The skeletal system includes the bones and their articulations. In addition to providing a bony framework, the skeletal system gives support and shape to the body. It provides protection for the internal organs, provides movement when acted upon by the muscles, manufactures blood cells, and stores mineral salts.

For study purposes, the 206 bones of the adult are divided into the 80 bones of the axial skeleton and the 126 bones of the appendicular skeleton. The axial skeleton includes the skull, vertebral column, ribs, and sternum. The appendicular skeleton includes the bones of the shoulder girdle, upper extremities, pelvic girdle, and lower extremities.

Bone is living tissue containing blood vessels and nerves within the hard bone structure. The osteocytes which form bone have the ability to select calcium and other minerals from blood and tissue fluid and to deposit the salts in the connective tissue fibers between cells. Bones become harder and brittle as age advances because there are higher proportions of minerals and fewer active osteocytes. The osteocytes in periosteum, which is rich in nerves and blood vessels, are active during growth and repair of injuries. The combination of hard and dense compact bone and porous cancellous bone produces maximum strength with minimal weight.

Bones are classified as long, short, flat, and irregular. Long bones in the extremities act as levers to produce motion when acted upon by muscles. Short bones, strong and compact, are in the wrist and ankle. Flat bones form the protective plates and provide broad surfaces for muscle attachments such as the shoulder blades and sternum. Irregular bones have many surfaces and fit into many locations such as the facial bones, vertebral and pelvic bones.

Long bones have a diaphysis and two epiphyseal extremities. The shaft is a heavy cylinder of compact bone with a central medullary cavity containing marrow, blood vessels, and nerves. Cancellous bone is located toward the epiphyses and is covered by a protecting layer of compact bone. Articular cartilage covers the joint surfaces at the ends of a long bone, providing a smooth contact surface in joint formation which gives some resilience for shock absorption. The periosteum, essential for bone nourishment and repair, is anchored to bone by connective tissue fibers. Bone repair is often inhibited when the periosteum is torn away or damaged in severe bone injury.

Projections on bones are often used as points of reference; in function, they serve as sites of muscle, tendon, or ligament attachment or as passageways for blood vessels and nerves. Because surface anatomy plays an important role in physical examination and spinal analysis, bony landmarks must be learned.

A fracture is a rupture or breaking of living bone. Fractures are often classified by type such as simple, with no external opening (closed), or compound, with an external opening (open). Fractures are also classified by patterns such as green stick, infraction, comminuted, crush, avulsion, impaction, double, spiral, oblique, transverse, fracture-dislocation, compression, or interarticular.

Dislocation refers to a displacement of a part, especially of a bone from its normal position wherein the articulating surfaces have lost contact. A dislocation is usually described in relation to the part which has moved and where it is found; eg, a subspinous dislocation is a dislocation of the head of the humerus into the space below the scapular spine.

A subluxation refers to a displacement of a part wherein the articulating surfaces have not lost contact; ie, a partial or incomplete dislocation. A subluxation may complicate, predispose, pre-exist, or otherwise attend other afflictions.

Several abnormalities related to bone besides fracture, dislocation, and subluxation offer pertinent diagnostic signs. For instance, congenital syphilis causes a sabre shin deformity in which the front edge of the tibia bows anteriorly. Paget's disease of bone can often be diagnosed upon observation alone of a prominent forehead, stooped gait, flared pelvis, and bowed legs. A rare hereditary disease of connective tissue, osteogenesis imprefectum, is featured by blue sclera and brittle bones that fracture easily and heal slowly. Tibial tenderness and subperiosteal hemorrhage are characteristic of scurvy. It is associated with corkscrew leg hairs and perifollicular petechial hemorrhages. Scurvy is more common than generally recognized, especially with alcoholism. New subperiosteal bone growth (hypertrophic pulmonary osteoarthropathy) is associated with pulmonary maligancies and characterized by rapidly progressing tibial or forearm compression pain wherein the growth process produces a warm, red streak over the bone involved. Osteomyelitis is associated with a draining skin sinus wherein the underlying bone is tender and the overlying skin presents warmth and erytherma. Bone fracture may lead to fat embolism characterized by a sudden attack from 36 to 48 hours after trauma of fever, apprehension, intense dyspnea, and a fine petechial rash over the neck and upper chest.


The Joints

A joint or articulation is a structure which holds together separate bones. Joints are classified according to the amount of movement they permit --immovable, slightly movable, or freely movable. Thus, articulations are classified according to their freedom of motion. The three basic types are the synarthroses, amphiarthroses, and diarthroses.

Synarthroses are immovable joints fixed by fibrous or connective tissue. Examples are the facial bones with the exception of the mandible, the sacral bones, and coccygeal bones. At one time during skeletal development, these joints had some movement, but as the bones matured they fused for stability. Most authorities consider the cranial bones as immovable or slightly movable joints.

Amphiarthoses are slightly movable joints joined by flattened fibrocartilage and held in place by strong ligaments.

Examples are the vertebral bodies, the sacroiliac joints, the symphysis pubis, and the lower tibiofibular joint of the ankle.

There are several types of diarthoses; joints capable of free motion that permit maximum motion. These joints have complex arrangements since they have joint cavities: joint capsule with its synovial membrane lining and synovial fluid.

A joint capsule is comprised of strong fibrous ligament bands which enclose the joint. The six types of disarthoses are briefly described as follows:

1. Gliding joints are those in which the articular surfaces in apposition are almost flat or the surface of one bone is concave while the articular surface of the other bone is concave (eg, vertebrae articular facets).

2. Hinge joints resemble the hinges of a door which permit flexion and extension. The elbow and knee joints are examples. Elbow joints allow forward movement: the anterior bone surfaces approach each other. Knee joints have backward movement: the posterior bone surfaces approach each other.

3. Condyloid joints allow an angular motion by a rounded end of a bone fitting into an elliptical cavity of another bone such as the radiocarpal articulation in the wrist.

4. Saddle joints are formed by the concave articular surface of one bone and the convex surface of another bone placed at right angles. Like the condyloid type of articulation, a saddle joint provides angular movement in two directions.

5. Pivot joints allow a semirotary movement as seen in the pivot action of the anterior ring of the atlas with the odontoid process of the axis. The distal ends of the radius and ulna also form a pivot joint for wrist rotation.

6. Ball-and-socket joints are formed by a socket-like end of one bone fitted into a cip-like cavity of another bone. The movement is pivotal with angular action and excursion in all directions; eg, the shoulder joint, which is the most freely movable joint in the body, and the hip joint. These joints permit flexion, extension, abduction, adduction, and rotation.

There are several types of joint motion: gliding and angular, flexion, extension, abduction, adduction, rotation, and circumduction. These actions have been discussed in the Introduction. Attempts to force joints to move beyond their normal limitations can be quite harmful to the integrity of the joint.

Some joint disorders are mechanical: the parts of the joint are displaced or subluxated. When the ligaments holding the joint together are partially torn or stretched, but the joint is not displaced, the injury is called a sprain. When muscles or tendons are injured by over stretching, the injury is called a strain. At some joint locations, the tendon connecting muscle to bone passes over a joint; eg, at the shoulder, elbow, knee, and heel. To reduce pressure, small fluid-containing bursa are formed over and around the tendon; and they may become inflammed: bursitis.

      Joint Swellings

Periarticular swellings are classified as:

(1) swellings arising in the joint proper,

(2) swellings derived from the bones adjoining the joint, or

(3) swellings originating in th extra-articular tissues around the joint.

In general, joint motion becomes restricted from either pain or mechanical disability. Intra-articular swellings impair both active and passive movements while extraarticular swellings impair one type of movement or none. Foreign bodies or fragments within a joint resulting in effusion are associated with intermittent motion restriction. Lesions such as Charcot's joint are absolutely painless and may portray a supernormal range of joint motion.

Joint swelling is the result of thickening of the synovial membrane or of excess fluid in the joint cavity. Such swelling is often obscured by bones, muscles, and tendons which overlie the joint cavity or its pouches; however, it is noticeable over thinly covered areas of the joint. For instance, swelling in the hip joint is almost impossible to detect. Swelling in the elbow is observed only on the posterior part on the sides of the olecronon process because the anterior surface of the elbow joint is thickly covered with muscles and the lateral aspects by strong collateral ligaments which prevent protrusion. For the same reasons, a wrist swelling is least noticeable when viewed from the front and radial side, and a knee swelling is least noticeable when viewed from the medial or posterior aspects.

Shape of the swelling corresponds to that of the synovial membrane distended in toto. For instance, when a subcrureal pouch becomes dilated, the knee joint swelling may extend as much as 7 inches above the joint line. Distention of the tabular process of endothelium about the long head of the biceps in the shoulder may present the enlargement over the surgical neck of the humerus.

Because of the relative position of various bones and associated relaxation of the muscles around joints, every joint has one position in which the synovial cavity attains the greatest dimensions. When tension increases in the synovial cavity because of effusion, the patient will adopt a position that affords the greatest relief. For instance, the following positions of the larger joints offer the greatest ease:

(1) hip: slight flexion, eversion, abduction,
(2) knee: slight flexion,
(3) elbow: flexion and mid-position,
(4) wrist: slight flexion, and
(5) ankle: plantar flexion and eversion.

Tendinitis, tenosynovitis, peritendinitis, and bursitis directly in a joint region are non-infectious inflammatory processes involving a tendon, a tendon sheath, or a bursa. They may be related to a specific single severe trauma or a series of microtraumas as often seen in piano players, typists, bricklayers, weightlifters, and tennis players from joint stress and fatigue. Nelson states that they may be the result of reduced microcirculation caused by reflex mechanisms. The symptoms are a gradual onset of pain radiating along the involved tendon upon active contraction or passive stretching. The swelling is localized and soft, and the area may present heat and redness.

      Fluctuation

All swellings should be tested for fluctuation if they are more than an inch in diameter. Testing for fluctuation must be made in two planes at right angles to each other. If a mass fluctuates in one plane, but not another; it is negative for swelling, as a swelling fluctuates in both planes. In testing for fluctuation, fat or muscle also transmit an impulse, but less perfectly than fluid.

Moderate swellings are tested for fluctuation by pressure exerted with the tip of one forefinger midway between the center and outer border of the swelling while the tip of the other forefinger is placed at an equal distance on the opposite side but remains stationary. The stationary finger moves passively from the pressure exerted by the action finger on the other side. Then reverse the procedure with the originally passive finger becoming the active finger and vice versa. If displacement takes place in two planes at right angles to each other, there is little doubt that the swelling contains fluid. When examining small swellings, it is often best to use two fingers of each hand.

A swelling less than an inch is difficult to test for fluctuation. In such a case, use Paget's test which consists of pressing the mass with a finger tip. A solid swelling is hardest in the center, while a cyst is softest in its center.

