General Spinal Biomechanics
From R. C. Schafer, DC, PhD, FICC's best-selling book:
“Clinical Biomechanics: Musculoskeletal Actions and Reactions”
Second Edition ~ Wiliams & Wilkins
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to chiropractic research. Please review the complete list of available books.Background The Spine as a Whole Topographic Landmarks Development of the Spine The Spinal Curves Spinal Stability Normal Spinal Movements The Vertebrae and Pertinent Osteology Functional Anatomy Basic Regional Differences The Vertebral Motion Unit The Vertebral Body Planes of Articulation The Intervertebral Foramina The Spinal Joints and Pertinent Arthrology The Vertebral Joints The Intervertebral Disc Area The Apophyseal Joints The Spinal Ligaments and Pertinent Syndesmology The Vertebral Canal and Related Tissues Cord-Canal Relationships Functional Anatomy The Spinal Nerves Sensory Manifestations Spinal Circulation and Pertinent Angiology Area Vasculature Cord Circulation Disc Nutrition The Spinal Muscles and Pertinent Myology The Postvertebral and Prevertebral Muscles Spinal Movements General Aspects of Vertebral Subluxations Types of Subluxations Gross Structural Alterations Precipitating Factors of Spinal Subluxations Effects of Spinal Subluxations Fundamental Considerations in Evaluating Idiopathic Spinal Pain Clinical Cautions Prevalent Theories Incidence General Aspects of Spinal Inspection and Palpation The Basic Factors Involved in Spinal Examination Selected Clinical Considerations General Aspects of Musculoskeletal Injury Spinal Instability Spinal Fixations Spinal Strains and Sprains Myalgia (Fibrositis) Bone Injuries Arthrotic Pathology Disc Degeneration, Protrusions, and Ruptures Referred Pain and Reflexes The Dynamic Craniospinal System Spinal Fractures and Dislocations Congenital Anomalies and Deformities of the Neck and Back Therapeutic Objectives
Part II: Clinical Biomechanics of the Spine and Pelvis
Chapter 6: General Spinal Biomechanics
This chapter discusses the vertebral column as a whole and serves as a foun- dation for the following three chapters that consider the regional aspects of the spine and pelvis. Emphasis here is on gross structure, function, spinal kinematics, and other general biomechanical implications.
The vertebral column is a mechanical marvel in that it must afford both rigidity and flexibility.
The Spine as a Whole
The segmental design of the vetebral column allows adequate motion among the head, trunk, and pelvis; affords protection of the spinal cord; transfers weight forces and bending moments of the upper body to the pelvis; offers a shockabsorbing apparatus; and serves as a pivot for the head. Without stabilization from the spine, the head and upper limbs could not move evenly, smoothly, or support the loads imposed upon them (Fig. 6.1).
Essentially because of its various adult curvatures, the bony spine is anatomically divided into the seven cervical vertebrae, the twelve thoracic vertebrae, the five lumbar vertebrae, and the ossified five sacral and four coccygeal segments. From C1 to S1, the articulating parts of these vertebrae are the vertebral bodies, which are separated by intervertebral discs (IVD's), and the posterior facet joints. The IVD's tend to be static weight-bearing joints, while the facets function as dynamic sliding and gliding joints.
The flexible vertebral column is balanced upon its base, the sacrum. In the erect position, weight is transferred across the sacroiliac joints to the ilia, then to the hips, and then to the lower extremities. In the sitting position, weight is transferred from the sacroiliac joints to the ilia, and then to the ischial tuberosities.
About 75% of spinal length is contributed by the vertebral bodies, while 25% of its length is composed of disc material. The contribution by the discs, however, is not spread evenly throughout the spine. About 20% of cervical and thoracic length is from disc height, while approximately 30% of lumbar length is from disc height. In all regions, the contribution by the discs diminishes with age.
Development of the Spine
In brief, development occurs in three stages: mesenchymal, chondrification, and ossification.
MESENCHYMAL AND CHONDRIFICATION ORIGINS
Just prior to the 4th week of embryonic development, a vertebral segment begins to develop as paired condensations of mesenchyme (somites) around the longitudinal notochord and dorsal neural tube. One or usually two chondrification centers appear (6 weeks) in the centrum and begin to form a cartilaginous model surrounded by anterior and posterior longitudinal ligaments which are complete by 7-8 weeks. Chondrification centers also form in the neural arches and costal processes. A thick ring of nonchrondrous cells establishes the model IVD around the longitudinal string of beaded notochordal segments (Fig. 6.2).
The approximate topographical landmarks in relation to the anatomy of the vertebral column and pelvis are as follows:Inion: Prominence, midline of occipital base. C1 About 1/2 inch inferior and slightly anterior of the mastoid process. C2 First prominent spinous process below the inion. C4 Hyoid bone. C6 Cricoid cartilage. C7 Second prominent spinous process below the inion. T1 Most prominent spinous process in the region. T2 Jugular notch. T5 Angle of Louis. T7 Inferior angle of the scapula, third prominent spinous process below inion. T10 Xiphoid process. L1 Transpyloric plane. L3 Umbilicus. L4 Iliac crests. L5 Transtubular plane. S2 Level with the posterior-superior iliac spines (PSIS's). Sciatic notch: about 2 inches inferior and 1 inch lateral to the PSIS. Ischial tuberosity: about 2 inches inferior to apex of coccyx, on a vertical line through the PSIS.
A vertebra at term is in three primary ossifying centers: the oval centrum and the two aspects of the neural arch. However, the ossification process is well under way by the 16th week of gestation. Each of the three parts are united by hyaline cartilage. A cartilaginous ring develops around the anterior and lateral periphery of the centrum-disc interface, which firmly anchors the anulus to the centrum (Fig. 6.3). The two halves of the arch ossify posteriorly by appositional growth during the first year of age in the cervical region and complete ossification in the lumbar region by age 8. The progression is from above downward. The centrum, which ossifies endochondrally, joins the arch during the 3rd to the 6th year in the lumbar area and firmly fuses between the 5th and 8th year in the cervical region. In contrast, the progression is from below upward. During development, the superior and inferior cortex of the centrum thickens in the middle, and, with a cartilaginous plate that is thicker at the periphery, forms the vertebral plateau.
Scale-like traction epiphyses on the tips of the spinous and transverse processes and ring-like pressure epiphyses on the superior and inferior aspects of the vertebral body appear obvious shortly after puberty (age 13–16) and fuse prior to the age of 25 to form a thickened periphery (Fig. 6.4). When ossified, this ring receives Sharpey's fibers of a disc's anulus laminations. Abnormal ossification leads to Scheuermann's disease.
The Spinal Curves
A curved column has increased resistance to compression forces. This is just as true in the spine as for a rib or long bone.
Most authorities consider the spine to have four major curves: anteriorly convex curves at the cervical and lumbar areas and anteriorly concave curves at the thoracic and sacral levels. Cailliet considers the coccyx to be curved, but this is usually considered an extension of the sacral curve. A few authorities consider the occipitoatlantal junction as a separate anteriorly convex curve. Regardless, the spinal curves offer the vertebral column increased flexibility and shock-absorbing capability while still maintaining an adequate degree of stiffness and stability between vertebral segments (Fig. 6.5).
STRUCTURAL VS FUNCTIONAL CURVES
The adult thoracic and sacral anteriorly concave curves are firm structural arcs as the result of their vertebral bodies being shorter anteriorly than posteriorly. The normal kyphosis of the adult thoracic and sacral curves is quite similar to that of the fetal spine. This is not true for the anteriorly convex cervical and lumbar regions where the curves are essentially the result of their soft-tissue wedge-shaped IVD's. It is for this reason that the cervical and lumbar curves readily flatten in the supine position, while the thoracic kyphosis reduces only a slight amount.
There is a clinical correlation of disc wedging to disc disease. Most disc lesions are found in the cervical and lumbar regions where the greatest degree of physiologic wedging occurs. This appears to be true in both hyperlordosis and an exceptionally flat cervical or lumbar curve.
EFFECT OF BIPEDISM
An adult discless spine would resemble that of the newborn. Since animals that walk on four legs and infants prior to assuming the erect position do not have the physiologic curves of the erect adult, it can be assumed that these curves are the result of bipedism. In the erect position, the lower lumbar area is especially subjected to considerable shearing stress.
Although the spine is often considered as the central pillar of the body, this is only true when the spine is viewed from the anterior or posterior aspect. When viewed laterally, the spine lies distinctly posterior to the thoracic body mass essentially because of the space-occupying heart (Fig. 6.6). It lies much more centrally in the cervical and lumbar regions. An abundance of body mass also lies anterior to the midline in the head which must be held by erector and check ligament strength if a thoracic "hump" or a flattened cervical curve are to be avoided.
From a balance standpoint, the seven cervical vertebrae and the five lumbar vertebrae arc anteriorly from the central gravity line to compensate for the twelve thoracic vertebrae curved posteriorly from the gravity line. The female spine, below the age of 40, arcs less than that of the male, and the thoracic arc increases with age regardless of gender.
The extent of deviation from the midline of the cervical and lumbar curves is controlled to a great extent by the strength of the antigravity extensors, the weakness of the flexors, and the ability of the flexors to stretch. Keep in mind that the fetus is curved like a crescent. When the infant gains the erect position, the anterior lumbar curve and pelvic tilt are governed essentially by the strength of the lumbar-pelvic erectors and how far the iliopsoas and iliacus will elongate.
THE BASE EFFECT
The greater the S1 or T1 angles, the sharper the lumbar or cervical curves must be to bring the spine back toward the center of gravity. Thus, the sacral angle and wedge shape of the L5 disc determine the angles of the lower lumbars and the compensatory upper lumbar angles, and the T1 plane and shape of its disc generally control the cervical curve. Ideally, this base effect would progress up the spine from the sacrum so that the odontoid process would be in line with the gravity line. However, because the thoracic area allows minimum A-P mobility, considerable stress is placed at the L1-T12 and T1-C7 junctions.
The stability of the spine depends upon a number of factors, but essentially it is maintained by the relationship of the vertical gravity line to the segments. When weight is in balance to the gravity line, muscular activity is minimal. When in a chronic unbalanced state, fatigue and structural deformity are induced (Fig. 6.7). This is readily brought out when vertebral asymmetry horizontally or a short leg produces a lateral tilt that must be compensated by scoliosis. In short time, the muscles on the concave side of the curve become fatigued, the vertebral bodies rotate toward the side of convexity, and the spinous processes rotate toward the side of concavity.
Head and trunk weight is fairly balanced in the frontal plane where the gravity line passes posterior to most of the centers of the cervical vertebral bodies, through the bodies at the cervicothoracic junction, anterior to the thoracic body centers, through the bodies at the thoracolumbar junction, and posterior to most of the lumbar body centers.
Because body mass is heavier anteriorly in the thoracic region, the thoracic curvature must arc posteriorly in compensation. This compensatory kyphosis is limited by restricted A-P thoracic motion and the posterior ligament straps. As muscles fatigue rapidly, the erectors have little influence. Most severe thoracic kyphoses result from collapse of the anterior vertebral bodies.
Since the lumbar spine carries more weight than any other region of the spine, it is the responsibility of this area to make major adjustments to load shifts from the gravity line. For example, thoracic kyphosis shifts the line anteriorly so that the lumbar area must increase its lordosis to prevent the body from falling forward. In this regard, the lumbar effect is secondary to the thoracic kyphosis. A similar effect is seen in late stages of pregnancy where a temporary increase in lumbar lordosis develops in adjustment to the increased anterior body mass. On the other hand, any condition that would tend to shift the center of gravity posteriorly would tend to flatten the lumbar curve.
These adjustments are in addition to the adjustments the lumbar vertebrae must make to the normally anteroinferior slant of the sacrum. As the sacrum is usually more oblique in females than in males, due to different pelvic design, lumbar compensations will usually be more pronounced in females.
Normal Spinal Movements
PLANES OF MOTION
Normal movements of a vertebral segment relative to its supporting structure below may be described in accordance with its ability to laterally flex on the coronal plane, rotate on the transverse plane, and anteroflex and retroextend on the sagittal plane (Fig. 6.8). To some degree, all vertebrae are able to function in all three dimensions; however, the magnitude of such movements varies to some degree in the different regions as well as in the transitional areas.
As the spine is normally curved in its A-P aspect, few spinal motion units move on a horizontal plane because few discs are parallel to the ground. Horizontal motion occurs only at the centers of the curves such as near the C5, T6, and L3 disc areas (Fig. 6.9).
EXTENT OF MOTION
In the A-P direction, male mobility usually exceeds female mobility. On the other hand, female mobility usually exceeds male mobility in lateral flexion.
Spinal motion between vertebrae takes place essentially at the fibrocartilaginous IVD and the zygapophyseal joints formed by the inferior facets of the superior vertebra and the superior facets of the inferior vertebra. Movement is also governed by the flexibility of the disc and the slope of the articulating facets. All spinal motions require free gliding of the articular facets. While motion of any one vertebra is quite minimal, the sum motion of the 24 vertebral segments is considerable.
The IVD's are relatively large in the cervical area in comparison to the size of their bodies. The inferior cervical bodies are concave and the superior bodies are convex in their A-P and lateral aspects to allow overlapping during quite free flexion, extension, and lateral bending. In the thoracic area, the IVD's are relatively smaller, flatter, and wedge-shaped as compared to their bodies. The discs are quite large in the lumbar area.
The anterior convexity of the cervical and lumbar regions decreases during flexion, and it is not uncommon for the cervical curvature to slightly reverse during complete flexion.
Flexion is the most pronounced spinal motion. About 75% of all spinal flexion below the neck occurs in the lumbar spine, and about 70% of all lumbar flexion occurs at the lumbosacral joint. Normally, the degree of lumbar flexion is up to and only slightly over the flattening of normal lordosis, thus total possible flexion must be achieved by hip rotation. In fact, some people can bend forward to touch the floor with little change in the spinal curves (Fig. 6.10).
ACTION AND BRAKE MECHANISMS
Flexion. During flexion, the IVD tends to compress at its anterior aspect, the inferior set of articular facets glide anterosuperiorly upon the mating set of superior facets of the vertebra below, and the range of motion is checked by the posterior anulus of the disc, the posterior longitudinal ligament, the intertransverse ligaments, the supraspinous ligament, the extensor muscles, and the dorsolumbar aponeurotic sheet of fascia.
Extension. Extension has a much lower magnitude than flexion. The IVD tends to compress at its posterior aspect, and the inferior set of articular facets glide posteroinferiorly upon the mating superior facets below. The motion is checked by the anterior anulus of the disc, the anterior longitudinal ligament, all the anterior and lateral muscles that contribute to flexion, the anterior fascia and visceral attachments, and probably spinous process and/or laminae jamming at maximum extension.
Rotation. Spinal rotation is limited by the planes of the articular facets, the thickness of the associated IVD's, and the resistance offered by the fibers of the disc's anulus and the vertebral ligaments under torsion.
Lateral Bending. Sideward abduction involves a degree of tilting of vertebral bodies on their discs. The anterior aspect of the vertebral bodies in the upper spine also rotate toward the side of convexity, the posterior aspect swings in the opposite direction, and the facets tend to slide open on the convex side and override on the concave side. The motion is checked by the intertransverse ligaments and intercostal tissues on the convex side, behind the fulcrum, and the apposition of ribs on the concave side in the thoracic region.
Coupling and Related Effects. Some motions restrict other motions and enhance still others. For example, flexion and extension restrict rotation and lateral bending ranges. Rotation decreases A-P motion and is accompanied by a degree of lateral flexion. Lateral flexion inhibits A-P motion, and it enhances cervical rotation towards the concave side and lumbar rotation towards the convex side.
The Vertebrae and Pertinent Osteology
When viewed as a whole, the entire vertebral column can be thought of as three segmented rods: a major pillar of anteriorly stacked vertebral bodies and discs, and two minor pillars of posteriorly stacked bilateral articular processes (Fig. 6.11). These tripod-arranged pillars progressively increase in size from C1 to L5 as a mechanical adaptation to increasingly progressive load to which the vertebrae are subjected in the erect position. Likewise, the compression strength of the vertebrae progressively increases from C1-L5.
A vertebra consists of a main body located anteriorly and a bony arch located posteriorly. The vertebral arch is composed of two bilateral, short, stout pedicles which join the arch to the vertebral body and two plate-like laminae which span the pedicles. In addition to their posterior articulating surfaces, each pedicle has superior and inferior rounded grooves which form the intervertebral foramina (IVF's) through which the spinal nerves pass. The arch supports two transverse, one spinous, and four articular processes.
Each aspect of a vertebra has a major function. The vertebral body serves as the weight-bearing aspect, the bilateral superior and inferior processes determine the direction of motion and restrict abnormal movement, the vertebral arch encases the spinal cord and its coverings, and the spinous and transverse processes serve as bony levers for muscle and ligament attachment.
Basic Regional Differences
In addition to differences in size, the first, second, and seventh cervical vertebrae are atypical; the wedge-shaped thoracic vertebrae have articular facets for the ribs; and the lumbar spine has mammary processes. There are also significant regional differences in the spinous processes, laminae, and transverse processes. Figures 6.12, 6.13, and 6.14 exhibit the major structures.
It is important to keep in mind that as much as one-third of a typical human spine shows some variation from the textbook "normal." This is often reflected in an increase or decrease in the number of vertebrae or ribs, malformed unions, abnormal facet facings and unilateral differences, and differences in curvature arcs.
In the cervical and lumbar regions, the spinous processes project fairly posterior except for a posterior tubercle that replaces the spinous process of the atlas. Cervical processes are usually bifid and of equal length in Caucasians but nonbifid in Negroes. The process of C7 is called the vertebra prominens, but it is sometimes shorter than that of the T1. In the thoracic region, the spinous processes are bifid, often of unequal length, and turned downward and overlap like shingles. This is most pronounced in the T2-T10 area. Consequently, extension is severely limited there, and A-P movements are made much more freely in the cervical and lumbar regions. The spinous processes of the lumbar spine resemble thick, relatively large, quadrilateral plates. The L5 segment has the smallest lumbar process.
The laminae overlap slightly in the cervical spine, overlap severely in the thoracic spine, and do not overlap at all in the lumbar region. When overlap is absent, bony protection is diminished. Similar gaps are also seen at the occipito-atlantal, atlanto-axial, lumbosacral, and sacrococcygeal junctions.
The cervical vertebrae contain foramina within their transverse processes for passage of the vertebral vessels. All channel the vertebral artery, vein, and sympathetic fibers except for the smaller C7 foramina which do not transmit the artery and are occasionally absent. With the exception of the wide transverse processes of the atlas and C7, the horizontal processes of C2-C6 are relatively small, fairly equal in width, located anterior to the facet joints, and turn inferior-anterior to overlap the IVF's. If a transverse process of C7 is as wide as or wider than that of T1, a cervical rib is often associated. The wide, thick, strong transverse processes of the thoracic spine arise posterior to the IVF's and articular processes, sit further posterior than those of the cervical or lumbar regions, serve as fulcra for the ribs (T1-T10) at their specialized transverse process facets, and act as lever arms for muscles and ligaments. The widths of the thoracic transverse processes progressively decrease caudally while those of the lumbar region increase to L3 and then slightly decrease at L4 and L5. The transverse processes of the lumbar spine project as thin plates that extend dorsolaterally in the upper region and progressively become more anterolateral as L5 is approached.
JOINTS OF LUSCHKA
Near the posterolateral aspect of the adult cervical IVD's, small, bilateral, oblique cavities often appear that can be mistaken for true synovial joints. These uncovertebral articular modifications are located between the superior surfaces of the uncinate processes and the corresponding lateral tips of the articular surface below. They are evident around 8–10 years of age in only some people, thus several authorities feel they represent degenerative changes in accommodation to stress.
The Vertebral Motion Unit
As it serves as the axial support of the trunk, the erect spinal column is a primary concern in static postural equilibrium. Since the body is never actually in a static state in life but exists in a state of "quiet dynamics" in the sta- tic postural attitude and a state of "active dynamics" in movement, the kinetic aspects of normal spinal biomechanics are an important consideration. Total spi- nal function is the sum of its individual component units.
An intervertebral "motion unit" consists of two vertebrae and their contiguous structures forming a set of articulations at one intervertebral level, thus conferring a quality and quantity of motion to the relationship of two vertebrae (Fig. 6.15). These units are firmly interconnected by the IVD and restraining ligaments and are activated by muscles that respond to both sensory and motor innervation.
The biomechanical efficiency of any one of the 25 vertebral motion units from atlas to sacrum can be described as that condition (individually and collectively) in which each gravitationally dependent segment above is (1) free to seek its normal resting position in relation to its supporting structure below, (2) free to move efficiently through its normal ranges of motion, and (3) free to return to its normal resting position after movement.
THE ANTERIOR PORTION
This includes the roughly cylindrical vertebral bodies, the hydraulic IVD, the anterior and posterior longitudinal ligaments, and the other associated soft tissues. This anterior portion is weight bearing, shock absorbing, and supportive, and it plays an essentially static role. At the slightly concave superior and inferior aspects of the vertebral body are the vertebral end plates. The anterior portion of the unit has very little sensory innervation. Changes or pathology affecting these structures, even though they may be quite spectacular in appearance on an x-ray film and may alter biomechanics and spinal mobility significantly, are seldom accompanied by much pain or other subjective discomfort in the local area.
THE POSTERIOR PORTION
The non-weight-bearing, tuning-fork-shaped, posterior aspect of a motion unit consists of the two pedicles, two laminae, neural foramina, articular processes and apophyseal articulations, the ligamenta flava and those that encapsulate the articulation, the spinous and transverse processes, the interspinous and supraspinous ligaments, and all the muscles and other attached soft-tissue structures (Fig. 6.16). The posterior portion of the motion units, which plays an essentially dynamic role, is rich in sensory and proprioceptive nerves. Thus, problems that affect these structures are usually painful.
The Vertebral Body
The vertebral body can be considered as a miniature long bone in structure; ie, a hard shell surrounding a spongy interior containing an array of crisscrossing trabeculae and red marrow. However, the cancellous portion of a vertebra is much thinner than that seen in a long bone.
VERTEBRAL BODY LOADING
Although some axial load is carried by the vertebral facets, the majority of compression load is borne by the vertebral bodies. Load upon a superior end plate is directed to the inferior end plate via the cancellous core and the cortical shell. Not only does the cancellous core share load distribution with the cortical shell, but during loading (especially at high rates) it serves as the main resistor of dynamic peak loads via its energy-absorbing trabeculae and marrow.
Core Strength. The cancellous core of the vertebral body provides 55% of its vertebral strength, and the cortical shell provides 45% of its strength up to the age of 40. This core strength sharply decreases after the age of 40 to about 35%, with 65% provided by the cortex. Beyond 60 years, however, this decrease in core strength is much more gradual. Bone strength appears to be directly related to mineral content, and a small loss of osseous tissue has a profound effect on bone strength. A 25% loss of osseous tissue decreases bone strength 50%. Comparative values of healthy vertebral bodies are offered in Figure 6.17.
Core Deformation. The cancellous core of a vertebral body can undergo up to 9.5% deformation prior to fracture, as compared to only 2% for the cortical shell. Thus, it is unlikely to have compression fractures of the core without fractures of the shell. Figure 6.18 depicts failure with and without a health disc.
CONSIDERATIONS IN INTERSPINAL POSTURE
The vertebral body deserves special consideration in evaluating interspinal posture because even though we usually think of its function as forming the anterior boundary of the neural canal and a slight contribution to the boundary of the foramen, almost any change in its size, shape, or position will alter these boundaries. Second, the vertebral body must be considered in its function as a contributor to the vertebral articulation for limited or excessive movement of this articulation influences the neural canal and the intervertebral foramen. In some instances, it is difficult to separate the change of the vertebral bodies from that of the IVD's.
Changes Relevant to Interspinal Posture. Changes of the medullary substance which influence interspinal posture include (1) loss of substance, (2) collapse, (3) comminuted fragmentation, (4) scalloping of margins, (5) wedging that may be triangular, quadrilateral, or trapezoid in shape, (6) biconcave deformity (cupping), (7) serrated formations, (8) irregular cartilaginous plates such as in osteochrondrosis or underdevelopment of the secondary ossification centers, (9) Schmorl's nodes, and (10) osteophytes.
