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Pain Beyond the Facet
September 8, 2015 by Dr Matthew D. Long
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Pain Beyond the Facet
September 8, 2015 by Dr Matthew D. Long
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Pain Beyond the Facet
September 8, 2015 by Dr Matthew D. Long
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When faced with a patient suffering from sciatica it is tempting to immediately presume that a disc protrusion is to blame - even more so if they demonstrate sensory loss or weakness. After all, what other structures could possibly compress the nerve roots? But is nerve root compression actually necessary to produce radiculopathy?
In truth, sciatica is a problem of chemistry. While protruded disc materials can certainly displace or compress their neighbouring nerve roots, it is the inflammatory chemistry that accompanies such lesions that really does the damage (1,2,3). Indeed, a simple annular tear can provoke significant damage if substances such as tumour necrosis factor-alpha (TNF-α) are able to leak through the outer wall and bathe adjacent neural tissue (4). These inflammatory cytokines have nasty habit of demyelinating nerve roots and causing intraneural fibrosis - all without signs of physical compression. It has also been suggested that these cytokines may induce scarring and adhesion formation - effectively tethering the nerve in a 'collar' of connective tissue (5) that continues to produce compression.
So we can see that perineural inflammation is a bad thing - but is this only a feature of disc herniation? Could other spinal structures have a similar effect?
When we consider the known origins of spinal pain, the humble facet joint is usually near the top of the list. Epidemiology tells us that the zygapophysial joints are the second most common source of chronic lower back pain, with an approximate 31% prevalence (6). However, there is still debate about the underlying nature of facet joint pain and the way in which it manifests. Is it an inflammatory condition? Should we use the term 'osteoarthritis' (implying an inflammatory disorder), or is 'osteoarthrosis' a more accurate description? Furthermore, we know that many individuals carry on their lives in a pain-free state, yet have significant osteoarthritic change evident on imaging studies (7). So is facet joint degeneration truly relevant?
While the process of osteoarthritis within the spine has long been considered largely painless, this is not always the case, and more recent findings have indeed confirmed that an inflammatory process does occur within degenerated spinal joints. Igarashi and colleagues (8) looked closely at the process of spinal degeneration and suggested that mechanical stresses occurring through joint instability or 'alignment abnormality' may occur to promote inflammatory changes within the joint and remodelling of subchondral bone, osteophyte formation and cartilage degeneration. They further examined the chemical constituents within the zygapophysial joints and noted many of the same cytokines that originate in disc tissue (such as TNF-α). According to Laplante and DePalma (9),
In truth, sciatica is a problem of chemistry. While protruded disc materials can certainly displace or compress their neighbouring nerve roots, it is the inflammatory chemistry that accompanies such lesions that really does the damage (1,2,3). Indeed, a simple annular tear can provoke significant damage if substances such as tumour necrosis factor-alpha (TNF-α) are able to leak through the outer wall and bathe adjacent neural tissue (4). These inflammatory cytokines have nasty habit of demyelinating nerve roots and causing intraneural fibrosis - all without signs of physical compression. It has also been suggested that these cytokines may induce scarring and adhesion formation - effectively tethering the nerve in a 'collar' of connective tissue (5) that continues to produce compression.
So we can see that perineural inflammation is a bad thing - but is this only a feature of disc herniation? Could other spinal structures have a similar effect?
When we consider the known origins of spinal pain, the humble facet joint is usually near the top of the list. Epidemiology tells us that the zygapophysial joints are the second most common source of chronic lower back pain, with an approximate 31% prevalence (6). However, there is still debate about the underlying nature of facet joint pain and the way in which it manifests. Is it an inflammatory condition? Should we use the term 'osteoarthritis' (implying an inflammatory disorder), or is 'osteoarthrosis' a more accurate description? Furthermore, we know that many individuals carry on their lives in a pain-free state, yet have significant osteoarthritic change evident on imaging studies (7). So is facet joint degeneration truly relevant?
While the process of osteoarthritis within the spine has long been considered largely painless, this is not always the case, and more recent findings have indeed confirmed that an inflammatory process does occur within degenerated spinal joints. Igarashi and colleagues (8) looked closely at the process of spinal degeneration and suggested that mechanical stresses occurring through joint instability or 'alignment abnormality' may occur to promote inflammatory changes within the joint and remodelling of subchondral bone, osteophyte formation and cartilage degeneration. They further examined the chemical constituents within the zygapophysial joints and noted many of the same cytokines that originate in disc tissue (such as TNF-α). According to Laplante and DePalma (9),
"As inflammation ensues, fluid and polymorphonuclear leukocyte infiltration, vasodilation, and venous congestion occur within the joint space, which results in pain-provoking capsular distention and neuronal sensitization of substance-P immunoreactive nerve fibers. If nociceptive input persists, then the development of peripheral and central sensitization and neuroplasticity can occur, which contributes to chronic z-joint pain."