In the knee, the examiner tests for "floating" of the patella over an effusion by surrounding the joint with the hands, which are pressed slightly toward each other to limit the escape of fluid in either direction, and then suddenly making quick pressure on the patella with one finger. If the examiner feels or hears the patella knock against the bone below and rebound as the pressure is released, fluid in abnormal quantity is present.

      Crepitus

There are several types of crepitus which characterize a specific type of lesion: bone crepitus, traumatic pulmonary emphysematous crepitus, joint crepitus, and tendosynovitis crepitations.

Bone fractures elicit an audible grating when the ends of the broken fragments rub against each other during movement. The crepitation from an epiphyseal separation resembles that of a broken bone but is softer in character than bone crepitus from a fracture.

A fractured rib in which a fragment of bone has pierced a lung allows air from the lung to escape into the subcutaneous tissues. Crepitus may be felt when the fingers are placed with mild pressure over the affected area.

Joint crepitus may be tested by placing a hand over the joint while passively moving the joint with the other hand. When coarse crepitations are transmitted to the palm of the palpating hand, osteoarthritis is usually involved. Other acute or chronic lesions present fine crepitations. To amplify the crepitations involved, it is often helpful to apply a stethoscope to the joint during the passive motions.

Crepitus may be felt over an effused joint following inflammation of the tendon sheath. In traumatic tendosynovitis of the extensor tendon sheaths of the foream, for example, test by grasping the arm above the wrist while instructing the patient to clench his fist and open his hand with rapid motion several times. The presence of effusion will result in a transmitable or audible crepitation.

      Pitting on Pressure

A suspicion of edema may be confirmed by applying thumb pressure over the area in cases of massive infiltrations and index-finger pressure in cases of localized swelling. This pressure should be maintained for about 15 seconds. A positive sign of edema is indicated by a depression in the area after the action thumb or finger is removed. The depression is often palpable with the finger tips even though it is not visible.

Pitting is a sign of liquid infiltration into the underlying tissues. Tenderness associated with pitting is indicative of inflammatory edema. While edema gives rise to a soft pitting, a degree of induration can be felt if pus is present.

      Local Temperature and Tenderness

In cases of inflammation, the presence of local heat is a valuable sign. This may be noted by passing the outstretched hand rapidly over the affected part to an unaffected part and back again. Any difference in warmth from the affected area to the unaffected area signifies an increase in local temperature.

Mild cases of joint involvement invariably present points of maximum tenderness which correspond to those regions of the endothelium most superficial. For example, they are elicited:

(1) in the knee on both sides of the patella,
(2) in the wrist over the anatomical snuffbox,
(3) in the elbow over the radiohumeral joint, and
(4) in the ankle at the anterior surface of the joint.

      Mechanical Stresses

Joint structure refers to the quality and quantity of the chemical consituents of bone and associated tissues to cope with the action of external and internal forces. A force that is applied which is greater than the structural resistance will fracture a bone or dislocate a joint. Stress is defined as the force exerted. While it requires from about 1,500 to 3,000 lbs to fracture the neck of the femur, a weight of only 20 lbs dropped upon it will have the same result.

Regardless what degree of force is induced upon a part, there is always a counteracting stress because for every action there must be a reaction. For instance, a downward pressure should equal an opposing upward thrust. A force pulling right should be equal to a pull toward the left, expressed in terms of centropedal and centrifugal force. A twisting force in one direction must be followed by an equal twisting force in the opposite direction. A force permitting a part to slide downward must be resisted by an adequate upward force. And a force tending to bend a structure along its axis must be resisted by a force equal to prevent such bending.

A pressure always results in a compression stress, and a pull causes a tensile stress which is an action directly opposed to compression. Tensile and compression stresses (axial stresses) operate along the axis of a part without altering it.

A force directed against a structure at an angle to its axis that permits one part to slide over the other is called a shearing stress. Both parts may be movable with the parts sliding in opposite directions or one part fixed. A spinal curvature in any direction involves a constant state of abnormal tension and compression of bones, cartilage, and muscles. Spinal bending involves the dual actions of tension, compression, and torsion.

The various body motions are not the sole result of muscular action alone; they're also the effect of the structure, balance, and position of the various bones forming the joints acted upon. This cooperative action of muscles and bones is the result of leverage, and levers operate according to mechanical laws.


Joint Biomechanics

Mechanics is the study of forces and their effects, and the application of these principles to the body in movement and at rest is termed biomechanics. A complete understanding of human biomechanics includes the mechanical principles involved, the physiologic considerations of muscle length-tension relations, and an understanding of the controlling neuromotor mechanisms and the sensory feedback apparatus. The more human biomechanics are understood, the better musculoskeletal disorders can be appreciated.

The effect of muscle contraction depends basically upon:

(1) the unique fiber arrangement which determines the relationship of force that the muscle can produce and the distance over which it can contract,
(2) the angle of pull, and
(3) the muscle location relative to the joint axis.

The resistance offered to the musculoskeletal forces may arise from gravity pull, friction, stationary structures, elasticity of structures, or manual resistance. The effectiveness of resistance or load is determined by the angle of the line of resistance applied and the distance of the load from the axis of the lever system involved. Gravity is the most common load upon the body and provides a line of force in a constant direction.

Knowledge of the mechanisms involved in an injury is necessary to evaluate an injury accurately. While forces of all types may cause subluxations, dislocations, and fractures, the biomechanical mechanisms involved determine the type and extent of the injury produced depending upon the applications of force and its resistance. For example, different applications of force may cause bending fractures, stress fractures, or compression fractures. When the examiner understands how an injury was caused, the tissues involved are more readily located and the injury extent is more quickly evaluated.

In any movement or injury, Sir Isaac Newton's three laws of mechanics apply:

(1) The Law of Inertia; a body remains at rest or in uniform motion until acted upon by an unbalanced or outside set of forces. When a body is at rest, the forces acting upon it must be completely balanced. When a body is in motion, it will continue to move until some force causes it to stop.

(2) The Law of Acceleration; the acceleration of a body is proportional to the unbalanced force acting upon it and inversely proportional to the mass of the body. A forceful push moves a small object rapidly. A light push on a large object moves it slowly.

(3) The Law of Reaction; for every action there is an equal and opposite reaction. The pushing against or lifting up of any object pushes against you or pulls down with equal force in a line directly opposite to that of your force. While a study of human biomechanics is beyond the scope of this text, a basic understanding is necessary to realize the implications involved in poor posture, deformity, and spinal dysarthrias.

      Joint Examination Basics

The major symptoms of musculoskeletal abnormality are pain, deformity, and functional limitation. Examination generally includes inspection; bony palpation; soft tissue palpation; determining the passive and active range of motion; testing muscle integrity and strength; testing superficial and deep reflexes; and investigating associated areas. These subjects will be discussed in the regional sections of the text; however, certain basics should be acknowledged:

1. Observation is the first step of the examination.   First look for gross abnormalities. Observe gait, and note any awkwardness in rhythm, weight shifting, or imbalance. Note any bone bowing, angulation, or tumor. If a specific joint is involved, observe any gross deformity or swelling from either:

   (1) fluid where a wave can be demonstrated, or
   (2) thickened synovial tissue where there is no wave but boggy tissue can be palpated.
   

   Acute inflammation will present itself as an area that is red and swollen. Inflammation associated with a red and swollen area suggests an acute synovitis. Inspect muscles for hypertrophy and atrophy, and note areas of ecchymoses which point to previous trauma.

2. Palpate the joint for masses and points of tenderness which may indicate osteoarthritis, synovitis, a torn ligament or meniscus. Palpate for muscle tone, fasiculations, and spasms. Fasciculations are isolated contractions of a portion of muscle fibers. Spasms are readily palpable, tender, and frequently accentuated during passive joint movement.
   
   Palpate bone for tenderness and masses. Bone tenderness suggests inflammation, tumor, or complications from trauma. A suggestion of bone inflammation is enhanced when the bone is percussed at a site distant from the point of tenderness and pain is felt at the site of tenderness rather than at the site of percussion.

3. Note character of pain.   Bone pain resulting from tumor or aneurysm is usually deep, constant, boring, more intense at night, and rarely relieved by rest or a change in position. Fracture pain is severe, throbbing, and aggravated by movement of the part. Pain from degenerative arthritis and muscular disorders is an aching type which is relieved by rest, aggravated by certain motions, and often accompanied by splinting and paresthesias. A sharp, severe pain (associated with muscle changes and sensory disturbances) radiating along the distribution of a nerve is characteristic of acute nerve compression. Referred pain is often associated with musculoskeletal disorders, as are somatosomatic, somatovisceral, and other reflexes.

4. Determine active and passive range of motion bilaterally, and palpate the joint simultaneously to determine presence of crepitation. Note bone integrity by its ability to resist a deforming force. It is important to remember that the examination of the musculoskeletal system must be greatly adapted in examining an acutely injured patient from that of a patient presenting nontraumatic complaints. For instance, active and passive range of spinal motion should not be conducted until after roentgenograms have demonstrated the mechanical integrity of the spine. Functional limitation may be the result of:

   (1) pain associated with movement,
   (2) bone or joint instability (eg, muscle weakness, fracture, torn ligament), or
   (3) restricted joint movement (eg, spasm, ankylosis).
   

5. Take circumference measurements at equal points above and below involved joints bilaterally and compare.

6. Test deep tendon reflexes. Upper limb muscles are supplied essentially by C2-T1; lower limb muscles by L1-S2.

      General Methods of Joint Examination

1. By inspection and palpation we detect:

   a.   Pain, tenderness, and heat in, near, or at a distance from the joint.
   
   b.   Enlargement: hard, probably bony; boggy, probably infiltration or thickening of capsule and periarticular structures; or fluctuating, probably fluid in the joint. Enlargement is generally unmistakable; but when there is much muscular atrophy between the joints, the joints may seem enlarged by contrast when in fact they are not. Fluid or semifluid exudates in joints may fill up and smooth out the natural depressions around the joint, or, if the exudate is large, may bulge out the joint pockets. In the knee joint, four eminences may take the place of the natural depressions, two above and two below the patella.
   
   c.   Irregularities of contour: osteophytes or lipping (attached to the bone); gouty tophi (not attached to the bone); constriction-line opposite the articulation; or protrusion of joint-pockets in large effusions, filling out of natural depressions. Irregularities of contour are easily recognized, provided the normal contour is familiar.
   
   d.   This is due to pain and effusion, muscular spasm, thickening or adhesions in the capsule and periarticular structures, obstruction by bony overgrowths or gouty tophi, or ankylosis.
   
   e.   Excessive motion as in extremity subluxation. This is recognized simply by contrast with the limits furnished us by our knowledge of anatomy and physiology of joint motion at different ages. When the bone and cartilage appear normal or are not grossly injured, we call the excessive motility of the joint a subluxation, but excessive motility may also be due (eg, as in Charcot's joints) to destruction of bone and other essentials of the joint.
   
   f.   Crepitus and creaking.   These are detected simply by resting one hand on the suspected joint, with the other hand putting the joint through its normal range of motions while the patient remains passive.
   
   g.   Free bodies in the joint.   These are not palpable externally and are recognized only by their symptoms, by roentgenology, and by operation.
   
   h.   Trophic lesions over or near a joint (cold, sweaty, mottled, cyanosed, white, or glossy skin; muscular atrophy).
   
   i.   Sinus formation: the sinus leading to necrosed bone, to gouty tophi, or abscess in or near the joint.
   
   j.   Distortion or malposition due to contractures in the muscles near the joint, to necrosis, to exudation, or to subluxation.
   
   k.   Telescoping of the joint with shortening (limb, toe, finger, or trunk). Shortening of a limb as evidence of joint lesion is tested by careful measurements. The vast majority of such measurements are made with reference of the hip joint. One method is to mark the tip of each ASIS with a skin pencil and likewise the tip of each inner malleolus. Then, with the patient lying prone on a flat table, the distance from the ASIS to the inner malleolus is measured with a tape on each side.