Changes Usually Irrelevant to Interspinal Posture. The internal structure or medullary portion of the vertebral body undergoes a number of changes that do not necessarily influence spinal posture. These include (1) lack of substance, (2) sclerosis, (3) condensation, (4) eburnation, (5) fasciculation, (6) osteoporosis, and (7) compression. Changes in the vertebral body that do not appreciably alter the A-P curve, neural canal, or foramina, but do denote limitation of movement or fixation, include marginal sclerosis or end plate sclerosis which may be in the form of lipping or spurring. Exostosis or marginal vertebral hypertrophy occurs following trauma or chronic abnormal weight-bearing changes much in the fashion as that which develops on the margin of the articular facet. These overgrowths may or may not produce encroachment of the spinal canal or foramina, depending upon location.
Other factors influencing size, shape, and position of the vertebral bodies include a long list of congenital anomalies such as hemivertebrae, osteochondrodystrophy, achondroplasia, and dyschondroplasia.
Planes of Articulation
Paired diarthrodial articular processes (zygapophyses) project from the vertebral arches. The superior processes (prezygapophyses) of the inferior vertebra contain articulating facets, which face somewhat posteriorly. They mate with the inferior processes (postzygapophyses) of the vertebra above which face somewhat anteriorly. Each articular facet is covered by a thin layer of hyaline cartilage which faces the synovial joint. Vertebrae facet angulation varies with the level of the spine.
Fisk states that these joints are more prone to osteoarthritic changes than any other joint in the body. "Evidence of disc degeneration precedes this arthritis in the lumbar spine, but there is no such relationship in the cervical spine." However, most authorities agree with Grieve that the presence of arthrotic changes in the facet planes does not, of itself, necessarily have any effect upon ranges of movement, neither does the presence of osteophytosis.
THE CERVICAL AREA
The plane of articulation is about perpendicular to the sagittal plane and inclined about 45° to the vertical plane in the cervical region. The lateral cervical gravity line extends from the apex of the odontoid process through the anterior aspect of T2. The relatively stable base between T1–T2 progressively changes upward so that the planes of articulation tend to be forced inferior, posterior, but not medially as in the thoracic and lumbar regions of the spine.
A horizontal locking type base of support at the atlantoaxial articulation is quite similar to that found at the lumbosacral area. The inferior articular surfaces of the atlas offer a bilateral, medial, and inferior slant which forces the atlas to move inward toward the odontoid to allow rotary movements of the head. Excessive A-P movement is stabilized by the anterior and posterior rings and check ligaments. The posteromedially slanted cup-like superior articular surfaces of the atlas help stabilize the occipital articulating surfaces. These concave facets allow free rocking for A-P nodding.
From C3 to C7, the almost flat and thus freely mobile articular processes are found at the junction of the pedicles and laminae. The inferior facets face downward and forward, and glide on the superior facets of the vertebra below which face upward and backward (Fig. 6.19). Maximum cervical A-P movement usually takes place between C5 and C6, and it is almost impossible to actively flex the neck without causing some flexion in the upper thoracic region.
THE THORACIC AREA
In the thoracic spine, the direction of the superior articulations is pos- terolateral, and the inferior processes face anteromedially. This slant comes closer to the vertical axis as the thoracic spine progresses caudally. The fa- cets are inclined about 60° to the vertical plane in the midthoracic spine. The articular planes of the thoracic vertebrae allow greater rotation but less flexion and extension than that seen in the more horizontal articular planes of the lumbar vertebra. Thoracic movement is restricted in all directions because of the attached rib cage. Gravitational forces fall upon the articular surfaces in such a manner as to force each vertebra more inferior, posterior, and medial until gravity brings the curve back toward the centered balance point.
THE LUMBAR AREA
The facets in the lumbar region describe moderately sloped surfaces rather than a single-plane angle as seen in the cervical and thoracic area and are fairly parallel to the vertical plane. The convex inferior facets mate with con- cave superior facets. From L1 to L5, the plane of the articular facets changes from mediolateral to anteroposterior and lie, for the most part, in the sagittal plane.
From the middle of the anterior surface of T12, the body's gravity line ex- tends downward to the anterior aspect of the sacral base. Weight distribution in the lumbar region is governed chiefly by the inclination of each vertebral body articulation. The lumbosacral articulations are slightly more horizontal than those above them. This allows greater A-P and lateral motion but affords less joint locking as compared to the vertebrae above.
The horizontal inclination of L5, spreading out toward the coronal plane, becomes progressively more vertical from L4 to L1 as the dorsolumbar articula- tion is approached. These changes in articular planes allow the lower back to bend and twist to accommodate gravitational force during movement. The upper lumbar joints are J-shaped when viewed from the lateral, thus their anterior aspect resists forward displacement.
The lateral center line of gravity falls upon the spinal points because of gradual changes in the angles of the inclined planes of the various articular surfaces. Van Dusen points out that this tends to force each lumbar vertebra more inferior, medial, and anterior or posterior until gravity brings the apex of the curve back toward the balancing point.
Body weight is borne ultimately in the lower back essentially by the L5 disc, sacral base, and sacroiliac joints. This weight is forced slightly anterior on the load surfaces to place the lateral pelvic gravity line at the anteroinferior aspect of S2. Gravitational weight during development wedges the sacrum between the innominates because of their peculiar laterally inclined planes that allow the sacrum to move inferior, anterior, and medial, coupled with the anteroinferior angulation of the sacral base.
Many of the abnormal orientations found in the lower spine can be attributed to the fact that the lumbar facet joints are not determined until the secondary curves are developed in the erect position. The stresses imposed during the development stage can easily lead to the high incidence of asymmetry.
FACET ANGLE VARIATIONS
An important influence on interspinal posture is that of the facet facing of each posterior intervertebral joint, with the alterations of the facings most commonly occurring in the lumbar and lower cervical regions. The facings are more frequently altered between L4 and L5 than at any other level in the verte- bral column.
Symmetric facets glide with little friction produced. However, if the facets deviate in their direction of movement, the unparallel articulating surfaces "scrub" upon one another. Articular variances of the processes and facets, over a period of time even in the absence of injury at the level of abnormality, will present thickening of the covering of the facet, referred to as marginal sclero- sis. This hardening process is usually followed by hypertrophy or exostosis and produces an appearance of an irregular articular surface when the facet is viewed in profile in roentgenography. Coexistent with this finding, the interar- ticular spaces gradually become narrowed, hazy, obscured, and even obliterated on x-ray films.
Since these various facet and interarticular manifestations are due to either chronic abnormal weight-bearing or specific trauma, the term arthrosis is used rather than posterior intervertebral osteoarthritis. It seems a more reaso- nable descriptor because of the implications of the suffix "itis". Although there may not be evidence of direct bony encroachment from the process of arth- rosis directly into the intervertebral foramina, one must consider that the pro- cess of arthrosis does produce a general narrowing of the diameters of the intervertebral foramina and hence produces interference with the normal expres- sion of nerve impulse transmission.
Normal articular angles in any text are approximations. There is consider- able variation from one person to another and from the transition of one region to another. For example, the transitional vertebra between the thoracic and lum- bar regions is usually given as T12, but it might be any vertebra from T9–L1 according to White/Panjabi.
Torsional Strength. The articulating processes and their capsular ligaments provide up to 45% of torsional strength of a vertebral motion unit, as contrasted with 45% by the disc and longitudinal ligaments and 10% by the interspinous lig- aments. These percentages will vary with different postures.
Compression Strength. The facets normally carry about 18% of a vertebra's total axial load but can contribute up to 33% of its compression strength, de- pending upon posture. The facets of a lower lordotic curve (C5–C7; L3–L5) carry more weight than those of other areas.
The Intervertebral Foramina
Generally, an intervertebral foramen is bounded above by the inferior pedicle notch of the superior vertebra, below by the superior pedicle notch of the inferior vertebra, anteriorly by the IVD and parts of the two vertebral bodies, and posteriorly by the superior and inferior articular processes.
Vertebrae move in the planes of their articulations, and it is at the level of the posterior intervertebral articulations along with their facets that most subluxations occur and influence the IVF's far more than any other articulations of the spinal column. Changes in the diameter of normal IVF's result in an ab- normal joint formation, which predisposes to subluxation as well as being a direct factor in altering the curves of the particular region of the spine in which this structural defect is found.
SIZE AND SHAPE
When viewed laterally, an IVF is generally elliptical in shape, with the diameter of its vertical axis about double its A–P dimension. Because of this, there is usually adequate space for changes in vertical dimension (eg, dynamic axial traction or compression, disc flattening) without injury to the IVF con- tents as long as there is adequate fat and fluid present. However, reduction of an already short transverse diameter can produce a number of noxious effects. For this reason, complete disc collapse vertically is often asymptomatic, while a slight posterolateral herniation may protrude upon the IVF and produce severe symptoms.
The Cervical Area. In the cervical region, the foramina are more in the shape of rounded gutters than orifices, averaging 1 cm in length. There is no IVF between the atlas and the occiput or between the atlas and the axis. The C1 nerve exits over the superior aspect of the posterior arch of the atlas in the vertebral artery sulcus. The C2 nerve exits between the inferior aspect of the posterior arch of the atlas and the superior aspect of pedicle of the axis. It then dangerously transverses the lateral atlantoaxial joint, anterior to the ligamentum flava. The C3–C8 nerves exit through short oval canals, which increase in size as they progress caudally. Cervical nerves, especially, fill the transverse diameter of the their IVF's. Thus, any disorder that reduces this dimension (eg, subluxation, osteophytes, disc herniation, edema) will undoubted- ly compromise the integrity of the IVF contents (Fig. 6.20).
The Thoracic Area. In the thoracic region, the pedicle notch of the vertebra above is quite deep, while that of the vertebra below is relatively shallow. The result is a pear-shaped canal with sharp bony edges that predispose to fibrotic changes from chronic irritation. The vertebral body and the disc of the superior vertebra form most of the IVF's anterior boundry.
The Lumbar Area. In the lumbar region, an IVF is shaped like a kidney bean. It takes considerable posterolateral disc protrusion to encroach the nerve exiting at the same level because the lumbar IVF's are relatively large. When herniation does cause trouble, it is usually due to pressure on the laterally placed nerve root on the vertebra above. Sunderland stresses the fact that the passage of the medial branch of the lumbar dorsal ramus and its accompanying vessels through the osseofibrous tunnel and the intimate relationship of the neurovascular bundle to the capsule of the apophyseal joint represents a poten- tial site of fixation and entrapment following pathologic changes involving the joint.
Each foramen is dynamic; widening and expanding with spinal motion, serving as a channel for nerve and vascular egress and ingress, and allowing compression and expansion of the lipoareolar bed. From one-third to one-half of the forami- nal opening is occupied by the spinal nerve root and its sheath, with the remaining portion filled essentially by fat, connective tissue, and various vessels.
The following specific structures are found in the IVF: the anterior nerve root, the posterior nerve root, a part of the dorsal nerve root ganglion, a bilaminar sleeve of dura and arachnoid membrane to the ganglion, a short contin- uation of the subarachnoid space with cerebrospinal fluid which ends just after the ganglion, the recurrent meningeal nerve, the spinal ramus artery, the inter- vertebral vein, and lymphatic vessels.
Factors That Change the Diameter. The typical factors modifying the diame- ters of the IVF's are (1) the disrelation of facet subluxation, (2) changes in the normal static curves of the spine, (3) the presence of induced abnormal cur- ves of the spine, (4) degenerative thinning, bulging, or extrusion of the related IVD, (5) swelling and sclerosing of the capsular ligaments and the interbody articulation, and (6) marginal proliferations of the vertebral bodies and articulations.
Consequences of Diameter Alteration. The above factors insult the viable contents of the IVF and subject its contents to physiologic compromise that results in nerve root pressure, traction, or torque; constriction of the spinal blood vessels; intraforaminal and paraforaminal edema; induration and sclerosing of the periarticular ligaments with incarcerating insult upon the contained receptors; forcing of the foraminal contents into protracted constriction and altered position; and such other consequences. Nerve tissue tolerates slow com- pression quite well without offering obvious symptoms. Acute phenomena are usually the result of friction, severe or repeated trauma, and encroachment from degenerative thickening or exostosis.
The Spinal Joints and Pertinent Arthrology
Each vertebral segment articulates with adjacent vertebrae and ribs through a complex system of joints, ligaments, and levers. The stability of the spine and pelvis is not due to its inherent ligamentous stability, which is meager as a whole, but through its dynamic neuromuscular structures and control system.
The Vertebral Joints
As many as 97 true-synovial diarthroses and an even greater number of amphiarthroses are involved in spinal movement. All these diarthroses are the gliding type except for the odontoid pivot joint on the atlas. Synarthroses are found only during development.
The dynamic functions of the spine are dependent upon seven articulations:1. Posterior intervertebral (synovial) 2. Vertebral bodies and IVD's (nonsynovial) 3. Costovertebral (synovial) 4. Uncovertebral joints of Luschka (synovial?) 5. Sacroiliac (nonsynovial) 6. Symphysis pubis (nonsynovial) 7. Iliofemoral (synovial).The fact that some of these joints are synovial and some are nonsynovial accounts for the expression of localized pain witnessed clinically in the synovial joints and the absence of pain in the nonsynovial types of articulation. The other contributing factor of pain elicitation is found in the sensory nerves of the periosteum or perichondrium. The posterior intervertebral articulations contain both synovial membrane and perichondrium, whereas the anterior vertebral body articulation contains neither of these two connective tissues.
The spine exhibits two main areas of articulation: at the vertebral body and at the vertebral arch. Two forms of nonsynovial amphiarthroses connect adjacent vertebral bodies: the IVD's represent symphyses, and the anterior and posterior longitudinal ligaments form syndesmoses. The articulations of the vertebral arches involve the apophyseal joints, the ligamentum flava, and the interspinous and intertransverse ligaments.
The Intervertebral Disc Area
The elasticity of the IVD's is diminished throughout the day as an individual remains in the upright position and the discs are subjected to compression forces producing dehydration. Thus, the length of the spine is gradually diminished so that a person is shorter at night than in the morning. In senility or from a premature breakdown in the disc's gel, disc thickness and elasticity are diminished, thus disc flexibility and resistance to jarring are lessened.
The IVD's are numbered by the vertebra above; spinal nerves, by the vertebra below. Thus, for example, a posterolaterally herniated C6 disc may affect the C7 nerve.
There is no true disc between the occiput and atlas or between the atlas and the axis. The L5 disc is considered the last disc, but rudimentary discs are sometimes present between the sacral segments, sacrococcygeal junction, and the coccygeal segments.
The joints between C3 and S1 vertebral bodies are unique symphyses formed by the opposing vertebral plateaus and the IVD. Each disc unit consists of three distinct parts: the end-plates, anulus fibrosus, and nucleus pulposus.
The End Plates. These are thin sheets of cortical bone and relatively tough hyaline cartilage that separate the disc from the vertebral body above and below. They tend to prevent herniation of the nucleus into the adjacent vertebral bodies (Fig. 6.21).
The Anulus Fibrosus. The peripheral part of the disc is composed of lamina- ted bands of concentric fibers. The apposing layers of fibers are angled (+/- 30°) in opposite oblique direction (criss-crossed). The fibers become angled less obliquely toward the periphery so that they are nearly vertical at the edge of the disc and almost horizontal near the core. In this manner, the anular fibers extending from one end-plate to the other serve as coiled springs that tend to hold the adjacent vertebral bodies together against the pressure of the nucleus. The anular fibers are loosely attached to the vertebral end plates centrally but strongly fixed to bone at the periphery (Sharpey's fibers). Fibers near the circumference blend into the posterior and anterior longitudinal ligaments.
The number of lamellae in the anulus is the same at all points around the disc. However, these fibers are distorted and compressed by the effect of posture on the secondary curve in the lumbar region, resulting in thickening of the anterior portion of the anulus.
The Anulus and Loading. The outer disc carries 25% of vertical compression forces. It is best designed to carry tension forces, while the nucleus is better constructed to carry compression loads. Anulus fibers are usually stouter and stronger anteriorly and centrally, thus contributing to the higher incidence of posterolateral herniation.
The Nucleus Pulposus. The central part of the disc is surrounded laterally by the central ring of the anulus and above and below by the vertebral plateaus (Fig. 6.22). It resembles a small, transparent, mucopolysaccharide gelatinous sphere (80–90% water) under both internal and external pressure that gives it considerable elastic rebound, and it is devoid of nerve fibers and blood vessels. Its shape allows motion in all directions. There is no definite structural interface between the nucleus and the anulus in the adult; ie, the tissues blend rather than appose. The nucleus is a remnant of the beaded string of intervertebral notochordal cells that did not degenerate.
The Nucleus and Loading. The ability of the nucleus to absorb and retain water under high imbibition pressure is unique to living tissue. As a ball bearing between two relatively flat surfaces, the nucleus allows six degrees of freedom. However, the extent of motion at any particular disc is limited by the various ligaments and facet planes. The nucleus, highly resistant to compression, carries or distributes the majority of axial compression forces. It transmits some forces horizontally to the anulus, and the amount increases when the spine is flexed and the load is increased as in lifting. Actual displacement of the nucleus occurs most often in severe scoliosis as a result of disc degeneration and the abnormal distribution of forces on the disc.
Regional Variables. Disc thickness varies in the different spinal regions as the result of the degree of curvature, load, vertebral body size, and hydrophilic capacity. Discs are thinnest in the cervical region and progressively thicken as the spine progresses caudally (Fig. 6.23). However, it is the ratio of disc thickness to vertebral body thickness that governs segmental mobility. This ratio is greatest in the cervical region and least in the thoracic area. The surface area of the nucleus (nucleus/anulus ratio) relative to the overall disc and the position of the nucleus relative to the midline also vary slightly according to spinal region (Fig. 6.24). Data from Kapandji and others in this regard are summarized in Table 6.1.
Table 6.1. Intervertebral Disc Regional Variables (Approximate)Average Disc:Body Nucleus:Anulus Position to Discs Thickness Ratio Ratio Vertical Axis Cervical 3 mm 2:5 4:7 57% nucleus Centered--Posterior Thoracic 5 mm 1:5 3:7 43% nucleus Posterior Lumbar 9 mm 1:3 4:6 67% nucleus Centered--Posterior
These facts are important as it has been shown that the IVD functions opti- mally, has the greatest resistance to stress, and allows optimum mobility when (1) the nucleus is located near the center of the disc, (2) the height of the disc is of normal proportions, (3) its dimensions are symmetrical, and (4) the disc is well hydrated.
The disc is subjected to a variety of loads: compression by gravity, push- ing; traction by being pulled; tensile stress by flexion, extension, lateral bending; torsion and shear by axial rotation; and various multiple combinations of each. Since the back muscles use the spine as a lever in maintaining balance, the forces upon the IVD's and vertebrae are much greater than the forces of the body weight above.
Disc Bulge. During spinal movement, the peripheral anulus bulges slightly posterior during extension, anteriorly during flexion, and towards the side of lateral bending. This is opposite to what some might think. Concurrent with bulging is disc contraction on the contralateral side (Poisson effect). The healthy nucleus remains near its normal position with only slight movement towards the anular bulge.
Preloading. Because the nucleus is strongly hydrophilic and encased, its pressure is never zero, even if completely unloaded. This "preloaded" factor offers an inherent tension which offers greater resistance to compression and lateral flexion forces. The "swollen" state of the nucleus also creates a constant pressure directed peripherally to the fibers of the anulus (Fig. 6.25). The hydrophilic characteristic of the nucleus decreases during constant load and advanced age, and this fact contributes to the reduction of spinal flexibility. The preload pressure of the nucleus is enhanced by about 30-lb of inherent pressure exerted by the anulus and intervertebral ligaments.
Loading. In the static position, the load on a disc is much greater than the superimposed body weight. This is the result of the center of gravity being anterior to the disc causing a bending moment that must be resisted by posterior muscle action that increases the compression force. During forward flexion, the L3 disc is subjected to about double the body weight above. If only a 45-lb external load is added (eg, a child being lifted), the disc carries a force three times the superimposed body weight. These pressures are substantially increased in the sitting position. During erect dynamic activities, disc forces rise to double static forces without the addition of external load.
Reaction to Axial Tension. When a vertebral motion unit is subjected to elon- gation (eg, during vertical stretching, A-P and lateral bending, rotation while flexed, mechanical traction, or hanging from a horizontal bar), the vertebral bodies tend to separate, the disc thickens, nuclear pressure reduces, and vertical anular fiber tension towards the periphery of the disc increases. Tensile loads produce perpendicular normal stresses that are readily absorbed by the criss-crossed anular layers and relatively larger parallel shear stress in the anulus that has little resistance. This is an early factor in most disc failures (Fig. 6.26).
Reaction to Axial Compression. When a vertebral motion unit is under axial compression (eg, body weight, with or without external load), the vertebral bodies tend to approximate, the disc flattens, nuclear pressure increases, the end plates are subjected to greater pressure, and anular fiber tension increases from forces projected laterally from the nucleus. Forces are normally transmitted evenly throughout the nucleus. The closed, pressurized container of the nucleus conforms to the law of Pascal which states that "any external force exerted on a unit area of a confined liquid is transmitted undiminished to every unit area of the interior of the containing vessel." The anular fibers are stressed somewhat vertically (compressive) and horizontally (tensive) but greater in line with their obliqueness (tensile). A disc is stiffer under compression than tension because nuclear pressure is increased under compression.
This centralized loading tends to deflect the end-plates away from the disc at the periphery so that the dimension of the disc increases centrally and the center of the end-plate becomes deformed. Such loading cannot produce disc rupture (unless the disc is burst by an unusually heavy and fast axial force) even if the disc is torn, but the disc does bulge (especially laterally and anteriorly) as it flattens. If excessive loading fractures an end-plate centrally, the nucleus tends to be driven into the vertebral body (traumatic Schmorl's node).
When compression load to a motion unit becomes excessive, the unit fails with fracture of the end-plate or vertebral body with little damage to the disc. Bending and torsional stresses appear to be more dangerous to disc integrity than axial loads. However, once a disc becomes degenerated, the stress of compression load substantially increases. Central end-plate fractures are more often associated with a healthy disc with a firm nucleus that generates maximum bending moments at the plate. In contrast, peripheral end-plate fractures are commonly associated with a degenerated nucleus where most forces are carried via the outer anulus.
Reaction to Asymmetrical Forces. When a disc is loaded unilaterally, the disc initially becomes wedge-shaped and the normally parallel vertebral plateaus form an angle (Fig. 6.27). This vertically stretches the anular fibers opposite to the weight-bearing side, but this action is quickly counteracted by opposite forces transmitted laterally from the nucleus to help the disc return to its normal shape. This self-stabilization factor is the product of a healthy nucleus and anulus working as a mechanical couple.
Reaction to Oblique Forces. When a load is applied obliquely to the superior vertebra of a motion unit, the force is resolved into (1) a vertical force that tends to flatten the disc directly under the point of application and to approximate the vertebrae, and (2) a horizontal force parallel to the plateaus that tends to move the upper vertebra towards the direction of force. This motion stretches the anular fibers in the direction of force that sets up a self-stabilizing couple effect.
Reaction to Flexion, Extension, and Lateral Forces. When the spine is sub- jected to bending loads during flexion, half of the disc on the convex side suffers tension, widening, and contraction, while the other half of the disc on the concave side suffers compression, thinning, and bulging (Fig. 6.28). Concurrently, and in opposite fashion, the nucleus bulges on the side of tension and contracts on the side of compression, which increases tension on the adjacent anulus. As mentioned, this creates a self-stabilizing counteracting flexion force to the motion unit that aids a return to the resting position. An opposite reaction is seen during spinal extension, where the nucleus bulges forward and tension is increased on the anterior anulus to establish a counterforce. During lateral flexion, the anulus and upper vertebra tilt toward the base on the side of abduction and the nucleus bulges away from the side of flexion.
Reaction to Rotary Forces. As mentioned, the apposing layers of anular fibers run alternately oblique in opposite directions. When a vertebra twists, the oblique fibers angled toward the direction of rotation become stretched, and the oblique fibers running against the direction of rotation tend to relax (Fig. 6.29). The greatest tension from stretch is seen centrally where the fibers are nearly horizontal. This increases nuclear pressure by compression in proportion to the amount of rotation and is the most frequent mechanism of traumatic disc rupture. At the transitional areas of the spine, these forces are often magnified by one region rotating clockwise while the other is firmly fixed or rotating counterclockwise (eg, scoliosis, shoveling, sports injuries).
Farfan's cadaver studies showed that lumbar rotation is associated with a anterolateral tilt that increases the distance between the lateral margins of the vertebral bodies on the side of convexity. This especially stretches the posterolateral anulus, and excessive rotation produces a bulging of part of the disc with a compensatory contraction of its contralateral aspect. The anular filaments may separate, causing the disc to lose some of its stiffness property and an inability of the vertebral segment to return to its normal position when the torsion stress is removed. If this were to happen in vivo, a chronic unstable rotational subluxation could be expected to result.