Obviously such joint inflammation is capable of producing local back pain, but what about sciatica? The answer appears to be 'yes'.
A study by Tachihara et al (10) was an elegantly performed investigation into the possible mechanisms by which the facet joints may induce radiculopathy. By injecting an adjuvant promoting TNF-α production the researchers were able to induce local inflammation within the L5-L6 facet joints of experimental rats. They then observed various behavioural factors (such as the presence of mechanical allodynia) and assessed for the presence of local TNF-α, as well as TNF-α affected neurons within the dorsal root ganglion. They further observed degenerative changes within the facet joints after a month, including surface irregularities, erosions and abrasions. Tachihara was able to observe that inflamed degenerated facet joints were quite capable of inducing radiculopathy in the subjects. However, the simple presence of a non-inflamed, degenerated zygapophysial joint was not sufficient to induce symptoms,
A study by Tachihara et al (10) was an elegantly performed investigation into the possible mechanisms by which the facet joints may induce radiculopathy. By injecting an adjuvant promoting TNF-α production the researchers were able to induce local inflammation within the L5-L6 facet joints of experimental rats. They then observed various behavioural factors (such as the presence of mechanical allodynia) and assessed for the presence of local TNF-α, as well as TNF-α affected neurons within the dorsal root ganglion. They further observed degenerative changes within the facet joints after a month, including surface irregularities, erosions and abrasions. Tachihara was able to observe that inflamed degenerated facet joints were quite capable of inducing radiculopathy in the subjects. However, the simple presence of a non-inflamed, degenerated zygapophysial joint was not sufficient to induce symptoms,
“These results suggest that degeneration of the facet joints without inflammation is unrelated to leg symptoms, corresponding to the clinical fact that some patients remain asymptomatic, despite degeneration of facet joints on diagnostic imaging.”
Tachihara went on to say,
“Inflammation occurring in a facet joint can spread to the epidural space in two ways: via immunologic mechanisms or via direct infiltration. With immunologic mechanisms, because inflamed synovium induces inflammatory cells in adjacent tissue, inflammatory cells enter the epidural space through inflammation-induced chemical factors. With direct infiltration, destruction of facet joint structures involved in spondylotic changes or increased permeability of vessels and synovium due to inflammation, thus allow inflammatory cell and chemical factors to directly infiltrate the epidural space via the ventral articular capsule.”
Such studies demonstrate that an inflamed zygapophysial joint could easily induce a true radiculopathy (as opposed to a more diffuse sclerotogenous referred pain), and thereby mimic a disc presentation. This reinforces the need to keep our diagnostic wits about us when assessing our patients, and avoid the temptation to simply assume that sciatica is always a feature of disc derangement. Furthermore, we should familiarise ourselves with the imaging methods available to help us make an accurate diagnosis. In a prior Clinical Clarity Blog article (here) we looked briefly at the role of MRI in detecting a facet joint synovitis - specifically the use of fat-suppression techniques. There are a number of options available to highlight facet joint effusion and it is worth discussing this with your local radiologist. Most commonly a 'Short tau inversion recovery' (STIR) sequence is sufficient to demonstrate the affected structures, and is easily performed in addition to the standard T1 and T2 images (11). If facet joint synovitis is evident then a grading system has been developed to quantify the extent of fluid migration. Czervionke and Fenton (12) classified the MRI appearances using the following scheme:
Grade 0: No signal abnormality
Grade 1: Signal abnormality confined to join capsule
Grade 2: Periarticular signal abnormality involving less than 50% of the perimeter of the joint
Grade 3: Periarticular signal abnormality involving more than 50% of the perimeter of the joint
Grade 4: Grade 3 with extension of signal abnormality into the intervertebral foramen, ligamentum flavum, pedicle, transverse process, or vertebral body
Grade 1: Signal abnormality confined to join capsule
Grade 2: Periarticular signal abnormality involving less than 50% of the perimeter of the joint
Grade 3: Periarticular signal abnormality involving more than 50% of the perimeter of the joint
Grade 4: Grade 3 with extension of signal abnormality into the intervertebral foramen, ligamentum flavum, pedicle, transverse process, or vertebral body
According to Czervionke and Fenton a grade 4 synovitis is capable of producing inflammatory radicular pain, as the exudate directly encompasses neural tissue. The images below are taken from their paper "Fat-saturated MR imaging in the detection of inflammatory facet arthropathy (facet synovitis) in the lumbar spine."
