BMC Musculoskelet Disord. 2010 Jul 8;11(1):155.
An estimated 80% of the population will suffer from low back pain at some point of their lives. 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. In addition to imposing upon patients’ quality of life, low back pain is of significant socioeconomic relevance because it may lead to a temporary loss of productivity, enormous medical and indirect costs, or even permanent disability.
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, acupuncture, back school and cognitive behavioral therapy. The two most common diseases involving chronic low back pain are discogenic low back pain, responsible for 39% of cases, and disc herniation, accounting for just less than 30% of low back pain 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. However, systematic reviews to date were unable to find sufficient evidence in the literature to support the use of this modality. A subsequent chart review of 94 patients suggests that motorized non-surgical spinal decompression may be effective in reducing chronic low back pain. 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 nonsurgical spinal decompression treatment protocol.
The goal of this study was therefore to determine if changes in low back pain, 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.
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 low back pain of at least 3 out of 10 on a verbal rating scale and was due to either discogenic low back pain or disc herniation according to a radiological diagnosis using standard medical definitions. Discogenic low back pain is most succinctly defined as a loss of lower back function with pain due to disc degeneration. Degenerative disc disease often emerges 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.
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 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?
During a two year period 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 age of 65 (± 15) years, a body mass index of 29 (± 5) kg/m2, and an average duration of low back pain of 12.5 (± 19) weeks with a score of 6.3 (± 2.2) on the VRS. 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. Low back pain decreased from 6.2 (± 2.2) to 1.6 (± 2.3) and disc height increased from 7.5 (± 1.7) to 8.8 (± 1.7) mm. There was a statistically significant correlation between the increase in disc height and a reduction in pain, with a 1 mm increase in disc height being associated with a reduction of 1.86 on the 11-point verbal rating scale. 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. 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 explanation for this correlation might be that 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. 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 low back pain, and imaging techniques can only offer a partial solution to the problem of making a causal diagnosis of low back pain. 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 low back pain, a CT scan permitting examination of the outline of the intervertebral discs at high resolution provided sufficient measurable evidence.
It has been demonstrated that low back pain can lead to muscle spasms that could directly perpetuate pain, 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. It is hypothesized that the pain-spasm-pain cycle is perpetuated by further 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.
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. 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 this 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 the authors 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 non-surgical 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 low back pain in younger patients. While the authors largely believe the range of muscle tone during nonsurgical 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.
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 non-surgical spinal decompression.
In this study of non-surgical spinal decompression for chronic discogenic low back pain the authors 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.