Reaction to Torsion and Shear. Several studies indicate that torsional stress is the type of stress most damaging to discs. Torsion forces in a disc produce horizontal and vertical shear stresses of equal magnitude that vary relative to the instantaneous axis of rotation. The most damaging shear forces are those perpendicular to fiber direction.
Resistance to torsion is offered essentially by the discs and facet joints, in almost equal proportion. In the lumbar spine, Farfan points out that the discs are not equally sensitive to torsional stress. The upper lumbar discs, which are fairly round, are more resistant to torsion than the lower kidney-shaped discs. An L5 that is deeply seated in the pelvis, has a large lumbosacral angle, or has short iliotransverse ligaments is quite protective against torsion. However, these same factors that protect against torsion will subject the area to greater axial forces (Fig. 6.30).
The shear stresses resulting from torsional loading are fairly concentrated along the periphery of the anulus with a much smaller amount located centrally. A disc has a high stiffness resistance to shear in the horizontal plane, thus it is rare that a nucleus would fail from shear load alone.
Creep and Relaxation Behavior. The viscoelastic properties of the disc offer it creep and relaxation behavior. The greater the load, the greater the deformation and the faster the rate of creep. A degenerated disc exhibits less viscoelasticity, less creep, and less capability of attenuating shocks and vibrations uniformly over the full surfaces of the end plates.
Fatigue and Hysteresis Properties. The viscoelastic nature of a disc offers other time-dependent properties such as fatigue and hysteresis, which vary in reaction whether the load is applied quickly with high amplitude (jerk) or slowly with a low magnitude (pressure fatigue failure). As the repair and regeneration capabilities of the avascular disc are low, the fatigue life of a disc is quite low when subjected to repetitive loading. On failure, the result is radial and circumferential tears. When a disc is subjected to repetitive cycles of load and unload (eg, hopping), the shock waves directed from the feet to the head are substantially absorbed by disc hysteresis. This effect is minimal in the T9-L2 area. It decreases when the load-unload cycle is prolonged (eg, constant bumping) and during old age when viscoelasticity is low.
The Apophyseal Joints
The articulating processes have synovial joint capsules that are strengthened by two strong anterior and posterior ligaments, with fibers running perpendicular to the facet plane. They attach just beyond the margin of the facets. They are quite loose and elastic in the cervical region to allow greater mobility without capsule stretch. They are tighter and stronger in the thoracic and lumbar regions.
The faces of the articular facets are covered by tough hyaline cartilage and separated by meniscus-like tabs of synovium that originate from the synovial lining. These tabs glide in and out of the joint during motion but are rarely nipped during joint jamming. The tabs appear to allow a degree of extra shockabsorbing and pressure-absorbing protection for the articular cartilage.
Vertebral tilting as seen in subluxations with disc wedging alters the relationship of apposing articular surfaces to produce a change in the direction of compressive forces on these joints. In contrast, severe rotation produces a jamming compression on ipsilateral facets and contralateral facet opening. When continuous compression is applied to any active and mobile joint, cartilaginous erosion followed by arthritis can be expected.
Possible pain-provoking mechanisms at the facet joints include capsular ligament sprain, facet jamming or fixation by subluxation, pinching of a synovial fringe, entrapment of a loose cartilaginous body in the joint, and cervical or lumbar meniscoid entrapment.
The Spinal Ligaments and Pertinent Syndesmology
In the spine as in the extremities, the purpose of a ligament is to limit or modify joint movement. The articulation between the adjacent vertebral bodies is supported by the anterior and posterior longitudinal ligaments. During dynamic actions, the resiliency of these ligaments offers a cushioning effect that does much to relieve stress on the anulus. The articulations of the vertebral arches are essentially supported by the ligamenta flava, supraspinous, interspinous, and intertransverse ligaments.
Groups of uniaxial fibrous ligaments link together vertebral segments, com- monly check axial tensile forces, and infrequently buckle under axial compres- sion (Fig. 6.31). They must be elastic enough to allow physiologic motion, strong enough to resist excessive motion, exhibit some pretension in the neutral state to provide some stability, and damping and ductile enough to absorb shock energy without permanent deformation.
The anterior and posterior longitudinal ligaments have intimate attachment to the vertebral bodies and disc spaces, exhibit slight in situ pretension, readily stretch with disc bulge, and lose much of their viscoelastic properties in old age. They extend from the base of the occiput to the sacrum, are strong against A-P stress, but may be sprained by excessive rotation.
Anterior Longitudinal Ligament. This ligament narrows at its origin at the occiput, widens as it descends, and is firmly attached to the atlas and the anterolateral surfaces of vertebrae periosteum. It narrows slightly at disc intervals and lightly attaches to the anterior surfaces of the IVD's. It is especially thick and narrow in the thoracic region, with some fibers extending over four or more vertebrae. Chronic traction of this ligament is believed to be the cause of anterior lipping of the vertebral body. In hyperextension (whiplash) injuries of the neck, the anterior ligaments become severely stretched.
Posterior Longitudinal Ligament. The posterior ligament covers the trans- verse ligament of the odontoid, body of the axis, and posterior surface of the vertebral bodies and discs, and finally attaches to the coccyx. It is firmly attached to the IVD's but separated from the vertebral bodies by the venous plexuses. It is also thicker in the thoracic region but widens rather than narrows at the disc level. As this ligament descends to the lumbar region, it begins to narrow so that at the S1 level it has only half its original width and offers a structural weakness to the disc posterolaterally. This is mechanically unfortunate for the discs at the lumbar area must carry severe loading forces, and this weakness contributes to a high incidence of posterolateral disc herniation at the lower lumbar area (Fig. 6.32).
Ligamentum Flava. This short, strong, yellow, highly elastic ligament covers the interlaminar spaces, spanning between the anterior surface of the lower lamina and the superoposterior surface of the higher vertebra, and serves as the posterior boundary of the spinal cord from C2 to S1. The heavy flat bands are separated at intervals in the midline by veins of the external and internal vertebral plexuses. The ligamentum flava readily stretches (35-45%) with spinal flexion, contracts (10%) without buckling in extension, and exhibits substantial in situ pretension (15%) in the neutral position that contributes to disc pretension. This ligamentous pretension prohibits buckling upon neutral relaxation but not upon spinal extension. With aging, some of the elastic fibers (highest proportion in the body) are replaced with fibrous tissue.
Interspinous and Supraspinous Ligaments. Tough posterior interspinous and supraspinous (supraspinal) ligaments join the posterior aspects of the spinous processes from the cervical to the sacral area and reach their maximum tension when the spine is flexed. Bursal formation between the interspinous and supraspinous ligaments is quite common. The interspinous ligaments are poorly developed in the cervical region, thin and narrow in the thoracic region, and relatively broad and thick in the lumbar area. They connect the root and apex of each process during most of life but frequently degenerate in the later years of life. The supraspinous ligaments, composed of thin fibrous bundles, extend down the tips of the spinous processes as a slender band. They are well developed in the cervical region and blend with interspinous fibers to be called the ligamentum nuchae.
Considerable low-back shear forces are witnessed in the erect position because of the lumbar lordosis. These forces are checked somewhat by a meager supraspinous ligament which passes posteriorly to the vertebral facets. However, neither the supraspinous ligament nor the facets have any effect upon compression forces.
Intertransverse Ligament. This thin ligament attaches between the horizontal surfaces of each transverse process, serving as a biomechanical long lever when tensed. The fibers are extremely sparse in the cervical and lumbar regions but well developed in the thoracic area where the fibers are closely intertwined with the deep layer of spinal muscles.
The Vertebral Canal and Related Tissues
The spinal cord, continuous with the medulla oblongata at the foramen magnum, is protected within the spine anteriorly by the posterior aspect of the vertebral body, posteriorly by the bony laminae, and laterally by the pedicles. Further protection and stability are provided by the cord's three membranes, the two fluid-filled spaces, the ligamentum flava and dentate ligaments, and the nerve roots. To accommodate necessary innervation for the limbs, the spinal cord is enlarged at the cervical segments (C4–T1), essentially to supply the brachial plexus, and the lumbosacral segments (L2–S3), essentially to supply the lumbar and sacral plexuses (Fig. 6.33). The average sagittal diameter of the adult cervical vertebral canal is 18 mm.
In reference to the origin of the 31 pairs of spinal nerves, a spinal cord "segment" does not necessarily correspond in height or location to its corresponding numbered vertebra and disc, spinal nerve, or the level of the spinous process. The cervical spine contains 8 cord segments; the thoracic spine, about 20 segments; and the lumbar spine, probably only some sacral and the coccygeal segments. The adult spinal cord can generally be considered to occupy only the upper two-thirds of the vertebral canal.
In the embryo, the spinal cord and vertebral canal are about equal in length until about the 10th week. Because the vertebral column grows faster than the spinal cord, this relationship does not persist. The cord terminates near the level of S1 at 24 weeks, the L3 disc at birth, the L2 disc at age 5, and higher in the adult. This is usually near the level of the L1 disc. Occasionally, it is seen at surgery to terminate in the adult as high as T12 or as low as L3. As the lower third of the vertebral column is approached, the length and obliquity of the nerve roots must progressively increase to reach their respective IVF's.
In the adult, the average linear measurements for the cord and canal are:Spinal Spinal Cord Canal Males 45 cm 70 cm Females 42 cm 60 cmThe vertebral canal increases in length during spinal flexion and lateral bending, and decreases in length during extension. This is considerably reduced because of the flexion-rotation coupling that occurs. Because of its substantial degree of flexibility, the cord easily adapts to the normal lengthening and shortening of the canal during movements.
The spinal cord is sheathed by three cylindrical membranes that extend from the foramen magnum to the midsacral region: the internal pia mater, the middle arachnoid, and the exterior dura mater (Fig. 6.34).
The Pia Mater. The highly vascular pia membrane covers the spinal cord proper. Its outer layer is composed of a loose network essentially of collagenous fibers, and its inner layer consists of a meshwork abundant with elastic fibers. Between these two layers is a fine network of blood vessels.
The Arachnoid. The delicate, transparent, web-like, avascular, elastic fibrous arachnoid parallels the dura mater and pia mater. It is separated from the dura membrane by a serous-fluid-filled potential subdural space that contains threads of connecting subdural trabeculae. It is separated from the pia membrane by a cerebrospinal-fluid-filled subarachnoid space that contains tiny venous plexuses and threads of connecting arachnoid trabeculae that become continuous with the outer collagenous pia membrane. When considered together, the pia mater and arachnoid are called the leptomeninges.
The Dura Mater. The tough, dense, outer connective-tissue dura mater is separated from the bony canal by a potential space filled with fat and veins, which helps to reduce friction and contributes to the absorption of shock energy. However, the dura is firmly attached at the foramen magnum, the bodies of C2 and C3, and in the remaining spine by bridging trabeculae. As well as enclosing the spinal cord, the dura also envelops the spinal roots, nerve, and ganglia as it passes through the IVF and becomes continuous with the epineurium.
The dura, arachnoid, and pia membranes tightly invest the spinal roots as well as the spinal cord, and their extensions surround the cauda equina and fuse at the external terminal filum.
THE DENTATE LIGAMENTS
The 20–21 dentate (sawtoothed) ligaments derive from thickened pia mater. They are inferiorly inclined and extend bilaterally between the anterior and posterior nerve roots from the foramen magnum to the T12–L1 area, penetrate the arachnoid and its fluid-filled spaces, and fix to the inner surface of the dura membrane (Fig. 6.35). They provide a unique pretensed suspension system against sudden jars. It is because of the dentate ligaments that the spinal cord and nerve roots, but not the rootlets, are put under tension during spinal movements.
THE SPINAL CORD PROPER
Cord Flexibility. Although dentate ligaments help to stabilize the spinal cord in a central position in the canal and help to protect against undue stretch, the cord is still flexible enough (10% of length) under small loads to move as much as 3/8 inch. The cord is quite elastic when deformed axially, but prone to severe damage if a vertebra is displaced horizontally.
A space-occupying sclerotic or fibrotic lesion will restrict the cord's mobility and extensibility and thus increase tensile, torsion, and compression stresses. The symptoms thus produced can be alleviated if the cord can be relaxed.
Grieve implies that if a biomechanical evaluation could be conducted at the microscopic level routinely in clinical practice, many neurologic disorders in which no mechanical component is suspected would be shown to have their origin in tension of nervous and vascular microtissues producing a reduction of conduit diameter that interferes with function. We should be reminded here that D. D. Palmer stated before the turn of the century that "chiropractic as a science is founded on tone."
Cord Folds. In its neutral state, the cord possesses accordion-like folds which flatten on stretch (flexion) and increase on relaxation (extension). This folding and unfolding mechanism is responsible for about 3/4 of the cord's change in length from full flexion to full extension. Once these folds have flattened during spinal flexion, the cord is subjected to direct tensile forces. As a rubber band, the diameter of the cord then reduces on stretch and increases on relaxation.
The Cervical Cord. Inasmuch as maximum cervical movement is located at the C5–C6 level and the spinal cord snugly fills the cervical canal, degenerative arthritic changes and disc herniations in this area may encroach upon the canal contents. As the cervical cord is at its maximum width at this level, injury may readily lead to neurologic damage.
The Lumbar Cord. The spinal cord ends near the L1 disc. Below this, the elements of the cauda equina are within the vertebral canal of the lumbar spine. The mobility of the cauda equina roots in the relatively large canal provides a safety factor not found in the cervical or thoracic regions. This safety factor, however, is minimized in spinal stenosis.
The Spinal Nerves
A single spinal nerve trunk is a mixture of several posterior sensory (afferent) and anterior motor (efferent) rootlets. The anterior fibers arise from cell bodies in the spinal cord's ventral gray horn, while the posterior fibers are from cell bodies in the spinal dorsal root ganglia that lie outside the cord and partially within the IVF. A ganglion usually rests against the pedicle. Except for C1 and C2 which do not have IVF's, the common trunk forms just outside the IVF, where it quickly divides into anterior and posterior rami (Fig. 6.36).
The posterior rami turn sharply backward to supply the spinal muscles and skin of the back. Sunderland feels that the passage of the cutaneous branches through the muscles and fascia of the back should not be overlooked as potential sites of entrapment. Such entrapment is most frequent of the greater occipital nerve and the cutaneous branches of the posterior rami of L1–L3 nerves.
A few posterior rami intermix branches but most remain segmental. The anterior rami run anterior and laterally, and most enter into plexuses or connect with sympathetic fibers via the rami communicantes, whereafter their specific identity is impossible to determine. In the fused sacral region, the anterior and posterior rami respectively exit the bony canal through the anterior and posterior foramina.
The nerve roots are not normally firmly attached to the margins of the IVF's, and thus are able to move about quite freely during spinal motions. However, fibrotic changes following the granulation tissue of irritation, especially in the lower cervical region, frequently fix the sleeve at one or more points which contributes to traction on the sheath and its contents during movement. These attachments increase in strength with aging and other degenerative changes.
Position in Foramina. In the cervical spine, the nerve root is anterior and inferior to the facets; in the thoracic spine, directly anterior to the facets (Fig. 6.37); and in the lumbar spine, anterior and superior to the facets, under the pedicles.
Foraminal Compression. The nerve root is often compressed in the IVF by a subluxated articular facet and less often by a herniated disc or a spur from the posterior aspect of the vertebral body. These disorders can be worsened by a state of spinal stenosis which narrows the vertebral canal and the tunnel by which the nerve roots must pass as they exit the IVF's.
Segmental Sensory Supply. The area of a vertebral motion unit derives high- threshold sensory fibers from:
The usually two fine branches of the recurrent (sinuvertebral) meningeal nerve, running anterior to the spinal nerve in the IVF. An autonomic branch from the paravertebral plexus accompanies the recurrent spinal nerve, usually within the same sheath. These supply the anterior dura, blood vessels of the spinal canal, posterior longitudinal ligament, cortex of the vertebral bodies, and the surface of the posterior anulus. No or fibers extremely few fibers enter the central disc. Communicating and linking branches extend across, up, and down at least one segment, and frequently produce radiating or referred symptoms.
The medial branch of the posterior primary ramus. These fibers supply the ligaments and muscles of the posterior aspect of the vertebral unit. As in all synovial joints, the capsules of the articular processes, their fat pads, and their intrinsic and extrinsic ligaments are richly endowed with pain and proprioception fibers. This nerve also sends communicating and linking branches across, up, and down at least a segment. Figure 6.38 depicts most pain sensitive and nonsensitive areas of the vertebral motion unit.
From this we can see that the vertebral joint itself receives innervation from rostral and caudal segments in addition to those from the local segment. This means that a segmentally arranged nerve supply (with its specific dermatomes, muscles, and reflexes) is not available to evaluate a particular vertebral motion unit with certainty.
Nerve Fiber Proportions. There are about three times more sensory fibers than motor fibers in the cervical area, one and a half more in the thoracic region, and twice as many in the lumbar area.
Pain Distribution. When the anterior root is irritated, pain is felt in the muscles supplied and often becomes self-perpetuating from the focal spasm produced (ie, a trigger-point syndrome) with myotomal distribution. When the posterior root is irritated, pain is felt in its dermatomal distribution.
As the autonomic nerve pathways innervating musculoskeletal tissues are intimately connected with the spinal nerves, one can appreciate that these systems do not operate in isolation (Fig. 6.39). Structural disorders in the spine frequently cause, contribute to, or mimic such "functional" disorders as Meniere's disease, causalgia, shoulder-hand syndrome, asthma, sphincter spasms, cluster headaches, angina, and a large variety of referred pains.
Spinal Circulation and Pertinent Angiology
All skeletal muscles have a rich blood supply consisting of an intricate network of capillaries. The arrangement of the capillary network is such that each muscle fiber is placed in relation to several (4 or 5) capillary vessels. Many of these capillaries are closed during rest, opening only on the demand of activity.
The average body contains about 62,000 miles of capillaries whose surface area totals 6,300 square miles. With these data in mind, it is understandable that strong muscular contractions can effect fatigue and soreness by obstructing capillary circulation to continuously working muscles.
THE ARTERIAL SYSTEM
An anterior artery, descending in the ventral median sulcus, and two posterior arteries, descending along the posterolateral sulcus, supply the spine (Fig. 6.40). The latter arise from either the vertebral arteries or the posteroinferior cerebellar arteries. These anterior and posterior axial conduits are often small, irregular, and must be reinforced at intervals by radicular arteries that branch from nearby spinal arteries arising outside the vertebral column.
In the cervical area, the vertebral artery runs in the foramen transversarium of the transverse processes of C2-C6 and offers branches to each segment. Similar arteries arise from the intercostal and lumbar arteries branching from the aorta. The lateral sacral arteries give branches to the sacral segments. In each instance, the segmental artery offers several anterior twigs to the front and sides of the vertebral body and posterior branches to the spinal muscles and IVF. After the latter branch passes through the IVF, it enters the vertebral canal and divides into three branches: (1) an anterior branch, which (a) supplies the posterior aspect of the vertebral body to anastomose with the lateral and anterior twigs of that part of the artery that did not enter the IVF, and (b) ascending and descending twigs; (2) an intermediate branch, which supplies the nerve root and spinal dura; and (3) a posterior branch, which supplies the vertebral arch, extradural contents, and dura.
THE VENOUS SYSTEM
The venous system of the spine (Batson's plexus) is a valveless plexus separate from that of the thoracoabdominal cavities. It is derived from the veins of the extremities, body wall, neck, and head. Any increase in intrathoracic or intra-abdominal pressure (eg, Valsalva maneuver) shunts venous blood to the vertebral system. This contributes to the spinal pain of many patients with structural spinal faults. The close tie between spinous venous pressure and neurologic integrity is clearly exhibited when the jugular compression test elicits paresthesia in the lower extremities.
Each cervical vertebral artery offers a branch at the brain stem to form a single anterior spinal artery which runs the length of the cord lying over the median fissure. It tapers as it courses downward in the thoracic cord and gives off central branches at intervals of about 2 mm which, in turn, branch both peripherally and centrally. The anterior spinal artery supplies all the cord with the exception of the posterior columns and posterior horns.
In addition, the vertebral arteries contribute a branch to unilateral posterior spinal arteries that form longitudinal plexiform channels as they progress caudally to supply the posterior columns and horns. The anterior spinal artery appears to be the main source of blood supply to the posterior arteries below the upper thoracic level.
The arterial system of the cord does not have extensive collateral circulation. It relies heavily on extraspinal radicular artery sources. Any interruption of these (eg, IVF encroachment) can produce serious neurologic damage. The superior portion of the anterior spinal artery is assisted by radicular arteries that enter through the IVF's of the midcervical, lower cervical, and upper thoracic levels. A large radicular artery (great spinal) enters between the T9 and L3 level and is believed to be responsible for one-fourth to one-half the blood supply of the cord below this level. A severe drop in blood pressure for 3–5 minutes can so compromise radicular circulation that necrosis of the thoracic neurons occurs.
The abundant veins of the spinal cord drain into the intervertebral veins which communicate with other plexuses. The immediate part of the system involves the (1) internal plexuses, whose pia branches drain the contents of the vertebral canal, vertebral arch, and posterior vertebral body and leave via the IVF; and (2) external plexuses, which drain the anterior and lateral aspects of the vertebral body and its associated tissues (Fig. 6.41). If the prostate is cancerous, pelvic blood returning to the heart via the vertebral plexuses rather than the inferior vena cava may initiate spinal metastasis.
The IVD or at least the nucleus pulposus is primitive mesenchymal tissue. Only during early life does it have a blood supply, namely a twig off the spinal artery of the corresponding level. This artery, which arises bilaterally, penetrates at the posterolateral aspect of the disc. In the early months of fetal life, it involutes and atrophies. Thereafter, discs obtain nutrition by means of canaliculus seepage and imbibition of adjacent fluids via the end plates and anulus. This does not mean that IVD's are biologically inert like cartilage. They have a high rate of metabolic activity that is dependent on the vascularity of the core of the vertebral bodies above and below (Fig. 6.42).
The Spinal Muscles and Pertinent Myology
Viewed simply, the entire spine can be contrasted with a flexible mast of a sailing ship sitting on the S1 deck, with the shoulder girdle viewed as a transverse spar. For support, there are several major triangles and inverted triangles of muscular and ligamentous check "guys" that link the mast to bony supports. When the pelvis tilts laterally downward (eg, gait, short leg), the guys automatically become taut to assist body equilibrium (Fig. 6.43). This design makes the spine a first-class lever system in which loading has a considerable mechanical advantage.
The Postvertebral and Prevertebral Muscles
The spinal muscles consist of a large number of quite small muscles arranged in a most complicated manner with converging and diverging fascicles. They are arbitrarily grouped by location or function, since they work in groups rather than individually, and only some of them have biomechanical significance in the spine.
The long muscles are placed superficially, the intermediate muscles lie deeper, and the short muscles occupy the deepest layer. The superficial and intermediate muscles are the extrinsic muscles of the back, concerned primarily with movements of the shoulder girdle, trunk, and respiration. The deep spinal muscles are the intrinsic muscles of the back, concerned primarily with segmental movements of the vertebral column.
THE DEEP POSTVERTEBRAL INTRINSIC LAYER
These small, short, intersegmental muscles play an important role in specific segmental movement. They include the interspinales, connecting adjacent spinous processes; intertransversarii, connecting adjacent transverse processes; rotatores, connecting the transverse process below to the laminae above; levatores costarum, connecting transverse processes to the ribs; and, deep to the semispinalis, the multifidi, which occupy the groove on each side of the spinous processes from the sacrum to the axis. Under the trapezius and rhomboids in the neck lie the splenius capitis and cervicis bandage-like muscles that arise medially from the C7–T6 spinous processes and ligamentum nuchae to attach laterally on the upper cervical transverse processes and the occiput.
Fisk believes that the deep and middle layers of spinal muscle especially are the site of "tennis elbow" type lesions, with all that this implies.
THE INTERMEDIATE POSTVERTEBRAL EXTRINSIC LAYER
These muscles arise from the transverse processes of each vertebra and attach to the spinous process of one or more vertebrae above. They consist of the semispinalis capitis in the occipital area, semispinalis cervicis in the cervical area, and semispinalis thoracis in the thoracic area. The serratus in- ferior, superior, and posterior are intermediate muscles usually discussed with the thorax rather than the spine.
