Annular pancreas

Modified from The Mechanics of Spinal Manipulation, in Herzog, W (Ed) Clinical Biomechanics of the Spine, Mosby Publishers, in Press

One of the most pressing scientific issues facing chiropractic remains the delineation of the subluxation. The problem is confounded by the appearance of good clinical response to chiropractic care for patients who have a number of defined pathologies. Yet, the pathology itself remains unchanged. Clinical descriptors of patients responding favorably to manipulation/adjustment are inadequate. They lack diagnostic sensitivity; that is, they are generic measures (e.g., posture, ROM, strength, myoelectric activity) known to be affected by a number of conditions, rather than being selective to subluxation. Reliability and validity issues are unresolved for some. Recently, renewed efforts have begun to develop animal models.

These investigations are important. But their development is guided by current uncertain hypotheses about the nature of the subluxation lesion. Each of the published hypotheses, when contrasted with the spectrum of patient presentations, appears incomplete. In many ways, our quandary is analogous to that of diabetes mellitus investigators of the 1930s. They could describe the classical patient presentation and provide intervention that was beneficial. They could not describe the functional pathology, later determined to be in the Langerhans cells of the pancreas. What is needed is a unified theory of motion segment dysfunction that accounts for the range of clinical observations and comorbidities.

Biomechanical evidence compiled in a number of laboratories over the past decade supports such a unified theory of subluxation. What follows is an effort to consolidate that evidence in discussion, leading to a buckling theory of motion segment behavior.

Motion Segment Buckling

Empirically, there exist structurally undefined abnormalities associated with symptoms that respond to the clinical application of manipulation. These can be described as functional spinal lesions (FSL) that alter the behavior of the motion segment or the functional spinal unit (FSU). The observations of motion segment buckling have promise for a unified theory that links clinical observations with evidence on mechanisms of action. Similarly, it helps explain clinical response from manipulation observed in patients with co-morbid pathologies; for example, degenerative disc disease, herniated disc, instability, facet arthrosis, and spinal stenosis.

In order to account for all of the situations where manipulation appears to have some benefit, a patchwork quilt of alternative hypotheses (nerve compression, facet irritation, synovial tags, muscle spasm, etc.) must be used. Each segregates elements of the clinical picture and offers a preferred mechnaism of action, but no single theory is able to explain the rich set of observations from patients that respond to manipulation methods. However, a more general understanding of FSU biomechanical behavior is available that permits specific signs and symptoms to be explained as a function of the circumstances of injury.1,2

In its simplest form, motion segment buckling behavior represents a local, uncontrolled mechanical response to spine load environment that manifests clinically as a set of symptoms. The nature of the clinical reply is dependent upon the tissue that has been stressed by the buckling event.

The macroscopic failure of a structure may be defined as occurring by one of two means: loss of continuity (e.g., fracture) or unacceptable deformation (e.g., degenerative spondylolisthesis). In general, deformed structures (i.e., degenerative scoliosis) may work well under limited circumstances, but tend to introduce undesirable tissue stress through the remainder of a joint's functional range. By definition, mechanical buckling is a failure of the structure to sustain its loan within bounds of acceptable displacement for a given task or posture.

Buckling of a structure, either for the motion segment itself or an entire functional spinal region (FSR), may be characterized as a displacement (deformation) that is disproportionate to the increment of load applied. The phenomenon has been observed experimentally in isolated thoracolumbar and lumbar spine regions with critical loads as low as 20 N(2) and 90 N(3), respectively. With activities of daily living, the intact spine may withstand loads as high as 18,000 N(4), because of well-coordinated and timely muscle activation. However, in vivo buckling behavior confined to a single FSU has been observed during heavy exertion.5 Ill-timed or insufficient muscular response du;ring a task leaves the spine unguarded and susceptible to sudden, local, disproportionate displacement and strain.

Wilder and colleagues6,7,8 were among the first to describe buckling of isolated spine segments while attempting to study constrained mechanical behavior. Their work has demonstrated a sensitivity of the FSU to the load application point, load vector, load rate, and load magnitude.9 Normally, loads applied to the spine result in displacement of the vertebrae in direct proportion to their magnitude. The inherent constitutive properties of the tissues, as well as the stiffening action of the local muscles, are responsible for the slope of the forcedisplacement curve. Fig. 31 shows a classical displace

displacement curve. Fig. 31 shows a classical displacement in response to incremental loads. Each added increment results in a nearly equal amount of displacemnt. Below the critical value, the unit displacement per increment is a very small proportion of the total available physiologic range. Across this interval, removal of the load results in an elastic rturn of the joint toward its neutral zone. At the critical load, the addition of another increment in load is associated with a sudden, large deformation that reorients the segment near its maximum normal limit of motion. Removal of the load at this point will not allow elastic repositioning to the original equilibrium configuration. Instead, it will establish a new equilibrium near the extreme position achieved by the buckling event. Such behavior has been described for both main and coupled motions.7

Similar responses have been recorded for entire lumbar FSRs.5 Figs. 32a & b demonstrate the effects of disc injury at LS5/S1 on the characteristics of buckling. In essence, injury allows large displacements to occur at slightly lower loads than will occur in healthy discs. However, the load necessary to reach the limit of displacemtn for each FSU is much lower.

