and data recorded on standard

collection forms. One height measurement was

taken by WM for each of the intervertebral discs under

study per CT scan. Accuracy of data was confirmed by a

second investigator (JP), but only one measurement was

made of each intervertebral disc per CT scan. All CT

scans analyzed were performed at least one hour after the

subject got out of bed. The first CT scan was performed

within two months before the initiation of the treatment,

and the second CT scan at least one day after or on the

day immediately before the final treatment session.

Exclusion criteria for enrollment in the study were any

patients with metastatic cancer; previous spinal fusion or

placement of stabilization hardware, instrumentation or

artificial discs; neurologic motor deficits; bladder or sexual

dysfunction; alcohol or drug abuse; or litigation for a

health-related claim (in process or pending for workers'

compensation or personal injury). Limitations of the spinal

decompression system also led to the exclusion of

patients with extremes of height (< 147 cm or > 203 cm)

and body weight (> 136 kg).

Treatment protocol

Patients received treatment with the DRX9000 (Axiom

Worldwide, Tampa, FL) as dictated by the intervention's

operating guidelines[11]. In short, the protocol typically

included 22 sessions of spinal decompression over a 6-

week period with 28-minute active treatment sessions. At

the start of each session, the patient is fitted with adjustable

lower and upper body harnesses and is lowered into

the supine position. To initiate active treatment the

machine then pulls the patient gently on the lower harness

while the upper harness remains stationary, thus distracting

the patient's spine. A safety button can be pushed

at any time by the patient to release all tension immediately.

Daily treatments, Monday through Friday, were

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performed for the first two weeks of treatment. The latter

four weeks consisted of treatments every other day, Monday,

Wednesday and Friday.

Initial decompression force was adjusted to patient tolerance,

starting at 4.54 kg (10 lbs) less than half their body

weight. If a patient described the decompression pull as

"strong or painful," this distraction force was decreased

by 10%-25%. In subsequent treatment sessions, the distraction

force was increased as tolerated to final levels of

4.54 kg to 9.07 kg (10 to 20 lbs) more than half their body

weight. Patients continued to use analgesics prescribed

by their physicians before enrollment, but were allowed

to use additional non-steroidal pain medication should

their pain increase temporarily and permitted to discontinue

pain medication as needed. During the routine

physical examination performed by WM prior to beginning

the non-surgical spinal decompression treatment

session, at the first and final visits maximal pain was evaluated

during a flexion-extension range of motion exam

with the question "How strong is your pain on a scale of

0-10 with 0 being no pain and 10 as bad as it could be?"

Variables

The first main outcome for this study was the change in

pain during a range of motion evaluation measured on an

11-point verbal rating scale (VRS), with 0 being no pain

and 10 being pain as excruciating as could be imagined,

before and after the 6-week spinal decompression treatment

regimen.

The second main outcome was the change in average

disc height as measured by CT scan. For each patient,

average disc height of L3-L4, L4-L5 and L5-S1 was calculated

before the first treatment session and at least one

day after or on the day before the last treatment session.

Statistical analysis and sample size estimation

We assumed data to be normally distributed unless

exploratory analyses suggested otherwise, in which case a

Kolmogorov-Smirnov test was to be applied. Since the

treatment effect was defined as the difference between

before and after the therapeutic intervention, a paired ttest

was applied to test whether there was a reduction in

pain and an increase in disc height. For the main hypothesis,

the correlation between disc height changes and low

back pain, we applied linear regression to quantify the

relationship with Pearson's correlation coefficient to

determine statistical significance.

Sample size estimations were performed to have sufficient

power to test with a two sided type I error of 0.05

and type II error of 0.2 (80% power). Given the sizeable

treatment effect reported in the retrospective chart

review and also in the prospective pilot study mentioned

in the introduction, we expected a reduction in range of

motion pain from 6 to 2, with a standard deviation of 2.5.

This resulted in a sample size estimation of only 5

patients. To test changes in disc height, we expected a

standard disc height of about 8 mm with diseased discs

being slightly more compressed, i.e. at about 7.5 mm, and

anticipated discs after the decompression treatment to

measure at about 8.25 mm. Assuming a standard deviation

of 1.0 mm, we estimated a required sample size of 16

patients in order to show a difference. The sample size for

the main hypothesis, that the degree of pain reduction is

associated with the amount of increase in disc height, was

more difficult to estimate since no previous study had

determined a correlation coefficient. Therefore, we chose

a coefficient of 0.5 for a conservative expectation, resulting

in a required sample size of 26 patients. Taking into

consideration the possibility of drop-outs, we aimed to

collect data from 30 patients.

During a two year period, Sept 19, 2005 to Aug 6, 2007, a

total of 103 patients were treated with the intervention,

but only 30 of those patients fulfilled the per protocol

inclusion and exclusion criteria for the analysis. The 30

participants consisted of 21 female and 9 male patients

with lumbar disc herniation. They had a mean (SD) age of

an average duration of LBP of 12.5 (± 19) weeks with a

score of 6.3 (± 2.2) on the VRS (Table 1). All 30 patients

had a disc prolapse and the majority (n = 25) also had

degenerative disc disease.

