Research Review By Dr. Josh Plener©

Audio:

Download MP3

Date Posted:

December 2020

Study Title:

The degenerative lumbar disc: not a disease, but still an important consideration for OMPT practice: a review of the history and science of discogenic instability

Authors:

Swanson B & Creighton D

Author's Affiliations:

Department of Rehabilitation Sciences, University of Hartford, Connecticut, USA

Publication Information:

Journal of Manual and Manipulative Therapy 2020; 28(4): 191-200. doi: 10.1080/10669817.2020.1758520.

Background Information:

The American Academy of Orthopedic Manual Physical Therapists (AAOMPT) recently released a position statement stating “[the] AAOMPT supports and encourages early physical therapy interventions with known effectiveness instead of high-risk procedures and medication, and strongly recommends that clinicians avoid using the diagnosis of degenerative disc disease” (1). This objection is based on several factors, specifically: 1) degenerative disc disease (DDD) is a common age-related observation and therefore not a disease; and 2) clinicians tend to overutilize diagnostic imaging to direct treatment, which is in conflict with the evidence.

However, the authors of this paper suggest that imaging findings can and should inform treatment decisions as one aspect of a broad clinical reasoning process. Past research and commentaries (2) have suggested that disc degeneration is a common finding in adults and “the choice of treatment doesn’t seem to matter as much as identifying an individual likely to respond” (3). Despite this, the International Society for the Study of The Lumbar Spine references DDD as the most common cause of low back pain (4). Pain arising from DDD has been suggested to result from the hallmarks of the degenerative process, such as tears of the annulus fibrosis, loss of disc height, alterations in loading and stability of the motion segment, and accompanying biochemical changes (4).

This narrative review aims to understand if the manual interventions used in clinical practice reflect the scientific evidence pertaining to the biomechanical aspects of DDD leading to pain, or whether the science has been ignored as the call grows to discard harmful diagnostic labels.

Summary:

Historical Perspective
 
Instability due to disc degeneration has been suggested to be a significant cause of low back pain, dating back to 1911 (5-9). In 1944, Knutsson was one of the first researchers to describe instability that results from early grade disc degeneration through side bending, flexion and extension stress radiographs (9). Future researchers discovered segmental instability secondary to disc degeneration in spine specimens during autopsy, and consistently found an association of instability with annular clefting and tears (10-12). Schmorl and Junghanns described discogenic instability using terms that eventually became known as anterolisthesis and retrolisthesis (13-14).

Mechanically, Ian Macnab defined disc degeneration as the breakdown in the mechanical integrity of the disc resulting in irregular and excessive spinal segmental motion leading to a loss of structural integrity (15-16). Later, Kirkaldy-Willis famously described the sequential three-phase pathophysiological spinal degeneration model which includes (17-18):
  1. Dysfunction
  2. Instability
  3. Stabilization
Furthermore, the advancement of magnetic resonance imaging allowed Pfirrmann to establish grades of disc degeneration (19). It is thought that understanding the grades of disc degeneration and its association with segmental instability is an important concept that manual therapists who utilize spinal manipulative therapy should know.

The Disc as a Pain Generator

Past research has supported the notion that the disc is a potential source of pain. Kuslich et al. stimulated local segmental tissues during decompression surgery and found that stimulating the annulus fibres provoked lower back pain in over two-thirds of patients (20). Furthermore, nerve fibres have been recorded both on the outer annulus and inner portions of degenerative discs, which is often accompanied by annular tears (21-23). This can result in the disc being more pain sensitive (20-22).

Healthy discs behave differently then degenerative discs. Due to the compact and stable collagen network, in addition to an abundance of proteoglycan aggrecan, healthy discs have a protective mechanism from nerve ingrowth (24). However, pathological discs have annular tears which disrupt the collagen complex, resulting in an inflammatory process leading to decreased proteoglycan. This process results in the upregulation of nerve growth factor following a disc injury, leading to nerve ingrowth into the disc (25-26). This becomes a vicious cycle as the abnormal stresses which occur due to the uneven load distributions imposed on pathological discs leads to further annular fibre tears (27). This continued cycle can lead to chronic inflammation and further degenerative changes (28).

