The Functional Spinal Lesion:
An Evidence-Based Model of Subluxation

This section is compiled by Frank M. Painter, D.C.
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FROM:   Topics In Clinical Chiropractic 2001 (Dec); 8 (1): 16–28 ~ FULL TEXT

John J. Triano, DC, PhD

Chiropractic Division, Texas Back Institute,
6300 W. Parker Road, Plano, TX 75093-7916

Purpose:   Theoretical foundations for the subluxation model are reviewed and compared with new evidence. Understanding the mechanisms of the lesion will further refine chiropractic theory and empower the elaboration of techniques to improve treatment outcomes and quality of patient care.

Methods:   Literature from multiple scientific and clinical disciplines was surveyed with emphasis on evidence related to the concepts of subluxation and manipulation.

Summary:   The buckling model builds on clinical observations and supplements them with both direct and indirect biomechanical evidence. This model does not preconceive or proscribe any source of symptoms, but is able to accommodate the multifaceted clinical presentations of patients who respond favorably to manipulation/adjustment. It also can sustain a variety of hypothetical and evidence-based challenges. These findings offer an opportunity to reconceptualize and refine theoretical models of the spinal lesion into a platform for scientific, clinical, and political advancement of the profession.

Key words:   biomechanics, orthopaedic manipulation, spine, theoretical models


Spinal manipulation and adjusting have a long history, stretching from ancient Greece through medieval England and the Far East. The chiropractic profession was founded on empirical observations suggesting a role for spinal structure influencing patients' function and health. A number of explanations on how the mechanics of vertebral subluxation/somatic dysfunction may impact physiology have been offered. [1, 2] Since 1975, with the first multidisciplinary scientific conference on the research status of spinal manipulation, the clinical science of manipulation has made substantial strides. Over 50 clinical trials have been completed, with a preponderance of evidence supporting the use of manipulation for management of acute back pain [3] and, to a lesser extent, subacute and chronic back pain, neck pain, and headache. [4–8] Internationally, several formal guidelines for the management of spine-related disorders now recommend manipulation/adjustment as a first line of care. In response to increased interest and the need for answers to fundamental questions, the chiropractic profession recently has begun to prioritize the development of theory and the definition of its unique body of knowledge as a discipline. [9]

While clinical evidence has begun to evolve, basic science data have lagged behind, due in part to a general lack of solid information on the pathophysiologic nature of spinal disorders in general. [10] Traditional pathophysiologic models, typical of health care, have failed to predict adequately spine injury, prevention, disease, or recovery. Although evidence exists for anatomic and degenerative abnormalities as potential pain generators, their presence alone is neither necessary nor sufficient to produce symptoms or disability. Similarly, normal structure can be present in an individual with disabling nociceptive pain. The focus of much research has been on morphology in addition to the processes of inflammation, pain mediation through peripheral and central mechanisms, and psychological factors influencing the degree to which patients suffer. [11–13] Speculation on neurophysiologic, kinetic, biomechanical, trophic, and psychosocial mechanisms of subluxation/spinal dysfunction abound in chiropractic literature as well, but remain primarily deductive. [14, 15] The present work reviews developments in the field of biomechanics that relate directly to the subluxation concept and its resolution through manipulation/adjustment. [16, 17] Understanding the mechanisms of the lesion development and of manipulation will further refine chiropractic theory and empower the elaboration of techniques to improve treatment outcomes and the quality of patient care.

      Concepts Underlying Clinical Biomechanics 

There are compelling reasons to study the fundamental mechanics of subluxation and spinal manipulation procedures, First, biomechanics is the language by which the spine – and joints in general – manifests its function. Through studies of successful treatment methods, for example, it may be possible to reconstruct the biomechanical elements of the underlying lesion or lesions leading to better treatment and prevention, Second, there is need to comprehend the loads that act on the spine during the administration of these procedures. On the one hand, we must respond to the legitimate concerns of society for generally safe procedures and warrant, in unequivocal terms, their trust. At the same time, detailed knowledge of the forces and moments that are induced by our procedures give us the tools by which we can better refine them and match procedures to patient need on an objective basis. Third, if we are to be more successful and convincing in communicating our model of health, we must be able to communicate in terms understandable to the broader communities of health care and policy makers. Last, with quantitative knowledge, we are able to develop high clinical standards for skill and training that are testable, [18–20] anchoring our claim for jurisdictional control of our science. [21]

Albert Einstein used an elegant refinement of the oft-quoted chiropractic philosophical notion of theory to "keep it simple." Einstein's version is paraphrased:

“everything should be made as simple as possible, but not simpler.” [22]

The biomechanics of forces and moments applied to the human body can be both mathematically and physiologically complex. The concepts of lesion development and its correction, however, are relatively straightforward with an understanding of some basic biomechanics. Such information is not simply heuristic but is pragmatically applied. Understanding how the effects of treatment may be affected by age, degeneration, and traumatic changes, combined with manipulation control strategies. [17, 23] provides a rich armamentarium for dealing with a wide variety of problems, from the simple to the complex.

      Biomechanical Characteristics Of Manipulation 

Manipulation uses externally applied forces and moments, targeting a joint assembly. [17, 24, 25] The procedures may be characterized by their biomechanics to supply a simple system that accommodates all of the available techniques. Table 1 summarizes these categories based on current scientific knowledge.

Table 1.   Manual procedures classified according to biomechanical characteristics. Loads listed represent published means, where larger sample sizes are available, or typical values for smaller samples.

Procedure type    Subgroup              Mode         Load                 Speed
Unloaded spinal   Continuous passive    Mechanical   Periodic [<20% BW,      
motion            motion (CPM)                       <5% BMI]             0.53 Hz
                  Flexion-distraction   Manual       Periodic             <0.50 Hz 

Mobilization Manual Periodic (~150 N*) <2.00 Hz High-velocity, low-amplitude manipulation procedures Manual Manual Impulse [<560 N, <140 msec <84 Nm] Mechanical assist CPM Manual + Periodic + Summed mechanical impulse Impulse hammer Manual + Impulse (<150 N*) <20 msec mechanical
* Typical value. BW = body weight; BMI = body mass index.

The high-velocity, low-amplitude procedure, most often considered the primary treatment used by chiropractors, [26] produces a brief impulse (100–300 msec) load [17, 25, 27–30] into the region of an osseous joint. In recent years, Herzog's group in Alberta, Canada, has provided evidence of absolute and relative intervertebral movements resulting from manipulation. [25, 31–33] The concept of Sandoz [34] that synovial joints may be stretched into the "paraphysiologic" joint range is supported. If cavitation (rapid separation of the joint surfaces with formation of an intra-articular gas bubble in the synovial space of the joint) occurs, an audible "pop" can often be heard. [35]

Brodeur [36] reviewed literature on joint cavitation, particularly the work of Sandoz [34] and Mierau et al [37] that studied the characteristics of cavitation in depth. Mierau et al's work provided the first experimental evidence of increased range of motion after joint cavitation. The boundary separating physiologic and paraphysiologic motion has not been mapped, and its exact relationship to cavitation is not known. Empirical experience suggests that cavitation also may occur before reaching the paraphysiologic space. Regardless of timing, biomechanical behavior of joint structures is known to change following manipulation/adjustment. [37–39] The advantage, from a biomechanical standpoint, of altered behavior of the joint is a shift in load-bearing stresses that are transmitted.