THE SUPERFICIAL POSTVERTEBRAL EXTRINSIC LAYER
The outer layer of spinal muscles consists of the iliocostalis (lumborum, thoracis, cervicis) laterally, which inserts at the rib angles and lower cervical transverse processes; longissimus (thoracis, cervicis, capitis), which inserts at thoracic transverse processes and ultimately reaches the skull (Fig. 6.44); and the underdeveloped flat spinalis (thoracis, cervicis, capitis) medially, which attaches its medial fibers at the thoracic spinous processes. These three muscle groups are collectively called the erector spinae and are involved in vertebral extension. The large lumbosacral portion of the erector spinae is frequently considered as one muscle, the sacrospinalis.
The superficial layer also includes the levator scapulae and rhomboids that are primarily involved in movements of the shoulder girdle.
The lateral portion of the erector spinae is called the iliocostalis system, composed of the iliocostalis cervicis, thoracis, and lumborum divisions. Their fibers arise from ribs and insert on higher ribs except in the cervical region where they attach to transverse processes of C4–C6.
The longissimus system also consists of cervis, thoracis, and lumborum divi- sions. Lower fibers arise from the common tendon of the erector spinae and insert into lower ribs and adjacent transverse processes. Middle fibers arise from upper thoracic transverse processes and attach at C2–C6 transverse processes. Capitis fibers arise on or near the articular processes of C4–C7 and insert at the mastoid area. The major role of the iliocostalis, longissimus, and serratus systems is played in respiration and not in spinal motion. The serratus posterior superior and inferior arise essentially from the upper and lower thoracic spinous processes and ligamentum nuchae and insert on upper and lower ribs.
THE PREVERTEBRAL MUSCLES
These are the four relatively large muscles that encase the abdominal area: the rectus abdominis, running vertically at the anterior midline; internal ob- lique; external oblique; and transverse abdominis (Fig. 6.45).
The approximate degrees of spinal motions for various vertebral segments are shown in Figure 6.46, and the important movers are shown in Figure 6.47.
The spinal extensors span the entire length of the vertebral column, originating from the laminae, transverse processes, and ribs as diagonal strips and inserting as multiple tendon inserts on the spinous processes. This group of muscles, known collectively as the erector spinae, has the sole function of restoring the flexed spine to neutral and controlling flexion momentum as an antagonist guard. Bilateral action by the splenius capitis, cervicis, rotatores, interspinales, and multifidi is also involved in spinal extension.
The erector bundles are subdivided by innumerable connective tissue planes, and the entire group is enveloped by strong fascia in the lumbar region that is strongly anchored to the transverse processes. This tends to spread a mechanical load over a large area.
As the erector spinae are the only muscles in the body supplied solely by the posterior rami of the spinal nerves, local pain, splinting, or unilateral weakness of this muscle points to spinal nerve involvement.
General Stability. A spine devoid of its muscles but containing all its ligaments is most unstable. The majority of stability of the spine can be attributed to the action of the spinal muscles. The guy-wire arrangement of the erector spinae provide ideal lateral stability for the spine. If defective, spinal deformity is the immediate result. This fact is readily confirmed when the unilateral loss of a few spinal nerves produces a severe scoliosis.
Static Balance. The erector spinae do not assist in maintaining static neutral balance. They are myographically inactive during erect stance. When in static equilibrium, we normally rest primarily on weight-bearing joints against ligament resistance. With the exception of extremely slight and intermittent iliopsoas, longissimus dorsi, and rotatores muscle action, little spinal activity is required. There is slightly more activity in the sitting position than in the standing posture.
The flexor muscles, developed most in the cervical and lumbar regions, are represented chiefly by the anterior longus coli and scalene muscles in the cervical area and the more lateral sternomastoid muscles, which are powerful assistants. In the lumbar region, the psoas major flexes the trunk on the thigh at the hip but has little effect on flexion of individual lumbar segments. The lumbar spine is essentially flexed by the anterior rectus abdominis with help from the lateral external and internal obliques. During typical flexion and extension, there is little change in the dorsal curve (Fig. 6.48).
The first 70° of forward bending is due to flexion of the lumbar segments, where the pelvis is locked by strong contraction of the gluteus maximus, medius, and hamstrings. The following 25° of flexion takes place by hip release and pelvic rotation (Fig. 6.10).
SPINAL LATERAL FLEXION
The quadratus lumborum and intertransversarii are probably the only purely lateral flexors of the spine. Additional lateral bending power is achieved by unilateral contraction of the spinal flexors and extensors.
Voluntary rotation is minimal in the lumbar region. The sternomastoid in the cervical area and the abdominal obliques in the trunk are usually considered the most powerful rotators. However, myographic studies have shown that the most active spinal muscles during axial rotation are the erector spinae on the side moving posteriorly and the musculi rotatores and multifidi on the side moving anteriorly. There is also activity of the ipsilateral splenius capitis, cervicis, gluteus medius, and tensor fascia lata.
General Aspects of Vertebral Subluxations
Abnormal spinal biomechanics clinically relates to the intervertebral subluxations and other spinal malfunctions that result in structural and physiologic inadequacies of the spinal column. This state is the condition of a vertebral motion unit that has lost its normal structural and/or functional integrity and is, therefore, unable to move from its normal resting position, to move properly through its normal range of motion, or to return to its normal resting position after movement.
Types of Subluxations
There are numerous methods of classifying vertebral subluxations. Each has its own rationale and each has had certain validity that has been a contribution to our understanding of this complex phenomenon.
CLINICAL CLASSES OF SUBLUXATION
The seven commonly recognized clinical types of subluxation are:
(1) functional subluxation, a functional and slight "off centering" with partial fixation in an otherwise normal articular bed;
(2) pathologic subluxation, an "off centering" derangement in an articular bed that has become deformed as the result of degenerative changes;
(3) traumatic subluxation, in consequence to an extraneous or intrinsic force and the associated muscle spasm;
(4) reflex subluxation, "off centering" induced by asymmetrical muscle contraction from aberrant visceral or somatic reflexes;
(5) defect subluxation, subluxation of an anomalous or developmentally defective spinal or pelvic segment;
(6) fixation subluxation, hypomobile fixation wherein a spinal or pelvic segment that is in a neutral position of mobility fails to fully participate in movement (Fig. 6.49);
(7) hypermobile subluxation, pathologic segmental increase in movement consequent to the loss of integrity of the retaining mechanism caused by trauma or degenerative pathology.
What is called a vertebral subluxation in chiropractic is the alteration of the normal dynamic, anatomic, or physiologic relationships of contiguous articular structures. The concept that an "off centered" and/or "fixated" vertebral or pelvic segment has a unique effect upon the neuromuscular bed that may be the cause of, aggravation of, or "triggering" of certain syndromes is a major contribution to health science by the chiropractic profession. This contribution has undergone considerable refinement since its inception, but this is not unique in the health sciences.
The degree of derangement of a bony segment within its articular bed may vary from a microtrauma to one that is macroscopic and quite readily discernible. It is always attended to some degree by articular dysfunction, neurologic insult, stressed muscles, tendons, and ligaments. Once produced, the lesion usually becomes a focus of sustained irritation from which a barrage of impulses stream into the spinal cord where internuncial neurons receive and relay them to motor pathways. The muscular contraction that provoked the subluxation originally is thereby reinforced, thus perpetuating both the subluxation and the pathologic process.
Confusion exists because the term chiropractic refers to both structural position (both static and dynamic) and related functional abnormalities (both static and dynamic), and a definition that serves one aspect does not necessarily serve another. In the words of Gillet, "Vertebrae do not slip out of place. They are not displaced out of their physiological boundaries. They have not gone out of their limits of motion. When we adjust subluxations, we do not replace vertebrae." As far back as the first chiropractic textbook published (1906), Smith et al fought the idea of "a bone out of place." They emphasized that "a simple subluxated vertebra differs from a normal vertebra only in its field of motion and the center of its field of motion" –a concept valid today.
The "off centering" referred to is usually far less in extent than the "near dislocation" used by medical orthopedists. In chiropractic semantics, this "off centering" may not even exist in the static spine as seen in the "subluxation" of fixation that produces an abnormal pivot within the normal physiologic range of motion or in the hypermobile segment that returns to a centered position in the neutral position. Conversely, an "off centered" vertebra that is not interfering with function is rarely considered a "subluxation" in clinical chiropractic.
To date, no one definition has been able to serve all that is implied in chiropractic. Osteopaths have used the term "vertebral lesion," but this jargon implies a pathologic or traumatic discontinuity of tissue or loss of function that may or may not exist with a "subluxation." Hildebrandt has used the term "dysarthria" in an attempt to imply the dynamic rather than the static "off centering" aspects of the motion unit, but even he realizes that this is often confused with the imperfect articulation of speech.
An accurate term could be devised, but this would require an extensive polysyllabic word that would be so cumbersome to use that it would be ignored by the mainstream of health science. Thus, until this dilemma is solved, the word "subluxation" will continue to be used.
MOTOR-UNIT CLASSES OF SUBLUXATIONS
The biomechanical element of the vertebral motion unit subluxation is classified by Hildebrandt/Howe in accord with its static or kinetic aspects and with the number of vertebral motion units involved.
Static Vertebral Motion-Unit Subluxation-Fixations
Flexion Subluxation. This is characterized by approximation of the vertebral bodies at the anterior and by separation of the vertebral bodies, facets, and spinous processes at the posterior. When found, it is indicative of irritative microtrauma to the anterior IVF; forced excursion of the nucleus pulposus and bulging of anular fibers; stretching of the posterior longitudinal, interspinal, and supraspinal ligaments; traction shearing stress of the synovia of the facet articulations; and biomechanical impropriety of the motion unit (Fig. 6.50).
Extension Subluxation. An extension subluxation is featured by separation of the vertebral bodies at the anterior and approximation of the vertebral bodies, facets, and spinous processes at the posterior. Such a subluxation points toward irritative microtrauma at the posterior IVF, forced excursion of the nucleus pulposus and bulging of the anulus, stretching of the anterior longitudinal ligament, imbrication of the facet articulations with compressive shearing stress to the synovia of the facet articulations, and biomechanical insult of the vertebral motion unit.
Lateral Flexion Subluxation. This is characterized by approximation of the vertebral bodies and facets on the side of flexion and separation of the vertebral bodies and facets on the side of extension. This type subluxation possibly indicates irritative microtrauma to the IVD on the side of flexion, imbrication of the facets and compressive shearing stress to the synovia on the side of flexion, forced excursion of the nucleus pulposus with bulging of the anulus, stretching of the anterior longitudinal ligament at its lateral aspect, and biomechanical impropriety of the vertebral motion unit (Fig. 6.51).
Rotational Subluxation. Such a subluxation is featured by rotary displace- ment of the vertebral bodies laterally and posteriorly on the side of rotation with torsion of the facet articulations in the direction opposite to vertebral body rotation. This situation signifies torsion binding of the anulus, decreased resiliency of the IVD due to torque compression of the anular fibers, torsion stretching of the anterior and posterior longitudinal ligaments, rotatory imbrication of the facets with reverse shearing stress to the synovia, and biomechanical insult of the vertebral motion unit.
Anterolisthesis Subluxation Without Spondylolysis. This is characterized by an anteroinferior excursion of the vertebral body at the anterior and by anterosuperior excursion of the vertebral body and facets at the posterior. It encourages irritative microtrauma at the anterior IVD, forward shearing stress to the anulus, stretching of the anterior and posterior longitudinal ligaments, imbrication of facets with forward shearing stress to the synovia, and biomechanical impropriety of the vertebral motion unit (Fig. 6.52).
Anterolisthesis Subluxation with Spondylolysis. This is featured by anterior excursion of the vertebral body independent of the posterior division of the motion unit. The posterior division of the unit remains in position with the structure below because of separation of the pars. It is characterized by irritative microtrauma to the posterior aspect of the IVD, forced excursion of the nucleus pulposus with bulging of the anulus, forward shearing stress of anular fibers, stretching of the anterior longitudinal ligament, and biomechanical insult of the vertebral motion unit.
Retrolisthesis Subluxation. Such a subluxation is featured by posteroinfer- ior excursion of the vertebral body and by posteroinferior excursion of the facets. This subluxation signifies irritative microtrauma to the posterior IVD, posterior shearing stress of the anulus, stretching of the anterior and posterior longitudinal ligaments, imbrication of the facets with posterior shearing stress to the synovia, and biomechanical impropriety of the vertebral motion unit.
Laterolisthesis Subluxation. This is characterized by lateral, superior, and posterior excursion of the vertebral body on the side of deviation and separation of the facets on the side of deviation with reverse torsion and approximation on the side opposite deviation. It suggests irritative microtrauma to the IVD on the side opposite deviation, lateral and posterior shearing stress to the anulus on the side of deviation, imbrication of facets and anterior shearing of the synovia on the side opposite deviation, and biomechanical insult to the vertebral motion unit (Fig. 6.53).
Decreased Interosseous Space Subluxation. This type is featured by narrowing of the vertical IVF space and inferior excursion of the facets. It is characterized by degeneration of the IVD with approximation of the vertebral bodies, traumatic compression of the IVD with possible herniation of the nucleus through an end plate, imbrication of the facets with compressive shearing stress to the synovia, compression of the contents of the IVF, and biomechanical impropriety of the vertebral motion unit.
Increased Interosseous Space Subluxation. This is characterized by superior excursion of the vertebral body and the facets. It results in inflammatory swelling or pathologic enlargement of the IVD, traction shearing stress to the anulus and the synovia of the facet articulations, stretching of the anterior and posterior longitudinal ligaments, and biomechanical insult to the vertebral motion unit (Fig. 6.54).
Foraminal Encroachment Subluxation. This type is featured by potential con- comitant findings of other types of subluxations with a possible relationship to osteophytic IVF spurs in conjunction with other types of subluxations. It features associated micro- and macro-traumas to the vertebral motion unit; compression, irritation, and swelling of the foraminal contents; osseous and soft-tissue primary degenerative processes of the vertebral motion unit structures; and interforaminal neurovascular insult effecting possible disseminated secondary pathophysiologic processes.
Costovertebral-Costotransverse Subluxation. The disorder features misalign- ment of the costal processes in relation to the vertebral bodies and transverse processes independent of vertebral motion unit subluxation (ie, primary) or misalignment of the costal processes in relation to the vertebral bodies and transverse processes as a result of vertebral subluxation (ie, secondary). These disorders present painful, difficult, and/or restricted respiratory movements of the ribs, shearing stress to the capsular ligaments and synovia, induction of a vertebral motion unit subluxation and/or contribute to a chronic subluxation, induction of spinal curvatures, aggravation of curvatures present, and irritations to the sympathetic ganglia and rami communicantes.
Sacroiliac Subluxation. This is characterized by misalignment of the sacrum in relation to the ilia independent of bilateral innominate involvement (ie, primary) or misalignment of the sacrum in relation to the ilia as a result of bilateral innominate involvement (ie, secondary). These situations encourage irritative microtrauma to the interarticular structures, induction of a subluxation and/or contribute to chronic subluxations, induction of spinal curvatures, aggravation of curvatures present, and biomechanical impropriety of the pelvis in static or dynamic postural accommodations.
Kinetic Vertebral Motion-Unit Subluxation-Fixations
Hypomobility and/or Fixation Subluxation. This common subluxation is charac- terized by fixation of the vertebral motion unit in relation to the supporting structure below and compensatory hypermobility of the vertebral motion unit above the level of fixation (Fig. 6.55). The irritative, excessive function of the hypermobile vertebral motion unit results in micro- or macro-trauma to the IVD, anterior and posterior longitudinal ligaments, periosteum, etc; muscular irritation, spasticity, muscle trauma, fatigue, etc; neurologic insult within the confines of the neural canal and IVF; vascular insult to the paraspinal and interforaminal blood vessels; and biomechanical impropriety of all vertebral motion units involved.
Hypermobility Subluxation. This is featured by a hypermobile vertebral motion unit in relation to a normally functioning or hypomobile motion unit below. It has the same features as that of a hypomobile and/or fixation subluxa- tion except for a possible traumatically loosened vertebral motion unit as opposed to compensatory hypermobility of a vertebral motion unit within its nor- mal range of motion.
Aberrant Movement Subluxation. This type of subluxation, frequently trauma- tic in origin, is characterized by movement of a vertebra "out of phase" with the segment above and below where two motion units are involved. It suggests microtrauma to both of the vertebral motion units involved, occlusion of the IVF's above and below the aberrant segment, shearing stress to the IVD's and synovia of both vertebral motion units, restriction of the neural canal, and bio- mechanical impropriety of both vertebral motion units (Fig. 6.56).
Gross Structural Alterations
Mechanical spinal disturbances can adversely affect the body in a number of ways such as (1) load stress on muscles leading to hypertrophy or atrophy and alterations of local muscle strength; (2) leverage stress at joints leading to weakness or sprain of ligaments, articular and intra-articular cartilage damage, and synovitis; and (3) compression stress or trauma of nerves leading to in- crease or decrease of normal conduction with consequent functional changes.
Compression stress on bone leads to sclerosis or alteration of its normal shape and internal architecture, and pressure stress on connective tissues leads to thickening or thinning. Various combinations of factors influence cartilage degeneration such as severe isolated or repeated minor trauma, chronic mechani- cal stress or tension, local circulatory excesses or deficiencies, idiopathic biochemical factors, developmental anomalies or malformations, nutritional fac- tors, and the inherited cellular quality of the cartilage.
The primary physical and mechanical factors that often negatively influence the body are gravity, pressure, weight load, inertia, compression, elasticity, leverage, movement, stretch, expansion, and contraction. With these forces in mind, a vertebral subluxation may be grossly determined by its structural alter- ations and manifestations.
Palpable alterations of the normal anatomic relationships of one joint to another are frequently found. These mechanical changes may occur in the static recumbent, sitting, or standing positions, or in various ranges of motion as the segments and their supporting tissues are put through either active or passive ranges of motion. Subluxations are also evident by the presence of certain objective or subjective signs and symptoms when the joint and tissues are put through various orthopedic tests. Overstress at the area of the zygapophyses and the attending inflammatory reaction may give rise to a moderate radiculitis.
Mechanical errors in position or motion may be brought about by structural alterations in the supporting tissues of the joint itself. These in turn may be brought about by: (1) genetic and developmental abnormalities causing asymmetry of the vertebrae, cartilage, muscular structure, etc; (2) various acquired disease processes within the joint such as arthritic degeneration, avascular necrosis, or a neuropathic process that causes the cartilage, bone, ligaments, or musculature to be structurally altered; (3) the resolution of macro- or micro-traumas, strains, sprains, or of other primary pathology may cause fibro- sis, degeneration, or other retrograde changes of a structural nature within the joints themselves.
These same processes not only develop within the vertebral column and its paravertebral tissues but also in the musculoskeletal tissues of the appendic- ular skeleton. Thus, similar lesions may exist remote from the spine which per- petuate neuropathic responses by their presence. When the cause is within the structures of the spine, the effects are more evident because of the close ana- tomic proximities and the functional importance of normal motion-unit activity or integrity to the various components of the nervous system.
Such structural faults are not, of course, the major criteria upon which a subluxation's presence and importance are based, for the body is able to adapt to many structural faults and diminish their influences upon it. Consequently, the signs and symptoms of neuropathic processes are more significant than struc- tural alterations. The major clinical importance is not the positional rela- tionship of the osseous segments, but the significance of the soft-tissue and functional changes that are causing or are affected by the alteration. The posi- tion of the segment is important because it suggests or reflects changes in the neuromusculoskeletal and visceral systems.
Posture can be defined as the relationship of each body structure to the entire structure (Fig. 6.57). Anatomists and neurologists no longer question the significance of the entire proprioceptive bed disposition in the ligamentous and myologic elements of the spine and pelvis.
Gravitational forces create subluxations and spinal distortions by the con- stant pull of body structures toward the center of the earth. Such distortions are increased by increasing the distance of the vertebrae from the center line of gravity and are decreased by decreasing the distance of the vertebrae from the center line of gravity. Thus, during spinal and pelvic analysis, it is imperative that spinal mechanics and structural deviation are interpreted from the gravitational center line if the body is to be returned to its normally balanced position.
Precipitating Factors of Spinal Subluxations
A vertebral subluxation may be either a cause or an effect, and the immedi- ate causes may be divided into two major categories: the unequal or asymmetrical muscular efforts upon the joint structures and the inequality in the supporting tissues of a particular joint such as the cartilage, IVD, ligaments, etc. Some form of internal or external stress is necessary to produce a subluxation to a degree sufficient to cause a state of dysfunction.
As discussed in Chapter 5, inequality in muscular balance (ipsilateral weak- ness and compensatory contralateral contraction) may be initiated by (1) trauma, (2) postural distortion phenomena, (3) psychomotor responses, (4) somatic and visceral responses, and (5) paralytic effects. Two other causes not previously discussed are (6) biochemical reactions and (7) stress factors, both of which may or may not overtly manifest biomechanically.
Acute or chronic hypo- or hyper-tonicity of musculature may be due to vari- ous biochemical changes within related tissues. This may be brought about by either local or general pathologies which may cause anoxia, ischemia, toxicity, etc, by foreign bodies, or by systemic fatigue-producing activities, nutritional deficiencies or excesses, caustic chemical exposure, ingestion of harmful chemi- cals, inhalation of noxious gases, microorganism toxins, abnormal glandular activity, excessive heat or cold, or electric shock affecting the chemical envi- ronment of cells histologically.
STRESS FACTORS RESULTING IN SUBLUXATION
Depending on the degree of stress produced, any internal or external stress factor involves the nervous system directly or indirectly, resulting in decreas- ed mobility of the vertebra of the involved neuromere. This decreased mobility may be the result of (1) muscle splinting, especially on the side of greatest stimulation according to Pfluger's law or (2) from abnormal weight distribution to the superior facets and other structures of the vertebrae involved.
Pfluger's law states that if a stimulus received by a sensory nerve extends to a motor nerve of the opposite side, contraction occurs only from corresponding muscles; and, if contraction is unequal bilaterally, the stronger contraction always takes place on the side that is stimulated. When affecting one or more vertebrae, this state of decreased mobility of the motion unit encourages nerve dysfunction leading to pathologic processes in the areas supplied by the affec- ted nerve root or neuromere depending upon the degree and chronicity of involve- ment.
Effects of Spinal Subluxations
Many spinal subluxations have more than one immediate cause and effect. Ab- normality of development may be complicated by degenerative joint disease, retrograde changes, inflammation, and muscle splinting, for example. The effects may be direct upon blood vessels and nerves, reflex in nature, etc. Therefore, a complicated and far-reaching series of interacting and interdependent changes occur which may be designated as a subluxation syndrome.
As a primary concept of chiropractic science, spinal subluxations may result in the development of disease states locally within the vertebral motion unit itself or throughout the body. These primary and secondary effects of subluxa- tions may be divided into three major categories:
The mechanical effect, motion, and balance of the local segment, or the effect upon the skeleton elsewhere, due to compensatory distortions and altera- tions as proprioceptive mechanisms attempt to correct the mechanics in the pres- ence of structural imbalance.
The effect of any localized condition occurring within the articulations due to interarticular stress and trauma (often microtrauma) such as irritation, inflammation, swelling, necrosis, and other degenerative changes.
The neurologic scope of subluxation effects may be grossly differentiated as nerve pressure, nerve stretch, nerve torsion, circulatory changes, meningeal irritations, cerebrospinal fluid flow alterations, alterations of proprioceptive responses and reflexes, traumatic insult to the rami communicantes or sympathe- tic ganglia, among many others.
The neurologic effects are undoubtedly the more important of the three from a clinical aspect.
There are 115 diarthroses within the spine and pelvis vulnerable to the abnormal movement related to subluxation. Each of these articulations is a site of proprioceptive sensitivity which under articular strain is insulted and provoked to express pain. As mentioned, a working hypothesis regarding segmental malposition is that the displacement fixation causes adjacent areas of the spine to become hypermobile, resulting in stress of adjacent motion units. Neurologic feedback may cause the elicitation of ACTH and a resulting increase in the production of corticosteroids as an adaptive mechanism, according to the Hans Selye stress concept. This may also be reflected by possible blood sugar changes.
EVENTS AT THE INTERVERTEBRAL FORAMINA
The normal cross-sectional area of an IVF leaves ample room for its neural contents. The IVF narrowing that occurs during spinal extension movements has little if any adverse effects. The channel contents are normally free to adjust to movements throughout the normal range of regional motion. Pathologic changes in and near the foramen may reduce its dimensions and lead to compression, but, as Sunderland points out, friction over osseofibrous irregularities or traction on a nerve or nerve roots fixed in the foramen by an adhesion is much more likely.
