Spinal Manipulation May Help Reduce Spinal Degenerative Joint Disease and Disability: PART I and II
SOURCE: Dynamic Chiropractic
By James Brantingham, DC, CCF , Randy Snyder, DC, CCFC, and David Biedebach, DC, CCFC
Has the hypomobile manipulable joint lesion been demonstrated to exist? Historically the manipulable joint lesion has, from the beginning of the chiropractic profession, been described as a painful stiff joint. [1, 2] Joint stiffness, commonly called hypomobility (also known in the chiropractic profession as “fixation”) has become by consensus one of the most important aspects of the manipulable joint lesion in the professions of chiropractic, osteopathy, and manual medicine. [3, 4] Nearly 100 years of clinical agreement between three separate professions supports the existence of such a lesion although research now supports its existence.
Loss of full, or global, range of motion in the lumbar or cervical spines is an indirect proof that the segmental hypomobile manipulable vertebral joint lesion exists, because it is a fact that loss of full global range of motion occurs and such stiffness is considered an objective factor in chronic back pain.  therefore, even if this decreased range of motion is a mixture of hypermobile and hypomobile joints (i.e., a mixture of loose and stiff joints) there must be intervertebral hypomobility for global hypomobility to exist. Randomized controlled trials of manipulation documenting decreased global range of motion, and post-treatment global range of motion are growing. [6-12]
A meta-analysis of clinical trials of spinal manipulation performed by Anderson et al., clearly and strongly demonstrated that spinal manipulation is effective in restoring or increasing global, and therefore segmental lumbar mobility. Mead et al., documented post-manipulation treatment restored or increased lumbar mobility: data proving that the hypomobile manipulable joint lesion must have existed prior to treatment, and that manipulation restored to these hypomobile joints fuller mobility (Fig 1.).  Other studies have documented similar results. Nansel and his associates have demonstrated in three, multiply blinded, controlled studies, in which goniometer measurements confirmed cervical range of motion or global end range asymmetries or hypomobility, that after chiropractic high velocity low amplitude manipulation, statistically significant increased mobility was restored to the global and therefore segmental hypomobility areas: proof that global and therefore segmental hypomobility was returned to more normal mobility by manipulation. [14-16]
Treated in HospitalTreated by Chiropractor
62 cm (302 patients)
85 cm (344 patients)
Adapted from Meade et al. 
Lumbar Flexion (cm at 6 weeks)
Hvidd claimed that prior to manipulation global and therefore segmental hypomobility could be documented by cervical spine stress x-rays; that post-manipulation, global and therefore segmental hypomobility, was returned to fuller or more normal mobility.  Betge and Leung performed cineradiographic studies and claimed to have documented vertebral joint hypomobility and post-manipulation, to have observed restoration of full or fuller mobility. [18, 19] Jirout examined 250 patients with pre and post-treatment stress x-rays and claimed that those with hypomobility who received manipulation had improved, fuller, or restored mobility.  Yeoman utilized 58 case studies performing blinded pre and post-manipulation measurements to document against previously defined normal values that post manipulation mobility was significantly greater than pre-manipulation data. Yeoman used templating techniques with extension and flexion cervical stress x-rays to document the existence of segmental hypomobility and restoration of mobility to hypomobile joints as well as secondary normalization of hypermobility (Fig. 2).  Does the hypomobile manipulable joint lesion exist? And can mobility be restored by manipulation? The answer appears to be yes.
Average intersegmental motion before and after therapy. Values for motion or change are ratios of the amount of glide or tilt (horizontal movement) over the sagittal mid-body diameter. Two examples given: Male Cases C2 C3 Pre-SMT (average) 0.26 0.27 Post-SMT (average) 0.37 0.37 Normal C2 C3 Values: 0.33 0.44 Adapted from Yeoman. 
Can the hypomobile manipulable joint lesion be diagnosed?
