The mechanical category of the VSC includes derangements or disorders of the somatic structures of the body that lead to altered joint structure and function. Derangement of the articular soft tissues and mechanical joint dysfunction may result from acute injury, repetitive-use injury, faulty posture or coordination, aging, immobilization, static overstress, congenital or developmental defects, or other primary disease states.*
Joint Malposition
Historically, the basis for subluxation was founded on the concept that traumatic events could lead to altered joint position and that this malposition would interfere with neurologic impulses. Both the chiropractic profession (through D.D. Palmer) and the osteo- pathic profession (through A.T. Still) have stressed joint position as an important quality for normal joint function.1,94
One of the oldest concepts from the literature on manipula- tion is the interdependence of structure and function. In other words, structure determines function and function determines structure. When there is a change in structure, there will be a change in function. Therefore, if a structural alteration is identi- fied, a functional change should also be perceived. When a spinal joint is either acutely traumatized or undergoes chronic repeti- tive stresses, it is assumed that asymmetric muscle tension is likely to develop and hold the joint in a position away from its neu- tral alignment. The central idea is that misaligned positions of skeletal components can result in movement limitations, associ- ated inflammatory changes, and irritation of nociceptors leading *References 15-23, 26, 30, 34, 50-54, 56, 75-93.
to pain. From a historical perspective, the chiropractic profession primarily viewed spinal subluxations as a structural failure that alters body function.95
The concept of static vertebral misalignment is difficult to sup- port, however. Triano cites evidence that there is no “normal posi- tion” between vertebrae in the sense of the historic subluxation argument.95 The spine and the component parts are not perfectly
symmetric in their development. Spinous processes in particular are quite prone to asymmetric growth. It is also very unlikely that one could palpate a displacement of a few millimeters or degrees based on the location of the spinous processes. Identification of joint malposition is typically through static palpation or radio- graphic mensuration. Both of these procedures have only fair to poor inter- and intraobserver agreement. Furthermore, there is no evidence that supports a change in alignment following manipu- lative intervention. Clearly the “bone-out-of-place” concept is not likely to be the sole explanation for subluxation.25,96
Joint Fixation (Hypomobility)
A more biologically plausible model of spinal joint pain incorpo- rates abnormal joint mechanics and postulates that vertebral hypo- mobility can cause pain and abnormal spinal mechanics because of changes in sensory input from spinal and paraspinal tissues. Work by Henderson and associates provide the first preliminary anatomic evidence that altered spinal mechanics may produce neuroplastic changes in the dorsal horn of the spinal cord.97-99 Their preliminary
data suggest that chronic vertebral hypomobility (fixation) at L4 through L6 in the rat affects synaptic density and morphology in the superficial dorsal horn of the L2 spinal cord level.99
Soft Tissue Injury and Repair. A commonly proposed source of joint fixation (hypomobility) and dysfunction is periarticular soft tissue injury with its resultant fibrosis and loss of elasticity and strength.15-22,54,56,57,75-77 Soft tissue injury and fibrosis may result from
acute or repetitive trauma to muscular, tendinous, myofascial, or lig- amentous tissue. Regardless of the mechanism of injury, an ensuing inflammatory response is triggered57 resulting in extracellular accu-
mulation of exudates and blood. Platelets then release thrombin- converting fibrinogen into fibrin, which organizes into collagenous scar tissue, resulting in a variety of soft tissue and articular adhesions. This process is considered to be nonspecific and often excessive in the case of traumatic NMS injuries.15,79 As a consequence, early con-
servative management is often directed at limiting the extent of the inflammatory response. Therapies directed at minimizing the extent of associated inflammatory exudates are helpful in reducing pain and muscle spasm and in promoting early pain-free mobilization and flexible repair.79,83-85,93,100-113 Aggressive early care and mobilization
provide the best opportunity for optimal healing and an early return to work for the patient. Bed rest and prolonged inactivity increase the chances of long-term disability and lost work time.103,105,114,115
The exudates that form as a byproduct of injury and inflam- mation set the stage for the next step in the process of connective tissue repair. They provide the matrix for the development of granulation tissue and scar formation. The formation of granu- lation tissue is predominantly carried out by the proliferation of fibroblasts and the synthesis and deposit of collagen tissue. The collagen is initially very poorly organized and must add addi- tional collagen cross-linkages and reorganize along planes of stress
to improve the tensile strength of the injured area. This process of repair and remodeling may take months and may result in less than optimal restoration and extensibility of the involved tissue. Immobilization slows the process of recovery, leading to loss of strength and flexibility and potential intra-articular fatty adhe- sions.75,76,83-93 Immobilization also leads to dehydration, causing
proteoglycans to approximate and stick together.83,84,88 If injury
or immobilization leads to decreased flexibility, therapies such as articular adjustments or joint mobilization should be directed toward the restoration of motion.15,79,82,102
Myofascial Cycle. Painful conditions capable of triggering per- sistent muscle hypotoncity are additional sources of restricted joint motion (Figure 3-1). Muscle contraction, once initiated, may become
MYOFASCIAL CYCLE Repetitive use Emotional tension Chronic postural stress Exposure to cold Visceral disease Joint dysfunction Pain Vasoconstriction ischemia Sustained contraction Fibrous reaction
Soft tissue contractures
Persistent joint and somatic dysfunction Uncoordinated movements
Physical trauma
Retained metabolites
Edema (inflammation) Muscle splinting
Joint dysfunction Myofascial syndromes Structural inadequacies MUSCLE
STRAIN
Figure 3-1 Myofascial conditions are triggered by many causes and can become self-perpetuating sources of pain, muscle spasm, and joint dysfunction.