   
   

2. Indirectly we may gain valuable information about the joints by noting:

   a.   General constitutional symptoms, their presence or absence. These include fever, chills, leucocytosis, glandular enlargement, albuminuria, and emaciation.
   
   b.   Blood analyses such as tuberculin and Wassermann reactions, bacterial presence or absence.
   
   c.   Disease of other organs, their presence or absence; ie, syphilis; tuberculosis; tabes and other chronic spinal-cord lesions; endocarditis; hemophilia; various acute infections such as gonorrhea, influenza, scarlatina, septicemia; and skin lesions such as psoriasis, purpura, hives, and herpes.
   
   d.   The course of the disease and the results of treatment.

      Muscle Spasm

Limitations of motion due to muscular spasm are seen with special frequency in tuberculosis joint disease and spinal dysarthrias, but may occur in almost any form of joint trouble, particularly the larger joints.

In the hip joint, two forms of spasm are important:

(1) that which is due to irritation of the psoas alone, and
(2) that in which all the muscles moving the joint are more or less contracted.

In pure psoas spasm, the thigh is usually somewhat flexed on the trunk, though this may be concealed by forward bending of the trunk. Very slight degrees of psoas spasm may be appreciable only when, with the patient lying prone, the examiner attempts hyperextension. In pure psoas spasm, the other motions of the hip (rotation, adduction, abduction, and flexion) are not impeded.

General spasm of the hip muscles is tested with the patient on the back upon a table or bed (a child may be tested on its mother's lap) and the leg flexed at a right angle, both at the knee and at the hip. Using the sound leg as a standard of comparison, the examiner then draws the knee away from the mid line (abduction), toward and past the mid line (adduction), and toward the patient's chest (flexion). Rotation is tested by holding the knee still and moving the foot away from the median line of the body or toward and across it.

General spasm of the spinal muscles guarding motion in the vertebral joints can be tested by watching the body attitude (eg, stiff, military carriage) and by efforts to bend the spine forward, backward, and to the sides. In most cases, we can witness limitation of these motions by asking the patient to stand with knees and hips stiff and then bend his trunk as far as he can in each of these four directions. If we are familiar with the average range of motility in each direction and at the different ages, this test is usually easy and rapid. Backward bending is the least satisfactory; and in doubtful cases, the patient should be prone while the examiner, standing over him, lifts the whole body by the feet.

In the joints of the shoulders, knees, elbows, wrists, ankles, toes, and fingers, there is usually no difficulty in testing for muscular spasm and no special directions are needed.

      Joint Restrictions

To distinguish muscular spasm from bony outgrowth as a cause of limited joint motion, notice that bony outgrowths (eg, in the hip) allow perfectly free motion up to a certain point, then motion is arrested suddenly, completely, and without great pain. Muscular spasm, on the contrary, checks motion a little from the onset, the resistance and pain gradually increases until the examiner's efforts are arrested at some point, vaguely determined by the examiner's strength and hard-heartedness and by the patient's ability to bear the pain.

Bony outgrowths may be obvious, as in Heberden's nodes; but if they are within the joint, they may be recognized only by the sudden arrest of an otherwise free joint motion at a certain point. In most cases, roentgenology is necessary. Protruding gouty tophi are identified positively by transferring a minute piece to a glass slide, teasing it in a drop of water, covering with a cover glass, and examining with a high-power dry lens and a partly closediaphragm. The sodium biurate crystals are characteristic.

Motions limited by capsular thickening and adhesions are not, as a rule, so painful after the first limbering-up process is over. There is no sudden arrest after a space of free mobility, but motion is limited from the first and usually in all directions, though the muscles around the joint are not rigid. The possibility of more or less limbering-out after active exercise (or passive motion) distinguishes this type of limitation.

In true ankylosis, there is no motility whatever.


Goniometry

The measurement of joint motion is an important evaluative procedure in physical examination of the joints for it offers an accurate record of joint motion and extent of disability as part of a patient's permanent record. The most common methods of measurement employ the goniometer, either the 180-degree system or the 360-degree system. Both systems depend on the fact that a long bone is like a lever rotating around a fulcrum; and when it moves, it describes the arc of a circle. It is this arc that is used in determining the amount of joint motion, and the goniometer is used to measure the angle produced between two bony segements when maximum motion in a particular plane has been made.

      Mensuration

Measurements are made of movement as it occurs around an axis perpendicular to one of the three body planes: sagittal, coronal, transverse:

1. Motions in a sagittal plane around a coronal axis include shoulder flexion, extension, internal and external rotation; elbow flexion and extension; wrist flexion and extension, fingers flexion and extension; hip flexion and extension; knee flexion and extension; ankle dorsiflexion and plantar flexion; and thumb abduction.

2. Motions in a coronal plane around a sagittal axis include shoulder abduction and adduction, wrist radial and ulnar deviation, thumb extension, hip abduction and adduction, and foot eversion and inversion.

3. Motions in a horizontal plane around a vertical axis include forearm supination and pronation, and hip internal and external rotation.

The goniometer consists of two levers (arms) with a protractor attached at the end of one arm and the other arm serves as a pointer. At the center of the protractor, an axis allows movement where the two arms join. The goniometer is applied to an extremity with its axis centered on the joint and its arms aligned with designated skeletal landmarks. For example when measuring the elbow for flexion and extension, one arm is aligned with the humerus and the other arm with the radius and the axis is at the elbow joint. The protractor would thus normally read 0° for extension and 150° for flexion because the forearm has moved in a total range of motion (ROM) in a sagittal plane of 150° from extension to flexion. The arc of motion is determined by subtracting 0° from 150°, thus a ROM of 150°. If a segment is in its neutral position at 180° and is moved to a maximum of 110°, the ROM would be 70°.

There is usually a locking nut for the fulcrum which can be tighten just before removing the goniometer from the body to assure holding an accurate reading. Because the scale has a 90° center, the readings achieved on the goniometer must be converted into degrees of arc of motion. When the goniometer arm begins at 90°, the below conversion factors are used:

Goniometer     Arc
Reading        of Motion

  90            0°

  100/80       10°

  110/70       20°

  120/60       30°

  130/50       40°

  140/40       50°

  150/30       60°

  160/20       70°

  170/10       80°

  180/0        90°

It is important to think of skeletal muscles as one part of a three-part nerve-muscle-skeleton unit. For example, a motor nerve is needed to stimulate muscle contraction; the muscle itself must be able to contract and to relax; and the power of the contraction must be transmitted to a bone or other attachment to produce the desired movement. When any one part of this three-part unit cannot function normally, the other two parts also lose their normal functional ability.

      Muscle Structure

Long, slender muscle cells form fibers; muscle fibers are grouped together into bundles; and muscle bundles are united to form an individual skeletal muscle. Each skeletal muscle is wrapped in an opaque connective tissue sheath, a form of fascia. This sheath encloses the blood vessels and nerves that stimulate and nourish the muscle cells. The fiber arrangement determines the line of pull of an individual muscle. Extensions of muscle sheath become continuous with tough connective tissue attachments such as the cord-like tendons or sheet-like aponeuroses which bind muscles to bones or to adjacent muscles.

      Muscle Function

Many neuromuscular and musculoskeletal disorders show evidence of disturbed muscle tone such as weakness or spasm, but weakness is the predominating pattern found in muscle testing. This is depicted as a compensatory spasm in the opposite, lateral, or antagonistic muscle.

When muscle fibers are stimulated by a nerve impulse to contract, the muscle shortens and pulls against its connective tissue attachment. One attachment is sometimes a fixed joint or anchor, and the direction of action is then toward it. When power of the muscle contraction is transmitted to bone or an adjacent muscle, movement occurs. As muscles produce movements by pulling on bones and since bones move at joints, most skeletal muscles attach to bones above and below a joint. Usually one bone is stabilized while the other bone moves. Muscles moving a part usually lie proximal to the part moved. For example, muscles moving the humerus originate in the shoulder, chest, and back; muscles moving the femur originate in the lumbar and pelvic region.

Muscles almost always act in groups rather than singly, and the coordinated action of several muscles produces movement; ie, while one group contracts, the other group relaxes, and vice versa. The muscle whose contraction produces the movement is called the prime mover. The muscle that relaxes is the antagonist. In flexion and extension of the forearm, for example, the biceps and triceps are alternately prime movers and antagonists.

It should be noted however that the concept that there is a form of true antagonism between the muscles that move the joint in one direction as opposed to those that move the joint in another direction is not exact. The action is better termed a reciprocal inhibition because the "antagonistic" muscle relaxes completely. Most muscles that demonstrate a reciprocal pattern do not necessarily have an antagonistic role; it is closer to that of a synergistic partner. Nervous coordination is so precise there is no need for muscles to act on antagonism.

Healthy muscle is characterized by active contraction in response to the reaction of the nervous system to the environment. This readiness to act, resulting in firing of motor units, as stimuli from the environment impose upon the nervous system is called muscle tone. Muscles that have lost their tone through lack of activity, through primary muscle disease, or through nerve damage become flaccid. The tone of muscles is due to the constant, steady contraction and relaxation of different muscle fibers in individual muscles which helps to maintain the "chemical engine" of the muscle cells. Even minor exercise helps to maintain tone by renewing blood supply to muscle cells.

Many normal and abnormal mechanisms can be explained in that a slightly stretched muscle contracts with a great amount of force, whereas a shortened muscle contracts with very little force.

While it appears during normal muscle contraction that all muscle fibers are in a smooth continuous muscle contraction, they are not. This appearance results from a totality of a series of small groups of fibers contracting at the same moment. In the members of these groups, the muscle fibers are supplied by the terminal branches of one nerve fiber or an axon whose cell body is in the anterior horn of the spinal gray matter. This nerve cell body plus the long axon extending within the motor nerve, plus all the terminal branches, and all the muscle fibers supplied to these branches comprise a "motor unit". Thus, the motor unit is a functional unit of striated muscle since an impulse descending from its axon causes all the muscle fibers of a particular motor unit to contract simultaneously. With the arrival of nerve impulses, usually below 50/sec, motor units contract sharply.

