Discogenic pain is pain originating from a damaged intervertebral disc, particularly due to degenerative disc disease. However, not all degenerated discs cause pain. Disc degeneration occurs naturally with age.
Once a fully degenerated disc no longer has any inflammatory proteins that can cause pain, the disc enters into a stable position. Hence, discogenic pain rarely occurs after 60 years of age.
Some of the basis for performing a discogram is to identify levels that may produce “discogenic pain” or “painful disc syndrome”, a controversial point. When the pain produced mimics the patient’s presenting pain, the pain is said to be “concordant.”
see also Thoracic discogenic pain.
The expressions of IL-1 and IL-6 in the discs of discogenic low back pain (DLBP) patients were significantly elevated and negatively correlated with the Modified Japanese Orthopaedic Association scale (mJOA) of low back pain 1).
Pro-inflammatory chemokines CCL5 and CXCL6 are released by induced degenerative discs, and CCL5 has been associated with discogenic back pain. A case-control study was performed, based on the Hong Kong Disc Degeneration Population-Based Cohort of Southern Chinese, to investigate if systemic levels of CCL5 and CXCL6 were elevated in subjects with disc degeneration compared to non-degenerated individuals. Eighty subjects were selected, 40 with no disc degeneration (control group; DDD score 0) and 40 with moderate/severe disc degeneration (disc degeneration group; DDD score ≥5) as noted on MRI. Subjects were matched for age, sex, body mass index and workload. Blood plasma samples were obtained from each individual, and levels of CCL5 and CXCL6 were measured. Secondary phenotypes of lumbar disc displacement and cervical disc changes were also assessed. CCL5 concentrations were significantly increased in the disc degeneration (mean: 19.8 ng/mL) compared to the control group (mean: 12.8 ng/mL) (p = 0.015). The degeneration group demonstrated higher levels of CXCL6 (mean: 56.9 pg/mL) compared to the control group (mean: 43.4 pg/mL) (p = 0.010). There was a trend towards elevated CCL5 levels with disc displacement in the degeneration group (p = 0.073). Cervical disc degeneration was not associated with elevated chemokine levels (p > 0.05). This is the first study to note that elevated systemic CCL5 and CXCL6 were associated with moderate/severe lumbar disc degeneration, further corroborating tissue studies of painful discs. These chemokines may be systemic biomarkers for the diagnosis and monitoring of disc degeneration 2).
The treatment of degenerative discogenic pain is controversial, and anterior lumbar fusion for the treatment of degenerative discogenic low back pain has also been a controversial topic for over a generation.
Discogenic pain can usually be successfully treated with non-surgical treatments, such as pain medication and physical therapy and exercise, but chronic discogenic pain that is severe and limits the individual's ability to function may need to be treated with surgery.
There are few evidence-based effective interventional treatment options available.
There are few high-quality studies evaluating nonoperative treatments for reducing discogenic low back pain. Although conclusions from several studies favor intervention over sham, it is unclear whether these interventions confer stable long-term benefit. There is some promise in newer modalities such as biacuplasty; however, more inclusive studies need to be performed 3).
A single-center study included 80 patients and followed them for 6 months. Transforaminal laser annuloplasty (TFLA, 37 patients) or intradiscal radiofrequency annuloplasty (IDRA, 43 patients) was performed. The main outcomes included pain scores, determined by the numeric rating scale (NRS), and Oswestry disability index (ODI), at pre-treatment and at post-treatment months 1 and 6.
The patients were grouped according to procedure. In all procedures, NRS and ODI scores were significantly decreased over time. Mean post-treatment pain scores at months 1 and 6 were significantly lower (P < 0.01) in both groups, and between-group differences were not significant. The ODI score was also significantly decreased compared with baseline. Among patients undergoing TFLA, 70.3% (n = 26) reported pain relief (NRS scores < 50% of baseline) at post-treatment 6 months, vs. 58.1% (n = 25) of those undergoing IDRA. There were no statistically significant differences between the groups in ODI reduction of > 40%.
The results indicate that annuloplasty is a reasonable treatment option for carefully selected patients with lower back and radicular pain of discogenic origin, and TFLA might be superior to IDRA in patients with discogenic low back pain 5).
Thirty-two consecutive patients were intradiscally injected with 2 mL of 0.5% bupivacaine (control group). Another 31 consecutive patients were intradiscally injected with 40 mg tocilizumab and 1-2 mL of 0.5% bupivacaine (tocilizumab group) at the same time. Prior to treatment, the vertebral origin of low back pain was confirmed in all patients based on pain provocation during discography and pain relief with 1 mL of 1% xylocaine. Numeric rating scale and Oswestry disability index scores were used to evaluate pain level before and after treatment between the 2 groups. The association between pain relief with tocilizumab and intervertebral disc degeneration grade was also determined.
At the end of the study (8 weeks after treatment), 30 patients in each group were evaluable. In the tocilizumab group, numeric rating scale and Oswestry disability index scores improved significantly at 2 and 4 weeks after treatment, respectively. Intervertebral disc degeneration was not associated with improvement of numeric rating scale score in the tocilizumab group. Local infection (i.e., discitis) was observed in 1 patient in the tocilizumab group.
The results demonstrate the clinical relevance of interleukin-6 in discogenic low back pain. Intradiscal tocilizumab injection was shown to exert a short-term analgesic effect in patients with discogenic low back pain. Further research is required to determine the long-term effects of intradiscal tocilizumab therapy in patients with discogenic low back pain 6).