Motion palpation as a diagnostic test to determine if a hypomobile joint exists shows mixed results. Some areas of the spine demonstrate degrees of intra and inter-examiner reliability and others do not.  Motion palpation of the spine and sacroiliac joints demonstrate, on balance, marginal to poor inter-examiner reliability and good to moderate intrarater reliability. [23-28] Manual palpation for vertebral misalignment and muscle tension appears to be unreliable.  Studies utilizing symptomatic patients point toward greater inter-examiner reliability when assessing for osseous and paraspinal soft tissue tenderness  or tenderness upon palpation of accessory posterior or anterior (joint play) movements.  In fact, the earliest chiropractic palpation techniques, dating back to founder D.D. Palmer, stressed posterior malalignment, and based upon this, lack of posterior to anterior movement. 
As previously noted, stress radiography shows some promise as a diagnostic tool for determining segmental hypomobility,  as does the goniometer; the goniometer also being capable of documenting restoration of mobility. [14-16] As Keating et al., have pointed out, there is a need to evaluate motion palpation using symptomatic, not asymptomatic patient population (as most previous studies have used asymptomatic student populations), and it is therefore too early to draw the firm conclusion as some have that motion palpation is of no value in diagnosing the hypomobile manipulable joint lesion.  It may well turn out that a combination of diagnostic tests such as palpation for stiffness tenderness, stress radiography, and goniometer measurements will best diagnose the hypomobile manipulable joint lesion. The ability to objectively diagnose the hypomobile manipulable joint lesion has improved but there is still a great deal of room for improvement.
Spinal Manipulation May Help Reduce Spinal Degenerative Joint Disease and Disability: PART II
By James Brantingham, DC, CCF , Randy Snyder, DC, CCFC and David Biedebach, DC, CCFC
Could the hypomobile manipulable joint lesion cause degenerative joint disease?
Kirkaldy-Willis believes that an episode of trauma many injure the posterior spinal joints and their associated surrounding soft tissues leading to sustained reactive muscle splitting and pain; if additional trauma or continuing postural or compressive stress is present, this stiff, painful joint, unless treated at this juncture to restore mobility, will lead to facet and disk degeneration or degenerative joint disease.  Studies which have induced hypomobility in animal joints by: placing tension springs over joints to restrict movement, producing constant compression and stiffness; making animals run on uphill treadmills producing compression, immobilizing joints, inducing post-surgical immobilization, and various other sundry methods have all led to the development of degenerative joint disease. [33-43] All of the above mechanisms result in loss of nutrition and fluid exchange leading to increasing stiffness and degenerative joint disease.
Loss of intermittent compression results in muscle, ligament, cartilage, and disc degeneration. [44, 45]
It is clear from the above that hypomobile animal joints develop degenerative joint disease but Junghanns, Baker, and Kirkaldy-Willis report similar degenerative changes in hypomobile human joints resulting from injury, trauma, and surgery, essentially the same degenerative changes as those seen in induced hypomobility in animals. [32, 46, 47] In fact, according to the work of Kapandji,  Salter,  Junghanns,  Baker,  Kirkaldy-Willis,  and Akeson,  the effects of hypomobility on human vertebral joints always results in an increased development of degenerative joint disease. It is well documented then that the nutrition and fluid exchange of cartilage, and to a somewhat lesser extent of muscle and ligament in animals as well as humans, is dependent on normal essentially full range mobility;  an observation reported by orthopedists for many years. 
Could the Hypomobility or Stiffness Which May Lead to Degenerative Joint Disease, a Known Predisposer to Injury and Disability, Produce a Positive Feedback Cycle of Further Stiffness-Injury-Degenerative Joint Disease?