When a vertebral motion unit is under constant stress, changes occur in adja-cent IVD's, ligaments, membranes, muscles, and other associated tissues which produce some degree of fixation. The adjacent IVF's are altered in size. As a rule, two of them become smaller than normal, and the other two become larger than normal. Nerve roots and other contents of the affected IVF's are subjected to insult at the smaller foramina and stretching at the larger fora- mina (Fig. 6.58).
Effects of Microtrauma. Initially, the zygapophyseal articular complex of a subluxated vertebral motor bed is subjected to the stress of "off centering" and is attended by the following aspects of microtrauma: (1) minute hemorrhage, transudation, and arteriovenous stagnation from the sluggish circulatory flow resulting from the motion unit's decreased mobility and arterial backup, (2) para-articular and paraforaminal traumatic edema, (3) eccentric compression stress upon the IVD and the zygapophyseal cartilages, (4) possible separation of minute fasciculi of the retaining fibers of the anulus, joint capsule, dural root sleeve, and nerve root sheath, (5) stress insult of the proprioceptive bed, (6) minute crushing of the periosteal margins with resultant proliferative irri- tation, and (7) minute tearing of the attachments of the dural root sleeves if they attach to the lining of the IVF.
Consequences. The following pathologic changes occur: (1) Extravasation and edema, along with the precipitation of fibrinogen into fibrin, result in interfascicular, foraminal, articular, and capsular thickening and adhesions that restrict fascicular glide, ingress and egress of the foraminal contents, and the competent movement of the vertebral segment within its articular bed. (2) Whenever there is extravasation, mineral salts are precipitated and infil- tration and sclerosing result. (3) Binding adhesions may develop between the dural root sleeves and the nerve roots within the interradicular foramen and between the spinal nerve root sheath and the inner margins of the IVF. (4) When subjected to microtrauma, mesenchymal connective tissue undergoes a relative rapid and extensive degenerative change with loss of functional integrity and substance.
Proprioceptive Responses and Reflexes. Perhaps the most significant effect is that of proprioceptive irritation. The musculoskeletal tissues and particu- larly the ligaments and paravertebral or intervertebral musculature of the spine are richly endowed with proprioceptive receptors. First, when overly stimulated by stretching, these neurons interpret the stimuli as somatic sensory stimula- tion which may be perceived as pain. Second, they may also send reflexes to their motor components and cause muscular changes within the paravertebral mus- cles or elsewhere in the soma supplied by the segment. Third, they may be interpreted as visceral sensory stimuli, whose visceromotor response alters cir- culatory changes, smooth muscle activity, glandular secretions, or trophic activity in the musculoskeletal tissues or viscera supplied. It is this vast ability of the proprioceptive sensory beds to influence motor changes, both of a somatomotor or visceromotor nature, that is perhaps the most universal effect of vertebral subluxation.
Direct Nerve Pressure. The nerve roots are normally well protected from trauma by the bony border of the IVF and the tough fibrous dura. However, Schaumburg shows that when distorted by degenerative bone and joint disease or a variety of space-occupying lesions, these same protective layers may damage the delicate neural structures. Direct nerve pressure may come from the misaligned osseous segment itself or from the various soft-tissue pathologies causing or affected by the mechanical fault such as contractures, adhesions, inflammatory residues, atrophies, cysts and tumors of related tissues. The direct physical nerve pressure may be responsible for motor alterations and sensory disturbances within this particular nerve and its innervated structures or cause other rami- fying reflexes.
Studies discussed by Sharpless show that the posterior nerve roots are about five times more susceptible to compression block than a peripheral nerve. As little as 10 mm Hg pressure held for 15-30 minutes reduces the compound action potentials of posterior roots to about half their initial value. This effect is probably due to mechanical deformation rather than ischemia since the larger fibers are blocked first. It is believed that anoxia affects the small fibers first.
Ganglion Irritation/Compression. Irritation/compression of a dorsal root ganglion may be a factor. The sensory dorsal root ganglion of each spinal nerve generally lies within the upper medial aspect of the IVF, a precarious position. Whenever the transverse diameter of the IVF is modified, the ganglion may be subject to compression and irritation. This is especially true at the cervical level where it tends to occupy the medial limits of the IVF and is thus vulner- able to and most likely to become involved in any changes in IVF diameter on any event of trauma or the manifold tissue processes of discogenic spondylosis. For example, an acute whiplash-like mishap to the cervical spine, especially of the hyperextension type, may force the vagus and the superior cervical sympathetic ganglion against the transverse processes of the atlas and axis, provoking the bizarre autonomic reactions that not uncommonly attend this condition.
Intraneural Effects. It is probable that any interference with or abnormal- ity of (1) the interstitial fluids in which the nerves lie and/or (2) the intra- cellular fluid of the nerve itself in the nerve axoplasm will cause a breakdown of the sodium pump mechanism that will prevent the normal flow of impulses along the nerve fibers concerned. These abnormal impulses refer to an overaction or underaction in the rate of impulse frequency along the nerve. Once a threshold stimulus has been reached, a nerve will fire in accordance with the all-or-none law.
Meningeal Irritations. Mechanical errors in motion and position may cause tractional effects upon the meningeal coverings of the cord or dural root sleeves that may produce mechanical pressure upon the neurons emanating from the cord itself. These may, therefore, cause the elicitation of abnormal neurologic motor effects or sensory interpretations.
Altered Nerve Root Level. Induced disrelation between position level and course direction of nerve root origin (spinal cord) and nerve root exit (IVF) is an important factor. Whenever there is subluxation, changes in normal curves, or the presence of abnormal curves, the relative levels of points of nerve root origin and exit are altered and the nerve root becomes vulnerable to encroach- ment compression or irritation. This is because whenever the normal curves of the spine are grossly modified (eg, kyphotic deviation of the cervical spine, lordotic exaggeration of the lumbar spine, scoliotic deformity especially at the cervicobrachial area and lumbosacral junction), the nerve root is forced to assume an unusual approximation to one or the other walls of the IVF. There- after, the least additional deviation may precipitate a nerve root irritation syndrome. In addition, a vertebral column affected with partial fixation of several segments when subjected to flexion, extension, and circumduction efforts will be attended by marked tension upon the dural root sleeves and the related spinal nerve radicles, especially the cauda equina (Fig. 6.59).
When for any reason one or more vertebral segments are embarrassed by ab- normal motor action, added articular and proprioceptive responsibility is imposed upon the segments above and below the involved area. Thus there is an extension of harmful effects that may have noticeable complications. In addi- tion, the phenomenon of bipedism neurologically necessitated the development of an ascending and descending reticular activating mechanism. It can be assumed that spinal and pelvic interosseous disrelation may overstimulate the ascending portion of the reticular activating mechanism. On the other hand, excessive attention stress may, by means of the descending portion, provoke overstimula- tion of the cellular elements in the anterior and lateral horns and provoke abnormal somatic and autonomic reactions.
Paraforaminal Adhesions. Paraforaminal adhesions as the result of stress and traumatic edema often result in a painful restriction of the normal back-and- forth glide (1/4–1/3 inch) of the nerve root within the IVF. Symptoms simulate a low-grade radiculitis: increased pain on movement, straining, and stretching; pain on changing positions and when placing the involved part in extension.
Circulatory Changes. Decreased mobility (eg, vertebral fixation) of a motion unit within its normal physiologic range of movement may cause sluggish lympha- tic or vascular circulation that is further influenced by mechanical pressure. This can cause chemical or physical changes within tissues such as anoxia, toxi- city, swelling, edema, etc, and the consequent derangement of normal function brought about by these disorders. Local irritation at the site of misalignment and a decreased ability to move produce an inflammatory reaction with edema leading to a disturbance in the normal exchange of nutrients and waste products between capillary and extracellular fluid. Added to this stasis is the probable factor of lactic acid buildup in the area as a result of acid leaking from the surrounding hypertonic muscles.
Local Toxicity Effects. The venous stagnation from arterial backup can pro- duce local toxicity. While toxic metabolic end products (eg, urea, uric acid, creatinine, lactic acid) accumulate in the stagnant tissue and congested capillary beds, there is also a corresponding decrease in nutrient and oxygen concentration in these fluids. Thus, the nerves emanating from the involved area will be deficient in necessary nutrients and quite possibly hypoxic as well. The buildup of metabolic waste products in the area of the IVF, may also alter the normal pH of local fluids causing a breakdown of Krebs' cycle, due to decreased oxygen and toxicity, which causes a partial breakdown of the sodium pump mecha- nism, resulting in an ionic imbalance. As the sodium pump can no longer maintain a normal ionic balance, the imbalance can result in a degree of erratic nerve conduction and edema in the tissues of the immediate area. This erratic nerve conduction may be exhibited in all nerves passing through the involved IVF and immediate area. When toxicity occurs in either the central or peripheral nervous systems, the formation of acetylcholine at the level of involvement will be interfered with and result in further disturbances due to increased nerve con- duction impairment. This situation along with the toxicity effects upon the nerve may well result in abnormal membrane permeability leading to dysfunction.
Cerebrospinal Fluid Flow Alterations. These refer to the mechanical effect upon the flow of cerebrospinal fluid within the central nervous system and perhaps within the peripheral nerve origins themselves. Cerebrospinal fluid stagnation possibly occurs in association because of the intimate relationship between spinal fluid and venous blood, contributing to toxicity in the nerve root area. According to some researchers, minute pressure on meninges alters the flow of cerebrospinal fluid and interferes with its ability to remove wastes and provide nutritional substances to the cord and nervous system. This may be either the effect of direct mechanical pressure or impairment of motion neces- sary for proper inflow and outflow of this nutrient material.
DISTAL NEUROLOGIC MANIFESTATIONS OF SUBLUXATIONS
Because of the effects of the subluxation's microtrauma and the consequent pathologic changes involved, the neurologic insult may result in (1) modifica- tion of the basic chronaxie; (2) alteration of normal impulse amplitude, wave length, and force intensity; and/or (3) extension of the refractory period.
The neurologic manifestations of a subluxation are not always indicated by the response the nervous system makes to irritation not external to it (ie, discernible in its immediate area), but rather from within the body. Thus, it can be an intrinsic source of neurologic irritation. This altered state of the nerve-fiber threshold and the impulse proper leads to dysfunction of the sen- sory, motor, vasomotor, and spinovisceral responses.
Somatic Responses. Dysfunctions in the somatic-sensory field include varying degrees of discomfort and pain, tension, superficial and deep tenderness, muscu- lar tone, periosteal tenderness, hyper- and hyp-esthesia, haptic sensations, acroparesthesia, formication, flushing, numbness, coldness, and postural fatigue. Dysfunctions in the somatomotor field include painful and especially proximal muscle spasms; abnormal muscular tone (from hypotonicity to spasm), weakness, atrophy, or degeneration in long-standing cases; sluggish and uncoor- dinated movements; paralyses; fasciculations, tics, and tremors.
Visceral Motor Responses. Visceromotor responses of the nervous system may be exhibited in several ways. For example:
Dysfunction in the vasomotor field include local swellings, angioneurotic edema, flushing, blanching, mucous membrane congestion, urticaria and dermato- graphia. Minor changes in the circulation of the skin can be measured by various heat sensitive devices, thermography, galvanometers, or infrared photography. Such changes often parallel circulatory changes in the deeper tissues as they too are affected by similar vasomotor responses.
Changes in the ability of the skin to secrete oils or perspiration which can be measured by various electrical means. These secretory errors may also be indicative of similar changes in deeper visceral tissues. Hyperhidrosis or dry- ness, as well as hyperesthesia or hypoesthesia, in a local area near the spine implies altered vasomotor activity in the subsequent spinal segment. Hyperesthe- sia and hyperhidrosis are usually associated with an increased flare (red response) to scratching and a decrease in electrical skin resistance.
Dysfunction in the spinovisceral field include visceral musculature ab- normalities, glandular and mucous membrane secretory malfunctions, and sphincter spasms of the detrusor muscles and myocardium.
Changes in the quality of tissue from trophic disturbances such as atro- phies, degenerations, thinning or discoloration of the skin, or other changes that reflect viscerotrophic abnormalities.
VISCERAL MANIFESTATIONS OF POSTURAL FAULTS
Postural faults, which may be either the cause or result of vertebral sub- luxations, are readily visualized in postural analysis. Pressure or stretching stress of viscera and their supports leads to disturbed visceral function and abnormal reflexes.
Abnormal body mechanics affecting the thoracic and abdominal cavities inter- fere with normal function by (1) abnormal efferent visceral stimuli reaching organs from the faciliated segment, (2) abnormal tensions and stretching of visceral supports, nerves, blood and lymph vessels, (3) venous pooling as the result of inactivity, diaphragm dysfunction, organ displacement, and sustained postural stress, or (4) abnormal vasomotor impulses to blood vessels. Blocking stress or irritation of blood vessels leads to ischemia or congestion.
There are many general effects to the body as a whole besides these local effects because each abnormal stress results in abnormal discharges of afferent impulses to the central nervous system with consequent hormonal reactions sys- temic in character. Also considered must be the associated emotional stress as the result of the local stress which contributes to the clinical picture.
Fundamental Considerations in Evaluating Idiopathic Spinal Pain
The general public associates the management of "backache" with chiropractic probably more than any other disorder because of the profession's reputation for offering relatively rapid relief by conservative means. This has been a "dual- edged sword" for it has contributed to the public's difficulty in associating chiropractic care with disorders far removed from the spine.
While most causes of spinal pain are best discussed in relation to particu- lar regions, some considerations are so general that they apply to all regions. These points will be covered later in this chapter.
Tunnel Thinking. A writer who uses an abundance of outlines, classifica- tions, charts, and graphs is considered well organized and a "good" teacher. It is easier to teach, to remember isolated facts, and to pass examinations when data are so depicted. It simplifies the complex. Unfortunately, such learning habits tend to develop compartmentalized thinking. There is probably no other area in clinical practice where the tendency is stronger to reduce patient pro- files to conform to preconceived notions than that of spinal pain. Granted, pat- terns do occur, and we will present them in this book as a basis for thought, but the exceptions may outweigh their textbook descriptions.
The Evasive "Normal". When Earl Rich was head of the Roentgenology Depart- ment at Lincoln Chiropractic College, after viewing thousands of spinal films, he felt that the typical adult spine contained about seven anomalies on the average. In clinical practice, we constantly search for the ideal normal and rarely find it. It seems that all we ever find are variations. Yet, we often hold in our minds a visualization of a necessary "normal" that we strive to attain for an individual which is often impossible. This creates an enigma.
This for That Concepts. Case failure is too often the result of "this for that" thinking in prejudiced diagnostics and therapeutics; eg, is this a "Type A" case, a "Class II" distortion, or a "routine" reaction? Orthopedists, espe- cially, often assume that every pain goes with some musculoskeletal derangement similar in severity to the patient's complaint. Such an iatrophysics approach completely ignores the body's holistic nature, adaptive ability, and individual normal variances to the preconceived "textbook norm."
STRUCTURAL VS FUNCTIONAL EMPHASIS
From a purely mechanical viewpoint, we commonly think of movement being the result of the shape of the planes of articulation, assuming that a certain shape causes certain motions. This contributes to assumptions that structure always governs function and that function is always dependent on structure. This, as are most clinical definites, is a half truth, because movement occurs long before ossification establishes the osseous planes. And this does not consider the many severe bumps and jars suffered during childhood.
The science and art of chiropractic orthopedics are concerned with the postural relationships of articular surfaces, both normal and abnormal, the ana- lysis of harmful influences on improper structural relationships, the diagnosis and correction as is possible of such abnormal relationships, and the management or prevention of disturbances resulting from such malrelationships.
Pure orthopedics is not concerned with function to a great extent, but concentrates upon structure with function playing a platonic role. From this strict structural viewpoint, function is dependent on structure and is regarded as secondary. The major emphasis is on the position of rest rather than the dynamics of articulation. However, although movements of mature joints are in- fluenced essentially by the design of the articular planes, these planes have attained their shape because of functional movements made during development. In addition, it is not rare to see a subluxation where movement has not accura- tely followed the normal plane of movement.
During the clinical analysis of structure, Lieb offers three postulates worthy of consideration. He points out quite accurately that (1) without struc- ture there is no function, (2) without correct structure there is not correct function, and (3) incorrect function, however, may adversely affect not only correct structure, but also seriously affect developing structures. Thus, struc- ture can be the effect of function, and function can be the effect of structure. There is no need to divide into "chicken and egg" camps if we stay with reality, in the "now."
In chiropractic, we view so many static x-ray films, see so many static diagrams in books and professional papers, and palpate so many patients in the relaxed position that it is often very difficult to think of a subluxation in its dynamic sense. And when we do, our visualization often represents a series of static "stills."
The doctor is misled who believes he can understand the patient's perception of pain. We can only seek to understand the patient's reaction to it. This is true whether the pain is isolated or generalized, local or referred. Although all pain does not have organic causes, there is no such thing as "imagined" pain.
Pain that can be purely isolated as a structural, functional, or an emotion- al effect is rare. More likely, all three are superimposed upon and interlaced with each other in various degrees of status. This is also true for neural, vas- cular, lymphatic, and hormonal mechanisms.
The four most common mechanisms producing spinal pain are IVD degeneration, posterior joint dysfunction, IVF pressure (compression or traction), and abnor- mal somatovisceral reflexes. It is important to differentiate local causes of spinal pain from diseases referring pain to the spinal area. Classes of selected vertebral causes of spinal pain are outlined in Table 6.2. Classes of selected pathologies simulating spinal pain are shown in Table 6.3. Again, these tables are offered as "thought provokers", not as boundaries.
Table 6.2. Classification of Selected Vertebral Causes of Spinal PainTRAUMATIC INFLAMMATORY ARTHROPATHY Dislocation Ankylosing spondylitis Fracture Collagen diseases Sprain Fibrositis Strain Focal sepsis Subluxation Gouty rheumatism Muscular rheumatism Osteochondritis INFECTION Panniculitis Brucella melitensis Psoriasis Escherichia coli Regional ileitis Staphylococcal Reiter's disease Tubercular Rheumatoid arthritis Ulcerative colitis DEVELOPMENTAL METABOLIC Hypermobility Osteomalacia Kyphosis Osteoporosis Lordosis Scoliosis SYSTEMIC Spondylolisthesi Secondary involvement of primary infection Various anomalies and general disease processes such as typhoid fever, brucellosis, actinomycosis, DEGENERATIVE influenza, smallpox, gout, blood Apophyseal osteoarthritis dyscrasias, alkaptonuria, and cancer. Cauda equina disorders Degenerative disc lesions MISCELLANEOUS Hyperostosis Iatrogenic causes such as unskilled Joint instability or ill-advised manipulation, myelography, Nerve root compression surgery with sub sequent adhesions, and Spinal cord diseases poorly fitted or prolonged use of supports. Psychogenic conversion syndromes. TUMOROUS Myelomatosis Secondary carcinoma IDIOPATHIC Paget's disease Rare bone diseases
Table 6.3. Classification of Selected Pathologies Simulating Spinal PainCERVICAL PAIN Malignant lymphadenopathy Pancoast tumor Subarachnoid hemorrhage Vertebral artery syndrome THORACIC PAIN Aortic aneurysm Bronchial carcinoma Cardiac enlargement Coronary artery disease Gallbladder disease Herpes zoster Hiatus hernia Pulmonary disease LUMBAR PAIN Aortic obstruction Colon carcinoma Disseminated sclerosis Endometriosis Hip disease Miscellaneous pelvic carcinoma Obstruction of iliac arteries Pancreatic carcinoma Peptic ulcer Rectal carcinoma Renal disease Short leg syndrome Spinal cord tumor MISCELLANEOUS Visceral diseases causing referred pain to the spine or pressure erosion Central nervous system diseases such as meningitis, poliomyelitis, syringomyelia, tetanus, spinal subarachnoid hemorrhage Psychogenic causes Iatrogenic manifestations.
Although there are many good theories, the actual cause of common neck or back pain remains unknown unless gross pathology can be demonstrated. There is no one type of subluxation picture or abnormality that is associated with all forms of spinal pain, nor does the presence of a subluxation or abnormality mean that the patient will have pain. Diagnosis must be approached with caution be- cause of the many structural, functional, and psychologic mechanisms that may be involved (Fig. 6.60).
We know that mechanical pressure (traction or compression) on axons or nerve trunks inhibit rather than excite. This blocking effect would appear to contraindicate spinal manipulation whose aim is to relieve pain caused by a stretched or compressed IVF. However, rapid transient mechanical distortions, such as would be aggravated during normal motion, depolarize nerve trunks and mechanoreceptors and produce impulse bursts of short duration. Other explanations include (1) soft-tissue receptors as the source of pain impulses, (2) vascular pulsations offering repeated transient mechanical stimuli to tensed or compressed roots, or (3) inflammation foci responsible for sustained neural discharge rather than that of mechanical forces.
Spinal pain not associated with gross trauma or obvious pathology has been common to mankind since the earliest civilizations. These common disorders have their highest incidence during middle age (30–50) and frequently originate near the more mobile areas of the spine (Oc–C1, L5–S1).
While the literature abounds with discussions on industrial and sports- related injuries, about 43% of musculoskeletal injuries occur in the home, 16% at work, 34% in public places and recreational areas, and 7% in automobiles. Regardless of the site of trauma, the common response includes inflammation and repair.
A relationship between the magnitude of loading and the degree of motion of the various spinal regions to the incidence of pain has been established. The cervical region, which has the second rank in pain incidence, has the highest degree of motion and the lowest weight load. In contrast, the lumbar region, which has the highest rank in pain incidence, has the second rank in mobility and the highest weight load. The relatively stiff thoracic region, which has the lowest rank in pain incidence, has the least range of mobility and the second rank of weight load.
General Aspects of Spinal Inspection and Palpation
The art and science of spinal examination, analysis, and diagnosis mandate that the patient be examined in more than one postural stance or position. The discovery of the indication of subluxations depends on multiple positions in which the spine is observed because certain lesions are more obvious in one attitude than in another. The (1) Adams position, (2) anatomic position, (3) prone position, and (4) supine position are suggested for a complete spinal analysis.
It is assumed that prior to mobilizing procedures any indication of frac- ture, dislocation, advanced arteriosclerosis, hemorrhage, or cord injury has been considered.
STATIC BONY PALPATION
The identification of the bony segments of the spine is done by palpating and counting. This requires the development of a refined tactile sense on the part of the examiner. It is important to count the vertebrae so to correlate and document the involved segment neurologically.
Since the 1890's, digital examination of the spinal column has been conduc- ted within chiropractic for evidence to determine "incorrect positioning" of one vertebra relative to another. For the most part today, static palpation seeks to determine only the probable locations of subluxations by the variations in mus- cular tonus, texture, and sensitivity (bone anomalies are far too frequent).
Healthy paravertebral tissue presents a normal texture, is not tender to moderate touch, and has no lasting soreness following minor trauma. However, local hyperalgesia, abnormal soft-tissue tone, and lasting soreness are common findings associated with subluxations. Adjacent soft tissues will frequently feel boggy or thickened near rigid muscle. These two signs alone represent a disturbance in local homeostasis. This may be the pathophysiologic result of trauma or the effect of changes induced by functional (visceral or psychologic) or other disturbances by way of the controlling and communicating neural, vascu- lar, lymphatic, or hormonal processes that determine homeostatic balance.
Resting muscle is electrically silent as shown by electromyography and re- laxed as shown by palpation. Conversely, muscle tissue near a subluxation is often active as shown by electromyography and spastic as shown by palpation. Propping the patient in different positions with pillows often will decrease electromyographic activity, but it does not appear to reduce the palpable firm- ness. This would indicate that the increased tone is not necessarily due to muscle contraction from nociceptive input. However, it is well established that irritation of the posterior joints and ligaments readily leads to reflex spasm of the erector spinae and other extensors.
In the absence of muscle contraction, one hypothesis is that this change in texture is the result of local fibrositis. And it has been shown that the cuta- neous pain threshold is significantly reduced in fibrositis. Other theories attribute it to a neurogenic inflammatory process or an interference with nor- mal axoplasmic flow resulting in abnormal neuron trophicity. Gillet feels it is a state of hypertonus of the autonomic mechanism, not far from normal, as there is often no pain (except on deep palpation) such as that exhibited in extremity muscle spasm.
It is possible, with practice, to palpate the comparative tone of the spinal intrinsic muscles. The rotatores or multifidi are the most easily palpated and are helpful in evaluating subluxations. The intertransversarii (levator costae in the thoracic area) are more difficult to palpate but are quite helpful indi- cators.