Buckling behavior is reactive under conditions much like those in which our patients find themselves. Buckling response is sensitive to the presence of degeneration and may arise from a single overloading event, or from prolonged static posture, followed by a small increment in load. Overload events that result in buckling may be rate-dependent. Exposure to vibration, a known risk factor for back disorder, enhances buckling. The production of clinical symptoms by the buckling mechanism has been documented under at least two

conditions. Wilder et al.7 imposed simulated seated vibrations on a healthy, intact disc as confirmed by discographyl. A combined flexion and lateral bend loading was applied. In both human cadaver and calf disc specimen, annular tears and disc herniations were produced in up to 75 percent of the cases tested to extreme. Cholewicki and McGill8 captured the occurrence of a painful bucling event while using videofluoroscopy to monitor lumbar spine kinematics during heavyweight lifting in a young volunteer.

The advantage of the buckling model over earlier ones is its ability to accommodate a variety of both hypothetical and evidence-based challenges. The model does not rely on a preconceived tissue's being the source of pain. Injury, neurogenic and non-neurogenic pain mechanisms, and the symptoms that may arise from the buckling event are dependent upon which tissues exceed injury threshold. Like the buckling itself, the painful tissue will be dependent on the prior health of the FSU and the nature, direction, and severity of the loading event. Thus, one can envision one or more of several possible mechanisms -for example, acute facet capsulitis from a sudden high compressive or shearing load, ligamentous or discal damage. Each possibility is based on the distribution of the peak forces and moments during buckling. Discogenic compression, with neurogenic or non-neurogenic inflammation of the nerve roots or the terminal nerve fibers of the disc, may result in either dermatomal or sclerotomal radiating pain. Finally, reflex spasm and altered motor control of both the proximal and distal muscle groups may be evoked. The increased structural stability acts to splint the area and restrict painful motion. At the same time, the model permits direct damage to other tissues in the region of the FSU, as may occur in a direct muscular strain/sprain or contact injury to the back or neck.

The buckling model builds upon the earlier clinical observations, supplemented by both direct and indirect biomechanical evidence. Perhaps its strongest feature is that it offers a testable form of hypothesis for the nature of the lesion that responds to manipulation. That lesion is conformable to specific forces and moments provided by manipulation in such a way that the symptom-generating mechanisms are reduced.

Future Legend.

Figure 31: Buckling behavior observed in an isolated lumbar FSU during flexion (F) and lateral flexion (LF) tasks. Displacements from constant increments of load are plotted. A linear force-displacement relationship exists both before and after the sudden shift to a new equilibrium orientation after the sixth increment. The new equilibrium is near the physiological limit of the FSU.

Figure 32b: Buckling behavior after injury to L5/S1 disc (after Crisco et al. 1992).

References:

1. Triano JJ. Interaction of spinal biomechanics and physiology. In: HaIdenman S (ed). Principles and practice of chiropractic, Norwalk, Appleton & Lange, 1992; pp. 242-252.

2 Cholewicki J, McGill SM. Mechanical stability of th in vivo lumbar spine: implications for injury and chronic low-back pain. Clin Biomech 1996; 11 (1): 1-15.

3. Crisco JJ III, Panjabi MM, Yamamoto I, Oxland TR. Euler stability of the human ligamentous lumbar spine. Part II experiement. Clin Biomech 1992; 7:27-52

4. Cholewicki J, McGill SM, Norman RW. Lumbar spine load during the lifting of extremely heavy weights. Med Sci Sports Exer 1991; 25 (10): 1179-1181.

5. Cholewicki J, McGill SM. Lumbar posterior ligament involvement during extremely heavy lifts estimated from fluoroscopic measurements. J Biomech 1991; 25 (1): 17-28.

6. Wilder DG, Pope MH, Frymoyer JW. Cyclic loading of the intervertebral motion segment. Proceedings of the tenth Northeast Bioengineering Conference, March 15-16, 1982. Dartmouth College, Hanover, New York: Institute of Electrical and Electronic Engineers.

7. Wilder DG, Pope MH, Frymoyer JW. The biomechanics of lumbar disc herniation and the effect of overload and instability. J Spinal Discord 1988; 1:16-52

8. Wilder DG, Pope MH, Seroussi RE, Dimnet J, Krag MH. The balance point of the intervertebral motion segment: An experimental study. Bull Hosp Jt Dis Orthop Inst. 49(2): 1989,155-169.

9. Pope MH, Wilder DG, Krag ME Biomechanics of the lum bar spine A. Basic principles. In: Frynwyer JW (ed). The adult spine- -principles and practice. New York, Raven Press, 1991; pp. 1487-1501.

Copyright American Chiropractic Association Dec 1999
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