      Theoretical Mechanics of Spinal Lesion and Dysfunction

Effective manipulation acts on a lesion that is conformable to specific forces and moments in such a way that mechanical stress concentrations resulting in symptoms are altered. Sustaining beneficial clinical effects depends on the ability for repair of any tissue damage and for return to the pre-injury function. Many independent hypotheses have been advanced to account for various aspects of the clinical presentations seen with patients that seem to respond favorably to treatment. The autonomy of each of these interpretations limits the ability to generalize to the spectrum of patients who seem to respond favorably when treated. This section reviews the principal features of the main theories and shows how each may be understood in the context of a unified theory of the lesion, based on biomechanical evidence.

Traditionally, the manipulable disorder (termed "subluxation" in chiropractic, "somatic dysfunction" in osteopathy, and "fixation" or "functional blockage" in manual medicine) has been characterized as a spinal joint strain/sprain with associated local and referred pain and muscle spasm. [40] This may be too narrow a perspective as will be shown in the material that follows. Spinal joint function is assumed to become restricted or deranged in some fashion, either as an isolated lesion at single or multiple levels, or in combination with other pathology. [16, 17] Several mechanisms for restricted function (fixation, blockage, hypomobility) have been proposed, but definitive work on their viability remains to be done. Proposed mechanisms for such hypomobility include the following:

  • Zygapophyseal joint entrapment of an inclusion or meniscoid (heavily innervated by nociceptors)

  • Anular fragment entrapment at the intervertebral disc that is innervated by nociceptors

  • Adhesions and scar formation from earlier injury and/or degenerative change resulting in stiffness and adaptive myofascial shortening

  • Hyperactive (spastic, hypertonic) deep intrinsic spinal musculature in unilateral, asymmetric patterns

Mechanisms of action from manipulation that have been proposed to affect mechanics include releasing entrapped synovial or disc tissues, reducing pain and restoring mobility, breaking adhesions, and stretching myofascial tissues. [40] Again, the effects on local tissues within the joint structures require much more research before they can be determined.

Clinically identifying the lesion requires deductive reasoning from the history and examination. The same data are often useful in selecting the preferred treatment method. Specific procedures are matched to the patient's condition through provocative testing [23] that evaluates the joint tolerance to a given technique. Modifications in manipulation loads transmitted through the lesioned segment can follow, based on knowledge of the local anatomy, pathology, and response to provocation. Such strategies are aimed at varying the effects of treatment and may include alterations to the patient's initial position in preparation for the procedure, using static or dynamic preload, or altering direction and amplitude of loading. All of these steps are mechanical in nature, and they involve an understanding of the biomechanical actions at the articulation when they are taken.

The core concepts describing the lesions have evolved from multiple sources and may carry different meanings to different groups, [2, 41, 42] Table 2 relates symptoms by presenting complaint, pathoanatomic diagnoses, or speculation on the symptom generator. Patients labeled with these descriptors may benefit from manipulation. [43] This observation raises several scientific considerations that might include the following:

  • What is the precise nature of the disorder being treated?

  • Are there subcategories of lesion that might better be treated by one form of manipulation over the others?

  • Might some patients respond better to one intervention compared with another?

  • Are there clinically observable characteristics of spinal dysfunction that allow for an accurate prognosis (based on response to treatment)?

Table 2.   Diagnostic terms that relate symptoms by presenting complaint, pathoanatomic diagnosis, or speculation on the symptom generator

Grouping factor             Diagnosis                                   
Hypothetical                Subluxation/subluxation complex 
concept                     Osteopathic lesion/somatic dysfunction 
                            Joint/segmental dysfunction 
                            Manipulable lesion

Pathoanatomy                Facet syndrome 
                            Disc bulge/protrusion/herniaion
                            Internal disc derangement 
                            Spinal stenosis 
                            Costovertebral syndrome 
                            Myofascial syndrome 

Complaint                   Low back pain/lumbalgia 
                            Neck pain!cervicalgia 
                            Thoracic pain 

      Modeling Spinal Lesions

Classical chiropractic theory favors the term "subluxation" to characterize the spinal lesion. Leach [44] and Gatterman [2] offered reviews of chiropractic reasoning incorporating indirect, sometimes remote, evidence from the literature to correlate or explain clinical observations. Traditional spinal lesion concepts reflect clinical observations. Most early concepts imply an independent lesion. However, more recent opinions acknowledge common comorbidity between subluxation and common pathoanatomic states. [14, 43, 45–47] Descriptive terminology such as subluxation syndrome or subluxation complex has been proposed in an attempt to better convey this concept. [2, 42]

In the fields of manual medicine and osteopathy, Dvorak and Dvorak, [48] Lewit, [49] and Greenman [50] argued similarly to explain clinical observations. Ignoring the syntax of respective schools of thought, [2, 15, 42] the similarities in concepts between the disciplines are striking. Over 106 different terms have been used to define the spinal lesion over the years, with agreement among authors occurring for only nine of them. The motivation for some of the terms seems less to foster scientific and clinical utility than to differentiate professional or philosophical domains. Figure 1 groups terms according to historical consensus regarding the speculative nature of the lesion itself. Over 60% of the proposed definitions reference physical constructs (mechanical/anatomic/structural). Over 20% are ambiguous, as the terms are self-referencing, incorporating the term (or a derivative) being defined.

Based on clinical observations, speculative mechanisms have included mechanical (eg, restricted range of motion), neurologic (eg, aberrant reflexes, hypertonicity), trophic (eg, inflammatory change), or even psychosocial (eg, stress in the form of muscle tension) [15] elements. A summary of the early writings of Palmer outline four required components of subluxation:

(1) articular misalignment,

(2) narrowing of the intervertebral foramen,

(3) nerve pressure, and

(4) interference with nerve function. [51]

While elements of this cascade may be present in any given case, Boone and Dobson [51] correctly point out that there is "insufficient," even contradictory, data for such a narrow and circumscribed model. Dishman [52] and Lantz [14, 53] expanded the Palmer model in an effort to account for pathomechanical, biochemical, and physiologic components without proscriptive focus on a given sequence.

Leach [44] and Mootz [15] supplement the hypotheses on subluxation seemingly to reconcile explanations shared with other disciplines that use manipulation methods (Table 3). Leach [44] suggests that subluxation is a form of manipulable lesion. Other modem terms include "somatic" or "segmental" dysfunction. [48, 50] Together they encompass a disturbance of the internal behavior of the functional spinal unit that is reversible. The lesion is an impairment of mobility caused by various forms of mechanical overload and may have remote effects, influencing the vascular, lymphatic, or neural elements. Regardless of origin, there appears to be a cross-discipline consensus that these altered biomechanical behaviors may manifest as local and/or remote clinical signs and symptoms.