The development of degenerative joint disease is an outcome of global and therefore segmental hypomobility, a reaction to chronic stiffness. Such degenerative joint disease can result in the development of complex combinations of hypo and hypermobility in spinal joints resulting in a positive feed back cycle leading to increasing global stiffness and further degeneration of joint tissues.  This increasing stiffness will predispose joints to injury and disability. Felton and O’Connell studied back injuries for the county of Los Angeles using law enforcement officers, firefighters, attorneys, investigators, lifeguards, and deputy marshals and came to the conclusion that decreased spinal mobility (decreased global and therefore segmental mobility) predisposes to increased spinal injury. 
Norgren et al., evaluated 5,093 Scandinavian soldiers to determine risk factors in producing back pain and clearly demonstrated that decreased spinal range of motion, particularly segmental mobility correlated with tenderness, was a predisposer to the increased incidence and severity of low back pain.  These studies clearly support the idea that global and therefore segmental hypomobility is a predisposer and precursor to increased injury and disability. The flip side of this equation is demonstrated in the Meade et al., study in which it was clearly demonstrated that in those low back pain patients who received chiropractic manipulation, and therefore attained documented superior restoration of mobility or increased global (and therefore segmental) mobility (as opposed to the control group of physical therapy patients), the chiropractic patients had less reoccurrences and complications, less need of additional treatment, and less disability. 
Patyn and Durinck in a controlled study followed the absenteeism rate for 12 months in 310 employees that received manipulation and 324 who received no treatment or standard medical treatment. The patients that received manipulation had 4.7 weeks of absenteeism, the other group 6.5 weeks of absenteeism (averages), clearly demonstrating that manipulation (which increases mobility) decreased disability. 
Summary and Conclusions
Has the hypomobile manipulation joint lesion been demonstrated to exist? The answer is yes. Can we diagnose the hypomobile manipulable joint lesion? Diagnosis is slowly improving, is only partial at this time, and needs improvement. After manipulative therapy have these hypomobile joints been demonstrated to have had their mobility increased or restored? The answer is yes. Can such hypomobility or stiffness develop into degenerative joint disease, lead to further hypomobility, further degenerative joint disease, and an increased predisposition to injury and disability? The answer is a qualified yes; additional research is needed to determine exactly what degree of hypomobility must develop to initiate the onset of degenerative joint disease and to predispose to injury and disability.  Such research and evidence could firmly establish that the hypomobile manipulable joint lesion is a developing pathology, in and of itself a developing disease, and a significant public health concern since, with diagnosis and manipulative treatment, injury, disability, and degenerative joint disease may not develop or develop less quickly. It is vital that the chiropractic scientific community perform this research and soon.
Can manipulation reverse global, and therefore segmental hypomobility, increase or restore mobility, possibly reverse, stop, or retard degenerative joint disease and lessen the predisposition to injury and disability? The answer appears to be yes.
REFERENCES: (PART I and II):
1. Palmer DD.
The Chiropractor’s Adjuster: The Science, Art and Philosophy of Chiropractic.
Reprinted by the Parker Chiropractic Resource Foundation, 1988. Portland, OR: Portland Printing House, 1910.
2. Smith OG, Langsworthy SM, Paxson MC.
Ceder Rapids, MI: Laurence Press, 1906.
3. Schafer RC, Faye LJ.
Motion Palpation and Chiropractic Technique.
Huntington Beach, CA: The Motion Palpation Institute, 1989.
4. Greenman PE.
Principles of Manual Medicine.
Baltimore: Williams and Wilkins, 1989.
5. Mellin G.
Correlations of spinal mobility with degree of chronic low back pain after correction for age and anthropometric factors.
Spine (Phila Pa 1976). 1987 Jun;12(5):464-8.
6. Meade TW, Byer S, Browne W, Townsend J, Frank AO.
Low Back Pain of Mechanical Origin: Randomised Comparison of Chiropractic and Hospital Outpatient Treatment
British Medical Journal 1990 (Jun 2); 300 (6737): 1431–1437
7. Howe DH, Newcombe RG, Wade MT.
Manipulation of the cervical spine — a pilot study.
J Royal Coll Gen Practitioners. 1983; 33: 574-79.