The quantity of muscle does not vary after birth. Exercise increases muscle quality, not quantity. Exercise causes muscles to become larger, stronger, and better developed. An increase in muscle size is hypertrophy; wasting away of muscles due to inactivity is atrophy. Activity is necessary to maintain normal muscle integrity.

A 15-year research project in Germany on the subject of muscle building has determined that the maximum contraction of a muscle, held for a matter of seconds, will cause the muscle to grow in strength at an average of 4% per week (NATIONAL HEALTH WORLD, 4/78). These scientists claim that the maximum contraction of a muscle is all that is necessary to strengthen, for example, slackened or weak abdominal muscles. An exercise for these muscles would include pulling in the stomach as far as possible and keep it until the muscles quiver, then letting the muscles relax. This exercise, performed once each day to these muscles or other muscles of the body, will increase the strength of the muscles 50% in 12 weeks according to the research conducted. Thus, evidence of disuse atrophy indicates a severe lack of activity of a muscle group.

During examination, it is important to realize that the ligaments play a much greater part in supporting loads than are generally thought. Electromyographic studies in situations involving fatigue from forces acting across a joint prove that muscles play only a secondary role. Such fatigue is basically a form of pain in the ligaments rather than the muscles. Thus, if the muscles involved in a problem are weak to begin with, there is a more immediate strain on the ligaments producing the characteristic fatigue syndrome.

Muscle contraction consumes food and oxygen and produces acids and heat. Acids accumulating as a result of continued activity contribute to fatigue which occurs most rapidly when contractions are frequent. It occurs slowly if rest periods are taken between contractions. Muscle activity is the major source of body heat.

      Evaluating Strength

Muscle testing demands attention to detail, a working knowledge of anatomy, a comprehensive knowledge of muscle function, joint motion, muscle origin and insertion, muscle antagnostic and agonistic action, and their role in fixation. It is a procedure that depends greatly upon the skill, knowledge, and experience of the examiner.

Muscle power is judged when there is:

(1) a complaint of weakness or incoordination, or

(2) need for an aid in subluxation analysis and in evaluating correction.

The following criteria are used in recording muscle strength:

• Grade 5   (100%, Normal) - Complete range of motion against gravity with full resistance.
  
  
• Grade 4  (75%, Good) - Complete range of motion against gravity with some resistance.
  
  
• Grade 3   (50%, Fair) - Complete range of motion against gravity.
  
  
• Grade 2  (25%, Poor) - Complete range of motion with gravity eliminated.
  
  
• Grade 1   (10%, Trace) - Evidence of slight contractility, but no joint motion.
  
  
• Grade 0  (0%, Zero) - No evidence of contractility.

The examiner should strive to evaluate one muscle at a time, thus the patient should be requested not to recruit allied muscles during resistance. The examiner must use extreme caution during resistance to avoid creating cramps, stretch injuries, or excessive fatigue. It should be noted that muscles often test differently in various positions such as from prone or supine to weight bearing.

The trouble with this method is the evaluation rests a great deal upon the subjective skill of the examiner. Thus it is important that the same examiner records initial and follow-up evaluations of the degree of "resistance". Until recently, the hand dynamometer and electromyograph were the only objective clinical instruments available to record the force of muscular contraction; however, recently more practical equipment has been developed.

The hand dynamometer offers the examiner four data:

(1) the strength of the grip muscles,
(2) the fatigue rate of the grip muscles,
(3) the recovery rate of these muscles, and
(4) a comparison between the muscles of the right and left hands. While initial readings are helpful in diagnosis, subsequent reading are helpful in determining rate of recovery.

In dynamometry, three readings are taken on each hand in sequence to show strength, fatigue, and recovery rates.

      Conditions Causing Muscle Weakness and Spasm

ATROPHY.   With the possible exception of spinal dysarthrias, disuse atrophy is the most common cause of muscle weakness. It may be the result of immobilization, an occupational lack of use, or disuse as a result from a painful injury, nerve disease, or primary muscle disease. Atrophy is demonstrated in evaluations of muscle strength as well as a decrease in bulk. Because of this decrease in mass, bilaterally compared circumferential measurements are helpful in evaluation when practical (eg, limb).

SPASTIC PARALYSIS.   Muscle weakness is often noted in patients who have lost the reflex inhibition of the smooth coordinate mechanism of muscle contraction as a result of any upper motor lesion that leaves the spinal reflex arc intact but interferes with the fine coordinating inhibitory and facilitory impulses. Although the muscles affected show weakness upon evaluation, they palpate tight and tense at rest (spastic paralysis). The reflexes are hyperactive.

Incoordination is the more common complaint rather than weakness and results from the varying degrees of strength between the prime movers and antagonists in addition to the neurologic disorder. Deformity by flexion contraction results when the flexors of a part remain strong while the extensors become weak. A child with cerebral palsy presents a typical spastic paralysis.

MUSCLE SPASM.   Muscle spasm is an involuntary and aberrant contraction of a muscle part or whole as a result of some excessive motor fiber stimulation such as irritation of:

(1) the anterior horn cells by the toxic elements of catabolic debris, accumulations consequent to faulty elimination, and circulatory disturbances,
(2) an encroached nerve root from subluxation, paraforaminal congestion, herneated disc, and/or ligamentous thickening,
(3) a nerve trunk or plexus; eg, piriformis, psoas major, scalenus anticus contraction,
(4) peripheral nerve branches; eg, common peroneus by contracted tensor fascia lata or occipital nerve by suboccipital spasm.

Spasm may also occur:

(1) as splinting secondary to injury as in sprain, avulsion fracture, and compression,
(2) within a muscle as the result of direct injury or irritation, often resulting from toxic accumulations; eg, toxic lumbago, or
(3) consequent to emotional or mental stress.

FLACCID PARALYSIS.   Flaccid paralysis is viewed as the opposite of spastic paralysis. The muscles feel small, atrophic, flabby, and the reflexes are decreased; however, here too muscle strength is diminished. Deformity occurs, but for a different reason. In flaccid paralysis, the normal muscles overcome the weakened muscles. A limb suffering a nerve palsy offers a typical example of flaccid paralysis.

MUSCLE RUPTURE.   Muscle rupture associated with non-penetrating wounds are seen in both the young and old. In youth, they occur when a muscle is suddenly stressed beyond its tensile strength and the muscle fails at the musculotendinous junction. Rupture is characterized by painful voluntary contraction, ecchymosis at an area of local tenderness, swelling, edema, and hemorrhage. Careful palpation will often reveal the defect. After the acute stage, persistent weakness remains and there is an increase in muscle bulk proximal to the rupture site upon contraction. In the elderly, muscle rupture occurs under minimal loads as a result of degeneration within the muscle's tendon. These ruptures are featured by considerably less pain, swelling, tenderness, and ecchymosis; however, they do present the later persistent weakness and increased bulk upon contraction.

MYOPATHY.   Weakness is usually proximal. Atrophy is usual except for hypertrophic calves. There is no fasciculation. Tendon jerks, tone, and direct myotatic response are decreased. Plantar reflex is normal, and there is no associated sensory loss.

MYASTHENIA GRAVIS.   Weakness is in the eye and throat, variable in the limbs. Atrophy is rare. There is no fasciculation. Tendon jerks, tone, direct myotatic response, and plantar reflex are normal. There is no associated sensory loss.

PERIODIC PARALYSIS.   Weakness is ascending. There is no atrophy or fasciculation. Tendon jerks and tone are absent. There is no direct myotatic response, plantar reflex, or associated sensory loss.

ROOT OR NERVE DISEASE.   Weakness is from lack of root or nerve innervation. Atrophy is present. Fasciculation is rarely evident. Tendon jerks and tone are decreased. Direct myotatic response is increased or normal. Plantar reflex is normal or depressed. Associated sensory loss is often in nerve or root distribution.

LOWER MOTOR NEURON SYNDROME.   Weakness is usually distal, but it can be generalized. Atrophy is prominent. Fasciculation is present. Tendon jerks are decreased. Tone is normal or decreased. Direct myotatic response is increased or normal. Plantar reflex is normal or depressed. There is no associated sensory loss.

UPPER MOTOR NEURON SYNDROME (CHRONIC).   Weakness in movements of distal parts is more evident. Atrophy is minimal, if any. There is no fasciculation. Tendon jerks are increased, and tone is spastic. Direct myotatic response is normal. There is an extensor plantar reflex. Associated sensory loss is sometimes seen as a result of other cerebral damage.

PARKINSONISM.   Weakness is a generalized hypokinesia. There is no atrophy or fasciculation. Tendon jerks are normal. There is a rigid tone, often cogwheeling. Direct myotatic response and plantar reflex are normal. There is no associated sensory loss.

CEREBELLAR DISEASE.   There is an ataxia most prominent in the limbs and a mild weakness. There is no weakness or fasciculation. Tendon jerks are normal (pendular), and tone is hypotonic. Direct myotatic response and plantar reflex are normal. There is no associated sensory loss.

      Trigger Points (Myodysneurias)

Trigger points are foci of stress inflammation which result in binding cobweb adhesions that incarcerate sensory nerve endings to produce sharp demarcation of pain especially upon pressure. They are primarily found in the "stress sites" of the myofascial planes of the erector muscles of the back, pelvis, neck, and shoulder girdle.

Thus, a trigger point is a small hypersensitive area in a myofascial structure from which impulses bombard the CNS and give rise to referred pain. The pain is initiated whenever the tigger site is stimulated by pressure, needling, extreme heat or cold, or motion that stretches the structure containing the trigger area. The resistance to stretching leads to apparent shortening of the affected muscle with limitation of motion and weakness. High-intensity discharges from a trigger area may be accompanied by vasoconstriction and other autonomic effects limited to the reference zone of pain.

A trigger area at a particular site gives rise to a consistent distribution of referred pain from person to person, indicating that the impulses follow fixed anatomic pathways. After evaluating about 1,000 patients with pain syndromes and myofascial trigger areas, Travell and Rinzler have diagramed patterns helpful in the diagnosis of myofascial pain sources: Head and Neck, Shoulder and Arm, Chest and Back, and Lower Extremity. Once the pain reference pattern of a muscle is known, it can be used to locate the muscle that is the source of the pain.

Trigger areas in myofascial structures can maintain pain cycles indefinitely; ie, the pain cycle may continue long after the precipitating cause has vanished because the mechanism that set the pain cycle in motion initially is not necessarily the same as that which keeps it going.

Myofascial trigger mechanisms may be initiated by direct trauma to muscle or joint, chronic muscular strain, chilling of fatigued muscles, acute myositis, arthritis, nerve root injury, visceral ischemia or dyskinesia, and hysteria. Predisposing factors may be general fatigue, low metabolic rate with creatinuria, chronic infection, and psychogenic stress. Protracted myofascial pain following activation of a trigger area is thought to depend upon a reflex pain cycle maintained by the trigger area.