Table 3.   Historical versus supplemented models of subluxation and the clinical observations associated with them

Historical model            Supplemental model       Clinical observations
Subluxation                 Subluxation complex      Local symptoms 
 • Vertebral misalignment    •  Kinesiopathology      •  Altered range of motion 
 • Narrowed IVF              •  Myopathology          •  Hypo/hypertonicity 
 • Nerve pressure            •  Neuropathology        •  Pain/paresthesia 
 • Nerve interference        •  Vascular pathology    •  Redness/swelling 
                             •  Connective tissue     •  Adhesions/degenerative change  
                                                       Remote symptoms 
                                                        •  Radicular symptoms 
                                                           - Pain 
                                                           - Paresthesia 
                                                           - Dysesthesia 
                                                           - Dysautonomia 
                                                        •  Radicular symptoms 
                                                        •  Organ dysponesis

IVF = intervertebral foramen.

      Biomechanical Concepts Relevant to Modeling the Spinal Lesion

Table 4 reviews biomechanical properties of living tissue that are relevant to modeling the spinal lesion. Posture and muscle activity, under normal conditions, are considered a response to the tasks being performed. However, a variety of postural choices may be available, dictating how loading of the spine actually occurs. Differing strategies may be effective in accomplishing the same task but may have different metabolic or mechanical costs. Typically, optimal postures minimize the local stresses by reducing muscular tension, joint compression, [54] or segmental displacement. [55]

Table 4.   Biomechanical properties of tissue that are relevant to modeling the spinal lesion

  • Balance point:   A small region within the neutral zone where, when a compressive load is applied, there is no movement. This location is uniquely different for each segment but generally near, but posterior to, the geometric center. It may be more right or left of the midline.

  • Coupled motion:   Complex motion involving components in all three cardinal planes (multi-planar).

  • Creep deformity:   A viscoelastic property of tissue that results in a time-dependent increase in strain when under constant load.

  • Dynamic equilibrium:   A condition where forces or moments acting on a structure invoke change in position or velocity that is mathematically offset by the inertial load created by its movement.

  • Elastic zone:   A subcomponent within the range of motion, generally away from its center, where there is a predictable relationship between the amounts of displacement that occur with a given applied load.

  • Functional spinal unit (FSU):   A mechanical linkage between two adjacent vertebrae and the intervening disc, connecting ligaments, and muscles.

  • Functional spidal region (FSR):   A complex mechanical linkage system of multiple functional spinal unit (FSU)s. The boundaries of an FSR vary with the task being performed and the identity of attaching muscles recruited.

  • Hysteresis:   The difference between rate of deformation of a tissue and its recovery in an elastic deformation. The amount of hysteresis reflects the amount of energy absorbed by the tissue.

  • Inertial load:   The effective force or moment generated by the effect of body segment mass in motion.

  • Motion segment buckling:   A local, uncontrolled mechanical response to spine load environment that manifests clinically as a set of spine-related symptoms.

  • Neutral zone:   A region of potential resting positions for the functional spinal unit (FSU). It is a subcomponent within the range of motion, generally near its center, in which very small applied loads result in relatively large displacement.

  • Normal segmental motion:   The boundaries of motion by a healthy functional spinal unit (FSU) are often noted as the normal range of motion. However, the behavior of the functional spinal unit (FSU) within its anatomic limits may vary based on the task, initial starting position, and order of recruitment of attached muscle.

  • Range of motion:   The sum of the neutral zone and elastic zone, on both sides of the center.

  • Static equilibrium:   The balance of forces and moments acting on a structure under static conditions that results in no change in its position, or, if moving, its velocity.

  • Stress concentration:   Localized increase in tissue stress resulting from change in the distribution of load to the tissue, dimension of the contact area between structures, or dimension of the load-bearing structure (eg, from creep deformity).

Recent, Relevant Biomechanical Research

      Spinal movement

Intersegmental motion is mechanically complex. The path of motion taken by an individual vertebra is determined by the geometry of the bone-disc-bone junction. Generally, there are common geometric features within functional spinal regions (FSRs) that guide coupling of multi-planar motions (Table 5). Geometry is not the only guiding factor, however. Movement may be modified, within limits, by muscle recruitment patterns, [56] the initial posture as a task begins, [57] tissue condition, [58] and so forth. That is, the coupled motions change ratio according to spinal region (eg, C2 rotation versus lateral bend at 3:2, decreasing to 1:7.5 at C7) [48] and whether the functional spinal unit (FSU) begins its motion in flexion or extension. [59]

Table 5.   Intrinsic limiting factors that influence mechanical functioning of vertebra

FSU geometry                 Vertebral dimensions  
                              •  Body height 
                              •  Pedicle length 
                              •  Facet orientation 
                              •  Articular height 
                             Soft tissue dimensions 
                              •  Disc fiber orientation and thickness 
                              •  Ligament lengths and thickness 
                              •  Muscle lines of action and strengths 

Tissue properties            Stiffnesses   
                              •  Axial 
                              •  Torsional 
                             Elastic modulus 


Tasks                        Moment loads 
                              •  Flexion 
                              •  Lateral bending 
                              •  Rotation 
                             Axial loads 
                              •  Compression/tension 
                              •  Anteroposterior shear 
                              •  Lateral shear

FSU = Functional spinal unit 

      Pelvic and sacroiliac motion

Pelvic motion exhibits even greater complexity. [60, 61] Body weight and the working loads from activity are transmitted downward and are balanced by reaction forces and moments from the lower extremity. Motion within the sacroiliac (SI) joints dampens descending loads [60] much the same as knee flexion suppresses shock to the spine from heel strike during gait. [62, 63] The direction of motions within the pelvic components, however, is not as straightforward as previously believed. Generally, behavior of the innominate has been held to correspond with ipsilateral movement of the pelvis and the lower extremity as a whole. [60, 64] Information that is more recent shows that this pattern is correct for only a portion of the population. Smidt et al [61] found considerable symmetry of pelvic movement during gait. The direction of SI motion, on the other hand, often varies from the expected pattern, falling into one of three subgroups. In one subgroup, the SI joints move in one direction only, regardless of the stride being taken. In a second group, the ilium moves in concert with the leading leg, while the remainder shifts that motion to the contralateral SI joint.

      Ligament stretches from coupled motions

Weight bearing and movement result in the loading of the spinal components. An intricate coordination apportions load sharing between both active and passive tissues. Distribution depends on the task, posture, and muscular fatigue. Flexion-relaxation phenomenon during trunk flexion is an example. [65, 66] As the lordosis of the lumbar spine straightens, the muscle activity controlling the movement ceases. The spine then "hangs" on its ligaments. Complex motions can result in high stresses to the spinal tissues, but only a few studies have focused on the load-sharing capacity. [67–72] Specific ligaments may be primarily responsible for controlling select movements when muscular action is not effective [72] Pure lumbar flexion produces stretching of the posterior ligaments. Twisting motions principally engage the capsular ligaments. Combined movement stretches the facet capsules and intertransverse and capsular ligaments, with relative sparing of the supraspinous and interspinous structures.

      Structural equilibrium

Mechanical failure can be defined as an excessive deformation or loss of continuity (fracture or tearing) of one or more of the tissues. [73] Degenerative spondylolisthesis might be considered a model of failure by deformation, whereas spondylolitic spondylolisthesis could serve as an example of failure by discontinuity. Under conditions of healthy function, mechanical equilibrium serves to transmit load without physical failure.