8. Evans OP, Burke MS, Lloyd KN, Roberts EE, Roberts GM.
Lumbar spinal manipulation on trial.
Rheumatol Rehabil 1978: 17: 46-59.
9. Rasmassen GG.
Manipulation in the treatment of low back pain: A randomized clinical trial.
Manuelle Medizin 1979; 1: 8-10.
10. Waagen GN, Haldeman S, Cook G, Lopez D, DeBoer KF.
Short term trial of chiropractic adjustment for the relief of chronic low back pain.
Manual Medigin 1986; 2: 63-7.
11. Zylbergold RS, Piper MC.
Lumbar disc disease: comparative analysis of physical therapy treatments.
Arch Phys Med Rehab. 1981; 62: 176-79.
12. Nwuga VCB.
Relative therapeutic efficacy of vertebral manipulation and conventional treatment in back pain management.
Am J Phys Med 1982; 61(6): 273-78.
13. Anderson R, Meeker WC, Wrick BE, Mootz RD, Kirk DH, Adams A.
A meta-analysis of clinical trials of spinal manipulation.
J Manipulative Physiol Ther 1989; 12: 419-27.
14. Nansel D, Jansen R, Cremata E, Ohami MSI, Holley D.
Effects of cervical adjustments on lateral-flexion passive end-range asymmetry and on blood pressure, heart rate, and plasma catecholamine levels.
J Manipulative Physiol Ther 1991; 14: 450-456.
15. Nansel DD, Peneff A, Quintoriaro J.
Effective of upper versus lower cervical adjustments with respect to the amerlioration of passive rotational versus lateral flexion and range asymmetries in otherwise asymptomatic subjects.
J Manipulative Physiol Ther 1992, 2: 99-105.
16. Hvidd H.
Functional radiography of the cervical spine.
Ann Swiss Chiro Association. 1963; 3: 37-65.
17. Betge G.
The value of cineradiographic motion studies in diagnosis of dysfunctions of the cervical spine.
Bul Euro Chiro Union 1977; 25 (2): 28-43.
18. Jirout J.
The effect of mobilization of the segmental blockage on the sagittal component of the reaction on lateroflexion of the cervical spine.
Neurology, March 1972: 210-215.
19. Yeomans SG.
The assessment of cervical intersegmental mobility before and after spinal manipulative therapy.
J Manipulative Physiol Ther 1992; 15; 106-114.
20. Banks SD, Willis JC.
Spinal manipulation: A review of the current literature.
Vol 4, number 3, October 1988: 1-3.
21. Keating JC, Bergmann TF, Jacobs GE, Bradley DA, Finer DC, Larson DC.
Inter examiner reliability of eight evaluative dimensions of lumbar segmental abnormality.
J Manipulative Physiol Ther 1990; 13: 463-470.
22. Panyer DM.
The reliability of lumbar motion palpation.
J Manipulative Physiol Ther 1992; 15: 518-524.
23. Haas M.
The reliability of reliability.
J Manipulative Phyiol Ther 1991; 14 (3): 199-208.
24. Haas M.
Statistical methodology for reliability studies.
J Manipulative Physio Ther 1991; 14 (2): 119-132.
25. Mior SA, King RS, McGregor M, Bernard M.
Intra- and interexaminer reliability of motion palpation in the cervical spine.
J Can Chiropractic Association 1985; 29: 195-8.
26. Carmichael JP.
Inter-examiner reliability of palpation for sacroiliac joint dysfunction.
J Manipulative Physiol Ther 1987; 10: 164-71.
27. Jull G, Bogduk N, Marsland A.
The accuracy of manual diagnosis for cervical zygapophysiol joint syndromes.
Med J Australia 1988; 148: 233-236.
28. Gonstead CS.
In W. Herbst, Gonstead Chiropractic Science and Art. USA:
SCI-CHI Publications; 1980.