The trigger points for the shoulder girdle are commonly located:

(1) immediately medial to the mastoid,
(2) immediately lateral to the spinous processes of C7-T1,2 (rhomboidii),
(3) under the trapezius over the trapezoid plexus,
(4) over the junction of the belly and tendon of the supraspinatus,
(5) in the quadrilateral space bounded by the humerus, the long head of the triceps, and the teres major and minor,
(6) at the deltoid insertion, and
(7) alongside the transverse process of T12.

The trigger points for the lumbosacral and sacroiliac articular complexes are commonly located:

(1) alongside the T12 spinous process,
(2) alongside the L5 spinous process,
(3) over the greater sciatic notch through the gluteal muscles,
(4) over the crest of the ilium,
(5) over the belly of the tensor fascia lata muscle,
(6) in the ischiorectal fossa apex, and
(7) at the sciatic outlet onto the back of the thigh from under the gluteus maximus.

Strains and Sprains

It should be noted that soft tissue damage is usually more painful and can be more serious than bone injury. Bone heals with calcium which is one of the substances of bone, whereas soft tissue heals with fibrous or scar tissue. The latter is different than the original soft tissue and lacks the elasticity or viability of the original tissue. Soft tissue takes longer to heal than bone tissue. Bone tissue may be actually stronger after the healing process has taken effect, whereas soft tissue is usually weaker after repair.

      Strains

A strain is damage to a muscle or tendon resulting from overuse or excessive stretching, direct trauma, and/or over-contraction against resistance. It can involve anything from a minor irritation of muscle fibers to an actual separation of the tendon from the bone structure. Strains are classified by either severity or by area. When classified by severity, the terms mild, moderate, and severe are generally applied. However, subacute and/or chronic strains may result in a myofascitis and/or myofibrositis. When classified by area, specific musculature are used such as gluteal, cervical paravertebral, intercostal, abdominal. If the muscles involved are of a nonspecific multiple nature surrounding a joint, the general area may be used as a descriptor such as a right iliofemoral strain, left knee strain, thoracocostal strain of T7-9.

In the typical simple strain, there is a small amount of internal bleeding and only a low-grade inflammatory reaction with swelling, collection of fluid in the local area, and a minor degree of involvement of the surrounding fibers. A severe strain is usually caused by a single severe injury where the tendon or muscle may be pulled apart or torn from the bone.

      Sprains

A sprain is an injury to a ligament which damages the fibers of the ligament or its attachments. The cause is primarily from forcing a range of motion beyond the power of a ligament to withstand the stress such as from over-stretching or over-exertion. The extent of damage depends upon the amount and duration of the force. Most sprains are classified as mild, moderate, or severe.

In a mild sprain, there is a small amount of internal bleeding in a localized area of the ligament with only a few fibers separated. No actual loss of function or reduced strength is present. Generally, the ligament requires no protection and is not weakened. It is characterized by tenderness over the ligament that is not marked at the bony insertion, by swelling, and by other symptoms of mild local inflammation. Joint instability is negligible.

A moderate sprain, however, results from a more severe tearing of the ligaments, although at least half of the fibers remain undamaged. This type of sprain shows some loss of function in the injured area even though the torn ligaments are not widely separated. They will join together again during the natural healing process unless the damage is great. If so, considerable scar tissue may form, and a permanent weakness of this section of the ligament may result.

A moderate sprain is characterized by a greater degree of symptoms than presented by a mild sprain, lack of normal ligamentous resistance on digital pressure, and increased joint movement on tension as seen with movement or manipulation. When a sprain is termed severe, it denotes a complete loss of function of the ligament caused by a force sufficient to pull it completely apart or tear it loose from the surrounding tissues. A severe sprain is characterized by a greater degree of symptoms than presented by a moderate sprain plus marked excessive joint motion indicating definite separation on tension or motion.

Sprains are classified by severity as acute, subacute, or chronic, or by the area of involvement such as cervical, thoracic, thoracocervical, brachiocervical, thoraco-costal, thoracolumbar, lumbar, lumbosacral, sacroiliac, or iliofemoral. Although the terms subacute and chronic may be diagnostic entities, these terms are confusing and an explanation of the subacute or chronic joint instability is more descriptive and desirable.

In differentiating sprain and strain, keep in mind that sprain involves the ligaments of a joint and strain involves the muscular and tendinous structures. Sprain usually elicits pain on movement of the affected joint even without muscular effort; strain elicits pain on muscular effort even without movement as in isometric contraction. However, any tissues may be strained in jury if the word "strain" is being used as a verb. When used as a noun or state of being, however, sprain refers to ligamentous injury and strain to muscular or tendinous injury.

      Complications in Strain and Sprain

The spine and extremity joints commonly suffer strains and sprains, which may be uncomplicated or complicated. For example, an uncomplicated spinal strain is a simple subluxation involving the muscular component primarily and does not contain any serious neurologic deficit. A complicated strain is accompanied by mild autonomic disturbances and may be associated with pre-existing arthropathy or discopathy, congenital deformities (osseous or muscular), systemic diseases (eg, diabetes mellitus), myofascitis, or age. An uncomplicated sprain is a ligamentous injury unaccompanied by any pre-existing pathology or injury to the spinal column contents. A complicated sprain is accompanied by pre-existing pathology or injury to the spinal column contents.

Complications result in strain/sprain when the tissues are abnormal or the general system is physiologically deficient at the time of injury because the lowered vitality of the locally damaged cells and the accumulation of exudate may provide fertile soil for the invasion of inflammatory processes and delayed repair.

Following are several direct complications of general musculoskeletal injury. Many of these conditions also occur, however, as specific primary entities.

1. Myositis is inflammation of a muscle; infectious myositis refers to a bacterial or viral infection, and toxic myositis results from chemical poisoning. The most common form of myositis is in response to trauma to the belly of an individual muscle. Myofascitis is an inflammation of muscle and its fascia, particularly of the fascial insertion of muscle to bone, and usually the result of trauma. Myositis ossificans is the conversion of a muscular area to bone, usually from a preceding hematoma. In addition to inflammation, a muscle can have a laceration (cut or tear), contusion (bruise without a tear, with or without ecchymosis), or hematoma (accumulation of blood).

2. Muscular spasm is an involuntary contraction of muscle; tonic spasm if persistent, clonic spasm if alternating. Severe muscle spasm, splinting, may be involved in a tonic spasm.

3. Tendinitis is inflammation of tendons or tendon-muscle attachments. It is more common to the short tendons without a sheath.

4. Tenosynovitis is an inflammation of tendon sheaths. It is more common than tendinitis when a sheath is present.

5. Bursitis is inflammation of a bursa. If it shows demonstrable calcium deposition, it is called calcific bursitis.

6. Capsulitis is inflammation of a joint capsule. If characterized by adhesions, it is called adhesive capsulitis.

7. Synovitis is inflammation of a synovial membrane. Tenosynovitis, capsulitis, and bursitis are all specific variations of synovitis.

8. Fibrositis is inflammatory hyperplasia of fibrous tissue, particularly of the muscle sheaths and fascial layers. It is sometimes referred to as muscular rheumatism. If the condition is noninflammatory, it is called fibrosis; if involving the ligaments surrounding a joint, periarticular fibrosis or fibrositis; if involving the musculature proper, myofibrosis or myofibrositis.

9. Radiculitis is inflammation of a nerve root, commonly causing pain over the distribution of a specific dermatome segment. The cause is commonly from osteoarthritis and/or degenerative disc changes resulting in foraminal occlusion. Pain is a constant symptom; it may be dull, sharp, shooting, constant, or paroxysmal. Three general symptoms recognized as cardinal signs of root pain are:

   (1) pain with body movement,
   (2) pain after such acts as coughing, sneezing, deep breathing, laughing, and
   (3) pain accompanied by dyskinesia after prolonged recumbency such as upon arising from bed in the morning. Radiculopathy is a nonspecific, noninflammatory irritation or disease of the nerve roots. The term is used when there are no positive neurological signs.

10. Paresthesia, abnormal sensory awareness over a specific area, is usually associated with minimal radicular irritation and presented over a dermatome segment.

11. Neuralgia is a general term for paroxysmal peripheral-nerve pain that usually extends along the course of one or more nerves. Radiculalgia is neuralgia of the nerve roots. Pain in neuralgia usually comes in attacks, and the nerve may or may not be pressure sensitive at points. Neuralgia is not necessarily associated with pathological nerve changes; thus muscle atrophy is not usually demonstrated. Most neuralgias attending musculoskeletal injuries are radiculitis in origin or reflex neuralgias and an inflammatory degeneration (neuritis) of the nerve proper is not present.

12. Extension or reflex neuralgia is an ache radiating along the course of a somatic sensory nerve as a referral from another source in the specific neuromere. It is differentiated from radiculitis in that it may not follow a specific dermatome.

13. Neuritis, inflammation of a peripheral nerve, is usually of a degenerative nature which may be grouped as mechanical, toxic (polyneuritis), metabolic (polyneuritis), and vascular. Pain is sharp and usually continuous. The nerve is sensitive to pressure throughout the whole or greater part of its course. Pain is rapidly followed by atrophy, anesthesia, and paralysis.

14. Myofascitis is inflammation of a muscle and its fascia, particularly of the fascial insertion of muscle to bone. Palpation of obscure pathology reveals small sensitive nodules which form in the fascial sheaths enveloping muscles or aggravated by overuse of the affected muscle or exposure to cold or chilly drafts.

15. Myofibrositis is the result of a prolonged or chronic injury with replacement by fibrous tissue. The result is stiffness or rigidity in muscle areas. Spinal distortion and subluxations, local diseases, autonomic reflexes, malformations, and developmental anomalies may be associated conditions with musculoskeletal injuries or they may attend, pre-exist, or predispose musculoskeletal injuries, as the above conditions may do. All these may exist as separate entities, the aftermath of previous injury or disease, or complicate the more recent condition.

Basic Pathology of the Neuromusculoskeletal Structures

CARTILAGE.   Cartilaginous and disc substance when traumatized will progressively undergo degenerative change with possible dehydration and fragmentation.

DISCS.   Repeated subluxations and the strain of mechanical and postural incompetence tend to weaken the annulus, and, in the cervical and lumbar spine areas especially, at the posterolateral aspects with possible bulging into the IVF.

LIGAMENTS AND TENDONS.   When a ligamentous or tendinous tissue is subjected to continuous strain and stress, it will become chronically inflammed and invaded by callogen substance and mineral salts. This results in sclerosing and even varying degrees of calcification; eg, iliotransverse and posterior atlantooccipital ligaments, supraspinatus tendon, and plantar aponeuroses. In addition, when ligamentous and tendinous tissues are subjected to acute traumatic strain, they will experience rupture of some of the comprising fasciculi which is attended by minute hemorrhages. Attempts at repair result in callogen tissue deposition and mineral invasion which also produce sclerosing and calcification. If the involved ligament possessed elastic fibers, there will be a definite shortening.