The balance of forces acting on a joint (static or dynamic equilibrium) must be maintained both during static postures and when there is movement. [74] In the static form, there is little to no motion and the inertial loads from the body segment masses are negligible. For normal activities of daily living, the inertial effects can be significant, and dynamic equilibrium becomes meaningful.

All of this may seem academic. However, it becomes clinically relevant during the normal day, for example, when a worker becomes fatigued. As trunk muscles tire, there is a redistribution of load to auxiliary muscles and ligaments [75] along with kinematic changes in spine behavior during lifting tasks. The motions in the primary direction decrease up to 10% while functional spidal region (FSR) coupled motions increase by as much as 50%. With repeated lifting tasks, similar changes are seen in the lower extremities when postural stability is lost. [76] The use of suboptimal strategies increases the risks for injury. [77]

Figure 2

Equilibrium of the functional spinal unit (FSU) is made even more interesting by the different behaviors of subregions within the normal intersegmental range of motion. The load-displacement curve (Figure 2), derived by applying measured loads while simultaneously recording motions, can illustrate the roles of particular spinal tissues. Load-displacement tests show that the range of motion is divided into a neutral zone and an elastic zone (see Table 4 for definitions). The ratio may vary from person to person; for example, at C2 the neutral zone may vary by as much as 21°. [78]

Work like that of Kumaresan et al, [79] Pintar et al, [80] Yoganandan and Pintar, [81] Luttges et al, [82] and Schultz et al [65, 83, 84] represent examples in which the properties and limiting factors of functional spinal unit (FSU)s and functional spidal region (FSR)s have been tested (Table 5). Stresses induced by lateral and posterior shear, axial compression, and flexion are absorbed primarily by the disc. The facets play a major role for anterior shear and axial torques with increasing contact forces. [85, 86]

Clinical Implications

      Spinal pain production

The interaction of biomechanics, biochemistry, and neurophysiology may explain complexities encountered in the management of spinal pain. Nociception related to the functional spinal lesion (FSL) is initiated by the mechanical event of buckling. The pain may be immediate from acute tissue insult or delayed from accumulated trauma or degeneration effects. Typically, treatments directed purely at moderating structural aspects of a patient's problem are frustrating. [11, 12] Local compressive, tensile, or shearing forces are responsible for acute injury. Tissue failure precipitates a cascade of biochemical and physiologic events and drives chronicity of the case. Secondary effects, resulting from the cascading biological responses, may become primary pain generators requiring additional modes of treatment. Persistent nociceptive pain may result in increased sensitivity of peripheral nerve endings (peripheral sensitization) and spinal cord neurons (central sensitization). Normal mechanical stimulus and movement then become painful. [87, 88] If the internal biochemical milieu of the disc degrades, the neurotoxicity of breakdown products (eg, phospholipase A2) develops a chemically mediated inflammation or irritation of neural elements. Under these sets of conditions, the patient may benefit most from a multidisciplinary treatment strategy. Chiropractic manipulation/adjustment is used to correct the mechanical element while analgesic/anti-inflammatory medication (oral or local joint/nerve injection) is given to resolve the biochemical component.

      Effects of mobility and immobilization

Movement maintains articular and periarticular tissue properties. The viscoelastic properties and ultimate strengths of the various tissue components are maintained by periodic deformation under different loads and speeds. Sustained or excessive repetitive load gradually invokes creep deformity, increasing tissue hysteresis and altering its ability to elastically rebound. [89] A 20–minute static bending task exhausts much of the elastic properties of the spine. After a 2–minute rest, it recovers only half of its normal stiffness. After 30 minutes, measurable joint laxity can be demonstrated. Prolonged static postures, even at low intensities, eventually become uncomfortable because of creep with local tissue stress concentration. [90] In practical terms, this means that heavy exertions should be avoided after prolonged static postures, particularly at the extremes of position. As mentioned earlier, muscle fatigue aggravates the risk by altering recruitment patterns and increasing coupled motions of the functional spidal region (FSR).

Under rapid loads, there is insufficient time for viscoelastic response. Tissue stress values are higher, and failure may occur at lower amplitudes than with sustained forces.

Repeated short periods of immobilization are as harmful as prolonged immobilization lasting up to 3 months. [91–93] A cascade of structural changes (Table 6) begins when the elastic potential of the tissues is not exercised. Without movement, physical shortening of the collagen fibers leads to periarticular fibrosis. Capsular tension increases, and the joint cartilage experiences a chronic increase in compressive stress. Fibrillation and atrophy of the articular cartilage may begin as early as 4 weeks. Videman [92] found similar cumulative effects from repeated short periods of immobilization in as little as 36 days.

Table 6.   Cascade of tissue changes that may result from relative immobilization of an articulation

Early changes                   Capsular contracture
                                Capsular adhesions

Later changes                   Muscular atrophy 
                                Fibrofatty joint infiltration 
                                Disuse osteoporosis 

Degenerative changes            Cartilage changes 
                                 •  Fibrillation 
                                 •  Erosion 
                                 •  Intracartilaginous cysts 

                                Degenerative arthritis

Symptoms                        Joint stiffness 
                                Joint pain 

      Effects of the neutral zone, hysteresis, and degeneration

The concept of a "normal" rest position for an functional spinal unit (FSU), as commonly represented for static and motion palpation procedures, is technically erroneous. Because of the neutral zone component of range of motion, a vertebra cannot be expected to reliably return to a fixed starting position in relation to its adjacent member. Differences in static resting positions are likely to occur in normal, healthy subjects. Fortunately, the variation for much of the spine is small. Specific ratios vary for each segment. In general, the neutral zone in the cervical spine is proportionately larger than in the lumbar spine. Hysteresis compounds the problem. Prolonged static posture, or repeated activity, results in a temporary shift in the stiffness properties that influence the ability of the vertebra to elastically return to a prescribed initial position. It is no wonder that reliability of static and motion palpation techniques has been so difficult to achieve. Schram [94] demonstrated this problem as early as 1982 when he attempted to measure pre- and post-treatment changes of location in the upper cervical spine vertebrae. The posttreatment location proved to be unpredictable and random.

All structural properties may be affected by the processes of aging and degenerative change, and they influence the potential to withstand stress and to repair. Yoganandan et al [95] demonstrated that degenerative disease reduces the capacity for structural loading by one half and the energy absorption by the intervertebral joint to one third. Recovery time frames may depart substantially from experimental evidence from acute injury, confounding long-term prognosis. Injury severity is not clinically quantifiable. Apparently serious injury may recover rapidly with no residual. Minor damage superimposed on degenerative disease may evoke a more severe early symptom picture that then recovers more quickly than expected. It also may evoke persistent symptoms because of the preexisting degenerative changes that prolong recovery. Making matters more complex clinically, psychosocial factors that different individuals display may lead to increased suffering and illness behaviors. [13]

Aging, like injury, is not a uniform process. [96] Age-related changes are an interplay of environmental and genetic factors. Aging reduces tissue compliance, strength, and physiologic endurance. [95, 97] Effects accelerate after age 76. Reduction in bone strength with age is well known. Bone density and strength decline in proportion to lean body mass. [98, 99] Static and dynamic muscular action decrease by 5% after age 45, Muscle endurance falls at a rate of 1% per year. Most muscle capacity changes result from the sedentary lifestyles that seem to go along with advancing age. [100–102]