a self-perpetuating source of pain and muscle hypotoncity.* Reactive splinting in the joint’s intrinsic muscles may further accentuate this process by blocking passive joint movement and the pain-inhibiting qualities of joint mechanoreceptor stimulation.120 Persistent contrac-
tions over time may develop into muscle contractures as a result of adaptational shortening and loss of elasticity from disuse or under- use. Although there is little direct evidence to support the belief that sustained muscle contraction is a feature of intervertebral dysfunc- tion, the concept of protective muscle splinting appears plausible.121
Maladies capable of producing acute muscle contraction are wide ranging; they include trauma, structural inadequacies, visceral dis- ease, emotional distress, and exposure to cold.122,123
Interarticular Derangements. A number of internal joint derangements have also been submitted as probable causes of joint locking and back pain. They include internal derange- ments of the intervertebral disc (IVD; intradiscal block), derange- ments of the posterior spinal joints (interarticular, intermeniscoid block),50,51,77,78,130-146 and compressive buckling injuries.12,13 They
are hypothesized to induce mechanical blockage to movement and unleveling of the motion segment, with resultant tension on the joint capsule, annulus, or both. The joint capsule and posterior annulus are pain-sensitive structures, and tension on these elements may induce additional painful muscle splinting, further accentuating the mechanical blockage and joint restric- tion. Mechanical joint dysfunction is therefore considered to be a significant and frequent cause of spinal pain and a potential source of spinal degeneration.
Interarticular Block. One source of derangement of the poste- rior joints is speculated to result from entrapment (Figure 3-2) or extrapment (Figure 3-3) of joint meniscoids or synovial folds.131-141
The intra-articular meniscoids are leaflike fibroadipose folds of syn- ovium that are attached to the inner surface of the joint capsule and project into the joint cavity. These meniscoids have been found to be present in all of the posterior joints of the spine.
Bogduk and Jull140 have suggested that extrapment of these
meniscoids may be one cause of restricted joint motion. They specu- late that the meniscoid may occasionally be pulled out of its resting position by the inferior articular process of a zygapophyseal joint as it moves upward during flexion. On attempted extension, the inferior articular process returns toward its neutral position, but the menis- coid, instead of re-entering the joint cavity, impacts against the edge of the articular cartilage and buckles, representing a space-occupying lesion under the capsule. Pain occurs as a result of capsular tension, and extension motion is restricted. The use of a distractive or joint gapping adjustive procedure may function to separate the articular surfaces and release the extrapped meniscoid (see Figure 3-3).140,147
Maigne78 and others77,116,137,148-152 have proposed a model of
interapophysary meniscus entrapment rather than extrapment. In this model the menisci are purportedly drawn into a position between the joint margins during poorly coordinated spinal move- ments or sustained stressful postures. With resumption of normal postures, pain resulting from impaction of the menisci or traction of the articular capsule induces reactive muscle splinting and joint locking. The development of a painful myofascial cycle is initiated as prolonged muscle contraction leads to muscle fatigue, ischemia, and more pain. If spasm and locking persist, the articular cartilage may mold around the capsular meniscus, causing it to become more rigidly incarcerated within the joint.116-118 To interrupt the cycle of
pain, muscle cramping, and joint locking, distractive adjustments have also been presented as a viable therapy capable of inducing joint separation, cavitation, and liberation of the entrapped menisci (see Figure 3-2).118 It is important to note that meniscoid derange-
ment is only one hypothetical cause of joint dysfunction. Meniscoid derangement is postulated to be a more likely source of joint dys- function in circumstances in which trivial trauma leads to acute joint irritation or locking and associated muscle spasm.139
Interdiscal Block. The mechanical derangements of the IVD that may lead to joint dysfunction are postulated to result from pathophysiologic changes associated with aging, degenerative disc disease, and trauma. Farfan153 has proposed a model of progres-
sive disc derangement based on repetitive rotational stress to the motion segment. He postulates that repetitive torsional loads of sufficient number and duration may, over time, lead to a fatigue injury in the outer annular fibers. The process would begin with circumferential distortion and separation in the outer annular fibers, followed by progression to radial fissuring and outward
A B
Impinged position
Normal position
Reduced: hard edge remaining remodels with time Reduced
Figure 3-2 Theory of meniscoid entrapment. A, Diagrammatic rep- resentation of meniscoid entrapment inducing flexion and extension malpositions, capsular tension, pain, and subsequent restrictions in spi- nal mobility. B, Manipulation of the joint separates the joint surfaces, allowing the meniscoid to return to a neutral position.