FASCIA.   In the biped human, the myofascial planes of the erectors of the neck, spine, and pelvis will become inflammed at the points of major strain and stress. Transudation and fibrin formation result to produce myofascial plane adhesions.

MUSCLE.   A muscle caused to be in traumatic or reflex spasm will become modestly inflammed. There may result some transudation precipitationn of fibrin, callogen, and mineral salt deposition, and, if extended, may result in a chronic myositis and myofibrosis.

BONE.   When subjected to weight bearing, occupational, or traumatic stress, bone will demineralize and undergo degenerative change resulting in deformity of the articulating surfaces. Concurrently, the attending excoriation of the articular periosteal margins will result in proliferative changes in the form of lipping and spur formations or eburnation.

DURAL ROOT SLEEVES.   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.

NERVES.   Stress, strain, and sprain at the area of the zygapophyses and the attending inflammatory reaction may give rise to a radiculitis of moderate disposition.

GANGLIONS.   An acute whiplash-like mishap to the cervical spine, especially of the hyperextension type, may traumatically 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.

      General Symptomatology

Abnormalities that may be discovered in disorders of the musculoskeletal system include:

(1) color changes such as ecchymoses and redness,
(2) local heat,
(3) soft tissue swelling from synovial thickening, periarticular swelling, or nodules,
(4) swelling from bony enlargement,
(5) deformity from abnormal bone angulation, subluxation, scoliosis, kyphosis, lordosis,
(6) wasting from atrophy or distrophy,
(7) tenderness on palpation,
(8) pain on motion,
(9) limitation of motion,
(10) joint instability, and
(11) carriage and gait abnormalities.

      Categories of Peripheral Joint Disease

Peripheral joint disease may be acute or chronic and local or general, allowing classification into acute monarthritis, acute polyarthritis, chronic monarthritis, and chronic polyarthritis. However, all cases cannot be grouped in such a fashion.

Acute Monarthritis: Gout, pseudogout, traumatic joint disease, osteoarthritis, infectious arthritis, rheumatoid arthritis, intermittent hydrarthrosis.

Acute Polyarthritis: Acute rheumatic fever, rheumatoid arthritis, other connective tissue diseases, infectious arthritis such as gonococcal, rheumatoid variants, palindromic rheumatism, gout, pseudogout, serum sickness, and sarcoidosis.

Chronic Monarthritis: Traumatic arthritis, osteoarthritis, infectious arthritis such as tubercular, gout, pseudogout, and neuropathic arthropathy.

Chronic Polyarthritis: Rheumatoid arthritis, other connective tissue diseases, rheumatoid variants, osteoarthritis, gouty arthritis, and sarcoidosis. Rheumatoid variants include such disorders as psoriatic arthritis, Reiter's syndrome, enteropathic arthropathy, etc.

      Common Causes of Myalgia

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.

Fibrositis and 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.

Tendinitis, Peritendinitis, and Capsulitis:   The history commonly presents an acute or insidious onset associated with trauma to or excessive strain of the involved area. Nelson, however, disputes 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 becomes painful without taruma, either overt or covert." The course is self-limiting, but joint deformity may result (eg, shoulder). There is local tenderness over the tendon insertion and around the joint. Motion limitation is common.

Drug-induced Myalgia:   There is a history of administration of steroids, diuretics, clofibrate, chloroquin, anticonvulsants, procainamide, etc, often wherein remissions can be associated with not taking the drug. Physical findings are usually negative, but there may be some pulmonary involvement.

Rheumatoid arthritis:   A history of severe muscular symptoms often precede articular symptoms such as severe pain and stiffness. Significant synovitis in the peripheral joints is common, as is muscle wasting and subcutaneous nodules.

Polymyalgia Rheumatica:   Most common in an elderly female whose history shows a relatively acute onset of aching and stiffness of the pelvic girdle, shoulder girdle, and proximal muscles. It may be the first indication of rheumatic arthritis, other connective tissue diseases, or of cancer. There is pain and tenderness of the proximal muscles without true weakness. Synovitis is minimal. A tenderness of the temporal artery is often associated.

Dermatomyositis, Scleroderma, Systemic Lupus Erythematosus, and Various Connective Tissue Diseases:   The history presents an insidious onset except in dermatomyositis. The course is variable. There is abnormal muscle tone, wasting, weakness, rash in lupus erythematosus and dermatomyositis, and skin induration in scleroderma.

      Reactions of Skeletal Muscle to Disease

Diseases and syndromes that affect the motor unit can be classified upon their clinical symptoms and findings such as weakness or hypotonia, periodic paralysis, fatigue, or cramping, stiffness, muscle contractions and myotonia.

Predominant hypotonia and widespread weakness may be from a fault in the (a) anterior horn cells, (b) motor nerve roots and peripheral nerves, or (c) at the myoneural junction, muscles, and unknown origins. Anterior horn cell dysfunction may be the result of a hereditary fault, congenital defect, trauma, toxic condition, an infective amyotrophy, an idiopathic amyotrophy, or cancer. Motor nerve roots and peripheral nerves may be involved from a genetically determined fault, trauma, toxic agent, an infection or inflammation, a metabolic disturbance, or an idiopathic polyneuropathy. Faults at the myoneural junction, muscles, or uncertain origins causing hypotonia and widespread weakness have their origin in myasthenia gravis with myopathy, tick paralysis, cholinergic paralysis, genetic influences, direct injury, toxic stress, infections, inflammations, metabolic disturbances, amyloidosis, and disuse atrophy.

Predominate periodic paralysis is seen in various forms: (a) primary finding of hypokalemia with secondary finding of hyperthyroidism, (b) primary hypokalemia and myotonia with secondary renal disease, (c) primary hyperkalemia with secondary hyperaldosteronism, (d) primary hyperkalemia and paramyotonia congenita with secondary pleoconial myopathy, and (e) normokalemia.

Predominate fatigue as a finding is characteristic of myasthenia gravis and the myasthenic syndrome. Myasthenia gravis may be of the transient neonatal or congenital-juvenile type or be associated with thyrotoxicosis or a thymic tumor. Myasthenic syndrome is seen in cancer or symptomatic myasthenia such as lupus erythematosus, hysteria, polymyositis, neurasthenia, adrenalectomy, anterior horn cell disease, chronic polyneuropathy, or neurasthenia.

Predominate cramps, stiffness, spasms, and myotonia may be from a fault in the (a) central nervous system (eg, tetanus, stiff-man syndrome), (b) anterior horns cells and peripheral nerves (eg, tetany, myokymia, neuromyotonia), or (c) myoneural junction, muscle, and uncertain origins. This third group may be the result of muscle contracture, myotonia, Schwartz-Jampel syndrome, malignant hyperpyrexia, myoglobinuric myopathies, relaxing-factor defect myopathy, or some mitochondrial disorder.

      Weakness Evaluated with Its Anatomical Origin

Weakness originating from a lesion at a particular anatomical site offers peculiar clinical findings:

Involvement of the Corticospinal Pathway:   The stretch reflexes are hyperactive, and there is increased resistance to passive motion. There are abnormal reflexes and sensory perceptions. Weakness is usually more pronounced than atrophy.

Involvement of the Anterior Horn Cells:   The stretch reflexes are absent or hypoactive. The weakness is generalized, but occasionally distal only. Weakness parallels the atrophy present.

Involvement of the Peripheral Nerves:   The stretch reflexes are absent or hypoactive. Weakness is usually distal but sometimes generally distributed. Weakness parallels the atrophy present. Muscle fasciculations are sometimes seen. Paresthesia and sensory changes are usually present.

Involvement of the Myoneural Junction:   Stretch reflexes are normal. Fatigue is greater than weakness, and strength returns quickly with rest after exertion. Muscle faciculations are rarely present. The disorder is usually seen first in the extraocular muscles, progressing in a variable, fluctuating course.

Involvement of the Muscle Fibers:   Stretch reflexes are absent or hypoactive, but the distal reflexes are usually normal. Weakness is proximal and parallels the atrophy present. Muscle fasciculations are rarely present.

Involvement of Function:   Stretch reflexes are normal, and there are no muscle fasciculations or atrophy. Cogwheel responses and slowness of motion are present. A positive Hoover's sign is present. There is a distinct overflow of activity and inconsistency in responses.

      Weakness or Paralysis Evaluated by Its Rate of Progression

Weakness or paralysis may have a fast, variable, or slow rate of progression and thus point toward specific conditions:

Disorders with a Fast Rate of Progression:   The muscular dystrophies, inflammatory myopathies, toxic myopathies, periodic paralysis, myasthenic syndromes, muscle tumors, a large variety of atrophies and neuropathies, amyotrophic lateral sclerosis, syringomyelia, and poliomyelitis.

Disorders with a Variable Rate of Progression:   The myoglobinuric myopathies, amyloid myopathy, sarcoidosis, infantile spinal muscular atrophy, myositis ossificans, and myasthenia gravis.

Disorders with a Slow or Static Rate of Progression:   The congenital myopathies, the endocrine myopathies, and the glycogen storage diseases.

      Weakness Evaluated by Its Site

The usual site of weakness may be generalized, essentially distal, essentially proximal, asymmetrical, or symmetrical in distribution.

Generalized Weakness from Fault in the Anterior Horn Cells:   Infantile spinal muscular atrophy, amyotrophy with arthrogryposis, poliomyelitis, and scapuloperoneal atrophy.

Generalized Weakness from Fault at the Myoneural Junction, Muscles, or of Unknown Origin:

(a) periodic paralysis, myasthenia gravis, myasthenic syndrome, steroid myopathy, and hyperthyroidism --in all of which there is little or no wasting;
(b) generalized myositis ossificans, congenital dystrophy with arthrogryposis, and the congenital myopathies --in all of which there is wasting.

Essentially Distal Weakness from Fault in the Anterior Horn Cells:   Amyotrophic lateral sclerosis.

Essentially Distal Weakness from Fault in the Peripheral Nerves:   Diabetic neuropathy, peroneal muscular atrophy, and hypertrophic interstitial neuropathy.

Essentially Distal Weakness from Fault at the Myoneural Junction, Muscles, or of Unknown Origin:   Myotonic dystrophy, distal and ocular myopathies.

Essentially Proximal Weakness from Fault in Anterior Horn Cells:   Familial spinal muscular atrophy.

Essentially Proximal Weakness from Fault at the Myoneural Junction, Muscles, or of Unknown Origin:   The muscular dystrophies, glycogen storage disease, poliomyelitis, and thyrotoxic myopathy.

Asymmetrical Weakness from Fault in Anterior Horn Cells:   Poliomyelitis.

Asymmetrical Weakness from Fault in the Peripheral Nerves:   Peripheral neuropathy.