Aging has serious effects on joint and disc cartilage, proteoglycan concentrations decrease, link proteins fragment, and the size of chondroitin sulfate chains reduce in articular cartilage. The osmotic pressure that retains water content within the matrix drops. [103] leading to roughening of the joint surface. Similarly, the intervertebral disc undergoes desiccation from loss of the mucopolysaccharides and osmotic pressure, Loss of disc height may or may not occur. [104] Clinically, changes appear as spondylosis, osteophyte formation, ligamentous and articular capsular hypertrophy, and osteoarthrosis. [105]

The nervous system also ages. Decreases occur in sensory sensitivity, reflex activity, and innervation of muscle spindles. [106] Collectively, these changes affect balance and posture, and how loads are distributed across a joint. [107, 108]

A Unified Theory of Spinal Lesions

The earlier review briefly described the patchwork of alternative hypotheses used to explain the rich set of observations from different patients that respond to manipulation methods. Empirically, structurally undefined abnormalities appear to respond to manipulation/adjustment. Often described by many terms, they might best be described as FSLs that alter the biomechanical behavior of the functional spinal unit (FSU). The FSL, arguably, may provide more general understanding of how such a wide range of signs and symptoms can be explained as a function of the circumstances of injury, [24, 55, 109] The simplest model that fits the various clinical observations is one of mechanical buckling within the functional spinal unit (FSU) or functional spidal region (FSR).

In simplest form, buckling behavior is a failure by unacceptable deformation for the operating conditions of the joint and the task being performed. It represents a local, uncontrolled mechanical response to a spinal loading environment that manifests clinically as a set of symptoms (Tables 3 and 4). Buckling may be characterized as a displacement that is disproportionate to the load imposed by the task. That is, when buckling occurs, the affected area of the spine reaches its maximum range under lower load conditions. It is operating at its extreme, out of phase with the demands of the task. A functional configuration operating at extremes results, by definition, in altered stress distribution within the functional spinal unit (FSU). But, does theoretical buckling occur in the real world? Is there independent evidence?

The concept of the FSL is similar to that of compressive buckling injury to the wrist. [110–112] The functional spinal unit (FSU) meets the biomechanical criteria for a multimuscular, biarticular chain that may be subject to "zigzag" collapse [112, 113] or buckling. Buckling in the spine is opposed only by appropriate muscle recruitment for a biomechanical task. The FSL begins with a mechanical overload. It may be either a single traumatic event or aggregate with multiple repetitions. Experiments [63, 114–116] have produced these effects in isolated spine segments under conditions where a single functional spinal unit (FSU) is incrementally loaded at the balance point. When a critical load is reached, the force-displacement behavior is interrupted by a disproportionately large displacement. The total distance, however, remains within the normal functional range.

Figure 3

Buckling in isolated functional spidal region (FSR)s occurs with critical loads as low as 20 N [55, 117] to 90 N. [59] Well-coordinated and timely muscle activation empowers activities of daily living. The intact spine may withstand loads as high as 18,000 N. [118] Ill-timed or insufficient muscle recruitment leaves the spine susceptible to sudden, local, disproportionate displacement and strain. Wilder and colleagues, [114–116] studying constrained mechanical behavior, first described buckling of isolated functional spinal unit (FSU)s. They demonstrated that functional spinal unit (FSU) buckling is sensitive to the loading site, direction, amplitude, and rate. [119] Figure 3 illustrates buckling behavior of isolated motion segments during pure flexion and lateral bending tests with the loads applied at the balance point. The displacement that occurs in an functional spinal unit (FSU) under a given load is dependent on the inherent constitutive properties of the tissues as well as the stiffening action of the local muscles.

Essentially, each added increment in load results in a proportionate displacement. Below the buckling value, the displacement per increment is a very small proportion of the total available physiologic range. At the critical buckling load, the addition of another increment meets with a sudden, large deformation that approaches its maximum normal range of motion. Removal of the load does not result in elastic recovery to the original equilibrium configuration. Instead, a new equilibrium, near the extreme position is achieved. Buckling has been observed both in main and coupled motions. [115] Cholewicki and McGill [120] captured a buckling event confined to a single functional spinal unit (FSU) in vivo during heavy exertion.

Similar responses have been documented for entire functional spidal region (FSR)s as well as segmental functional spinal unit (FSU)s. [59] The magnitude of loads necessary to reach the limit of displacement for each functional spinal unit (FSU) is predictably much lower than characteristic of functional spidal region (FSR)s. Buckling response is sensitive to degeneration, which seems to allow it to occur earlier and reach maximum displacement under lower loads. Exposure to vibration, a known risk for the spine, also enhances buckling.

Summary and Conclusion

The language of the spine is biomechanics. Both normal and abnormal functions express themselves in these terms. Recasting theoretical considerations of the subluxation/FSL likewise carries significant advantages. First, it helps to demystify subluxation as a heuristic concept that has neither been seen nor measured. Second, it helps reveal methods by which it may be defined scientifically and monitored clinically. Third, it empowers credible communication, grounded on tangible evidence that can help influence public policy makers and the remaining scientific skeptics. Fourth, it helps lay a foundation to stronger scientific investigation of clinical effects. Finally, a biomechanical understanding of the FSL permits the development of new strategies to refme its prevention, treatment, and resolution.

An advantage of using motion-segment buckling over current hypotheses as a basis for modeling rests on the fact that this model does not preconceive or proscribe any source of symptoms but is able to accommodate the multifaceted clinical presentations of patients who respond favorably to manipulation/adjustment. It also can sustain a variety of both hypothetical and evidence-based challenges. For example, injuries (neurogenic and non-neurogenic pain mechanisms) with potentially local or remote symptoms are dependent entirely on which tissues exceed injury thresholds. Like the buckling itself, the painful tissue response will be dependent on prior health and the nature, direction, and severity of the stresses distributed to it.

Thus, the clinical appearances can be many. They may include acute facet capsulitis from a sudden high compressive or shearing load, ligamentous damage, or discal damage. Discogenic tearing, with neurogenic or non-neurogenic inflammation of the nerve roots or the terminal nerve fibers of the anular material, may result in either dennatomal or sclerotomal radiating pain. Reflex spasm and altered motor control of both the proximal and distal muscle groups may begin. Periarticular tissues also may receive direct damage as with muscular strain/sprain or contact injury to the back or neck. The buckling model builds on clinical observations, supplementing them with both direct and indirect biomechanical evidence. These findings offer an opportunity to reconceptualize and refine theoretical models of the spinal lesion into a platform for scientific, clinical, and political advancement of the profession.