Figure 1. Grading of facet synovitis: fat-saturated contrast-enhanced T1-weighted images. (a) Grade 1 facet synovitis on the right at L3-4 level, with enhancement of the posterior facet capsule (single arrow on right side of patient). Enhancement of the left facet capsule and adjacent soft tissues (two arrows on patient’s left) indicate grade 2 facet synovitis on the left. (b) Grade 2. Contrast enhancement of tissues (arrows) extending around posterior margin of the right L4-5 facets. (c) Grade 3. Contrast enhancement within the facets and tissues around the facets (arrows) involves greater than 50% of the facet perimeter on the right at the L3-4 level. (d) Grade 4. Enhancement involves the tissues (arrows) surrounding the right L4- 5 facets and extends into the right L4-5 neural foramen surrounding the right L4 dorsal root ganglion (DRG). Note grade 3 facet synovitis on the left at this level but the enhancement does not extend into the left neural foramen. From Czervionke and Fenton (Pain Medicine)
Ever since Mixter and Barr (13) discovered the herniated nucleus pulposus in 1934, and ushered in the 'Dynasty of the Disc', most clinicians have viewed radiculopathy as a cardinal sign of disc lesion. Unfortunately, this has had a number of consequences. Firstly, many patients have undergone unnecessary disc surgery to reduce presumptive compression from an otherwise benign disc bulge. Secondly, many chiropractors have been challenged to justify their care of an individual suffering from dermatomal leg pain and a suspected disc lesion - sometimes losing care of the patient as a result. So it is imperative that we familiarise ourselves with the latest literature and imaging techniques, so that we can help our patients navigate the complex waters of spinal pain diagnosis.
Something to think about...
Dr Matthew D. Long
BSc (Syd) M.Chiro (Macq)
Something to think about...
Dr Matthew D. Long
BSc (Syd) M.Chiro (Macq)
References:
1. Yamashita, M., Ohtori, S., Koshi, T., Inoue, G., Yamauchi, K., Suzuki, M., & Takahashi, K. (2008). Tumor necrosis factor-alpha in the nucleus pulposus mediates radicular pain, but not increase of inflammatory peptide, associated with nerve damage in mice. Spine, 33(17), 1836–1842. http://doi.org/10.1097/BRS.0b013e31817bab2a
2. Genevay, S., Finckh, A., Payer, M., Mezin, F., Tessitore, E., Gabay, C., & Guerne, P. A. (2008). Elevated levels of tumor necrosis factor-alpha in periradicular fat tissue in patients with radiculopathy from herniated disc. Spine, 33(19), 2041–2046. http://doi.org/10.1097/BRS.0b013e318183bb86
3. Murata, Y., Nannmark, U., Rydevik, B., Takahashi, K., & Olmarker, K. (2008). The role of tumor necrosis factor-alpha in apoptosis of dorsal root ganglion cells induced by herniated nucleus pulposus in rats. Spine, 33(2), 155–162. http://doi.org/10.1097/BRS.0b013e3181605518
4. Peng, B., Wu, W., Li, Z., Guo, J., & Wang, X. (2007). Chemical radiculitis. Pain, 127(1-2), 11–16. http://doi.org/10.1016/j.pain.2006.06.034
5. Kobayashi, S., Takeno, K., Yayama, T., Awara, K., Miyazaki, T., Guerrero, A., & Baba, H. (2010). Pathomechanisms of sciatica in lumbar disc herniation: effect of periradicular adhesive tissue on electrophysiological values by an intraoperative straight leg raising test. Spine, 35(22), 2004–2014. http://doi.org/10.1097/BRS.0b013e3181d4164d
6. Manchikanti, L., Boswell, M. V., Singh, V., Pampati, V., Damron, K. S., & Beyer, C. D. (2004). Prevalence of facet joint pain in chronic spinal pain of cervical, thoracic, and lumbar regions. BMC Musculoskelet Disord, 5, 15. doi:10.1186/1471-2474-5-15
7. Schwarzer, A. C., Wang, S. C., O'Driscoll, D., Harrington, T., Bogduk, N., & Laurent, R. (1995). The ability of computed tomography to identify a painful zygapophysial joint in patients with chronic low back pain. Spine, 20(8), 907–912.
8. Igarashi, A., Kikuchi, S., Konno, S., & Olmarker, K. (2004). Inflammatory cytokines released from the facet joint tissue in degenerative lumbar spinal disorders. Spine, 29(19), 2091–2095.