The maximum force during the first treatment was on

average 33.9 (± 6.8) kg and gradually increased during

subsequent treatment visits to 52.4 (± 7.6) kg (Table 2).

Low back pain decreased from 6.2 (± 2.2) to 1.6 (± 2.3, p

< 0.001) and disc height increased from 7.5 (± 1.7) to 8.8

(± 1.7) mm (p < 0.001) (Figures 1 and 2).

There was a statistically significant correlation between

the increase in disc height and a reduction in pain (r =

0.36, p = 0.044), with a 1 mm increase in disc height being

associated with a reduction of 1.86 on the 11-point verbal

rating scale (Fig. 3). No adverse events were reported during

the treatment period.

In this cohort study we extracted data from 30 patients

with discogenic low back pain and found an average

reduction in pain from 6.2 to 1.6 after non-surgical spinal

decompression. This level of pain relief is consistent with

two previous studies using DRX9000 to decrease chronic

low back pain[10,11]. However, here we systematically

investigated the change in disc height before and after the

treatment, and were able to show that increases in disc

height correlated with increased pain relief. A mechanical

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spinal decompression reduces the pressure on the discs.

This relief of stress would simultaneously promote regeneration

of diseased and compressed discs and increase

lumbar disc height, with the latter reducing load on the

facet joints.

It is well recognized that continuous pressure on vertebral

discs decreases their height. Humans are taller in the

morning after the discs decompress while the body is

supine overnight and shorter in the evening after the

discs have borne weight during daily activity[12]. Interestingly,

this effect occurs quite rapidly so that the majority

of height-loss in a day occurs within the first hour of

arising. Therefore, all CT scans analyzed in this study

were performed at least one hour after the subject got out

of bed. The first CT scan was performed within two

months before the initiation of the treatment and at least

one day after or the day immediately before the final

treatment session.

A clear diagnosis cannot be made in approximately 80%

of cases of LBP, and imaging techniques can only offer a

partial solution to the problem of making a causal diagnosis

of LBP[13]. One might argue that a CT scan is not

as sensitive a measure of disc height as an MRI scan

because it images soft tissues poorly and cannot examine

internal disc morphology. However, because the primary

objective was to establish an observable correlation

between disc height increase and decreased LBP, a CT

scan permitting examination of the outline of the intervertebral

discs at high resolution provided sufficient measurable

evidence[14].

It has been demonstrated that low back pain can lead to

muscle spasms that could directly perpetuate pain,[15] or

induce pain within the disc as nerve fibers have been

described to grow into the inner part of the annulus

fibrosus or nucleus pulposus[16]. It is hypothesized that

the pain-spasm-pain cycle[15] is perpetuated by further

Age (yr) 64.4 (±14.9)

Height (cm) 166.1 (±8.5)

Weight (kg) 80.5 (±14.4)

Gender (F/M) 70% (21/9)

Average disk height, pre-treatment (mm) 7.5 (±1.7)

Pain, palpation (before first visit, 0-10) 6.2 (±2.2)

Pain, range of motion (before first visit, 0-10) 6.2 (±2.2)

Pain duration (weeks) 12.5 (±19.4)

Herniation (simple) 5

Herniation (with degenerative disk disease) 25

L3-L4 & L4-L5 (15-20°) 1

L4-L5 (15°) 11

L4-L5 & L5-S1 (10-15°) 6

L5-S1 (10°) 12

Maximal traction force (kg) 33.9 (±6.8) 52.4 (±7.7)

Pain, palpation (0-10) 6.2 (±2.2) 1.6 (±2.3) -4.5 (±2.7), <0.001

Pain, range of motion (0-10) 6.2 (±2.2) 1.6 (±2.3) -4.5 (±2.7), <0.001

Average disk height (mm) 7.5 (±1.7) 8.8 (±1.7) 1.3 (±0.5), <0.001

2

3

Pre-treatment Post-treatment

Average disc height (mm)

0 0

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reduction in disc height, which also simultaneously

aggravates the facet joint. In either case, dampened pressure

on the disc should facilitate the regeneration of the

disc and assuage facet joint stress. In fact, it has been

described that non-surgical spinal decompression

mechanically creates negative intradiscal pressures, and it

is speculated that this supports disc regeneration, though

this remains controversial[5].

Pain measurement relies first and foremost on patient

report. Taking into account the subjectivity inherent in

this process, it was noted that a cut-off point, or rather

the change in pain score necessary for detecting a clinically

important difference in an individual patient, was

needed to identify responders and non-responders to

analgesia. Farrar et al reported that on average a reduction

in pain intensity of at least 2 points on the NRS

serves as a clinically significant change[17]. Using this

standard, in this cohort study this intervention had a success

rate of over 75% (pain decreased by more than 2 out

of 11 in 23 out of 30 patients). In our analysis, each millimeter

of increase in disc height was associated with pain

relief of roughly 2 points on the scale, a clinically important

difference according to the aforementioned report.