Muscle tone evaluation requires precise knowledge of anatomy and much prac- tice at the technique of gliding the fingertips transversely across the muscle fibers with the skin of the patient moving as part of the fingertip. For the rotatores, the glide is axially along the side of and very close to the spinous process at the muscle insertion. Hyperesthesia will also often be located here (or less frequently, paresthesia), which induces even further muscle contraction by reacting to the pressure of the palpating fingertips.
Gonstead advises to search for areas of edema in sites of poor tissue tone which feel softer to the touch than normal areas. These areas are often found at or near the level of involvement.
Since pain from nerve roots or pathways is referred toward the periphery, the entire nerve leading from the area should be explored where possible. In addition, tenderness, masses, spasms, local temperature, areas of excessive moisture or dryness, their size and character, and other points should be noted.
The Basic Factors Involved in Spinal Examination
Whether spinal or extraspinal, musculoskeletal symptoms may be the first clues in the diagnosis of poor structural or stress adaptation. The most common musculoskeletal symptoms are joint stiffness, joint swelling, and joint pain. The nature of the damage usually depends on the direction of the applied force on bones and the manner in which these bones are attached to other structures.
The examination of the musculoskeletal system is different for an acutely injured patient than for a patient presenting nontraumatic complaints. For instance, active and passive ranges of spinal motion should not be conducted until after roentgenograms have demonstrated the mechanical integrity of the joint. During spinal analysis, the major motions evaluated are flexion, exten- sion, right and left lateral flexion, and right and left rotation. Motion of a superior segment is described in terms of the segment beneath it.
Although regional examination will be discussed in future chapters, certain basic points are appropriate here.
Normal Rotation. When the spine is in a neutral standing or sitting posi- tion, the anterior surface of a vertebral body in the lower spine will rotate to the side opposite the lateroflexion with the vertebral bodies tending to crawl out from under the load. This pattern of function usually takes place within multiple spinal segments, but dysfunction will occur when ligaments and muscles attached to and affecting the vertebral articulations are shortened or lengthen- ed to effect restricted or excessive motion of one or more segments. When the neutral position is resumed, each spinal joint should return to its "normal" position.
Scoliotic Rotation. The direction of vertebral rotation is determined by inspection and dynamic palpation of the transverse processes, with one trans- verse process being more posterior on the side toward which the vertebra has rotated. If one or more segments are rotated to one side in the neutral posi- tion, lateroflexion will usually be noted on the side opposite the rotation. In spinal flexion, the segment rotated will be laterally flexed to the same side with a loss in its ability to bend forward. During spinal extension, the segment is rotated to the same side and is inhibited in bending backward.
Motion Restriction. Functional limitation may be the result of pain associ- ated with movement (Fig. 6.61), joint instability, or restricted joint movement by muscular spasm or hypertonicity, ligamentous or capsule shortening, bony ankylosis, thickening or adhesions in the periarticular structures, or obstruc- tion by bony overgrowths or gouty tophi.
Excessive Motion. Excessive motion such as in joint tears is recognized simply by contrast with the limits furnished us by our knowledge of anatomy and physiology of joint motion at different ages. These are extremely rare except in cases of severe trauma such as in athletic injuries, vehicular accidents, or falls from great heights. The more common cause in the spine is the hypermobil- ity felt adjacent to an area of hypomobility.
Caution. Although a patient may actively move freely through all gross ranges of motion, this is not necessarily proof of segmental freedom. Such a conclusion is an error commonly made by general practitioners. Careful one-by- one static and dynamic palpation of the vertebral segments will often reveal extremely tender sites (previously unknown to the patient) and numerous segmen- tal fixations in one or more planes. With the exception of ankylosing spondylo- sis or some other generalized disorder of the spine, gross mobility evaluation of large regions of the spine have little clinical significance that can be applied to corrective therapy. Such evaluations are of more interest to insurance companies than to health science.
EVALUATING GROSS JOINT MOTION AND STRENGTH
The range of motion for any particular spinal area is usually recorded in degrees by a goniometer with comparable measurement of the opposite side noted. When asymmetry of motion range is observed, the examiner must determine whether the side with the greatest movement is weak or the side with less motion is restricted. Testing the strength of a group of muscles is made by carrying the spinal region to the extreme of allowed movement permitted by the antagonist muscles after which the examiner resists an active maximum effort by the patient to contract the muscles being tested. Strength is recorded bilaterally from Grade 5 to Grade 0.
Case Management. No injury is static. It continues to produce harmful effects on the injured person until either the injury or the person is defeated. As these effects are systemic as well as local, the response to injury is also both systemic and local. For this reason, injuries and their effects must be evaluated from the standpoint that the whole person is injured and not from the view that an otherwise well person is afflicted with a local defect or that only a part of the individual is affected.
Since the effects of injury and the body's efforts to defeat them are con- stantly changing, the doctor cannot rely on infrequent observations or one major symptom in evaluating the condition of the patient, especially one seriously disabled. Repeated observations must be made and indications of the patient's condition must be considered to obtain as clear a picture as possible of the patient's status and the treatment required at the moment the particular obser- vation is made.
Rehabilitation. After acute symptoms subside, a gradual rehabilitation program can be initiated which encourages the inflammatory reaction of resolu- tion to pass quickly and reduce fibrous thickening of tissues. A great deal of atrophy, muscle weakness, and fibrous induration can be eliminated by applying progressive rehabilitation as soon as possible. Naturally, timing must be coor- dinated with the type of injury; ie, bone injuries require longer support and rehabilitation procedures than do soft-tissue injuries.
Posttraumatic Functional Stiffness Prevention. We recognize that enforced inactivity following major surgery leaves an indurated scar of thick fibrous tissue that remains tight and uncomfortable for a considerable time after surgery. Likewise, severe joint injury inevitably results in overabundant scar tissue from necessary immobilization. Even minor disorders treated with long- term immobilization develop scar tissue which permanently restricts function. On the other hand, uncomplicated surgery, wounds, and sprains followed by ambula- tion in a day or two result in a cicatrix which is not tight, but rather soft and pliable. This same principle applies to spinal joint injuries. It would appear to be a worthy objective, if not mandatory, to carefully control rehabil- itation towards full return of function with minimal scar tissue and fixation.
Selected Clinical Considerations
An understanding of fundamental normal spinal kinematics is vital to compre- hend the factors necessary in clinical diagnosis and case management of most spinal disorders.
General Aspects of Musculoskeletal Injury
The initial treatment of acute spinal injury does not differ greatly from that of other musculoskeletal injuries except for special concern for the nerve roots, pathways, and spinal cord.
THE STAGES OF HEALING
After any severe strain or sprain, there is undoubtedly a degree of soft-tissue microhemorrhage. Resolution begins after bleeding stops to organize minute thrombi to form the richly vasculated granulation tissue which allows:
The inflammatory stage where the white blood cells dissolve extravasated blood elements and tissue debris, characterized by swelling and local tenderness.
The reparative stage where the network of fibrin and the fibroblasts begin the reparative process, characterized by local heat, redness, and diffuse tenderness.
The toughening stage of fibrous deposition and chronic inflammatory reac- tion, characterized by palpable thickening and induration in the area of reac- tion, with tenderness progressively diminishing (Fig. 6.62).
CARE DURING THE HEALING PROCESS
After displacement has been corrected or a fixation has been released, nothing should be done during the complicated healing stage that might disrupt the natural process. Firth continually reminded his students that "there is too much fiddling with the spine." The injury itself is all the local stimulation necessary for maximum response. Direct massage, heat, hydrocollators, whirlpool baths, ultrasonics, enzymes, etc, are usually contraindicated as they only add additional stimulation to an already maximally stimulated area.
The best procedure is to anticipate each step in the healing process and provide the opportunity for natural processes to express themselves. This is not to say that if a variation is seen at one of the normal stages of healing that treatment should not be varied accordingly. Increased local heat and tenderness during a later stage indicate an infectious process.
Good care during healing requires repeated inspection and sometimes external support:
(1) Periodic and regular appraisal can usually be made simply through inspection and palpation. When dealing with many injuries, one becomes astute in seeing and feeling the various stages of healing.
(2) Continuous support during the resolution stage may be provided by external measures without impairing the natural healing process.
The term spinal instability refers to that state of a vertebral segment which cannot maintain its normal relationships with its contiguous structures under normal loading conditions for the individual. The results are possible irritation of the nerve, root, or cord; intolerable pain; and degenerative structural alterations. The cause can be trauma, disease, or can be iatrogenic from misapplied surgery or manipulation.
Several authorities feel that the first sign of disc disease is that of abnormal motion on flexion. Macnab attributes most pain associated with disc lesions to be from repetitive ligamentous strain due to chronic hyperextension of the posterior vertebral joints and the resulting arthritis. Farfan believes the more advanced changes found in disc disease (eg, marginal osteophytes, degenerated facets, pseudospondylolisthesis) are also due to mechanical stresses. Both Macnab and Farfan consider these changes to be the result of segmental instability.
Hypermobility is permitted by ligamentous laxity, disc degeneration, and remolding of the posterior articulations (Fig. 6.63). It may be primary (ie, localized trauma or pathology limited to one or more motion units) or secondary. These secondary factors include those resulting from a primary problem often far removed from the spine such as lower limb asymmetries, eccentric weight bearing, misuse or overuse of spinal tissues associated with postural-occupational stresses, and system-oriented disorders such as hypoglycemia that may increase the degree of spinal curvatures through chronic fatigue.
As segmental instability requires stabilization, the primary question in diagnosis is locating and determining the primary problem or maladaption that is overloading and chronically stretching the involved motion unit. A hypermobile unit is not tightened by spinal adjustment. It is often self-correcting once its cause is removed.
Hypermobility is the variant of subluxation that is most apparent in roent- genography. The overt signs include traction spurs, interruption of Hadley's "S" curve, excessive A-P body shift at extremes of flexion and extension, abnormal opening and closing of disc space during lateral bending, appearance of segmental hyperextension on neutral lateral films, change in articular relations to the joint-body line, reactive spondylosis and arthrosis, etc.
A hypermobile subluxation indicates laxity of the holding elements –a positional relationship of two vertebrae in which their bodies or apophyseal joint surfaces or both are in a position that they could never occupy during any phase of a normal physiologic movement. It is particularly obvious in spondylolisthesis, laterolisthesis, and retrolisthesis, and in excessive disc space gapping in the sagittal or frontal plane. Instability in these cases becomes even more obvious at the extremes of movement, hence the value of carefully conducted stress films if they are not contraindicated.
These subluxations are relatively permanent; but on top of and/or below such an irreversible subluxation, a fixation subluxation in one or more particular arcs of movement (eg, forward flexion from an internal disc derangement) may be exhibited. Thus, this subluxation, which is often not roentgenographically demonstrable, is a dysfunction clinically discernible through motion and muscle palpation.
All subluxations appear to follow a progression. For example, a spondylolisthetic vertebra may start off with essentially normal mechanics, then slowly become hypermobile with middle age. An evident subluxation must be viewed in the context of the entire clinical picture, and this functional classification is clinically oriented.
A spinal articulation may be fixed, totally or partially, in its neutral position, or it may be fixed anywhere within its range of A-P, lateral flexion, or rotational motion. Thus, a fixation is not synonymous with a subluxation but a state superimposed upon a subluxation. If an articular subluxation is not fixed, it undoubtedly would reduce itself automatically in most cases during normal spinal motions.
In compensation to a local area of fixation, adjacent joints are forced to assume roles of increased mobility (hyperkinesia) leading to clinical instability. Also, when an unilateral articulation is partially fixated, its contralateral partner is forced to assume the role of both via pivotal hypermobility about an abnormal axis. Invariably, it will be at the site of excessive mobility that is symptomatic rather than the site of the cause of the abnormal movement. Gillet believes that one exception to this is the suboccipital area, which he feels is often involved in a multimuscular state of fixation.
Total fixation is most frequently found at the occipitoatlantal, lower thoracic, and sacroiliac articulations. In most instances, however, mobility is not restricted in all directions. The earlier a fixation is corrected, the less chance there is for chronic degenerative changes to occur and the greatest change in mobility can be noted after adjustment.
CAUSE AND EFFECT RELATIONSHIPS
Both spinal and extraspinal subluxations and fixations can be primary causes or secondary effects of each other.
Subluxation as the Primary Entity. In a situation of trauma, a vertebra can be forced out of its normal alignment and jammed into an abnormal position of unrest. Trauma inevitably is associated with severe, protective, phasic muscular spasm. In time, the related muscles will become hypertonic via postural reflexes in their effort to correct the situation, even when the phasic fibers relax. The related paravertebral ligaments will shorten to accommodate their restricted need for mobility. Here, fixation is secondary to the subluxation. Its state is usually acute and unilateral.
This same type of subluxation is seen secondary to peripheral irritation (eg, visceral irritation), where the subluxation is sustained via sensory or autonomic input to the efferent neurons via cord interneurons. Since the nervous system is not a one-way street, it is often difficult to determine if the subluxation here is a contributing cause or a complicating effect.
Fixation as the Primary Entity. Severe muscular contraction, from whatever stimuli, can lock a segment or pull a vertebra out of its position of rest. This site of primary fixation is, in turn, usually an adaptive secondary mechanism to a vertebral anomaly or asymmetry, a unilateral short leg (structural or functional), a remote adaptive mechanism to an acute subluxation that has been corrected, habitual postural imbalance (eg, occupational or otherwise), or unilateral overdevelopment. Here, the associated subluxation is secondary to the fixation. It is usually chronic and bilateral.
We can therefore appreciate that a subluxation or fixation can be locally primary or secondary. One type can be found at one site and the other type at another site, and one type can be superimposed upon the other at the same site. The complex, highly integrated human body is not a diagnostic "rose garden". However, a thorough knowledge of biomechanics and the neural mechanisms involved will do much to clear the confusion.
TYPES OF FIXATION
Four major mechanisms are involved in articular fixation: muscular, ligamentous, intra-articular, and osseous. These mechanism may occur singularly but more often they occur in combination, and they may occur in one motion unit or several.
The mechanisms that hold a vertebra in subluxation are varied and often controversial. Smith et al held that the cause was a muscular or ligamentous fixation. In 1923, Downing described the osetopathic lesion in similar terms. Other causes have been contributed to bony impingement (Palmer), trigger points (Travell), viscerosomatic reflexes (Bennett), articular adhesions (Stoddard), capsular adhesions (Mennell), disc displacement (Cyriax), nuclear displacements (Barge), meniscoid fragments (Schmorl/Junghans), synovial tabs (Haddley), acquired apophyseal asymmetry (Caplans), and various combinations of these factors.
Each region of the spine appears to have its peculiar characteristics in regard to fixation development. Certain muscles have a greater tendency to hypertonicity, and certain ligaments have a greater tendency to shortening. These characteristics which depend upon their physical properties and functional roles will be discussed in future chapters. Obviously, the type of fixation and degree of degeneration present, among other factors, determine the magnitude of adjustment force necessary for freeing the fixation.
Contracted musculature will fixate a vertebral segment. To appreciate the mechanisms involved, two points should be kept in mind that have been previously discussed:
Muscles receive dual efferent innervation:
(1) via the large phasic high-threshold neurons that provide intermittent voluntary or reflex impulses of short duration and fast velocity for movement and
(2) via the smaller postural lower-threshold neurons that provide reflex impulses of longer duration and slower conduction to maintain constant muscle tone. Activity of the latter is essentially sustained by the stretch reflex.
Phasic unilateral muscle contraction produces an automatic relaxation of its antagonists and a temporary abolition of the antagonists' postural tone via reciprocal inhibition.
A dynamic adjustment that would increase the distance between muscle origin and insertion elongates the contracted muscle fibers and encourages relaxation. On the other hand, a slow manipulation would elicit resistance via the stretch reflex.
Muscular fixations in the spine are the most numerous, the most symptomatic, the most liable to be unilateral, and the most visible in terms of "displace- ment." Fortunately, they are the easiest to correct by either direct or indirect means. Unfortunately, they are the most liable to return. A long-standing state of hypertonicity will lead to fibrotic degenerative changes. Thus, for practical purposes, such a muscle or muscle group acts and responds to treatment as would ligamentous tissue.
Acute reflex muscular fixations are usually the product of another site of chronic fixation-generating noxious reflexes. Thus, they often disappear imme- diately when the primary site is normalized. They are also the most likely to exhibit a predictable specific pattern in response to a primary remote site of chronic fixation. The hypertonicity is usually restricted to the short muscles, but the long muscles are occasionally involved.
PARAVERTEBRAL LIGAMENTOUS MECHANISMS
Shortened ligamentous tissue will fixate a vertebral segment. It is the nature of ligamentous tissue to adapt (shorten) itself to the range of motion used by the individual. While muscle contraction may be unilateral or bilateral, ligamentous shortening not occurring in the midline is almost always bilateral, with one side usually shorter than the other. Ligamentous fixations always produce a degree of torsion, and only a slight increase in mobility is appreciated immediately after adjustment.
Chronic hypomobile fixation of any diarthrodial joint results in para-articular ligamentous shortening and eventual joint cartilage degeneration. This degenerative process is usually initiated by a readily correctable state, poorly defined as joint "glueing" and similar to the early adhesive state of "frozen shoulder" capsulitis. Early proper adjustment breaks the seal and encourages a rapid return of mobility.
Shortening of capsular ligaments tends to restrict motions other than rotation, but the effect of capsular shortening is much more pronounced in the extraspinal joints than in the spine. Because body joints are coupled in kinematic chains, the effects of extraspinal fixations may be referred to the spine.
Bony ankylosis is the ultimate mechanism of fixation. Since it is usually the result of advanced pathologic processes and adaptive in nature, it does not fall into the realm of correctable fixation. Freeing a pure ankylosis will generally cause more harm than good, and thus is contraindicated (eg, rheumatoid arthritis).
Fibrous ankylosis, common to thoracic degenerative changes, does not contraindicate manipulation. However, fibrous tissues adapt slowly and correc- tion takes frequent care utilizing many different types of therapy over many months, if not years, to see an appreciable structural change.
Spinal Strains and Sprains
Healthy muscle function includes contraction for power production to over- come intrinsic and extrinsic loading. Equally important is a muscle's capability to relax contraction (physiologic elasticity) and yield to passive stretch (phy- sical elasticity). Coordination is the result of strength and physiologic elas- ticity in proper relation, interplay, and sensory regulation. Muscle function, dysfunction, and rehabilitative therapy are shown in Table 6.4, adapted basically from Kraus' data.
Table 6.4. Basic Muscle Function, Dysfunction, and Rehabilitative TherapyFunction Dysfunction Therapy Strength Weakness Exercises against resistance Physiologic elasticity Spasticity Relaxing exercises, autosuggestion, biofeedback therapy, postural correction Spasm Pain relief, "gate" blockage tech- niques, relaxing exercises Tension Relaxing exercises, psychotherapy, hypnotherapy, hydrotherapy Physical elasticity Contracture Stretching exercises, joint mobiliza- tion Coordination Incoordination Strengthening and relaxation exer- cises, coordination training and practice.
General spasm of the spinal muscles guarding motion in the vertebral joints can be viewed by watching body attitude (eg, stiff carriage) and by efforts to bend the spine forward, backward, and to the sides. If we are familiar with the average range of motility in each direction and at different ages, this test is usually easy and rapid. Isolated segmental spasms, however, cannot be determined by such screening tests.
Management. To relieve severe muscle spasm prior to adjustive therapy, heat is helpful, but cold and vapo-coolant sprays have sometimes been shown to be more effective. The effects of traction are often dramatic but sometimes short lived if a herniated disc is involved. A predisposing joint weakness may be present that requires special stabilization.
Passive Stretch. Mild passive stretch is an excellent method of reducing spasm in the long muscles, but heavy passive stretch destroys the beneficial reflexes. For example, hypertonic erector muscles of the spine can be simply relaxed by placing the patient prone on a split headpiece adjusting table and tilting the abdominal and pelvic section upward to flex the spine. The weight of the structures above and below the midpoint of the flexed spine have a mild stretching effect, both cephally and caudally. The muscles should relax within 2-3 minutes. Thumb pressure, placed on a trigger area, is then directed towards the muscle's attachment and held for a few moments until relaxation is complete. Psoas or quadriceps spasm, for example, can be relaxed with Bragard's test by holding the straight leg for a minute or two in extension and dorsiflexing the foot.
Spinal strains are afflictions of the young and healthy where strong back muscles guard the segments. When stressed, the pain and tenderness will exhibit away from the midline unless the erector spinae are involved. Older people with a degree of disc degeneration will inevitably manifest symptoms of posterior joint stress rather than muscle injury.
Tendinitis is not as common in the spine as it is in the extremities, but it does occur with strenuous effort. As the result of the vascular reaction and local edema, point tenderness is found at the musculotendinous junction or at the attachment to bone.
No modality will strengthen a muscle or permanently shorten a lax muscle. Only exercise will do that. Various techniques may be applied to relax a muscle, but only active and passive stretching exercises will lengthen a shortened muscle.
Gelb points out that "restoring muscles to their physiologic resting length is a three-dimensional concept; it entails placing the origin and the insertion of the muscles in correct three-dimensional relationship."
After a muscle has been strained, Goodheart's research found that heavy pressure over the origin or insertion of the affected muscle will elicit a normalization response in the comparatively weakened muscle. This state of weakness after strain appears to be the result of a microavulsion of the tendoperiosteal connection. The following technique is essentially used on weak hypertonic muscles created by overstretch injuries:
The isolated muscle is tested and noted for comparative weakness, hypertonia, and/or shortening. If strain to the tendoperiosteal site has occurred, the muscular origin and insertion will be tender. The site is selected which appears to be the most tender, either origin or insertion. The pads of two or three fingers are applied on the muscle's tendon or point of attachment. Pressure is directed from the muscle toward the point of origin or insertion. If partial rupture has occurred, it may be necessary to strap the muscle somewhat prior to therapy. If relaxation of a reactive muscle is desired, pressure is applied gently at first and slowly increased to just below the patient's tolerance (2-3 lb). Initial heavy pressure can be extremely painful and tends to increase spasm.
The correct pressure utilizes the Golgi tendon receptor reflex to induce muscle relaxation. This pressure is maintained for 30–60 seconds until the muscle relaxes and is allowed to lengthen, then it is held for approximately 10 seconds after the muscle has appeared to relax. The muscle is then re-examined unless severity prohibits re-testing. In some cases, small sensitive nodules noted on palpation near the affected muscle's origin and/or insertion disappear within 24 hours after successful treatment. When hypertonicity is normalized, the patient is given instructions in proper stretching exercises.
During the range of normal physiologic movement, the vertebrae move quite freely. Once the range of motion is approached, the spinal ligaments provide important protection by resisting forces and absorbing energy before they fail. When either a spinal or an extremity segment is subjected to excessive tensile load, failure is at either the bone or the ligament (Fig. 6.64). Note: Usually, bone fails first with loading at a slow rate, and ligaments fail first with loading at a rapid rate.
Sprung Spine. The final degrees of spinal flexion are checked essentially by the posterior fibers of the anulus and the posterior capsules. If the disc is dehydrated (degenerated), an abnormal degree of flexion is allowed. A sudden, forceful spinal flexion when the pelvis is fixed may rupture one or more supraspinous ligament fibers (eg, buttock falls). Pain is localized and rarely radiates.
POSTERIOR JOINT INJURIES
The stability of the posterior synovial joints is primarily established by action of surrounding musculature. Excessive joint stress results in strained muscles and sprained ligaments. When stress is chronic, degenerative changes occur. Joints anywhere in the body are usually injured from a direct stress leading to connective-tissue contusion and a possible degree of intra-articular fracture. The force is often an unexpected one where protective mechanisms have not been put in force, or it may be so excessive that protective mechanisms fail.
Synovial lining is slightly phagocytic, regenerative if damaged, and secretes synovial fluid which is a nutritive lubricant that has bacteriostatic and anticoagulant characteristics. This anticoagulant effect may result in poor repair in a situation of intra-articular fracture where the fracture line is exposed to synovial fluid (eg, apophyseal facets).
Myalgia or muscular rheumatism is a generalized term referring to aching muscles associated with stiffness, tenderness, and varying degrees of disability increased by active motion. Rare is the person who has not suffered some form of stiff neck, dorsodynia, lumbago, or sore extremity muscles after unusual exertion or chilling. It appears to be the most common form of persistently recurring pain other than headaches.
Fibrositis is a better term than myalgia since the nonspecific inflammatory changes occur chiefly in the white fibrous connective tissue of tendons, muscles, nerve sheaths, fascia, periosteum, joint capsule, and ligaments. These changes include hypothermic edema and proliferation of white fibrous connective tissue as a result of chilling, toxic influences, acute trauma, chronic strain, or physical fatigue.