A B C D
Figure 3-3 Theory of meniscoid extrapment. A, On flexion, the inferior articular process of a zygapophyseal joint moves upward, taking a meniscoid with it. B, On attempted extension, the inferior articular process returns toward its neutral position, but the meniscoid, instead of reentering the joint cavity, buckles against the edge of the articular cartilage, forming a space-occupying lesion under the capsule. C, Manipulation gaps the joint and allowing the meniscoid to return to its neutral resting position (D).
migration of nuclear material. Another view postulates that disc derangement, fissuring, and herniation begin in the innermost annular rings and progresses outward.154
The rate of fatigue and injury depends on the duration and magnitude of the force applied. In the individual with disrupted segmental biomechanics, the process is potentially accelerated as an altered axis of movement leads to increased rotational strain on the IVD. Postmortem dissection studies of degenerated discs have indeed identified radial fissures in the annulus fibrosus. Cyriax155
believes that displaced nuclear material along an incomplete fis- sure is the source of joint fixation. Nuclear migration along these radial fissures has also been demonstrated by computed tomogra- phy (CT) discography and correlated with patient pain.156
Interwoven in the natural history of degenerative disc disease may be episodes of acute mechanical back pain and joint lock- ing. Maigne78 and others23,129-131 have postulated that incidents of
blockage may occur during efforts of trunk flexion as nuclear frag- ments become lodged in fissures in the posterior annulus (inter- discal block) (Figure 3-4). Consequently, tension on the posterior annulus and other mobile elements of the involved motion seg- ment are produced, initiating local muscle guarding and joint lock- ing. Cyriax126 proposes that these lesions may induce tension on
the dura mater, inducing lower back pain (LBP) and muscle splint- ing. Once local pain and muscle splinting are initiated, a self-per- petuating cycle of pain, cramping, and joint locking may result.
Adjustive therapy has been proposed as a viable treatment for interrupting this cycle of acute back pain and joint locking. In addi- tion to the distractive effect on the posterior joints, adjustive ther- apy is thought to have a potential direct effect on the IVD, either by directing the fragmented nuclear material back toward a more central position or by forcing the nuclear fragment toward a less mechanically and neurologically insulting position (see Figures 4-18 and 4-19). Of course there are spinal joints (atlanto-occipital and atlantoaxial articulations) that do not have IVDs, and they are common sites of dysfunction. This clearly indicates that IVD derangement is not the sole source of spinal joint subluxation or dysfunction.
Compressive Buckling Injury. Triano suggests that a causal factor for a manipulable lesion may be a compressive buckling injury.12,13 Intersegmental buckling is likely the result of some error
in neuromuscular control that fails either to provide adequate pre- stability to the segment or to respond appropriately with muscle
activation to a perturbation.157 When a mechanical overload to
spinal functional units occurs, either as a single traumatic event or cumulative events, a critical buckling load may be reached. Individual structural elements (disc, facet, ligament, nerve, mus- cle) may experience concentration of local stresses with reduced functional limits and symptom production specific to the tissue affected. The result is a state of dysfunction that may lead to local inflammatory or biomechanical changes.158,159
Each joint possesses some inherent stability resulting from the stiffness of the ligaments and joint capsule. Further stability and control are provided by the neuromuscular system and faulty motor control may lead to inappropriate levels of muscle force and stiffness at a given spinal segment. This may compromise seg- mental stability at that level,160 leading to transient intersegmen-
tal buckling.161 The segment briefly exceeds its safe physiologic
motion, which leads to loading of the surrounding soft tissues (ligaments, IVD, etc.).157 Furthermore, exposure to vibration and
previous disc injury may augment the buckling event. The result of intersegmental buckling is asymmetric positioning of the ver- tebra that is maintained by the intrinsic muscles producing hypo- mobility of the functional unit.