9. Laplante, B. L., & DePalma, M. J. (2012). Spine Osteoarthritis. PM & R, 4(S), S28–S36. http://doi.org/10.1016/j.pmrj.2012.03.005
10. Tachihara, H., Kikuchi, S.-I., Konno, S.-I., & Sekiguchi, M. (2007). Does facet joint inflammation induce radiculopathy?: An investigation using a rat model of lumbar facet joint inflammation. Spine, 32(4), 406–412. http://doi.org/10.1097/01.brs.0000255094.08805.2f
11. Kotsenas, A. L. (2012). Imaging of Posterior Element Axial Pain Generators. Radiologic Clinics of North America, 50(4), 705–730. http://doi.org/10.1016/j.rcl.2012.04.008
12. Czervionke, L. F., & Fenton, D. S. (2008). Fat-saturated MR imaging in the detection of inflammatory facet arthropathy (facet synovitis) in the lumbar spine. Pain Medicine (Malden, Mass), 9(4), 400–406. http://doi.org/10.1111/j.1526-4637.2007.00313.x
13. Mixter, W.J. and Barr, J.S. (1934) Rupture of the intervertebral disc with involvement of the spinal cord. N Engl J Med 211: 210-214.
1. Yamashita, M., Ohtori, S., Koshi, T., Inoue, G., Yamauchi, K., Suzuki, M., & Takahashi, K. (2008). Tumor necrosis factor-alpha in the nucleus pulposus mediates radicular pain, but not increase of inflammatory peptide, associated with nerve damage in mice. Spine, 33(17), 1836–1842. http://doi.org/10.1097/BRS.0b013e31817bab2a
2. Genevay, S., Finckh, A., Payer, M., Mezin, F., Tessitore, E., Gabay, C., & Guerne, P. A. (2008). Elevated levels of tumor necrosis factor-alpha in periradicular fat tissue in patients with radiculopathy from herniated disc. Spine, 33(19), 2041–2046. http://doi.org/10.1097/BRS.0b013e318183bb86
3. Murata, Y., Nannmark, U., Rydevik, B., Takahashi, K., & Olmarker, K. (2008). The role of tumor necrosis factor-alpha in apoptosis of dorsal root ganglion cells induced by herniated nucleus pulposus in rats. Spine, 33(2), 155–162. http://doi.org/10.1097/BRS.0b013e3181605518
4. Peng, B., Wu, W., Li, Z., Guo, J., & Wang, X. (2007). Chemical radiculitis. Pain, 127(1-2), 11–16. http://doi.org/10.1016/j.pain.2006.06.034
5. Kobayashi, S., Takeno, K., Yayama, T., Awara, K., Miyazaki, T., Guerrero, A., & Baba, H. (2010). Pathomechanisms of sciatica in lumbar disc herniation: effect of periradicular adhesive tissue on electrophysiological values by an intraoperative straight leg raising test. Spine, 35(22), 2004–2014. http://doi.org/10.1097/BRS.0b013e3181d4164d
6. Manchikanti, L., Boswell, M. V., Singh, V., Pampati, V., Damron, K. S., & Beyer, C. D. (2004). Prevalence of facet joint pain in chronic spinal pain of cervical, thoracic, and lumbar regions. BMC Musculoskelet Disord, 5, 15. doi:10.1186/1471-2474-5-15
7. Schwarzer, A. C., Wang, S. C., O'Driscoll, D., Harrington, T., Bogduk, N., & Laurent, R. (1995). The ability of computed tomography to identify a painful zygapophysial joint in patients with chronic low back pain. Spine, 20(8), 907–912.
8. Igarashi, A., Kikuchi, S., Konno, S., & Olmarker, K. (2004). Inflammatory cytokines released from the facet joint tissue in degenerative lumbar spinal disorders. Spine, 29(19), 2091–2095.
9. Laplante, B. L., & DePalma, M. J. (2012). Spine Osteoarthritis. PM & R, 4(S), S28–S36. http://doi.org/10.1016/j.pmrj.2012.03.005
10. Tachihara, H., Kikuchi, S.-I., Konno, S.-I., & Sekiguchi, M. (2007). Does facet joint inflammation induce radiculopathy?: An investigation using a rat model of lumbar facet joint inflammation. Spine, 32(4), 406–412. http://doi.org/10.1097/01.brs.0000255094.08805.2f
11. Kotsenas, A. L. (2012). Imaging of Posterior Element Axial Pain Generators. Radiologic Clinics of North America, 50(4), 705–730. http://doi.org/10.1016/j.rcl.2012.04.008
12. Czervionke, L. F., & Fenton, D. S. (2008). Fat-saturated MR imaging in the detection of inflammatory facet arthropathy (facet synovitis) in the lumbar spine. Pain Medicine (Malden, Mass), 9(4), 400–406. http://doi.org/10.1111/j.1526-4637.2007.00313.x
13. Mixter, W.J. and Barr, J.S. (1934) Rupture of the intervertebral disc with involvement of the spinal cord. N Engl J Med 211: 210-214.