The Disc as a Source of Instability

When thinking about instability, one has to consider range of motion (ROM) and the neutral zone. ROM is movement which is limited by passive osseoligamentous structures, where the neutral zone is an inherently unstable area that requires neuromuscular control due to the minimal internal resistance to movement (29-30). The neutral zone is defined by the point in movement where resistance is first detected. From a clinical perspective, changes in the neutral zone are believed to be closely linked to clinical instability. One method to determine if clinical instability is present is a ratio of neutral zone/range of motion, as the neutral zone is expressed as a percentage of the full range of motion (29, 31). Since intervertebral discs provide the majority of intrinsic resistance to small spinal movement, and segmental instability arises from discogenic degenerative changes, enlargement of the neutral zone has been described as being more indicative of instability then range of motion changes (32-36).

Furthermore, disc dehydration and endplate disruption, which are typical of disc degeneration, have been shown to increase the neutral zone (37). The loss of disc height due to DDD leads to buckling of the longitudinal ligaments, resulting in ligamentous tension occurring later then in a healthy segment (38). This alters the ability of ligaments to protect against excessive motion. Fujiwara et al. demonstrated that disc degeneration was associated with spinal motion changes, particularly increases in lateral bending and rotation with disc degeneration grades of 1 to 3, but not grade 4 disc degeneration (39). Tanaka et al. demonstrated an increase in flexion, extension and rotation range of motion concurrent with annulus fibrosus tears (40). Kettler et al. determined that with an increase in the neutral zone motion, stability with bending increased but axial rotational stability decreased (41).

Axial Rotation as a Source of Annular Stress

Past work has demonstrated that forced rotation beyond 3 degrees may produce structural damage, in particular annular tears (42). However, it has also been observed that axial rotation in segments with disc degeneration is greater than 3 degrees (31,38). In addition, Acaroglu et al. demonstrated that axial rotation produced the largest strain across the posterolateral aspect of the disc (43).

Under normal conditions, the facet joints act as a protective mechanism, limiting axial rotation to < 3 degrees (44). However, if axial rotation occurs with flexion, stress to the annulus fibres increase as flexion produces a pre-load of the posterior annulus fibres (42, 44). Therefore, the facet joints in flexion are less protective against axial rotation (42, 44, 45).

Considerations for Discogenic Stresses During Manual Therapy

In a porcine model, 500 N of force applied at a healthy L4 transverse process resulted in 3.2 degrees of rotation, but if applied at the facet joint resulted in only 1.9 degrees of rotation (46). Normal lumbar manipulation forces range between 400 to 1400 N, with longer levers resulting in greater increases in rotation at the segment (47).

During manipulation and mobilization, maximal intradiscal pressure on the rotating side has been shown to be greater than the contralateral side. Furthermore, the rate of intradiscal pressure increased by 33-58% during manipulation, therefore demonstrating a more instant impact to discs (48). The asymmetrical mechanical loading of degenerated discs has shown that annular forces, annular stress and intradiscal pressure are higher in degenerated discs then healthy discs during rotary manipulation procedures (49).

In addition, disc degeneration leads to alterations in the axis of rotation. The axis of rotation migrates posterior or closer to the facet joints, placing more stress through the facet joints (37). It has been shown that higher grades of disc degeneration results in greater forces in the contralateral facet joints when axial rotation is applied, placing greater stress on the posterolateral annulus (37).

Clinical Application & Conclusions:

The research discussed in this paper states that:
  • Rotation forces stress the annulus
  • Flexion minimizes the ability of the facets to limit rotation
  • Disc degeneration allows for greater rotation to occur
  • Disc degeneration results in a decreased ability of the annulus to tolerate rotational stress
With the above in mind, the authors ask whether treatments that include rotational manipulations to the lumbar spine are appropriate to perform in patients with DDD. The literature that is presented suggests that in the presence of early disc degeneration, manual therapists need to be cautious when applying rotary lumbar manipulations. The authors suggest alternative manual therapy interventions such as oscillatory spinal manual therapy interventions, distraction and stabilization. Oscillatory spinal manual therapy interventions are often applied for the purposes of sensory modulation and therefore will not compromise the structural integrity of a motion segment affected by disc degeneration (3, 50). Distraction and stabilization have been suggested to assist with disc rehydration and potential regeneration (51-52). Distractive force manipulation may be more effective for degenerative spinal conditions due to the generation of lower forces within the disc, which may be safer than rotary manipulations (53-58).