Asymmetrical Weakness from Fault at the Myoneural Junction, Muscles, or of Unknown Origin:   Periodic paralysis.

Symmetrical Weakness from Fault in the Anterior Horn Cells:   Scapuloperoneal, infantile spinal muscular, and familial spinal muscular atrophies; and amyotrophic lateral sclerosis.

Symmetrical Weakness from Fault at the Myoneural Junction, Muscles, or of Unknown Origin:   The muscular dystrophies, glycogen storage disease, poliomyositis, and thyrotoxic, ocular, and congenital myopathies.

      Comparative Evaluation of Disuse Atrophy with Denervated Atrophy

Disuse Atrophy:   Moderate reduction in visible muscle size, mild to moderate diminished muscle strength (with paralysis in upper motor neuron lesions), normal tendon reflexes (hyperactive after initial shock in cases of upper motor neuron lesions), normal response to direct muscle stimulation, mild and slowly progressing atrophy. Pottenger shows that visceral malfunction can also produce these symptoms.

Denervation Atrophy:   Rapid reduction in visible muscle size, zero voluntary muscle strength, absent tendon reflexes, no response to direct brief muscle stimulation, and rapidly progressing atrophy.

      Disorders of Growing Bone

The so-called growing pains in children are usually the result of either joint overactivity which disappears with rest or of an epiphyseal disorder. Thus, it is vital to diagnosis joint and epiphyseal disorders early so that correction can be made before the young patient's future posture and well being are molded.

Normal postural balance depends upon the state of the epiphyses to a great extent because they form the future permanent skeleton. The epiphyses are functionally classed into three types:

(1) The pressure epiphyses, which influence osseous growth, are found at the ends of long bones, and transmit body load from one structure to another.
(2) The traction epiphyses, whose function are to serve as points of attachment for tendons and ligaments. And
(3) atavistic epiphyses, which serve to support and protect vital organs.

Disorders of growing bone can be classified into three general groups:

(1) disturbances in the general growth and development of bone such as premature ossification or delayed ossification,
(2) acquired epiphyseal lesions, and
(3) traumatic epiphyseal lesions.

Premature bone ossification is the result of an accelerated growth rate characterized by a large but otherwise normal skeleton such as seen in giantism. Delayed cartilage growth or the conversion of cartilage into bone is seen in chondrodystrophy and cretinism.

Epiphyseal lesions result from a local ischemia producing an aseptic subchondral necrosis. They are most commonly found involved in the epiphyses of the femoral head, anterior tubercle of the tibia, head of the second metatarsal and tarsal navicular of the foot, and the lunate of the hand. Traumatic lesions of the epiphyses can range from a simple dislocation to a severe osteochondritis.

      Disorders of Bone Calcification

These conditions offer few physical signs until greatly advanced: usually diagnosed from x-ray films.

Local bone atrophy (osteoporosis) is seen most commonly in bone atrophy from disuse, post-traumatic bone atrophy, Sudeck's atrophy, radiation atrophy, peripheral-vascular bone atrophy, gouty bone atrophy, arthritic atrophy, antibiotic bone atrophy, bone atrophy from celiac disease, and hemiatrophy. General bone atrophy is seen as the result of the physiologic changes occurring with senile osteoporosis and menopausal osteoporosis. Entities of generalized pathological bone atrophy include osteomalacia, rickets, osteitis fibrosa cystica, osteoporosis melolytica, and osteogenesis imperfecta.

A large number of disorders of calcified bone are recognized on x-ray films that are also most difficult to detect by physical signs in the early stages. These conditions include osteosclerosis, osteopetrosis, osteopoikilosis, melorheostosis, ivory vertebra, infantile cortical hyperostosis, cranial hyperostosis, calcified costal cartilages, soft tissue calcareous deposits, calcification of the thyroid cartilage, calcified lymph nodes, lipoid calcification, cerebral calcifications, calcified hematoma, and calcification of blood vessels such as in medial sclerosis of Monckeberg, arteriosclerosis, and phleboliths. Calcification of muscle tissue is seen in traumatic myositis ossificans and myositis ossificans progressiva in children. Widespread calcific deposits are noted in Werner's syndrome, calcinosis, calcinosis circumscripta, and calcinosis interstialis. Peritendonitis calcificans (bursitis) is often associated with bursitis of the following types: subacrominal, subdeltoid, olecronon, radiohumeral (tennis elbow), knee, hip, iliopsoas, deep and superfical trochanteric, ischiogluteal, and heel.

      Osteogenic Tumors

tumor is any neoplastic growth originating from the body tissues that appears to disregard the natural laws of body economy and to serve no useful purpose. Abnormal bone growths arise from either hypertrophy (increased cellular size) or hyperplasia (increased cellular quantity). Clinically, neoplasms are classed as either benign (nondestructive) or malignant (destructive).

Benign tumors are localized, grow by accretion, enlarge in one direction which is usually that of least resistance, and remain free and unattached to surrounding soft tissues. They take definite shapes such as spherical, ovoid, or polypoid, which can sometimes be palpated and distinguished from adjacent tissues. Complications from a benign tumor arise from calcification or degeneration of the growth by cystic formation, fracture, and fragmentation from aseptic necrosis.

Malignant tumors destroy normal cells while at the same time producing poor immitations which enter and wander through the blood and lymph channels invading distant tissues and there producing secondary malignant growths (metastases). Bone metastases are often secondary to primary cancer of the breast, thyroid, gastrointestinal tract, genitourinary tract, and lungs. Common sites are at the proximal end of the femur and humerus, the vertebrae, pelvis, ribs, and skull.

      The Arthritides

ATROPHIC ARTHRITIS (artrophic, rheumatoid) is an inflammation of a joint(s) involving the synovia and periarticular tissues, rarefaction and atrophy of the osseous structures, characterized by pain, swelling, restricted mobility of the joint, and termination in ankylosis. Two types must be recognized:

(1) a monarticular form, secondary usually to tabes or syringomyelia (Charcot's joint, neuropathic joint), and other diseases of the spinal cord; and

(2) a polyarticular primary form (rheumatoid arthritis, ankylosing arthritis). In both, the distinguishing characteristic is atrophy and destruction of cartilage, bone, and joint membrane --a process which in the early stages can be identified only by roentgenology.

Signs are joint swelling from synovial thickening and/or inflammatory effusion, local heat, redness, tenderness, atrophic changes, motion limitation because of pain or spasm of the flexor muscles, and flexor deformity of the involved joint(s) because of fibrous contractures of the periarticular soft tissues or due to joint destruction. Joint instability may be present because of destruction of cartilage and bone or from tendon(s) rupture. Occasionally, fibrous nodules may be noted in the phalangeal joints of the hand. Early symptoms include fatigue, muscle stiffness, and vasomotor disturbances. The disorder usually begins in one joint and spreads to other joints such as the knees, elbows, wrists, hips, and small joints of the feet. Associated manifestations may include carditis with significant murmurs, cardiomegaly, pericarditis, polyarthritis, chorea, erythema marginatum, and subcutaneous nodules. Pain ceases upon anklysosis. There may be a history of rheumatic fever, arthralgias, or fever.

The monarticular form generally has a rapid and painless course with semifluctuant swelling secondary to a cord lesion such as locomotor ataxia. A large joint is almost always affected, and the joint shows abnormal mobility. The bones often can be felt to grate.

The primary polyarticular form usually begins in the fingers and often occurs symmetrically in corresponding joints of both hands at the same time. The joints are boggy, enlarged, and spindle shaped owing to the rapid atrophy of the interossei muscles, often abundantly white, apparently fluctuant, and show trophic skin lesions such as glossy skin, sweating, and mottling. The terminal finger joints are rarely swollen. Late in the course of the disease, a ring of constriction often marks the line of articulation. Pain is not severe until motion is attempted or unless the joint is jarred and stirred up by some trauma. The changes progress slowly and attack new and larger joints, moving centrally from the periphery. At any stage, the process may become arrested, but usually not until ankylosis or contractures have occurred in one or many joints. Flexion of fingers with hyperextension of the terminal joints and deflection to the ulnar side are common deformities.

REITER'S SYNDROME is an atypical form of arthritis featured by polyarthritis, conjunctivitis, urethritis, fever, and inflammatory effusion into the joints.

STILL'S DISEASE (juvenile arthritis deformans, rheumatica arthritica juvenilis) is a chronic progressive polyarthritis of children characterized by intermittent pain, possible pericardial and pleural effusion, swelling and stiffness of one or more joints in the early stages that terminates in ankylosis and deformity. Enlargement of the lymph glands, spleen, and/or liver may be noted.

HYPERTROPHIC ARTHRITIS (osteoarthritis, degenerative arthritis) refers to a chronic degenerative disease of articular cartilage and bone. It is seen in x-ray films of most people to some degree past the age of 40 years. Unlike atrophic arthritis, it is not due to a specific focus of infection, but rather to trauma or stress upon weight-bearing joints from postural or occupational stress. Signs include redness, increased warmth if the joint is secondarily inflammed from trauma, joint effusion without palpable synovial thickening, joint margin bony enlargement, Heberden's nodes on distal interphalangeal joints, and tenderness over joint bursae and tendon insertions. There is pain on motion, palpable crepitus on passive motion, and joint instability from loosening of capsule and loss of cartilage.

The condition occurs mostly in elderly people. New bone is deposited around the edges of articular cartilage forming an irregular ring or lip near the joint. These osteophytic spurs are the distinguishing feature. The attachments of the ligaments (eg, anterior lateral ligament of the spine or cotyloid ligament in the hip joint) furnish another favorite site for the bony deposits. There is no ankylosis, and motion is limited only by the collision of bony spurs in joint margins.

1. In the terminal finger joints (Heberden's nodes), the process may remain for years without extending to any other articulation and without producing any discomfort.
   
   

2. The disease may be limited to the hip joint (malum coxae senilis) or to any other single joint, producing purely mechanical disturbances by movement limitation. There is no considerable muscle spasm, and motion is quite free up to a certain point at which it suddenly "locks" by the interference of the bony outgrowths. Pain and swelling are slight unless trauma stirs up a synovitis. The chief complaint is stiffness.

TRAUMATIC ARTHRITIS presents signs of possible ecchymosis, soft tissue swelling of periarticular tissue that may be limited to effusion within the capsule depending upon the severity of trauma, and tenderness on pressure. Motion is usually limited because of pain, and there will be joint instability if the injury is sufficient to tear a tendon or joint capsule.

MALUM COXAE SENILIS is a localized degenerative arthritis of the hip occurring after the age of 50 from trauma to an old adolescent epiphyseal disorder of the hip or reduced congenital dislocation. The patient reports a dull ache in the hip, thigh, or knee upon arising in the morning which decreases with activity. Signs and symptoms are slightly restricted joint action, increased pain on bearing weight, muscular spasm resulting in leg flexion and adduction, a limping gait, a shortened leg on the involved side, constant fatigue, and hip crepitus. As the disorder progresses, pain radiates along the anterior (occasionally posterior) part of the thigh to the knee. The trochanteric process is accentuated and externally rotated, thus referring stress to the lower back and sacroiliac joint on the affected side. Chronic backache, spinal distortion, and pelvic tilt are commonly associated. In some cases, the hip will become permanently ankylosed by spurs and lippings, relieving the pain.