  1. Patterson MM, Steinmetz JE.
    Long-lasting alterations of spinal reflexes: a potential basis for somatic dysfunction.
    Man Med. 1986;2:38-42

  2. Gatterman MI. Foundations of Chiropractic: Subluxation.
    St. Louis: Mosby; 1995.

  3. Bigos S, Bower O, Braen G, et al.
    Acute Low Back Problems in Adults. Clinical Practice Guideline No. 14.
    Rockville, MD: Agency for Health Care Policy and Research,
    Public Health Service, U.S. Department of Health and Human Services; 1994

  4. Bronfort G.
    Spinal manipulation: current state of research and its indications.
    Neurol Clin. 1999;17(1 ):91-111

  5. Triano JJ, McGregor M, Hondras MA, Brennan PC.
    Manipulative Therapy Versus Education Programs in Chronic Low Back Pain
    Spine (Phila Pa 1976). 1995 (Apr 15); 20 (8): 948–955

  6. Shekelle PG, Adams AH, Chassin MR.
    The Appropriateness of Spinal Manipulation for Low-Back Pain.
    Indications and Ratings by an All Chiropractic Expert Panel

    Santa Monica, CA: The RAND Corporation; 1992. R-4025/3-CCRlFCER.

  7. van Tulder MW, Koes BW, Bouter LM.
    Conservative treatment of acute and chronic nonspecific low back pain: a systematic review of randomized controlled trials of the most common interventions.
    Spine. 1997;22(18):2128-2156

  8. Bronfort G.
    Efficacy of Manual Therapies of the Spine.
    Amsterdam: Vrije Universiteit, EM GO Institute; 1997

  9. Meeker WC.
    Concepts germane to an evidence-based application of chiropractic theory.
    Top Clin Chiro. 2000;7(1):67-73

  10. Haldeman S.
    Presidential address, North American Spine Society: failure of the pathology model to predict back pain.
    Spine. 1990;15:718-724

  11. Saal JS.
    The role of inflammation in lumbar pain.
    Spine. 1995;20(16):1821-1827

  12. Saal JA.
    The pathophysiology of painful lumbar disorder: symposium introduction.
    Spine. 1995;20(16):1803

  13. Waddell G, Main CJ, Morris EW, DiPaola M, Gray IC.
    Chronic low back pain, psychologic distress, and illness behavior.
    Spine. 1984;9:209-213

  14. Lantz CA.
    A Review of the Evolution of Chiropractic Concepts of Subluxation
    Topics in Clinical Chiropractic 1995: 2 (2): 1-10

  15. Mootz RD.
    Theoretical models of chiropractic subluxation.
    In: Gatterman MI, ed. Foundations of Chiropractic: Subluxation.
    St. Louis: Mosby; 1995:176-189

  16. Triano J.
    The mechanics of spinal manipulation.
    In: HerzogW, ed. Clinical Biomechanics of Spinal Manipulation.
    New York: Churchill Livingstone; 2000:92-190

  17. Triano J.
    Biomechanics of spinal manipulation.
    Spine. 2001;1 (1). In press

  18. Byfield D.
    Cervical spine: manipulative skill and performance considerations.
    Eur J Chiro. 1991 ;39:45-52

  19. Triano J, Skogsbergh G, Mior S, Sportelli L.
    Biomechanical Parameters of Skill in Lumbar SMT.
    Proceedings of the International Conference on Spinal Manipulation, Palm Springs, California.
    Arlington, VA: Foundation for Chiropractic Education and Research; 1994.

  20. Triano J, McGregor M, Skosbergh D, Mior S, Sportelli L.
    Rating of Skill in SMT.
    Proceedings of 'the International Conference on Spinal Manipulation, Palm Springs, California.
    Arlington, VA: Foundation for Chiropractic Education and Research; 1994.

  21. Triano JJ.
    Chiropractic personnel in the 21 st century depends on the strategy today.
    Top Clin Chiro. 2000;7(1):27-32

  22. Einstein A,
    listed in Accessed on March 4, 2001.

  23. Triano JJ, McGregor M, Skogsbergh DR.
    Use of chiropractic manipulation in lumbar rehabilitation.
    J Rehabil Res Oev. 1997;34(4):25-36

  24. Triano JJ.
    Studies on the biomechanical effect of a spinal adjustment.
    J Manipulative Physiol Ther. 1992;15(1 ):71-75

  25. Herzog W.
    Mechanical and physiological responses to spinal manipulative treatments.
    J Neuromusculoskel Syst. 1995;3:1-9

  26. Christensen MG, Kerkhoff D, Kollasch MW.
    Job Analysis of Chiropractic 2000
    Greeley (CO): National Board of Chiropractic Examiners, 2000.

  27. Herzog W.
    Biomechanical studies of spinal manipulative therapy [Invited review paper],
    J Can Chiro Assoc. 1991 ;35:156-164

  28. Kawchuk GN, Herzog W.
    Biomechanical characterization (fingerprinting) of five novel methods of cervical spinal manipulation.
    J Manipulative Physiol Ther. 1993;16:573-577

  29. Triano J, Schultz AB.
    Loads transmitted during lumbosacral spinal manipulative therapy.
    Spine. 1997;22(17):1955-1964

  30. Triano JJ.
    Biomechanical Analysis of Motions and Loads during Spinal Manipulation.
    Ann Arbor: University of Michigan; 1998.

  31. Gal JM, Herzog W, Kawchuk GN, Conway PJ, Zhang Y.
    Forces and relative vertebral movements during SMT to unembalmed post-rigor human cadavers: peculiarities associated with joint cavitation.
    J Manipulative Physiol Ther. 1995;18(1 ):4-9

  32. Kawchuk G, Herzog W.
    A new technique of tissue stiffness (compliance) assessment: its reliability, accuracy, and comparison with an existing method.
    J Manipulative Physiol Ther. 1996;19(1 ):13-18

  33. Gal J, Herzog W, Kawchuk G.
    Movements of vertebrae during manipulative thrusts to unembalmed human cadavers.
    J Manipulative Physiol Ther. 1997;20:30-40

  34. Sandoz R.
    The physical mechanisms and effect of spinal adjustments.
    Ann Swiss Chiro Assoc. 1976; 6: 91-141.

  35. Conway PJW, Herzog W, Zhang Y.
    Forces required to cause cavitation during spinal manipulation of the thoracic spine.
    Clin Biomech.1993; 8: 210-214.

  36. Brodeur RR.
    The audible release associated with joint manipulation.
    J Manipulative Physiol Ther. 1995; 18: 155-164.

  37. Mierau D, Cassidy JD, Bowen V.
    Manipulation and mobilization of the third metacarpophalangeal joint.
    Man Med. 1988; 3: 135-140.

  38. Nansel D, Crernata E, Carleson R, Szalazak M.
    Effect of unilateral spinal adjustments on goniometrically-assessed cervical lateral-flexion end-range asymmetries in otherwise asymptomatic subjects.
    J Manipulative Physiol Ther. 1989;12(6):419-427.

  39. Nansel D, Peneff A, Cremata E, Carlson J.
    Time Course Considerations for the Effect of Lower Cervical Adjustments with Respect to the
    Amelioration of Cervical Lateral Flexion Passive End–range Asymmetries,
    and on Blood Pressure, Heart Rate, and Plasma Catecholamine Levels

    J Manipulative Physiol Ther 1991 (Oct); 14 (8): 450–456

  40. Vernon HT.
    Biological Rationale for Possible Effects of Manipulation (Chapter 6)
    In: Chiropractic in the United States: Training, Practice, and Research
    Rockville, Md: Agency for Health Care Policy and Research,
    Public Health Service, US Dept of Health and Human Services; 1997.
    AHCPR publication 98-N002.

