Lumbar Spine Segmental Mobility & Stability

[KenNiemann]

Arch Phys Med Rehabil. 2005 Sep;86(9):1745-52. Related Articles, Links


Lumbar spine segmental mobility assessment: an examination of validity for determining intervention strategies in patients with low back pain.

Fritz JM, Whitman JM, Childs JD.

Division of Physical Therapy, University of Utah, and Clinical Outcomes Research Scientist, Intermountain Health Care, Salt Lake City, UT 84108, USA.

OBJECTIVE: To examine the predictive validity of posterior-anterior (PA) mobility testing in a group of patients with low back pain (LBP). DESIGN: Randomized controlled trial. SETTING: Outpatient physical therapy clinics. PARTICIPANTS: Patients with LBP (N=131; mean age +/- standard deviation, 33.9+/-10.9 y; range, 19-59 y), and a median symptom duration of 27 days (range, 1-5941 d). Patients completed a baseline examination, including PA mobility testing, and were categorized with respect to both hypomobility and hypermobility (present or absent), and treated for 4 weeks. INTERVENTION: Seventy patients were randomized to an intervention involving manipulation and 61 to a stabilization exercise intervention. MAIN OUTCOME MEASURES: Oswestry Disability Questionnaire (ODQ) scores were collected at baseline and after 4 weeks. Three-way repeated measures analyses of variance (ANOVAs) were performed to assess the effect of mobility categorization and intervention group on the change on the ODQ with time. Number-needed-to-treat (NNT) statistics were calculated. RESULTS: Ninety-three (71.0%) patients were judged to have hypomobility present and 15 (11.5%) were judged with hypermobility present. The ANOVAs resulted in significant interaction effects. Pairwise comparisons showed greater improvements among patients receiving manipulation categorized with hypomobility present versus absent (mean difference, 23.7%; 95% confidence interval [CI], 5.1%-42.4%), and among patients receiving stabilization categorized with hypermobility present versus absent (mean difference, 36.4%; 95% CI, 10.3%-69.3%). For patients with hypomobility, failure rates were 26% with manipulation and 74.4% with stabilization (NNT=2.1; 95% CI, 1.6-3.5). For patients with hypermobility, failure rates were 83.3% and 22.2% for manipulation and stabilization, respectively (NNT=1.6; 95% CI, 1.2-10.2). CONCLUSIONS: Patients with LBP judged to have lumbar hypomobility experienced greater benefit from an intervention including manipulation; those judged to have hypermobility were more likely to benefit from a stabilization exercise program.

[KenNiemann]

Hrysomallis & Goodman, A review of resistance exercise and posture realignment, J Strength Cond Res 2001;15(3):385-90, for a review.

The skeletal structure of the spine is inherently unstable, and incapable of carrying the loads imposed on it (1,2). The ligamentous cervical spine cannot carry the load of the skull (3) and as little as a 2-kilogram load at the first thoracic segment has been shown to
cause instability and buckling of the spine (2). Soft tissues, primarily muscles, are necessary to prevent instability and carry the loads imposed on the spine (1). Ligaments contribute little to primary spinal stability (4,5), acting as sensors for the activation of muscles first, and then as secondary stabilizers (6). It is
muscles that provide motion and are the primary stabilizers of posture, and the spine. In a relatively simple model of the thoracolumbar spine which included the stabilizing effect of muscles, a physiological load 20 times greater than that which caused buckling
in the skeletal spine resulted in only minimal muscle activations to support and stabilize the passive spine (7).

This is all, pretty much, done through passive *resting tone*, known as thixotropy. There is an academic argument whether even quiet standing is due to resting tone.

1. Panjabi M, Abumi K, Duranceau J, Oxland T. Spinal stability and intersegmental muscle forces; a biomechanical model. Spine 1989;14(2):194-200.

2. Panjabi MM. The stabilizing system of the spine. Part I. Function, dysfunction, adaptation, and enhancement. J Spinal Disorders 1992;5(4):383-389.

3. Panjabi MM, Cholewicki J, Nibu K, Grauer J, Babat LB, Dvorak J. Critical load of the human cervical spine: an in vitro experimental study. Clin Biomech (Bristol, Avon) 1998 Jan;13(1):11-17.