Clinical Joint Instability and Hypermobility
Joint dysfunction resulting from soft tissue injury or degeneration does not necessarily result in joint hypomobility. Disturbances of function of the vertebral column can also result from a loss of joint stability. Joint derangement and dysfunction resulting from a loss of joint stability are commonly referred to as joint hypermobility or clinical joint instability. Both terms are often used interchangeably, and there is no standard for defining these terms. Definitions vary among clinicians and authors and between the clinical and biome- chanical literature.162,163
Although numerous definitions abound, all seem to incorporate a loss of stiffness or sensorimotor control affecting the joints’ stabiliz- ing structures.162-165 The loss of stiffness is clinically relevant if exces-
sive or aberrant movements lead to pain, progressive deformity, or compromised neurologic structures. Movement can be abnormal in quality (abnormal coupling) or in quantity (increased movement).
Attempts have been made to distinguish clinical joint instabil- ity from hypermobility (Table 3-1). The differences are a reflection of the structures involved and degree of pathologic change in the joints’ stabilizing structures. Hypermobile joints are assumed to be stable under normal physiologic loads. Hypermobile joints dem- onstrate increased segmental mobility, but they maintain normal patterns of movement. Hypermobility may be in one plane and not associated with any abnormal translational movements.166,167
In contrast, patients with clinically unstable joints have been postulated to have ineffective neural motor control or more advanced changes in the joints’ stabilizing structures.168 Damage to
these structures leads to abnormal patterns of coupled and trans- lational movements and possible multiple planes of aberrant joint movement. Clinical joint instability should not be equated with gross orthopedic instability resulting from fracture or dislocation.
There is little doubt that clinical spinal joint instability exists, but current methods lack the necessary sensitivity and specificity for clearly identifying its contributions to back pain.162 Clinical
opinion suggests that the typical presentation is one of recurring
Figure 3-4 Interdiscal block. Illustration of nuclear material migrat- ing into internal annular fissures, producing tension on the posterior annulus.
episodes of marked back pain, often initiated by trivial events such as bending or twisting. Global movements are often limited and may demonstrate a painful arc with abnormal patterns of devia- tion or hitching. Symptoms often resolve within several days, only to recur at a later date.165
Physical examination tools are limited but increasing.162,168
Manual palpation of passive posteroanterior glide has been suggested as one physical means of testing for excessive shear and instability. One recent investigation did demonstrate that prone posterior-to-anterior (P-A) passive joint play (JP) evalu- ation of the spine can accurately identify abnormal segmental translation as compared with a reference standard of flexion extension radiographs.169 This test demonstrated good speci-
ficity (89%) but poor sensitivity (29%), with a positive likeli- hood ratio of 2:52. Both the P-A passive segmental mobility assessment and the prone “instability test” were predictive of which patients with low back pain (LBP) would benefit from a lumbar exercise stabilization program.168 The prone instabil-
ity test requires the patient to lie in a prone position on an examination table with his or her feet on the floor. The doctor applies segment-passive P-A pressure and, if pain is produced, the patient is asked to raise his or her feet off the floor. If pain is diminished, the test is consider positive and indicative of segmental instability.
Dynamic flexion-extension and lateral bending radiographs are the most commonly used radiographic methods for detecting end-range instability, but they do not provide information about quality of movement during the midrange of segmental motion.162
Methods using transducers or markers placed over bony land- marks have not demonstrated effective results as a consequence of the skin motion artifact. Methods using pins embedded in the spinous processes to measure movement have adequate accuracy, but these methods are invasive and are not practical for clinical use.162
In the absence of gold standard diagnostic tools for detect- ing spinal joint instability, the chiropractor should pay close attention to the clinical presentation, including history and manual examination, and consider instability in a patient who has recurring episodes of back pain with only temporary relief from manipulation. Suspicion of instability may be reinforced by dynamic x-ray flexion-extension examination, but this pro- cedure may have false-negative results. When instability is still