In addition, fluid exchange is vital in order to maintain disc nutrition, however hallmark features of DDD include a decrease in the diffusion of water and loss of proteoglycans (59). One treatment option to counter this is posterior to anterior glide mobilization that may improve disc hydration (60-62), however posterior to anterior mobilizations may also increase neutral zone shear (at least temporarily?) (63-65). Another possibility is prone extension exercises which may improve hydration (60-61), but neutral zone shear may (again) increase and significant degeneration may cause the nucleus to bulge posteriorly instead of anteriorly as in healthy and minimally degenerated discs (66-67). Another possible treatment is mid-range mobilization and traction which are theorized to improve hydration and reduce spinal flexibility (6), countering the increased instability in disc dehydration.

An increase in the neutral zone results in increased local musculature activation (29), with the multifidus shown to create up to two thirds of stability. Since the 1990s, researchers have documented that first time backpain causes immediate changes in the multifidus and spontaneous recovery of the multifidus doesn’t happen unless patients perform strengthening exercises (68). DDD has been shown to result in fatty infiltration of the multifidus, regardless of age (69). Evidence supports the notion of exercise improving the function of the multifidus muscles, with stabilization exercises demonstrating a more favorable outcome when compared to general lumbar range of motion exercises (68, 70, 71).

The authors of the paper make clear that they don’t want people ignoring imaging findings in spinal pain patients who have yet to reach the stabilization phase of Kirkaldy Willis’s pathophysiological model. They contend that basic science supports the biomechanical and physiological cycle of degeneration, and therefore manual therapists must utilize this information in practice.

Reviewer’s note: This article was very interesting, and the authors did a good job at showcasing the research in support of their particular beliefs. However, the authors focused solely on the bio- aspect of the biopsychosocial model. The research is unequivocal that a biopsychosocial model is required in order to properly treat patients with spinal pain. Therefore, a reductionist approach, as the authors took in this paper, may cause more harm than good when examining the whole patient. Individuals with low back pain may have pain originating from degenerative disc disease, however emphasising the importance of some manual therapy techniques and denouncing others based on the evidence provided may be too far a leap at this time. Every patient is unique and if clinicians utilize patient-centered care, they can alter manual therapy set-ups in order to maximize patient comfort and benefit.

Study Methods:

This paper was a narrative review and therefore, no statistical analysis was conducted nor was a specific description of their methodology provided.

Study Strengths / Weaknesses:

Strengths:
  • The authors did a good job at utilizing research in order to convey their viewpoint.
  • The authors did a good job at summarizing the available research on the topic.
Weaknesses:
  • The authors only focused on the biomedical model of DDD and failed to discuss the psychosocial aspects.
  • The authors did not state any research that contradicted their viewpoint, which would have been helpful for the reader and provided more balance to this paper. For example, the authors didn’t discuss research that shows imaging findings of DDD are present in symptomatic and asymptomatic patients.
  • The authors also did not discuss the quality and the level of research that supports their claims, such as the role of oscillatory techniques to rehydrate discs.
  • The authors used a narrative review approach instead of performing a systematic review, therefore the articles may have been cherry picked.

Additional References:

  1. Emerson A, Naze G, Mabry LM, et al. AAOMPT opposes the use of the term degenerative disc disease. Accessed 2020 Apr 11. Available at: https://aaompt.org/Main/Public_Resources/Position_Statements/Main/About_Us/Position_Statements.aspx?hkey=03f5a333-f28d-4715-b355-cb25fa9bac2c.
  2. Lewis JS, Cook CE, Hoffmann TC, et al. The elephant in the room: too much medicine in musculoskeletal practice. J Orthop Sports Phys Ther. 2020; 50(1): 1–4.
  3. Bialosky JE, Bishop MD, Price DD, et al. The mechanisms of manual therapy in the treatment of musculoskeletal pain: a comprehensive model. Man Ther. 2009; 14(5): 531–538.
  4. Venkatesh PKMC, Bolger C. Lumbar spine online textbook. Section 12, chapter 5: motion preservation for lumbar disc degeneration. International Society for the Study of the Lumbar Spine. Towson, MD: Data Trace Publishing; 2019. http://www.wheelessonline.com/ ISSLS/section-12-chapter-5-motion-preservation-forlumbar- disc-degeneration/.
  5. Wong D, Transfeldt E. Macnab’s Backache. 4th ed. Baltimore/London: Lippincott Williams & Wilkins; 2007.
  6. Goldthwait JE. The lumbo-sacral articulation; an explanation of many cases of “Lumbago,” “Sciatica” and Paraplegia. Boston Med Surg J. 1911; 164(11): 365–372.
  7. Johnson JRRW. Posterior luxations of the lumbosacral joint. J Bone Joint Surg. 1934; 16(4): 867–876.
  8. Smith AD. Posterior displacement of the fifth lumbar vertebra. J Bone Joint Surg. 1934; 16(4): 877–888.
  9. Knutsson F. The instability associated with disk degeneration in the lumbar spine. Acta Radiol. 1944;25 (5–6):593–609.
  10. Friberg S. Anatomical studies on lumbar disc degeneration. Acta Orthop Scand. 1948; 17 (1–4): 224–230.
  11. Friberg S, Hirsch C. Anatomical and clinical studies on lumbar disc degeneration. Acta Orthop Scand. 1949; 19(2): 222–242.
  12. Harris R, Macnab I. Structural changes in the lumbar intervertebral discs: their relationship to low back pain and sciatica. J Bone Joint Surg Br. 1954; 36-B(2): 304–322.
  13. Schmorl G, Junghanns H. Die Gesunde und Kranke Wirbels, Rontgenbild. Leipzig: Georg Thieme Verlag; 1932.
  14. Schmorl G, Junghanns H. Die Gesunde und die Kranke Wirbels Klinik. Stuttgart: Georg Thieme Verlag; 1953.
  15. Macnab I. The traction spur. An indicator of segmental instability. J Bone Joint Surg Am. 1971; 53(4): 663–670.
  16. Macnab I. Backache. Baltimore/London: Williams & Wilkens; 1977.
  17. Kirkaldy-Willis W, Farfan H. Instability of the lumbar spine. Clin Orthop Relat Res. 1982; 165: 110–123.
  18. Kirkaldy-Willis W, Wedge J, Yong-Hing K, et al. Pathology and pathogenesis of lumbar spondylosis and stenosis. Spine (Phila PA 1976). 1978; 3(4): 319–328.
  19. Pfirrmann CW, Metzdorf A, Zanetti M, et al. Magnetic resonance classification of lumbar intervertebral disc degeneration. Spine (Phila PA 1976). 2001; 26(17): 1873–1878.
  20. Kuslich S, Ulstrom C, Michael C. The tissue origin of low back pain and sciatica: a report of pain response to tissue stimulation during operations on the lumbar spine using local anesthesia. Orthop Clin North Am. 1991; 22(2): 181.
  21. Malinsky J. The ontogenetic development of nerve terminations in the intervertebral discs of man (histology of intervertebral discs, 11th communication). Cells Tissues Organs. 1959; 38(1–2): 96–113.
  22. Yoshizawa H, O’Brien JP, Thomas Smith W, et al. The neuropathology of intervertebral discs removed for low-back pain. J Pathol. 1980; 132(2): 95–104.
  23. Shinohara H. A study on lumbar disc lesion significance of histology of free nerve endings in lumbar disc. J Jpn Orthop Assoc. 1970; 44: 553–570.
  24. Johnson WE, Caterson B, Eisenstein SM, et al. Human intervertebral disc aggrecan inhibits nerve growth in vitro. Arthritis Rheum. 2002; 46(10): 2658–2664.
  25. Aoki Y, Takahashi Y, Ohtori S, et al. Distribution and immunocytochemical characterization of dorsal root ganglion neurons innervating the lumbar intervertebral disc in rats: a review. Life Sci. 2004; 74(21): 2627–2642.
  26. Yamauchi K, Inoue G, Koshi T, et al. Nerve growth factor of cultured medium extracted from human degenerative nucleus pulposus promotes sensory nerve growth and induces substance p in vitro. Spine (Phila PA 1976). 2009; 34(21): 2263–2269.