4. Solomonow M, Zhou B-H, Baratta RV, Lu Y, Harris M. Biomechanics of increased exposure to lumbar injury caused by cyclic loading: Part 1. Loss of reflexive muscular stabilization. Spine 1999;24(23):2426-2434.

5. Cholewicki J, McGill SM. Lumbar posterior ligament involvement during extremely heavy lifts estimated from fluoroscopic measurements. J Biomechanics 1992;25(1):17-28.

6. Williams M, Solomonow M, Zhou BH, Baratta RV, Harris M. Multifidus Spasms Elicited by Prolonged Lumbar Flexion. Spine 2000 Nov 15;25(22):2916-2924.

7. Kiefer A. Shirazi-Adl A, Parnianpour M. On the stability of human spine in neutral postures. Eur Spine J 1997;6:45-53.

8. Koumantakis GA, Watson PJ, Oldham JA. Trunk muscle stabilization training plus general exercise versus general exercise only: randomized controlled trial of patients with recurrent low back pain.Phys Ther. 2005 Mar;85(3):209-25.

9. Lindgren K-A, Sihvonen T, Leino E, et al. Exercise therapy effects on functional radiographic findings and segmental electromyographic activity in lumbar spine instability. Arch Phys Med Rehabil. 1993;74:933–939.

10. Bullock-Saxton J, Murphy D, Norris C, Richardson C, Tunnell P. The muscle designation debate: the experts respond. J Bodywork Move Ther 2000;4(4):225-241

11. Wittink H, Hoskins Michel T, Wagner A, Sukiennik A, Rogers W. Deconditioning in patients with chronic low back pain: fact or fiction? Spine 2000 Sep 1;2(17):2221-8.

12. Verbunt JA, Seelen HA, Vlaeyen JW, van de Heijden GJ, Heuts PH, Pons K, Knottnerus AJ. Disuse and deconditioning in chronic low back pain: concepts
and hypotheses on contributing mechanisms. Eur J Pain 2003;7(1):9-21.

13. Picavet HS, Schuit AJ. Physical inactivity: a risk factor for low back pain in the general population? J Epidemiol Community Health 2003 Jul;57(7):517-8.

14. Verbunt JA, Seelen HA, Vlaeyen JW, Van Der Heijden GJ, Knottnerus JA. Fear of injury and physical deconditioning in patients with chronic low back
pain. Arch Phys Med Rehabil. 2003 Aug;84(8):1227-32


15. Indahl A, Haldorsen EH, Holm S, Reikeras O, Hursin H. Five-year follow-up study of a controlled clinical trial using light mobilization and an informative approach to low back pain. Spine 1998;23:2625-2630.

16. Liebenson CS. Improving activity tolerance in pain patients: A cognitive-behavorial approach to reactivation. Top Clin Chiropr 2000;7(4): 6-14.

17. Liebenson CS. Motivating pain patients to become more active. Journal of Bodywork and Movement Therapies, 3;143-146, 1999.

19. Moore JE, Von Korff M, Cherkin D,et al. A randomized trial of a cognitive-behavioral program for enhancing back pain self-care in a primary care
setting. Pain 2000;88:145–53.

20. Waddell G: A new clinical model for the treatment of low-back pain. Spine 12:634, 1987.

21. Victorian WorkAuthority – Clinical Framework -
www.workcover.vic.gov.au/dir090/vwa/home.nsf/pages/chiropractors

[KenNiemann]

No Magic Bullet?

[KenNiemann]

Hurwitz EL, Morgenstern H, Chiao C. Effects of Recreational Physical Activity and Back Exercises on Low Back Pain and Psychological Distress: Findings from the UCLA Low Back Pain Study. Am J Public Health 2005; 95:1817-1824.

Biering-Sorensen F. Physical measurements as risk indicators for low-back trouble over a one-year period. Spine 1984;9(2):106-119.

Bullock-Saxton J, Murphy D, Norris C, Richardson C, Tunnell P. The muscle designation debate: the experts respond. J Bodywork Move Ther 2000;4(4):225-241.