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 explanation for this correlation might be that the non-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 LBP, and imaging techniques can only offer a partial solution to the problem of making a causal diagnosis of LBP. 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.
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 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 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 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 pain shows an r2 = .13, while statistically significant, there 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 need for a randomized placebo-controlled trial to establish a more concrete relationship between the anatomical 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 non-surgical 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 long-term 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.