  27. Lotz JC, Colliou OK, Chin JR, et al. Volvo award winner in biomechanical studies. Spine (Phila PA 1976). 1998; 23(23): 2493–2506.
  28. Ulrich JA, Liebenberg EC, Thuillier DU, et al. ISSLS prize winner: repeated disc injury causes persistent inflammation. Spine (Phila PA 1976). 2007; 32(25): 2812–2819.
  29. Panjabi MM. The stabilizing system of the spine. Part II. Neutral zone and instability hypothesis. J Spinal Disord. 1992; 5(4): 390.
  30. Adams MA. editor. Biomechanics of the intervertebral disc, vertebra and ligaments. Szpalski M GR, Pope MH, eds. Lumbar Segmental Instability. Philadelphia: Lippincott Williams & Wilkins; 1999.
  31. Mimura M, Panjabi M, Oxland T, et al. Disc degeneration affects the multidirectional flexibility of the lumbar spine. Spine (Phila PA 1976). 1994; 19(12): 1371–1380.
  32. Adams M, Dolan P, Hutton W. The lumbar spine in backward bending. Spine (Phila PA 1976). 1988; 13(9): 1019–1026.
  33. Adams M, Hutton W, Stott J. The resistance to flexion of the lumbar intervertebral joint. Spine (Phila PA 1976). 1980; 5(3): 245–253.
  34. Sato H, Kikuchi S. The natural history of radiographic instability of the lumbar spine. Spine (Phila PA 1976). 1993; 18(Supplement): 2075–2079.
  35. Brown MD, Holmes DC, Heiner AD. Measurement of cadaver lumbar spine motion segment stiffness. Spine (Phila PA 1976). 2002; 27(9): 918–922.
  36. Weiler P, King J, Gertzbein S. Analysis of sagittal plane instability of the lumbar Soine in Vivo. Spine (Phila PA 1976). 1990; 15(12): 1300–1306.
  37. Zhao F, Pollintine P, Hole BD, et al. Discogenic origins of spinal instability. Spine (Phila PA 1976). 2005; 30(23): 2621–2630.
  38. Rohlmann A, Zander T, Schmidt H, et al. Analysis of the influence of disc degeneration on the mechanical behavior of a lumbar motion segment using the finite element method. J Biomech. 2006; 39(13): 2484–2490.
  39. Fujiwara A, Lim T-H, An HS, et al. The effect of disc degeneration and facet joint osteoarthritis on the segmental flexibility of the lumbar spine. Spine (Phila PA 1976). 2000; 25(23): 3036–3044.
  40. Tanaka N, An HS, Lim T-H, et al. The relationship between disc degeneration and flexibility of the lumbar spine. Spine J. 2001; 1(1): 47–56.
  41. Kettler A, Rohlmann F, Ring C, et al. Do early stages of lumbar intervertebral disc degeneration really cause instability? Evaluation of an in vitro database. Eur Spine J. 2011; 20(4): 578–584.
  42. Pearcy M. Inferred strains in the intervertebral discs during physiological movements. Man Med. 1990; 5: 68–71.
  43. Acaroglu ER, Latridis JC, Setton LA, et al. Degeneration and aging affect the tensile behavior of human lumbar anulus fibrosus. Spine (Phila PA 1976). 1995; 20(24): 2690–2701.
  44. Bogduk N. The lumbar disc and low back pain. Neurosurg Clin N Am. 1991; 2(4): 791–806.
  45. Ahmed AM, Duncan NA, Burke DL. The effect of facet geometry on the axial torque-rotation response of lumbar motion segments. Spine (Phila PA 1976). 1990; 15(5): 391–401.
  46. Funabashi M, Nougarou F, Descarreaux M, et al. Influence of spinal manipulative therapy force magnitude and application site on spinal tissue loading: a biomechanical robotic serial dissection study in porcine motion segments. J Manipulative Physiol Ther. 2017; 40(6):387–396.
  47. Owens EF Jr., Hosek RS, Mullin L, et al. Thrustmagnitudes, rates, and 3-dimensional directions delivered in simulated lumbar spine high-velocity, low-amplitude manipulation. J Manipulative Physiol Ther. 2017; 40(6): 411–419.
  48. Wang F, Zhang J, Feng W, et al. Comparison of human lumbar disc pressure characteristics during simulated spinal manipulation vs. spinal mobilization. Mol Med Rep. 2018; 18(6): 5709–5716.
  49. Li L, Shen T, Li Y-K. A finite element analysis of stress distribution and disk displacement in response to lumbar rotation manipulation in the sitting and side-lying positions. J Manipulative Physiol Ther. 2017; 40(8): 580–586.
  50. Zusman M, Edwards B, Donaghy A. Investigation of a proposed mechanism for the relief of spinal pain with passive joint movement. J Manual Med. 1989; 4: 58–61.
  51. Cho BY, Murovic J, Park KW, et al. Lumbar disc rehydration post implantation of a posterior dynamic stabilization system: case report. J Neurosurg Spine. 2010; 13(5): 576–580.