Thermal and barometric changes, vitamin B deficiency, chemical intoxication, metabolic imbalances, as well as dampness and respiratory infection are important precipitating factors. Focal infection is often an important factor as is a malfunctioning colon. Regardless, the mode factor is via the capillary circulation and the nervous system.
The early state is one of effusion with a localized inflammatory serofibrinous exudate causing puffy swelling. The exudate may be absorbed or organized by fibroblast invasion and proliferation of fibrous tissue. In the latter stage of fibrous thickening, fibrous bands and nodules sometimes form in the muscles and fascia as adhesions and press on arterioles and nerve filaments producing contracture and atrophy.
Such a condition is undoubtedly a part of the arthritic syndrome which has a wide variety of manifestations. For example, intramuscular fibrositis (myositis, myofascitis, muscular rheumatism), bursal fibrositis (bursitis), perineural fibrositis or interstitial neuritis (eg, sciatica), periarticular fibrositis (capsulitis, capsular rheumatism), tendinous fibrositis (Dupuytren's fibrositis), or subcutaneous fibrositis (panniculitis).
While any disease that primarily affects joints may cause an associated poorly localized aching in a muscle or muscles, the following conditions are those which usually present muscle pain with minimal or no articular involvement.
Infection: The patient reports an acute onset associated with fever and other signs of infection.
Tendinitis, Peritendinitis, and Capsulitis: The history commonly presents an acute or insidious onset associated with trauma to or excessive strain of the involved region. Some investigators, however, dispute this, feeling that many times there is no overt trauma involved. Bennett contends visceral irritation produces local skeletal vasoconstriction which sets up spasm, joint irritation, etc. Thus, a joint or tendon may become painful without trauma, either overt or covert. The course is self-limiting, but joint deformity may result. There is local tenderness over the tendon insertion and around the joint. Motion limitation is common.
Psychogenic Rheumatism: The history presents poorly localized muscle pain, more commonly reported by females. The course is chronic, nonprogressive, and nondeforming. There is diffuse or localized areas of muscle tenderness.
Drug-Induced Myalgia: There is a history of administration of steroids, diu- retics, anticonvulsants, etc, often where remissions can be associated with not taking the drug. Physical findings are usually negative, but there may be some pulmonary involvement.
Other causes include rheumatoid arthritis, polymyalgia rheumatica, dermatomyositis, scleroderma, systemic lupus erythematosus, and various connectivetissue diseases.
COMBINED WEAKNESS AND TENSION
Muscle inactivity produces weakness and stiffness that lead to a large variety of muscle problems (eg, atrophy), and irritation leads to emotional imbalance and spinal tension syndromes. Kraus feels that "if both underexercise and over-irritation coincide, and if the physical response to stimuli is inhibited or prevented, the chronic, repeated inhibitions of the fight-or-flight response contribute to disease."
The normal response to stimulation (eg, pain, fear) is an increase in epinephrine release, an increase in muscular tension, heart beat, blood pressure, respiratory rate, and a shifting of blood volume peripherally. If this normal response is inhibited over a prolonged period, Kraus states that this enhances hypokinetic disease.
In normal relaxed attitudes, the tonic muscles contract only to the degree necessary for the posture desired, and the phasic muscles relax. During chronic stress, many phasic muscles remain in a constant state of residual tension as a guard against some psychic perception of danger. If this contraction becomes severe, pain results which produces increased contraction and a noxious cycle of spasm–pain–spasm occurs. Prolonged spasm leads to contracture because the muscle's physical elastic property diminishes, resulting in restricted yield to stretch and possible fiber tearing under heavy loading.
Whenever possible, the underlying cause must be found and eliminated, and treatment is often a challenge. The first concern should be to remove neural and circulatory interference. In regard to adjunctive therapies, relaxation, heat, dietary supplementation, low salt intake, support of the affected part, contrast baths, exercise, counterirritation, acupuncture, and massage all help somewhat but seldom completely.
When subjected to weight-bearing, traumatic, or occupational stress, bone demineralizes and undergoes degenerative changes resulting in deformity of the articulating surfaces. Concurrently, the attending excoriation of the articular periosteal margins results in proliferative changes in the form of lipping, spur formation, or eburnation that may or may not restrict segmental mobility and function.
Certain simple contusions which involve subcutaneous tissues overlying bone and the periosteum are often referred to as "bone bruises." They are not common to the spine except to the spinous processes as most of the osseous structures are well padded by muscle. Because the periosteum is richly endowed with nerves and vessels, severe bruises and fractures are quite painful despite lack of roentgenographic evidence. When the periosteum is affected, tenderness will be present long after true soft-tissue tenderness has eased, sometimes for several months. Wherever the site, the individual is disabled or considerably hampered as long as tenderness exists. Pain from any cause produces a protective reflex spasm of the phasic muscles that restricts mobility.
A discussion of spinal pathology is beyond the scope of this text except where these disorders have direct biomechanical implications in diagnosis or conservative therapy. This is not to say that biomechanical mechanisms may not be superimposed or involved as contributing factors in the clinical pictures of cord diseases, tumors, cysts, connective tissue diseases, infection, metabolic disturbances, birth defects, etc.
Certain pathologic processes, however, cannot be separated from their biomechanical implications; eg, bone damage, traumatic arthritis, disc degeneration and hernias, root compression, spinal stenosis, and structural deformities. These will be briefly discussed in this section and future chapters when appropriate.
When trauma is the chief factor, an acute arthritis may be induced. The extent of the local reaction is relative to the severity of the injury and the resistance of the tissues. Repeated injuries from excessive joint stress may cause pathologic reactions or produce derangements within the joint. Or arthritis resulting from a single severe injury, especially if improperly treated, may be indefinitely prolonged and result in chronic symptoms and permanent disability (Fig. 6.65).
Acute traumatic arthritis presents signs of pain, possible ecchymosis, and soft-tissue swelling of periarticular tissue. Motion is usually limited because of pain, and there is joint instability if the force is strong enough to tear a tendon or joint capsule. Intra-articular fractures and fragments are infrequently associated. The prognosis is excellent in those receiving efficient treatment; however, a subacute arthritis may, at times, persist indefinitely.
Periostitis is infrequently associated with spinal joint injury. It is the result of violent muscle strain which damages the periosteum. If severe enough to detach a chip of periosteum, a degree of hematoma develops. The bruised area is extremely tender and movements are restricted. Physical examination makes one suspicious of fracture, but early roentgenographic findings are negative. Later, ossification of the hematoma is exhibited by induration of the swelling and new bone formation.
"KISSING" SPINOUS PROCESSES
If the disc is well hydrated, the spinous processes do not touch on normal extension. However, if the disc is degenerated and thinned, chronic apposition of the spinous processes frequently produces bursal development in adaptation (Fig. 6.66). Chronic stress, usually at the center of lordotic curves, can lead to a picture of bursitis similar to that found in the extremities, but major symptoms are more likely to come from the disc or posterior articular processes. The bursal involvement is usually subclinical and imposes itself upon the total picture as a contributing factor.
The earliest symptoms and signs of acute bone or joint infection are local pain and tenderness in the periarticular region. The patient has extreme difficulty or refuses to move the area. The cardinal signs of infection may appear much later than pain and tenderness, and often never appear. Roentgenograms are of little help in arriving at an early diagnosis; when evidence is obvious, the disease is chronic. Sometimes comparative films exhibit slight soft-tissue evidence.
Joint infection may be the result of a rare penetrating wound, but it is commonly blood borne. A degree of hematoma or hemarthrosis is an invitation to a subclinical blood-borne condition to manifest. Persistent pain following adequate treatment may indicate the presence of a secondary low-grade and asymptomatic infection or irritation in spite of blood reports to the contrary. In such cases, suspicion should be directed toward a distant focus of infection.
In the cancellous part of an osteoporotic vertebra, there is greater loss of horizontal trabeculae than vertical trabeculae. This factor, rarely viewed on roentgenographs, has a profound effect on vertebral strength.
Disc Degeneration, Protrusions, and Ruptures
In the absence of severe trauma, disc height is a reflection of disc hydra- tion. As dehydration increases with age and late degeneration, the nucleus tends to lose its turgor, and disc height can be used as an indication of these two factors. But this is not to say that advanced degeneration cannot be found in a disc of normal height. The tip of the superior articular facet should not reach a line extending backward from the undersurface of the vertebral body above (Macnab's joint body line) if disc degeneration is absent.
THE DEGENERATIVE PROCESS
The degenerative process usually begins in the nuclear substance and then extends into the anulus and the end plate. When this degenerative process be- gins, abnormal movements result. This weakening process eventually involves the retaining fibers of Sharpey, the interbody articulations of Luschka, and the criss-crossing intertwining fibroelastic fasciculi comprising the laminae of the anulus (Fig. 6.67). From here, the process extends into the periosteal arti- cular margins from traction strain, resulting in proliferative changes that end in eburnation, lipping, and even osteophytosis (traction spur type).
This entire conglomerate of events may be referred to as a degenerative pro- liferative arthrosis of the spine or discogenic spondylosis. As a consequence to this process, we may list the following:
Detachment of a segment of the end plate and a weakening of the anulus fibrosis. This disrupts the integrity of the confining ring of the anulus, most frequently at one of the posterolateral aspects with possible prolapse or even frank nuclear herniation between the vertebral body and the displaced piece of hyaline cartilage (Fig. 6.68).
A loosening of the retaining mechanism of the IVD as well as the entire motion unit resulting in disc prolapse and hyperkinesis of the vertebral segment from an undue gravitational weight-bearing pathologic interosseous disrelation- ship (eg, subluxation). Because weight is now imposed through the displaced plate onto the vascular spongiosa, a zone of necrosis occurs and the nucleus dips into the vertebral body (Schmorl node).
An undue traumatic stress upon the ligamentous retaining mechanism with traumatic insult inflicted upon the proprioceptive bed. This usually occurs pos- terolaterally where the anular fibers are weakest and support by the posterior longitudinal ligament is deficient. Such insult results in nagging pain and asymmetrical reflex spasm of those muscles that relate to the vertebral segment of the motor bed involved.
Biochemical Factors. Interference with normal anular fiber synthesis results in increased polymerization. This and the associated increased fluid pressure of the nucleus increase intradisc tension, leading to nuclear degeneration, pro- lapse, and anular herniation.
Immunologic Factors. It is hypothesized that during the degenerative process destroyed tissue stimulates an autoimmune inflammatory response which may or may not involve the nerve roots. This may account for episodes of pain exacerbations and remissions. Inflammation, granulation, and fibrosis are part of the result- ing picture.
DISC PROTRUSIONS AND RUPTURES
Inasmuch as the IVD has sensory fibers only at its posterior superficial aspect, most exacerbating and remitting spinal pain cannot be attributed to the disc itself. Rather, involvement of the sensitive articular facets and IVF con- tents is much more likely.
Types of Intervertebral Disc Pathology. The consequences of the degenerative process have been discussed. To gain a broader viewpoint, another method of classifying the various types of IVD pathology is to review Charnley's seven types:
Type I: acute sprain, usually from unexpected loading (see Fig. 6.64). There are usually severe pain and muscle spasm. Nonsciatic referred pain is commonly associated. There may be rupture of some of the peripheral or central anular fibers, slight end plate fracture, and stress to the capsular or interspinous ligaments and posterior arch muscle fibers. Lasegue's straight-leg raising test is negative.
Type II: a nontraumatic, idiopathic, sudden intake of fluid by the nucleus pulposus, causing irritation of the peripheral anular fibers because of the nuclear pressure being transmitted horizontally. There are back pain and muscle spasm without referred pain or sciatica. Lasegue's test is negative.
Type III: slight abnormal bulging of some of the posterolateral fibers with slight IVF encroachment. In addition to local back pain, pain may be referred into the sacroiliac area, buttocks, hip, and posterior thigh. There is no neuro- muscular deficit, and Lasegue's sign is negative (Fig. 6.69).
Type IV: herniation of part of the nucleus into the peripheral anulus which, in turn, bulges into the vertebral canal. There is local back pain increased with Valsalva's straining maneuvers, true sciatica, and a positive Lasegue's test. These are signs of irritation of a nerve root (Fig. 6.70).
Type V: floating nuclear fragment. This chronic condition is sometimes asso- ciated with disc degeneration. There are episodes of back pain, with or without sciatica, depending upon the position of the fragment and the magnitude of stress (Fig. 6.71).
Type VI: anchored nuclear fragment. This is often the aftermath of Type V where the nucleus is fixed within the peripheral anulus or vertebral canal with probable IVF encroachment. The nerve root becomes chronically irritated from mechanical pressure, chemical irritation, autoimmune response, or a combination of these factors. There is true sciatica with a positive Lasegue's sign. A nar- rowing of the IVD space is usually associated (Fig. 6.72).
Type VII: advanced disc degeneration. When a disc is not well hydrated and nourished, it is unable to serve its hydraulic function. Disc narrowing and arthritic processes of the vertebral bodies are invariably associated (Fig. 6.73). Symptoms vary from severe to none, and they may be chronic or intermittent.
Management. In Type I, II, or III disorders, correction of related articular subluxation-fixation, rest without immobilization, and relief of pain are usual- ly all that are necessary for acute-stage resolution. Bed rest should be on a firm mattress to minimize bending moments; in the side position, a soft pillow should be used between the knees to reduce torsion. Traction and careful mobili- zation are often helpful additional adjuncts with Type IV disorders. If rest and adjustments do not move the fragment into a nonsensitive position in Type V conditions, referral for surgical excision may be necessary. Due to the anchored position of Type VI disorders, conservative measures such as manipulation and traction often fail unless the fixation can be released and replaced in a nonsensitive position with a force that does not injure other tissues. If pain is severe in Type VII disorders and does not respond to conservative measures, referral for arthrodesis may be the only alternative.
Occupational Considerations in Disc Disorders. With the exception of nurs- ing, most occupations associated with heavy lifting, carrying, pushing, or pulling do not appear to be directly associated with acute disc disorders. When failure does occur, it is usually associated with an unexpected exertion. Golf, bowling, or baseball accidents are sometimes associated with disc failure, but disc disorders are not common to most sports. On the contrary, women in late pregnancy and people over 5 years in a sedentary occupation (eg, executives, typists) have a high incidence of trouble. Race or body weight does not seem to be a factor. Traveling salesmen and tractor, truck, and other motor equipment drivers have a high incidence of disc herniations. This is probably attributed to several factors: IVD pressure increases in the sitting position, driving subjects the spine to constant "thumping" and vibrations (ie, load fatigue), the extended position of the lower extremities, and the lack of postural variation. An increased spinal intraosseous blood pressure is commonly associated with complaints of low back pain.
When a patient fails to find relief from customary therapy, misguided ex- tended pursuit is often justified on the basis of explanations currently in vogue. These often include facet impingement on the nerve root, motion unit instability, IVF encroachment by a disc fragment, pedicular kinking, nerve root fibrositis, or pseudoarthrosis. Such conditions may in fact exist, but they should not justify failure to seek other causes (eg, referred pain). Chronic root compression with its signs of functional loss is not a common syndrome.
During their exit from the IVF, the nerve roots often lie fairly close to the inner edge of the superior facet. In subluxation, the superior process can override the surface of the inferior process and produce direct irritation of the root by the inferior process, with or without compression, during motion. Direct compression can also result by the root being caught between the inferior process and the body of the superior vertebra or caught between a hypertrophied inferior process and the superior body.
This is associated with chronic IVD degeneration where the disc space is quite thin and the vertebral bodies approximate each other asymmetrically from either lateral disc collapse or a laterally tilted vertebral body (eg, scoliosis). As the superior vertebral body descends, it may impose its pedicle on the exiting nerve root. Macnab feels that the most common mechanism is that the nerve root becomes entrapped in the gutter formed by a wide lateral protrusion of the disc and the superior pedicle (Fig. 6.74).
This type of compression usually occurs from arthritic hypertrophy of the superior articular facet. The bony mass compresses the nerve root which exits beneath the medial border of the superior articular facet. The root is caught between the posterior aspect of the vertebral body and the facet.
Axial compression is never a problem with a healthy, well-hydrated disc. If the disc space narrows considerably, the spinal canal can be narrowed in the midline by several mechanisms. Typically, these include posterior subluxation of the superior vertebra, anterior subluxation of the inferior vertebra, a diffuse posterior anular protrusion or rupture, kinking of the ligamentum flavum and thickened capsules from laminae shingling, arthritic hypertrophy of the superior processes, or a combination of these factors.
It should be kept in mind, however, that the IVF is usually quite roomy. There can be complete disc collapse without any degree of compression. Also, there can be considerable compression on a root without any overt signs of malfunction if the pressure develops slowly. Entrapment, from whatever cause, can be encouraged by a transforaminal ligament, an adhesion, or an overgrowth, especially in the lumbar region, which restricts the normal mobility of the root in the IVF.
Spinal stenosis can present a bony root entrapment syndrome. Narrowing of the spinal canal can occur either laterally or in the midline of the canal. If it occurs laterally, compression of the nerve roots can result from foraminal impingement (ie, subluxation), pedicular kinking, or subarticular entrapment. If it occurs in the midline, compression of the cord or cauda equina can result.
Referred Pain and Reflexes
Todd has stated: "In holding up its own weights, the body may exert muscular effort far beyond what is really called for; and it can continue to do this because of its reservoir of energy. But in so doing, if the parts are held out of alignment and away from the axis of gravity, peculiar strains are put upon the spinal structure, which may give way with results of a quite unforeseen and disastrous nature. Sometimes the end results are remote from the site of strain; and, moreover, symptoms may be misleading because of the nature of referred and reflected pain."
Pain in one region of the body may indicate disease elsewhere because nerve supply often overlaps; eg, pain associated with the ureter can result in reflex spasm of the lumbar muscles. Such pain radiates to distant parts of the body depending upon the intensity of the stimulus, amplitude of the afferent impulse, and the excitatory state of the spinal cord at the level into which the noxious impulses enter.
Visceral disease or dysfunction frequently refers pain to the spinal seg- ments supplying the involved viscera and also alters the function of other viscera sharing the same nerve supply. In addition, the probability of somatic dysfunction occurring in segmentally involved areas causing visceral dysfunction or of other somatic structures sharing the same nerve supply should be consider- ed. The nervous system is not a one-way street: somatosomatic, somatovisceral, viscerovisceral, and viscersomatic reflexes must be considered. For example, Lieb shows a number of before-and-after full spine roentgenographs in which severe spinal scoliosis, lordosis, and kyphosis have been greatly reduced solely through the correction of dental occlusion.
Headaches, the most frequent malfunctional symptom in America today, are usually attributed to tension, migraine, abnormal sinus, tumor, vascular disor- ders, or hysteria. Often neglected causes are overall postural strain and trauma to the cervical spine. Headaches caused by viscerosomatic reflexes from the gallbladder, stomach, and duodenum are much more common than suspected. Nausea or vomiting with headaches is usually considered to have a neurologic basis of a vascular nature; however, a vagal disturbance due to upper cervical function may be the offender.
Cervical reflexes can be easily overlooked. Vertigo makes basilar insuffici- ency or Meniere's syndrome suspect, but vertebral artery ischemia due to upper cervical dysfunction or an occipitoatlantal subluxation secondary to scoliosis may be the reason. In blackout spells of an unexplained nature, epilepsy and arterial occlusive disease are suspect, but cervical somatic dysfunction invol- ving the cervical ganglia may be the cause. Numbness or tingling in the hands is seen in a number of neuropathies. However, the cause may be musculoskeletal in origin such as degenerative disc disease or somatic dysfunction of the cervical spine, brachial plexus entrapment due to clavicular and upper rib abnormality, or carpal tunnel syndrome. In a lower cervical motion-unit dysfunction resulting in brachial distribution symptoms, there are somatosomatic reflexes which have afferents from and efferents to the soma.
Gallbladder disease associated with referred pain near the right scapular tip is an example of viscerosomatic reflexes having afferents from a viscus and efferents to a somatic area. Frequently overlooked is the gallbladder reflex causing cardiac arrhythmia. However, several diseases may refer pain to the back, shoulder, or arm other than the gallbladder; for example, coronary artery disease, empyema, pneumothorax, pericarditis, mediastinal lesions, peptic ulcer, diaphragmatic hernia, perisplenitis, and subphrenic abscess. In coronary occlu- sion associated with nausea and vomiting, there are viscerovisceral reflexes which have afferents from a viscus and efferents to a viscus. Pain radiating to the arm may also be a reflex from brachial neuropathy caused by dysfunction or degenerative disease of the cervical spine or a trigger point.
Several common chest symptoms may indicate visceral disease or as often referred musculoskeletal problems. Ventilatory impairment is usually suspected in dyspnea, but it may be the result of rib-cage dysfunction, spondylitis, or paravertebral muscle spasm and pain. Air hunger at rest is a cardinal sign of anxiety and often seen in chronic obstructive pulmonary disease; it is, however, also a reflex sign of rib-cage dysfunction of a musculoskeletal nature. Chest pain points to coronary insufficiency, dissecting aneurysm, or may be of esopha- geal or pleural origin; but chest pain may also be the result of somatic rib- cage dysfunction, trigger points of the thorax, costochondral or costovertebral strain, or be referred pain from the gallbladder, stomach, duodenum, or pancreas.
In chest pains associated with a cough, pulmonary infections, pneumonia, lung abscess, and bronchitis are usually suspected, along with pleuritis and lung or pleural tumors. Reflex considerations would include costovertebral dys- function, costochondral dysfunction or separation, or rib fracture. In cough with chest pain, one normally thinks of acute or chronic infection, chronic bronchitis, bronchial tumor, pulmonary embolism, broncholith, bronchiectasis, postnasal discharge, or the inhalation of irritants. However, reflexes from cla- vicular strain affecting recurrent laryngeal nerves, cervical subluxation, or cerumen impaction should not be overlooked.
REFERRED PAIN AND TENDERNESS
Both somatic and visceral afferents are capable of acting on common pools of spinal cord neurons that are subject to summation, enhancing, and inhibiting effects.
Irritation from either pathologic or traumatic processes can refer pain and/or tenderness locally, distally, or both. Because tenderness can be re- ferred, some examiners are misled into believing that the site of irritation must be at the site of palpable tenderness. This often leads to misdiagnosis. The richly innervated posterior joint facets especially may send signals above, below, and outward from the focal site of irritation.
In some cases, a paravertebral inflammatory reaction need not be of infec- tion but of irritation from malfunction in a part of the gastrointestinal tract that reflexly produces vasospasm in the joint and hence pain. We must be aware that irritation produced by malfunction of a viscus can produce many symptoms difficult to diagnose.
Zones of hyperalgesia, often associated with cutaneous vasoconstriction and hypermyotonia, are more commonly associated with acute and subacute visceral disease rather than are chronic disorders. The afferent fibers occupying the pre- and post-ganglionic pathways of the autonomic system from soma and viscera have a general segmental arrangement. The segmental distribution of referred pain and tenderness in soma and visceral dysfunction is usually listed as follows:Head and neck: T1-T5 Upper limb: T2-T5 Lower limb: T10-T12 Aorta (arch area): C3-C4, T1-T3 Aorta (thoracic): T4-T7 Bladder body: S1-S4 Bladder neck: T11-L2 Breast: T4-5 Bronchi: T2-T4 Colon (transverse): T9-T10 Colon (descending): T11-T12 Epididymis: T11-L1 Esophagus (caudal): T5-T8 Heart: C3-C4, T1-T5 Intestines (small): T9-T10 Intestines (large, upper): T11-T12 Kidney: T10-L1 Liver and gallbladder: C3-C4, T6-T10, especially T7-T9 Lungs: C3-C4, T1-T10, especially T3-T5 Ovary: T10-T11 Pancreas: T6-T10, especially T8 Peritoneum: T5-T12 Pleura: T2-T12 Prostate: T10-T12, L3, S1-S3 Rectum: S2-S4 Scrotum and testis: T10-T12 Spleen: T6-T10 Stomach: C3-C4; cardiac portion, T6-T7; pyloric portion, T8-T10 Suprarenal area: T11-L1 Ureter: T12-L2 Uterine body: T10-L1 Uterine neck: T12-L1, S1-S4.Note: Authorities differ somewhat as to exact levels, and variances of a segment above or below are commonly stated by different authorities.