29. Palmer DD, Palmer BJ.
The science of chiropractic 1906.
Reprinted by the Parker Chiropractic Resource Foundation, 1988.
30. Kirkaldy-Willis WH.
Managing Low Back Pain. 2nd ed. New York:
Churchill Livingstone, 1978.
31. Gritzka TL, Fry LR, Cheeseman RL, and La Vigne A.
Deterioration of articular cartilage caused by continuous compression in a moving rabbit joint: A light and electron microscope study.
J Bone and Joint Surg 1973; 55A(8): 1698-1720.
34. Videman T, Eronen E, and Canolin T:
Effect of motion load changes on tendon tissues and articular cartilage.
Scand J Work Environ Health 1979; 5 (suppl. 3): 56-67.
35. Evans EB, Eggers GWN, Butler JK, and Blumel J.
Experimental immobilization and remobilization of rat knee joints.
J Bone and Joint Surg 1960; 42A: 737.
36. Hall MC.
Cartilage changes after experimental immobilization of the knee joint of the young rat.
J Bone and Joint Surg 1963; 45A: 36.
37. Troyer H.
The effect of short term immobilization on the rabbit knee joint cartilage: A histochemical study.
Clin Orthop 1975; 107: 249.
38. Mooney V, and Ferguson A.
The influence of immobilization and motion on the formation of fibrocartilage in the repair granuloma after joint resection in the rabbit.
J Bone and Joint Surg 1966; 48A: 1145
39. Holm S, Nachemson A.
Variations in the nutrition of the canine intervertebral disc induced by motion.
Spine 1983; 8(8): 866-74.
40. Radin El, Burr DB.
Hypothesis: Joints can heal.
Sem Arth Rheum 1984: 13(3): 293-302.
41. Saaf J.
Effects of exercise on adult articular cartilage — an experimental study on guinea pigs with relevance to the continuous regeneration of adult cartilage.
Acta Orthop Scand 1950; (Suppl.11): 1-69.
43. Hohl M, Luck JV.
Fractures of the tibial condyle — a clinical and experimental study.
J Bone and Joint Surg 1956; 38A: 1001.
44. Kapandji IA.
The Physiology of the Joints. Vol III: The Trunk and the Vertebral Column.
New York: Churchill Livingstone 1974.
45. Salter RB:
Textbook of Disorders and Injuries of the Musculoskeletal System.
Baltimore, MD: Williams & Wilkins Co. 1970.
46. Junghans H.
Clinical Implications of Normal Biomechanical Stresses on Spinal Function.
English Language edition edited by Hans J. Hager.
Rockville, MD. Aspen Publishing 1990.
47. Baker W de C, Thomas TG, Kirkaldy-Willis WH.
Changes in the cartilage of the posterior intervertebral joints after anterior fusion.
J Bone Joint Surg 1969: 518: 736.
48. Akeson WH, Amiel D, Woo S.
Immobility effects of synovial joint: The pathomechanics of joint contracture.
Bioheology 1980: 17: 95-100.
49. Grieve GP.
Common Vertebral Joint Problems.
New York: Churchill Livingstone, 1981.
50. Turek SL.
Orthopedics Principles and Their Application.
Philadelphia: J.B. Lippincott Co. 1984.
51. Felton JS, O’Conell ER.
Muscular performance test results and back injuries.
In: Cerquiglinis Venerando A, Wartenweiler J, Editors: Biomechanics III.
Basel-Karger 1973: 50-55.
52. Norgren B, Schele R, Linvooth K.
Evaluation and prediction of back pain during military field service.
Scand J Rehab Med 1980: 12: 1-8.
53. Patyn J, Durink JR.
Effect of manual medicine on absenteeism.
J Manual Med 1991; 6: 49-53.
54. Hubka MJ.
Joint fixation and degenerative joint disease.
“The Subluxation Complex” seminar notes.
Los Angeles College of Chiropractic 1992.