  41. Bernard TN Jr. Kirkaldy-Willis
    WHO Recognizing specific characteristics of nonspecific low back pain.
    Clin Orthop. 1987;217:266-280.

  42. Gatterman MI.
    Advances in subluxation terminology and usage.
    In: Lawrence DJ, Cassidy JD, McGregor M, Meeker WC, Vernon HT, eds.
    Advances in Chiropractic. St. Louis: Mosby-Year Book; 1995:461-470.

  43. Triano J.
    The subluxation complex: outcome measure of chiropractic diagnosis and treatment.
    J Chiro Tech. 1990;2(3):114-117.

  44. Leach R.
    The Chiropractic Theories: A Synopsis of Research. 3rd ed.
    Baltimore: Williams & Wilkins; 1994.

  45. Faye LJ.
    Motion Palpation of the Spine. Huntington Beach, CA:
    Motion Palpation Institute; 1983.

  46. Mootz RD.
    Chiropractic theories: current understanding of vertebral subluxation and manipulable spinal lesions.
    In: Sweere, ed. Chiropractic Family Practice, Volume I.
    Gaithersburg, MD: Aspen Publishers, Inc; 1992.

  47. Lantz CA.
    The vertebral subluxation complex.
    In: Gatterman MI, ed. Foundations of Chiropractic: Subluxation.
    St. Louis: Mosby; 1995:149-174.

  48. Dvorak J, Dvorak V.
    Manual Medicine Diagnostics.
    New York: Thieme Medical Publishers; 1990.

  49. Lewit K.
    Manipulative Therapy in Rehabilitation of the Locomotor System.
    London: Butterworth; 1987.

  50. Greenman PE.
    Principles of Manual Medicine.
    Baltimore: Williams & Wilkins; 1989.

  51. Boone, WR and Dobson, GJ.
    A Proposed Vertebral Subluxation Model Reflecting Traditional Concepts
    and Recent Advances in Health and Science

    Journal of Vertebral Subluxation Research 1996 (Aug); 1 (1): 1–12

  52. Dishman RW.
    Review of the Literature Supporting a Scientific Basis for the Chiropractic Subluxation Complex
    J Manipulative Physiol Ther 1985 (Sep); 8 (3): 163–174

  53. C Lantz
    The Vertebral Subluxation Complex PART 1:
    An Introduction to the Model and Kinesiological Component

    Chiropractic Research Journal 1989; 1 (3): 23-36

  54. Schultz AB. Biomechanics of the human spine and trunk.
    In: Skalak R, Chien S, eds. Handbook of Bioengineering.
    New York: McGraw-Hili; 1987:41.9-41.17.

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

  56. Winters JM, Woo SL-Y.
    Multiple Muscle Systems-Biomechanics and Movement Organization.
    New York: Springer-Verlag; 1990.

  57. Panjabi MM, Yamamoto I, Ox land TR, Crisco ll.
    How does posture affect coupling in the lumbar spine?
    Spine. 1989;14(9):1002-1011.

  58. Panjabi MM, KragM, ChungT.
    Effects of disc injury on mechanical behavior of the human spine.
    Spine. 1984;9(7):713.

  59. Crisco Jj III, Panjabi MM, Yamamoto I, Oxland TR.
    Euler stability of the human ligamentous lumbar spine. Part II experiment.
    Clin Biomech. 1992;7:27-32.

  60. Alderink GJ.
    The sacroiliac joint: review of anatomy, mechanics and function.
    J Orthop Sports Phys Ther. 1991 ;13:71-84.

  61. Smidt GL, Mcquade K, Wei SH, Barakatt E.
    Sacroiliac kinematics for reciprocal straddle positions.
    Spine. 1995;20(9):1047-1054.

  62. Lafortune MA, Lake MJ, Hennig EM.
    Differential shock transmission response of the human body to impact severity and lower limb posture.
    J Biomech. 1996;29(12):1531-1537.

  63. Ogon M, Bender BR, Hooper DM, et al.
    A dynamic approach to spinal instability. Part II: hesitation and giving-way during interspinal motion.
    Spine. 1997;22(24):2859-2866.

  64. Dontigny RL.
    Function and pathomechanics of the sacroiliac joint. a review.
    Phys Ther. 1985;65(1 ):35-44.

  65. Triano ll. Schultz AB.
    Correlation of objective measure of trunk motion and muscle function with low-back disability ratings.
    Spine. 1987;12(6):561-565.

  66. Toussaint HM, de Winter AF, de Haas Y.
    Flexion relaxation during lifting: implications for torque production by muscle activity and tissue strain at the lumbosacral joint.
    J Biomech. 1995;28(2):199- 210.

  67. Panjabi MM, Goel VK, Walter SD.
    Errors in kinematic parameters of a planar joint: guidelines for optimal experimental design.
    J Biomech. 1982;15:537.

  68. Panjabi MM, Abumi K, Duranceau J, Crisco Jj, Kramer K.
    A biomechanical study of partial and complete facetectomies of the lumbar spine.
    Proceedings of the 12th Annual Society of Biomechanics, Urbana-Champagne, Illinois, 1988.

  69. Goel VI( Fromknecht SJ, Nishiyama K.
    The role of lumbar spinal elements in flexion.
    Spine. 1985;10(6):516-523.

  70. Hedtmann A, Steffen R, Methfessel J.
    Measurement of human lumbar spine ligaments during loaded and unloaded motion.
    Spine. 1989;14(2):175-185.

  71. Mykleburst JB, Pintar F, Yoganadan N.
    Tensile strength of spinal ligaments.
    Spine. 1988;13(5):526-531.

  72. Gudavalli MR, Triano JJ.
    Effects of combined motions on the posterior ligaments of the lumbar spine.
    J Neuromusculosketal Sys. 1998;1 (1).

  73. Boresi AP, Sidebottom OM.
    Advanced Mechanics of Materials. 4th ed.
    New York: John Wiley & Sons; 1985.

  74. Triano JJ.
    Biomechanics of manipulation.
    In: Herzog W, ed. The Clinical Biomechanics of Spinal Manipulation.
    St. Louis: Mosby; 2000.

  75. Parnianpour M, Nordin M, Kahanovitz N, Frankel V.
    The triaxial coupling of torque generation of trunk muscles during isometric exertions and the effect of fatiguing isoinertial movements on the motor output and movement patterns.
    Spine. 1988;13(9):982-992.

  76. Sparto PJ, Parnianpour M, Reinsel TE, Simon S.
    The effect of fatigue on multijoint kinematics: coordination and postural stability during repetitive lift tasks.
    J Orthop Phys Ther. 1997;25(1 ):3-12.

  77. Potvin JR.
    The Influences of Fatigue on Hypothesized Mechanisms of Injury to the Low Back during Repetitive Lifting.
    Ontario, Canada: University of Waterloo; 1992.

  78. Wen N, Lavaste F, Santin Il. Lassau jP.
    Three-dimensional biomechanical properties of the human cervical spine in vitro I. Analysis of normal motion.
    Spine j. 1993;2(2):2-11.