MYOFASCIAL TRIGGER AREAS
In addition to the cutaneous hyperalgesia just discussed, visceral or somatic trigger-point irritation can produce a degree of spasm of the paravertebral muscles ipsilaterally in 2–3 segments on the same side as the entering afferent. However, if the irritation is severe, this effect will spread up, down, and contralateral (eg, renal colic). In this regard, Stoddard reminds us that the sharp "textbook" demarcation made between the somatic and autonomic nervous systems is erroneous.
Kraus states that the frequent result of chronic muscle tension and spasm is trigger-point development. The result is referred pain on pressure over the trigger area, hyperalgesia, joint stiffness, movement limitation, weakness, and autonomic dysfunction occurring in the area of reference (target area). Once one muscle has been affected by trigger points, its whole system of related antagonists and synergists is affected. This muscular dysfunction leads to episodes of tension, spasm, radiating pain, and more trigger points unless proper therapy is offered.
Predisposing Factors. The conditions that appear to predispose myofascial trigger mechanisms near the spine include chronic strain as the result of prolonged repetitive movement, subluxation, fatigue, tension, infection, neural lesions, nutritional deficiencies, syndromes of the menopause or male climacteric, and hypometabolism with creatinuria.
Precipitating Factors. The most common precipitating factor, according to Travell, is thought to be motion that produces stretching of the tissue containing the focal spot. This ignites a self-perpetuating cycle of pain–spasm–pain that may persist even after the precipitating cause has been removed (eg, subluxation). Other precipitating factors include acute trauma, an inflammatory process, unusual or excessive exercise, chills, IVD herniation producing nerve root pressure, immobilization, and severe anxiety.
OTHER COMMON REFLEX IRRITATIONS
Many sensory disturbances can be caused by reflex irritation of somatic musculoskeletal tissues in addition to nerve root involvements and/or peripheral irritations. These symptoms lack the typical features of nerve root involvement such as observed in cervical compression tests and usually do not create significant motor changes. They often arise from inflammatory tissues or fibrotic muscles, tendons, or ligaments which characteristically act as trigger areas. That is, their stimulation (eg, with deep pressure) initiates the reflex pain.
Some of the typical reflex neuralgias are listed in the following examples:
Marked hypertonicity and tenderness of the occipital musculature and the consequent C1 or C2 neuralgia associated with upper cervical subluxations.
Hypertonicity and tenderness of the muscles and tendons of the rotator cuff consequent to rotator cuff tendinitis and associated with referred pain into the posterolateral arm. These manifestations are often aggravated by cervical subluxation and spondyloarthrosis.
Hypertonicity and tenderness of the musculature around the scapula common to the scapulocostal syndrome. These areas often cause reflex pain down the ulnar side of the upper extremity and are often aggravated by a sectional thoracic scoliosis and thoracocostal subluxations or duodenal malfunction.
Hypertonicity and tenderness of the piriformis which may cause a posterior sciatic reflex neuralgia and even peripheral nerve pressure. This is common to many sacral subluxations or gonadal irritation and malfunction.
Hypertonicity and tenderness of the gluteal musculature and sacroiliac ligaments which may reflect pain over the sciatic trajectory. Such disorders are often caused or affected by sacroiliac subluxations or reflexes from pelvic congestion.
Hypertonicity and tenderness of the tensor fascia latae and the consequent reflex pain down the lateral thigh associated with iliofemoral tendinitis and innominate subluxation.
The Dynamic Craniospinal System
While the cranial sutures are immovable in cadavers and anatomic specimens, they are slightly movable in the living body, although it is often taught that they are not. The two uniting and five intervening layers between the edges of adjacent bones in the skull offer a strong bond of union but one which will permit definite but limited movement. This movement is necessary for the tissue respiration of the brain and spinal cord and controlled by the following structures and motions:
(1) the inherent motility of the brain and spinal cord,
(2) the fluctuations of the cerebrospinal fluid,
(3) the mobility of the intracranial and intraspinal membranes,
(4) the articular mobility of the cranial bones, and
(5) the involuntary mobility of the sacrum between the ilia. Lay and others report this based upon the separate research of Sutherland, Becker, and Retzlaff.
INVOLUNTARY CRANIAL MOTION
Every organ in the body exhibits a pulsation or inherent rhythmic action which features a slow, worm-like movement. The brain and spinal cord are no ex- ceptions to this, manifesting a slow, rhythmic coiling and uncoiling of the hemispheres and a longitudinal movement of the spinal cord within the spinal dura. This combined motility of the central nervous system (CNS) and movement of the cerebrospinal fluid manifest as a hydrodynamic activity (pump) and a bio- electric interchange (dynamo). Upon very light palpation of the cranium, this pulsation can be felt to have a rate of about 10 to 14 cycles per minute. It is the result of the pull of the dural membranes, the fluctuating cerebrospinal fluid, and the inherent motility of the CNS.
The sphenobasilar symphysis appears to be the key cranial articulation. Prior to 25 years of age, it has a cartilaginous union; after 25, it has the re- siliency of cancellous bone. Flexion of both the sphenoid and occiput increases the dorsal convexity and results in elevation of the phenobasilar symphysis towards the vertex. Extension does just the reverse. In other words, flexion of the midline bones appears as a slight increase in convexity; extension, a slight decrease in convexity. The occiput, sphenoid, ethmoid, and vomer are primarily involved. The paired bones move in synchronized internal and external rotation with the midline bones, especially the temporals, parietals, and maxillae.
INVOLUNTARY SACRAL MOTION
In addition to normal voluntary and postural motions of the sacrum between the ilia, the sacrum responds to the inherent motility of the CNS, fluctuation of the cerebrospinal fluid, and pull of the intracranial and intraspinal membra- nes in a similar fashion as do the cranial bones. Upon light palpation, it is felt as a slight rocking synchronized with cranial motions.
Since all voluntary and involuntary systems are encased in fascial envelopes connected directly or indirectly to the base of the skull through the cervical, thoracic, abdominal, pelvic, and appendicular fascial connections, all organs are subjected to this rhythm in addition to the rhythms of their particular voluntary or involuntary activity throughout life. The spine, pelvis, and extre- mities affect the head and dental occlusion via the temporals as there is a direct dura attachment of the sacrum to the cervical spine and occiput.
Spinal Fractures and Dislocations
Generally, ligaments are stronger than bone against most forces. Bone is weakest in lines of tensile stress, second weakest in lines of shear, and strongest in lines of compression. Once healed, a fractured vertebra will often (50%) be able to sustain equal or higher loads before failure.
Especially in the cervical spine, the anterosuperior or anteroinferior rim of a vertebral body, which is firmly anchored to the adjacent anulus, is readily fractured in either extension (tension) or flexion (shear) injuries. In compression overload, the end plate usually fails first (Fig. 6.75). Posttrauma- tic narrowing of an IVD interspace points to anulus failure and suggests a pic- ture of shear or tensile stress.
The greatest torsional stiffness of the spine is found at the thoracic- lumbar transition, which is usually at the T12–L1 disc. The highest stress con- centrations are found at these segments, as witnessed in the high incidence of fractures at this area.
Common sites of spinal fractures and dislocations and their mechanisms of injury will be discussed in future chapters.
Congenital Anomalies and Deformities of the Neck and Back
We speak of a functional norm, yet in clinical practice, we usually find variations. Simon was referring to dental anomalies when he stated that "all we ever find are variations; an exact ideal normal does not exist, cannot exist. And this is our enigma; in theory we will never find the normal, in practice we forever feel its need and apply it constantly." This same precept can be applied to the spine, to any structure.
A large variety of overt spinal malformations may be witnessed on occasion. Their brief descriptions are listed below:
Anomalous formation of the spinous process: when two touch, the condition is called Bastrup's disease.
Basilar invagination or impression: elevation and softening of the posterior cerebellar fossa with the atlas protruding above Chamberlain's line (a line across the hard palate to the posterior margin of the foramen magnum).
Cervical rib: rib or portion of rib from C7 or another cervical vertebra.
Failure of fusion: occurring at an articular process, a spinous process, transverse process, or epiphyseal plate (limbus bone).
Hemivertebra: failure of differentiation of an individual vertebra; failure of one half of a vertebral body to develop, leaving the other half in a parasagittal position.
Lumbarization: growth of S1 as a separate lumbar segment, may be pseudo or true, bilateral or unilateral.
Occipital vertebra: a morphologic structure resembling a vertebral segment which surrounds the foramen magnum.
Os odontoideum: congenital nonunion of the odontoid with the body of the axis.
Ossiculum terminale: nonunion of the secondary ossification center at the tip of the dens.
Overdevelopment or elongation of the transverse process: usually of L5 or C7, and may cause a bursa to form and give rise to bursitis.
Paramastoid process: bony column arising from the transverse process of the atlas which articulates with the base of the skull at the jugular process.
Platybasia: flattening of the basilar angle to an excess of 150° (135° is normal) without invagination of the posterior cranial fossa; a softening of the anterior cerebellar fossa with an increase in Martin's basilar angle (a line drawn from the root of the nares, to the anterior clinoid process, to the anterior border of the foramen magnum).
Ponticulus lateralis: a bony arch extending from the superior articulating surface of the atlas to its transverse process.
Ponticulus posticus: ossification of the posterior portion of the atlantooccipital ligament.
Sacralization: growth of L5 to S1, may be pseudo (false) or true, bilateral or unilateral (Fig. 6.76).
Sagittal clefted vertebrae: bifid vertebrae; failure of unification of the laterally placed primary ossification centers of the vertebral bodies.
Spina bifida occulta: failure of the neural arch to close in the posterior midline without protrusion of elements of the spinal canal and often associated with tropism. It is the most common developmental abnormality of a vertebra, usually located at the L5 or S1 level, and often associated with a patch of hair overlying the defect. The defect is seen to some degree in 10% of the population. If several vertebrae are involved, the defect is termed rachischisis and frequently associated with a variable degree of neurologic disorder.
Spondylolysis: defect in the pars interarticularis that usually leads to anterior displacement of the vertebral body (spondylolisthesis) later in life.
Spondyloschesis: separation of the pars interarticularis; isthmus separation where the pars interarticularis fails to ossify. Most consider it to be a failure of ossification of a fatigue fracture. It may be bilateral or unilateral, with or without spondylolisthesis.
Sprengel's deformity: congenital elevation of the scapula with adduction and downward rotation of the scapula attended by kyphoscoliosis of the brachiocervical spine.
Supernumerary vertebral segments: congenital development of additional vertebral segments.
Third condyle: an arch on the anterior margin of the foramen magnum which articulates with the odontoid in cases of an occipital vertebra.
Tropism: asymmetrical or anomalous development of a zygapophysis, usually seen as a sagittal disposition of the lumbosacral facets.
Vertebral fusion: examples include
(1) Klippel-Feil syndrome, a synostosis (growing together) of vertebrae of the cervical spine, characterized by a short neck, low hairline, limited neck movement, and sometimes by scoliosis, spina bifida and Sprengel's deformity,
(2) block vertebra, congenital synostosis of other vertebrae such as the thoracics or lumbars,
(3) atlanto-occipital (occipitalization) fusion of the atlas with the base of the skull,
(4) para-occipital process, a bony connection between the occiput and the first transverse process, lying close to the condyle.
The aims of therapy naturally change with the needs of the individual patient. The general objectives of therapeutic clinical biomechanics include the relief of pain, the reduction of muscular hypertonicity and spasm, the improvement of mobility, the improvement of soft-tissue pliability, the improvement of stabilization, the improvement of segmental structural alignment, and the improvement of overall body balance. These objectives imply the normalization of neural, vascular, lymphatic, and hormonal mechanisms for proper metabolic homeostasis.
MANIPULATION AND MOTION BARRIERS
All types of joint manipulation impose static and dynamic forces across joint surfaces.
Within its anatomic range of motion, a normal vertebra exhibits
(1) a voluntary active range,
(2) an involuntary passive range, and a
(3) slight paraphysiologic motion at the end of the passive range which is determined by ligamentous laxity and elasticity. These ranges, depicted in Figure 6.77, are utilized in therapeutic exercise, mobilization, and adjustive techniques.
To appreciate this, an understanding of the barrier concept is necessary. When a joint is passively tested for range of motion, the examiner will note increasing resistance to motion referred to as a "bind" or the physiologic motion barrier. When the joint is carried past this point, the added motion becomes painful to the patient. This point is referred to as the anatomic motion barrier. In evaluating the degrees of passive motion, joints should be moved near but not fully to the anatomic motion barrier. Thus, joint motion evaluation is accomplished by passively carrying the joint(s) through a range of motion until the motion barrier is encountered, and then recording the degrees of movement allowed.
Active motion usually exists from the neutral position to the point of tissue resistance, while passive motion extends past this to near the elastic barrier. Grice points out that the usual objective of mobilization techniques is to restore the normal range of passive joint motion from the neutral position to the normal elastic barrier. Thus, it is longer in range than that of active motion and to the maximum point of passive motion. The objective of mobilization (stretching) techniques is to restore motion from the neutral position to the elastic barrier. Most osteopathic "leverage" techniques are conducted within this range, as are many chiropractic extremity techniques. In contrast, dynamic specific chiropractic spinal adjustments are usually carried a step further into the paraphysiologic range, often to the anatomic limit, but the duration of the application of force is only a fraction of a second.
SPECIFIC CHIROPRACTIC ADJUSTMENTS
The biomechanic objective here is to restore motion throughout the active, passive, and paraphysiologic range of motion. Because of the dynamic forces involved, such techniques must carefully consider the exact geometric plane of articulation (normal or abnormal), asymmetry, the force magnitude to be applied, the direction of force, torque, coupling mechanisms, the state of the holding elements (eg, spastic muscles, articular fixations, stiffness and damping factors), the integrity of the check ligaments (eg, stretched, shortened), and any underlying pathologic processes (eg, sclerotic, arthrotic, osteoporotic) of the structures directly or indirectly involved. As local temperature, trabeculae arrangement, density, nutrition, etc, are variables that affect the material properties of tissues, these factors must also be considered.
Skilled spinal adjustments often involve the breaking of the synovial seal of the posterior joints which results in an audible "snap." While some feel this is of little significance, most authorities feel that breaking the joint seal permits an increase in mobility (particularly that not under voluntary control) from 15–20 minutes –allowing the segment to normalize its position.
Unsuccessful manipulations that result in increased pain rarely present an audible joint release, while successful adjustments usually result in an immediate sense of relief even though pain and spasm are still present, a reduction in palpable hypertonicity, an improvement in joint motion, and are followed by a gradual reduction in symptoms.
In view of our previous discussions on compensatory patterns, adaptive biomechanical responses, and reflex spasms, Gillet warns: Never readjust subluxations that already have been corrected without searching for the causes of their recurrence. If a correction must be made several times within a period of several days, it can usually be assumed that this site is secondary to a more primary area somewhere else in the body. Granted some positive influence can be made on this side of the neural cycle, but it cannot be considered good clinical judgment if treatment is limited to this site.
When manipulation is applied to any joint, changes in muscle, tendon, capsule, and ligamentous tension stimulate mechanoreceptors embedded within the affected stretched tissues.
Types and Function. The apophyseal joints of the spine contain three of the four types of sensory mechanoreceptors that are stimulated by tissue tension. The four types are described by Wyke as follows:
Type I: These are globular corpuscles, thinly encapsulated, embedded in three-dimensional grape-like clusters of 3-8 corpuscles. They are found in the outer layers of joint capsules, originating from small myelinated nerve fibers. These very low-threshold, slowly adapting biologic transducers are stimulated by slight increases in both static and dynamic local tissue stretching. They readily respond during active and passive manipulation. Their firing frequency, occurring even during joint rest and immobilization from static tension, is increased during capsule tension and decreased during capsule relaxation. Thus, their degree of activity is proportional to and signal the velocity, direction, and amplitude of joint movement (ie, tissue stretch).
Type II: These consist of conical receptors, thickly encapsulated, found individually or in clusters of 2-4 corpuscles. They are located in the deep subsynovial layers of joint capsules and articular fat pads, originating from medium-size myelinated nerve fibers. They have a low threshold as do Type I receptors but adapt readily to dynamic tension changes and do not fire during joint rest. These receptors signal that joint motion has been initiated, but offer no information as to joint velocity, direction, or amplitude of movement. During the ipsilateral tissue stretch of activity, they produce only short bursts of impulses that blend into Type I impulses; while simultaneously, impulses from the contralateral relaxed ligamentous fibers are greatly reduced in the Type I tonic nerve fibers. During axial traction, however, Type I discharges remain proportional to the tension force.
Type III: These are relatively large fusiform receptors, thinly encap- sulated, found individually or in clusters of 2-3 corpuscles. They are sited at the surface of extremity joint ligaments, collaterally and intrinsically, originating from large myelinated nerve fibers. These high-threshold receptors are absent in intrinsic vertebral ligaments but are affected indirectly within the extremities during spinal motion. They adapt slowly to dynamic changes in tissue tone but fire continuously when activated by severe dynamic changes of tissue tone.
Type IV: These are the nociceptive receptors, and they have two subtypes:
One subtype is the three-dimensional plexuses of unmyelinated nerve fibers found embedded in joint capsules, articular fat pads, and the outer coat of joint blood vessels, but absent in menisci and discs, synovial tissue, and articular cartilage. They comprise the articular nociceptive system that is normally inactive during joint rest but activated during joint motion or chemical irritation (eg, inflammation), thus providing the major source of joint pain.
The other subtype is the free unmyelinated nerve endings found weaving between collateral and intrinsic joint ligament fibers of both axial and appendicular joints.
Both forms originate from tiny myelinated and unmyelinated nerve fibers, are extremely high-threshold, are nonadapting, are highly sensitive to abnormal tissue metabolites, and have an intimate morphologic relationship with the other types of joint receptors.
Central Effects. The afferent discharges from Type I and II capsule recep- tors especially offer important effects during professional manipulation or traction. Wyke describes reflex, pain suppression, and position perception effects.
Reflex effects. The afferent nerve fibers of articular receptors transmit polysynaptically with fusiform motor neurons within the central nervous system. Connection with alpha neurons is absent. The circuits contribute to the activity messages produced at the fusiform muscle spindle receptors, thus affecting muscle tone and the stretch reflexes of voluntary muscle. Specific joint manipulation affects muscle activity both locally (ipsilateral and contralateral) and remote because the afferent nerve fibers from the mechanoreceptors involved give off collateral branches that are distributed both segmentally and intersegmentally. Thus, joint manipulation and traction produce reflex muscle tone changes (via motion unit facilitation and inhibition) so often seen in clinical application of various techniques.
Pain supression effects. If Type IV receptors are involved in a joint disorder involving the capsule or ligaments, polysynaptic afferent impulses are transmitted to alpha fibers of the local muscle motor pools to produce abnormal reflex activity. Pain is simultaneously manifested by neural synapses within the basal nucleus of the spinal cord's gray matter to ascending tracts to the limbic areas of the cerebral cortex. This spinal "gate" can regulate the central flow of nociceptive transmission if affected by inhibitory peripheral receptor impulses. Type I, II, and III receptors offer fibers within the dorsal roots that enter the posterior horns of the cord. They synapse with neurons of the apical spinal nucleus that connect with presynaptic terminals of the nociceptive afferent fibers located in basal nuclei. Because the apical interneurons release an inhibitory transmitter substance at the synapse, nociceptive impulses are inhibited. Thus, muscle stretching and joint manipulation (as well as compression, cold, acumassage, and deep vibration) produce peripheral receptor stimulation that creates presynaptic inhibition of nociceptive activity in the basal nucleus to dampen the central perception of pain. These pathways are more active during youth than old age, and this possibly explains why certain manipulative techniques are more effective in the young than in the elderly. Regardless, the relief of pain through reflexogenic mechanisms provides an important therapy in nonmedical case management by utilizing manipulative and cutaneous electronic stimulation techniques.
Positional effects. Messages from Type I receptors make a significant contribution to postural and kinesthetic perception. They arise from the dorsal and dorsolateral columns of the spinal cord and finally are relayed through complex synaptic relays to the parietal and paracentral regions of the cerebral cortex. It is for this reason that loss of Type I receptor activity (spinal or extraspinal) from traumatic, inflammatory, or degenerative joint processes manifests in abnormalities of posture, gait, and specific joint movement because of inhibited kinesthetic perception.
Most patients in pain follow instructions to the letter. Once pain diminishes, a functional "deafness" often appears in the patient. This is especially witnessed in the areas of preventive counseling and ergonomic advice. Rare is the practitioner who is not frequently exasperated by such a patient.
Properly supervised stretching exercises will do much to rehabilitate the patient with areas of spinal stress associated with hypertonic muscles and shortened ligaments. Although strength developing exercises would be beneficial to strengthen the spine, the typical nonathletic patient will not follow them to the length of time necessary, and possibly their benefit has been overemphasized in the literature. In fact, the flexion exercises recommended by some writers apply the same forces as those seen in improper lifting. One can hardly think of an isotonic exercise that would not increase intradisc pressure.
Isometric exercise would appear to be the most beneficial during the postacute stage. Such exercise has the least effect upon the large sensory receptors that provoke spasm. This subject will be discussed further in the next chapter.
When home regimens of therapeutic exercise are advised, there must be some way the physician can monitor compliance. To evaluate progress solely on the word of the patient will usually result in frustrating confusion. Children can be supervised by parents, but who is there to monitor the parent?
The general objectives of any therapeutic exercise program should be to
(1) relieve pain and improve function,
(2) relax unnecessary musculature,
(3) increase strength to that necessary for the individual's lifestyle,
(4) obtain flexibility within the required ranges of movement,
(5) remove metabolic waste accumulations by improving circulation,
(6) gain smooth, efficient, coordinated motion, and
(7) develop the kinesthetic sense of good alignment.
If the gate theory of pain is correct, heat, massage, and transcutaneous sensory overload applied by any means are effective temporary methods in inhibiting the transmission of painful stimuli. This seems especially true if the pain is initiated by an inflammatory or reflex condition. The involved muscles should not be actively moved during therapy as this would stimulate the large receptors and provoke spasm. Even if the gate theory is not absolute, we do know by experience that the reduction of muscle spasm is comforting to the patient and tends to reduce acute distortion.
Traction is one of the oldest methods used in the treatment of spinal distress and deformities (Fig. 6.78). However, as is true of all therapeutics, there are indications and contraindications. For example, traction may tend to relieve or irritate a disc protrusion (Fig. 6.79), depending upon the relationship of the hernia to the nerve root.
Immobilization supports provide a distinct advantage in therapeutics, but they should never be applied without careful consideration of the biomechanical and physiologic objectives involved (Fig. 6.80). Their primary purposes are to afford rest, support, balance, and corrective mechanical forces. Braces are not a panacea but neither should they be avoided because of some ill-founded dogma.
What is the pathologic state of the spine? What mechanical alterations are to be achieved by the support? What type of forces are necessary and how are they to be applied? Where is the greatest force to be applied? What motions should be restricted, and which should be allowed freedom? These questions must be answered as well as prognosis of the residual effect and psychologic impact the support will have on the patient.
REHABILITATION FOLLOWING SPINAL DISTRESS
After acute stress or during recuperation of a chronic disorder, stretched ligaments make one or more vertebral motion units relatively unstable. Until the restricting ligaments accommodate, and most are slow to adapt to a new range of motion, there is always predisposition to reinjury. This may or may not require temporary support and/or a regimen of therapeutic exercise. Keep in mind that much of spinal stability is provided by musculature (Fig. 6.81). In most spinal disorders, there is unilateral weakness or hypertonicity present that provides a constant tendency towards segmental rotation until bilateral balance is relatively permanent.
The patient must be thoroughly counseled in the efficient biomechanics of normal living; eg, stance and sitting posture, arising from the sitting and recumbent positions, rest, sleeping positions, proper pillow and mattress use, driving position, entering and leaving an automobile, working postures, ideal pushing and pulling techniques (Fig. 6.82), lifting and bending procedures, proper footwear, appropriate therapeutic exercises, home therapies, etc, and what activities should be avoided. Case management cannot be restricted to the few minutes at the doctor's office.
Just because an ideal adjustment has been made, it is no indication that the vertebra will hold this new position without assistance. Except for those seen following a severe accident, most subluxations seen in practice are not new occurrences. They are acute manifestations of a chronic problem, often where soft tissues have shortened unilaterally and stretched contralaterally. A degree of ligamentous stretching must accompany any degree of stress or any form of corrective mobilization else there would be no separation of the fixation. Several minutes of rest following adjustment will at least allow the elastic fibers to accommodate. During this time of postadjustment rest, warmth can often be used effectively to help reduce associated muscular spasm and hypertonicity and to bring nutrients to the area and remove metabolic ash. To adjust a patient and send him rapidly on his way, only to repeat the process visit after visit, is not professional case management. It smacks of quackery.