However, not all patients responded equally. This raises

the question of inter-individual variability and might be

addressed by taking into account the heterogeneity of

lumbar spine muscle strength acting as a counterforce to

the external distraction. Even though the DRX9000

machine has an integrated sensor to detect counterforces,

non-surgical spinal decompression can only work if lumbar

spine muscles are relaxed. Another reason for different

inter-individual response rates could be the age of the

patients. However, in sub-analyses (not described) we did

not find a correlation between age and treatment success.

With regards to the elderly cohort of patients analyzed in

this retrospective study, it is possible that a younger

patient population might respond differently to the nonsurgical

spinal decompression treatment given that they

would generally have less disc degeneration, be more

active, and have less co-morbidity than the elderly population

studied here. Yet this is a hypothesis that remains

to be tested in a future prospective study investigating

therapies to alleviate LBP in younger patients. While we

largely believe the range of muscle tone during non-surgical

spinal decompression to be the main reason for different

treatment effects, other reasons for variability could

be differing stages and degrees of degenerative disc disease,

an assortment of activity levels, and a wide spectrum

of concomitant treatments ranging from

chiropractic interventions and pain medication cocktails.

One limitation of this study is the lack of a control

group. This is especially relevant for herniated discs,

because of the significant rate of spontaneous recovery[

18,19]. A control group would have been absolutely

necessary if the primary objective was to establish a

causal relationship proving that the increase in disc

height is due to the non-surgical spinal decompression;

however, our primary objective was rather to demonstrate

the correlation between increased disc height and

reduction of pain. Thus, irrespective of a control group,

this is the first study that provides evidence of an association

between an anatomical correlate, change in disc

height, with pain relief over time. Even so, it is possible

the placebo effect may have contributed to the perception

of having decreased pain. Given that the correlation

between the increase of disc height and the reduction of

is room for an argument suggesting that perhaps the placebo

effect played a role in the positive outcome. Both

limitations of the current retrospective study indicate the

disc changes attributed to the non-surgical spinal decompression

intervention and the reduction of LBP.

Patients with chronic discogenic low back pain are usually

on a wide range of analgesics, and pain and analgesic

consumption is generally positively correlated. As a

result, interventions that reduce pain typically lead to a

reduced consumption of analgesics and thus counteract

the treatment effect of the intervention (suppressor

effect). The fact that a significant reduction of pain was

observed even though analgesics were not controlled for

corroborates the observation of pain relief through nonsurgical

spinal decompression.

Finally, the follow-up period was too short to comment

on the permanency of pain relief. However, this was not

within the scope of this study and the duration of the

effect is not essential to substantiate our primary finding

that restoration of disc height through non-surgical spinal

decompression is associated with decreased discogenic

low-back pain. The next step will be to obtain longterm

results, e.g. 1 or 2 years after the last treatment

cycle, to a) investigate whether treatment effects are long

lasting and to b) more importantly, establish whether

there is a long term correlation between disc height

increase and pain reduction.

In this study of non-surgical spinal decompression for

chronic discogenic low back pain we were able to demonstrate

an association between the restoration of disc

height and pain relief. The correlation of these variables

suggests that pain reduction may be mediated, at least in

part, through a restoration of disc height. These results

call for a randomized placebo-controlled trial to substantiate

the efficacy and elucidate the mechanism of this

promising treatment modality.

Competing interests

The authors themselves declare that they have no competing interests.

NEMA Research is a Clinical Research Organization that is involved in evidencebased

research development and was the lead sponsor implementing the protocol

for this clinical trial on behalf of Axiom-Worldwide.

Authors' contributions

CA contributed to the statistical analysis and drafting the manuscript, OSC contributed

to the statistical analysis of the data, WM is responsible for the assessments

made, data collection, and data review, CR performed statistical analysis

and assisted with writing the manuscript, AM assisted with drafting the manuscript,

EG contributed to drafting, editing, and formatting the manuscript, MS

contributed to drafting and editing the manuscript, JVP performed the data

review. All authors read and approved the final manuscript.

Author Details

Perioperative Care, University of California San Francisco, San Francisco,

Johns Hopkins University, Baltimore, Maryland, & Department of Anesthesia,

Georgetown University School of Medicine, Washington, DC, USA

References

chronic low back pain: a review of the evidence for an American Pain

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9. Clarke JA, van Tulder MW, Blomberg SE, de Vet HC, van der Heijden GJ,

outpatients with chronic discogenic low back pain with the DRX9000:

Prospective Evaluation of the Efficacy of Spinal Decompression via the

tomography-evaluated features of spinal degeneration: prevalence,

of changes in chronic pain intensity measured on an 11-point

disk herniation: MR imaging assessment of natural history in patients

Pre-publication history

The pre-publication history for this paper can be accessed here:

http://www.biomedcentral.com/1471-2474/11/155/prepub

doi: 10.1186/1471-2474-11-155

spinal decompression is associated with decreased discogenic low back

Received: 14 October 2009 Accepted: 8 July 2010

Published: 8 July 2010