  79. Kumaresan S, Yoganandan N, Pintar FA, Voo LM, Cusick JF, Larson SJ.
    Finite element modeling of cervical laminectomy with graded facetectomy.
    J Spinal Disord. 1997;10(1 ):40-46.

  80. Pintar FA, Yoganadan N, Pesigan M, Reinartz J, Sances A, Cusick JF.
    Cervical vertebral strain measurements under axial and eccentric loading.
    J Biomech fng. 1995;117(4):474-478.

  81. Yoganandan N, Pintar FA.
    Inertial loading of the human cervical spine.
    J Biomech fng. 1997;119(3):237-240.

  82. Luttges M, Stodieck LS, Beel JA.
    Post-injury changes in the biomechanics of nerves and roots in mice.
    J Manipulative Physiol Ther. 1986;9(2):89-98.

  83. Miller JA, Schmatz C, Schultz AB.
    Lumbar disc degeneration: correlation with age, sex, and spine level in 600 autopsy speciment.
    Spine. 1988;13:173-178.

  84. Moroney SP, Schultz AB, Ashton-Miller JA, Andersson GBJ.
    Load-displacement properties of cervical spine segments.
    J Biomech. 1988;21 (9):769-779.

  85. Shirazi-Adl A.
    Finite-element evaluation of contact loads on facets of an L2-L3 lumbar segment in complex loads.
    Spine. 1991 ;16(5):533-541.

  86. Kasra M, Shirazi-Adl A, Droun G.
    Dynamics of human lumbar intervertebral joints: experimental and finite-element investigations.
    Spine. 1992;17(1 ):93-1 02.

  87. Cavanaugh JM.
    Neural mechanisms of lumbar pain.
    Spine. 1995;20(16):1804-1809.

  88. Cavanaugh JM, Ozaktay AC, Ymashita HT.
    Lumbar facet pain: biomechanics, neuroanatomy and neurophysiology.
    J Biomech. 1996;29(9):1117-1129.

  89. McGill SM.
    The biomechanics of low back injury: implications on current practice in industry and the clinic.
    J Biomech. 1997;30(5):465-475.

  90. Chaffin DB, Andersson GB.
    Occupational Biomechanics.
    New York: John Wiley & Sons; 1991 :215-239.

  91. Enneking WF, Horowitz M.
    The intra-articular effects of immobilization on the human knee.
    J Bone joint Surg Am. 1972; 54 (5): 973-985.

  92. Videman T.
    Experimental models of osteoarthritis: the role of immobilization.
    Clin Biomech. 1987;2:223-229.

  93. Salter RB.
    The biologic concept of continuous passive motion of synovial joints. The first 18 years of basic research and its clinical application.
    Clin Orthop. 1989;242:12-25.

  94. Schram S.
    Error limitations in X-ray kinematics of the spine.
    J Manipulative Physiol Ther. 1982;5(1 ):5-1 O.

  95. Yoganandan N, Ray G, Pintar FA, Mykleburst JB, Sances A Jr. S
    Stiffness and strain energy criteria to evaluate the threshold of injury to an intervertebral joint.
    J Biomech. 1989;32(2):135-142.

  96. Neugarten B.
    Adaptation and the life cycle.
    Counseling Psychol. 1976;6:16.

  97. Courtney AC, Hayes We, Gibson LJ.
    Age-related differences in post-yield damage in human contrical bone experiment and model.
    J Biomech. 1996;29(1 ):1463-1471.

  98. Heaney RP.
    Prevention of Osteoporotic Fracture in Women. The Osteoporotic Syndrome.
    New York: Wiley-Liss; 1993:89.

  99. Eskinazi D, Parfitt A.
    Alternative, complementary or integrative medicine: can a journal take the lead?
    Integr Med. 1998;1 (2): 75-76.

  100. Ikai M, Fukunaga T.
    Calculation of muscle strength per unit cross-sectional area of human muscle by means of ultrasonic measurement.
    Int Z Angew Physiol. 1968;26(1 ):26-32.

  101. Aoyagi A, Shepard R.
    Aging and muscle function.
    Sports Med. 1992;14:376.

  102. MacLennan WJ, Hall MR, Timothy ll. Robinson M.
    Is weakness in old age due to muscle wasting.
    Ageing. 1980;9(3):188-192.

  103. Brandt DK, Fife RS.
    Aging in relation to the pathogenesis of osteoarthritis.
    Clin Rheum Dis. 1986;12(1 ):114-130.

  104. Twomey LT, Taylor JR.
    Age changes in lumbar vertebrae and intervertebral discs.
    Clin Orthop. 1987;224:97-104.

  105. Oegama TR, Bradford DS.
    The inter-relationship of facet joint osteoarthritis and degenerative disc disease.
    Br J Rheumatol. 1991 ;30(suppll):16-20.

  106. Baker Pc.
    The aging neuromuscular system.
    Semin Neurol. 1989; 9 (1): 50-59.

  107. Woollacott MH.
    Age-related changes in posture and movement.
    J Gerontol. 1993;48:56~60S.

  108. Kaufman T.
    Posture and age.
    Top Geriatr Rehabil. 1987;2:13.

  109. Triano JJ.
    Interaction of spinal biomechanics and physiology.
    In: Haldeman S, ed. Principles and Practice of Chiropractic.
    Norwalk: Appleton & Lange; 1992:225-257.

  110. Kauer JMG.
    Functional anatomy of the wrist.
    Clin Orthop. 1980;149:9.

  111. Kauer JMG.
    The mechanisms of the carpal joint.
    Clin Orthop. 1986;202:16.

  112. Landsmeer JMF.
    Studies in the anatomy of articulation. I. The equilibrium of the "intercalated" bone.
    Acta Morphol NeeriScand. 1961;3:287-321.

  113. Kaptchuk TJ, Landsmeer JMF.
    Functional anatomy of the wrist. In: Tubiana R, ed.
    The Hand. Philadelphia: W.B. Saunders Co; 1981.

  114. Wilder DG, Pope MH, Frymoyer, JW.
    Cyclic Loading of the Intervertebral Motion Segment. Proceedings of the 10th Northeast Bioengineering Conference,
    Dartmouth College, Hanover, New York, 1982.

  115. WilderDG, PopeMH, FrymoyerJW.
    The biomechanics of lumbar disc herniation and the effect of overload and instability.
    J Spinal Disord. 1988; 1 :16-32.

  116. Wilder DG, Pope MH, Seroussi RE, Dimnet J, Krag MH.
    The balance point of the intervertebral motion segment: an experimental study.
    Bull Hosp it Dis. 1989;49(2):155-169.

  117. Cholewicki J, McGill SM, Norman RW,
    Comparison of muscle forces and joint load from an optimization and EMG assisted lumbar spine model: towards development of a hybrid approach.
    J Biomech. 1995;28(3):321-331.

  118. Cholewicki J, Mcgill SM, Norman RW.
    Lumbar spine load during the lifting of extremely heavy weights.
    Med Sci Sports fxerc. 1991 ;23(10):1179-1181.

  119. Pope MH, Wilder DG, Krag MH.
    Biomechanics of the lumbar spine A. Basic principles.
    In: Frymoyer JW, ed. The Adult Spine - Principles and Practice.
    New York: Raven Press; 1991 :1487-1501.

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


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