  52. Yilmaz A, Senturk S, Sasani M, et al. Disc rehydration after dynamic stabilization: a report of 59 cases. Asian Spine J. 2017; 11(3): 348.
  53. Gay RE, Ilharreborde B, Zhao KD, et al. Stress in lumbar intervertebral discs during distraction: a cadaveric study. Spine J. 2008; 8(6): 982–990.
  54. Sheng B, Yi-Kai L,Wei-dong Z. Effect of simulating lumbar manipulations on lumbar nucleus pulposus pressures. J Manipulative Physiol Ther. 2002; 25(5): 8A–11A.
  55. Ramos G, Martin W. Effects of vertebral axial decompression on intradiscal pressure. J Neurosurg. 1994; 81(3): 350–353.
  56. Gudavalli M, Cox J, Baker J Intervertebral disc pressure changes during the flexion-distraction procedure. Paper presented at: International Society for the Study of the Lumbar Spine Conference, Singapore, 1997.
  57. Andersson G, Schultz AB, Nachemson A. Intervertebral disc pressures during traction. Scand J Rehabil Med Suppl. 1983; 9(2): 88–91.
  58. Gay RE, Bronfort G, Evans RL. Distraction manipulation of the lumbar spine: a review of the literature. J Manipulative Physiol Ther. 2005; 28(4): 266–273.
  59. Johannessen W, Vresilovic EJ, Wright AC, et al. Intervertebral disc mechanics are restored following cyclic loading and unloaded recovery. Ann Biomed Eng. 2004; 32(1): 70–76.
  60. Beattie PF, Arnot CF, Donley JW, et al. The immediate reduction in low back pain intensity following lumbar joint mobilization and prone press-ups is associated with increased diffusion of water in the L5-S1 intervertebral disc. J Orthop Sports Phys Ther. 2010; 40(5): 256–264.
  61. Beattie PF, Donley JW, Arnot CF, et al. The change in the diffusion of water in normal and degenerative lumbar intervertebral discs following joint mobilization compared to prone lying. J Orthop Sports Phys Ther. 2009; 39(1): 4–11.
  62. Beattie PF, Morgan PS, Peters D. Diffusion-weighted magnetic resonance imaging of normal and degenerative lumbar intervertebral discs: a new method to potentially quantify the physiologic effect of physical therapy intervention. J Orthop Sports Phys Ther. 2008; 38(2): 42–49.
  63. Panjabi MM. The stabilizing system of the spine. Part I. Function, dysfunction, adaptation, and enhancement. J Spinal Disord. 1992; 5(4): 383.
  64. Porterfield J, DeRosa C. Structural and functional considerations of the lumbopelvic musculature. Mechanical low back pain: perspectives in functional anatomy. Philadelphia, PA: WB Saunders; 1991. p. 47–82.
  65. Rabin A, Shashua A, PizemK, et al. The interrater reliability of physical examination tests that may predict the outcome or suggest the need for lumbar stabilization exercises. J Orthop Sports Phys Ther. 2013; 43(2): 83–90.
  66. Fennell AJ, Jones AP, Hukins DW. Migration of the nucleus pulposus within the intervertebral disc during flexion and extension of the spine. Spine (Phila PA 1976). 1996; 21(23): 2753–2757.
  67. Beattie PF, Brooks WM, Rothstein JM, et al. Effect of lordosis on the position of the nucleus pulposus in supine subjects. A study using magnetic resonance imaging. Spine (Phila PA 1976). 1994; 19(18): 2096–2102.
  68. Hides JA, Richardson CA, Jull GA. Multifidus muscle recovery is not automatic after resolution of acute, first-episode low back pain. Spine (Phila PA 1976). 1996; 21(23): 2763–2769.
  69. Shahidi B, Parra CL, Berry DB, et al. Contribution of lumbar spine pathology and age to paraspinal muscle size and fatty infiltration. Spine (Phila PA 1976). 2017; 42(8): 616.
  70. Danneels L, Vanderstraeten G, Cambier D, et al. Effects of three different training modalities on the cross sectional area of the lumbar multifidus muscle in patients with chronic low back pain. Br J Sports Med. 2001; 35 (3): 186–191.
  71. O’Sullivan PB, Phyty GDM, Twomey LT, et al. Evaluation of specific stabilizing exercise in the treatment of chronic low back pain with radiologic diagnosis of spondylolysis or spondylolisthesis. Spine (Phila PA 1976). 1997; 22(24): 2959–2967.

Contact Tech Support  Contact Dr. Shawn Thistle
 
RRS Education on Facebook Dr. Shawn Thistle on Twitter Dr. Shawn Thistle on LinkedIn Find RRS Education on Instagram RRS Education (Research Review Service)