PYOGENIC ARTHRITIS (acute infectious arthritis, suppurative arthritis, pyoarthrosis) refers to an acute infectious (usually virulent) arthritis of a joint that more often involves the knee or hip. During the early serous stage, there is little pain on rest or swelling. The joint is hot, usually flexed, and painful on severe movement. A mild fever increases in the serofibrinous stage as do the other symptoms. In the latter suppurative stage, there are extreme systemic reactions such as high fever, marked leucocytosis, joint pain and induration from the thickened periarticular soft tissues.

All varieties of acute infectious arthritis are distinguished from the other types of arthritis by:

(1) the absence of any marked bone lesions in most cases with the exception that virulent infections (especially those due to pneumococci or gonnococci) may destroy cartilage and bone and end in true bone ankylosis; and

(2) the tendency to recovery in the great majority of cases.

The milder idiopathic forms are often called "rheumatism" when a specific organism producing them is unknown. Between this group and those known as "rheumatism", there is no clear pathologic distinction. Mild infections with streptococci may leave the joint sound. Virulent infections may lead to crippling through fibrous adhesions. On the other hand, arthritis of "rheumatic" (ie, streptococci) origin may end in suppuration, crippling the joint with adhesions; though in most cases, it leaves a sound joint.

All members of the infectious group of joint lesions present the local signs of inflammation and the constitutional signs of infection. All may be complicated by endocarditis; but in those of streptococci origin (rheumatic), this complication is especially common. There is no bony hypertrophy, bone destruction in most cases with the exception of the virulent infections mentioned previously, sinus formation, or marked irregularities of contour. A general enlargement (more or less spindle shaped, owing to the periarticular thickening and muscular atrophy, is the rule. The joint motions are limited chiefly by pain and effusion; muscular spasm is not prominent.

One or many large or small joints may be affected in any of the varieties of infectious arthritis, though the gonorrheal organism is apt to lodge in a few joints and the "rheumatic" organism in many joints, while the typhoid poison has a predilection for the spine.

TUBERCULOUS ARTHRITIS is a localized, progressive destriction of one or more joints secondary to a primary tubercular lesion. Localization of the infection results in the formation of tubercles, tissue granulation, abscess formation, and bone destruction. A fibrinous exudate forms over the cartilage involved during the first (hyperemic) stage where there is pain, muscle spasm, and restricted joint motion. The second stage is characterized by slow atrophy and decalcification. The third stage presents on x-ray film eroded and sequestrated articular cartilage with marked softening of the underlying bone. The reparative stage features the formation of fibrous tissue and ankylosis.

Tubercular infection usually begins as an osteitis and involves the joint secondarily by extension. The primary characteristics of joint tuberculosis are:

(1) slow progress, with gradual enlargement and disabling of the joint;
(2) muscular spasm, especially in disease of the hip or vertebrae;
(3) evidences of low-grade inflammation such as moderate heat, swelling, pain, and tenderness;
(4) abscess and sinus formation;
(5) malpositions such as shortening of one leg in hip joint disease, angular backward projection in spinal disease, and subluxations in the knee joint; and
(6) bone necrosis as shown by x-ray films. The order of frequency in the different joints is as follows: spine, hip, knee, wrist, and shoulder.

In deep-seated hip-joint involvement, diagnosis has to depend largely on shortening of the limb and on the presence of limitation of all the hip motions by muscular spasm unless the disease is of long standing and manifests itself by abscesses burrowing to the surface. Usually these abscesses point in the upper anterior thigh, but they may open behind the great trochanter, below the gluteus maximus, or at any point in the vicinity of the hip. Besides muscular shortening, spasm, and abscess formation, we get some diagnostic aid from the general and vague symptoms present in this, as in many other joint lesions, such as enlargement (felt as thickening about the great trochanter), muscular atrophy, pain, tenderness, and crepitus.

GONORRHEAL ARTHRITIS results from a gonorrheal infection of the joints arising in from 2 or 3 weeks after the primary infection. Four types are recognized: serous, dry, serofibrinous, and suppurative. All types except the dry type present a clinical picture of suppurative arthritis. The dry type begins with periarticular edema, joint rheumatism, and "fleeting" pains in a number of joints prior to localization. It is usually associated with males between the ages of 20 and 30 years. Often a single joint is attacked such as the knee or less commonly in the hip, ankle, or wrist.

GOUTY ARTHRITIS refers to the deposits of urate of sodium in the soft structures around the joint. These deposits, like those in the ear, are close beneath the skin or perforate it. They somewhat resemble the nodes of hypertrophic arthritis, but are not attached to the bone and can be moved about in the soft structures over them. X-ray examination shows considerable destruction of bone in the vacinity of the tophi.

PNEUMONOCOCCAL ARTHRITIS, secondary to pneumonia particularly in children and alcoholics, is a rare monarticular complication. It usually involves a hip. The clinical picture is often one of a mild suppurative arthritis complicating pneumonia.

MENINGOCOCCAL ARTHRITIS is a monarticular (sometimes polyarticular) arthritis often following the administartion of antimeningococcal serum. The picture is that of suppurative arthritis with a history of meningitis.

HYPERTROPHIC PULMONARY OSTEOARTHROPATHY (clubbing, Marie-Bamberger disease, osteophytosis) is a disorder of the bones and soft tissues, particularly the fingers, featuring a tufting of the terminal phalanges, nonspecific periosteitis, and soft tissue swelling wherein the fingers appear "clubbed". It is secondary to a chronic suppurative disease of the lungs, but the exact mechanism involved is not understood. The joints become effused with fluid but the articular cartilage is unaffected. Only in extremely severe cases does the periosteum of the long bones become involved.

The finger clubbing is a nonpainful, symmetrical enlargement of the finger ends. The nails show thickened ridges, are markedly convex, and appear slightly cyanotic. Similar changes may be noted in the toenails. Wrists and ankles may be swollen due to joint effusion. The spine is rarely affected in this manner.

HEMOPHILIC ARTHRITIS.   A chronic stiffening and enlargement of the joint, resembling in many respects the joint of hypertrophic arthritis, but often accompanied by the formation of fibrous adhesions, ensues in some cases of hemophilia, presumably as a result of frequent hemorrhages and serous oozings in the joint. The diagnosis depends on the evidence of hemophilia, the age of the patient, and the absence of infection as a causative factor.

      Reticuloendothelial Disorders

GAUCHER'S DISEASE (large cell splenomegaly, kerasin-liporeticulosis) is a rare childhood disease featuring deposits of cerebroside kerasin in the hyper-plastic reticulum cells of the reticuloendothelial system resulting in splenomegaly, heptomegaly without ascites, hypochromic anemia, and unique bone marrow changes. Because of the enlarged spleen, pain radiates from the upper abdomen down to the left thigh. A mild jaundice may be present. Thrombocytopenia results in hemorrhages, central-type spastic contractures and tremors occur, and there is a marked retardation of growth in the long bones from malnutrition causing dwarfism. Early death is the rule.

CHRISTIAN'S SYNDROME (lipoid granulomatosis, xanthomatosis) refers to a disorder of the reticuloendothelial system where cholesterol deposits and esters enter the hyperplastic reticulum cells. The disorder features diabetes insipidus, exophthalmos, and bone changes especially in the cranium. The disease begins insidiously with physical and mental retardation. Xanthomata skin lesions often occur. Gingivitis is common and early. The liver, spleen, and lymph nodes may be enlarged.

LETTERER-SIVE'S DISEASE is a more severe form of Christian's syndrome seen in the very young.

NIEMANN-PICK'S DISEASE (histiocytosis) refers to an acute infancy disorder involving the reticuloendothelial system that features lipid deposition in the hyperplastic reticulum cells. Signs include physical and mental retardation, marked splenohepatomegaly with or without ascites, anemia, brownish skin pigmentation, and a rapid course until death which is usually prior to bone changes.

EOSINOPHILIC GRANULOMA of bone is a localized destructive lesion of the shaft of a long bone which is cystic and hemorrhagic. There is no abscess formation, the periosteal reaction is minimal, there is no central bone expansion, but there may be a slight cortical erosion. Spontaneous fracture may be associated. The pain is localized, and swelling and tenderness are present at the site of involvement. Muscle spasm and atrophy develop. However, the disorder may be completely asymptomatic except on roentgenology.

      Mycotic and Parasitic Bone Infections

A swelling of granulation tissue may develop in any tissue during the late stages of a specific infection as the infection begins to localize. Examples of such localized macroscopic swellings are the gumma of syphilis, the tuberculoma of tuberculosis, the nodules of leprosy, and the various granulomata of actinomycosis, blastomycosis, yaws, streptothricosis, leishmaniasis, and nonspecific cocci infections.

Regardless of the specific etiological factor, the mechanism involved includes:

(1) Invasion and infection with the immediate formation of granulation tissue.
(2) A degenerative stage in which necrosis develops slowly and insidiously, wherein the central zone of granuloma undergoes an aging transformation to become a cheese-like mass called "caseation" which is infiltrated with enzymes that change it into a fluid consistency (liquefaction). Hence
(3) the formation of an abscess encapsulated by a layer of granulation tissue. The inflammatory process may spread to the surface during this stage forming an ulcer or sinus.
(4) The final reparative stage is featured by the absorption or discharge of the purulent material with eventual healing by scar tissue or calcification.

Fungi are plants that mature in irregular and differentiated clusters having a parasitic or saprophytic nature and are classified as:

(1) yeast-like organisms such as those associated with moniliasis, blastomycosis, coccidiosis, and sporotrichosis;
(2) mold-like organisms which, except for those causing asperillosis, are nonpathogenic; and
(3) higher forms of fungi causing actinomycosis.

      The Spine

a.   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.

b.   Tropism:   asymmetrical or anomalous development of a zygapophysis (articular facet); usually seen as a saggital disposition of the lumbosacral facets.

c.   Sacralization:   growth of L5 to S1, may be pseudo (false) or true, bilateral or unilateral.

d.   Lumbarization:   growth of S1 as a separate lumbar segment, may be pseudo or true, bilateral or unilateral.

e.   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 stress fracture. It may be bilateral or unilateral, with or without spondylolisthesis.

f.   Overdevelopment or elongation of the transverse process:   usually of L5 or C7, and may cause bursa to form and give rise to bursitis.

g.   Anomalous formation of spinous process:   when two touch, the condition is called Baastrup's disease.

h.   Failure of fusion:   articular process, spinous process, transverse process, or epiphyseal plate (limbus bone).

i.   Vertebral fusion:

(1) Klippel-Feil syndrome, a synostosis (growing together) of vertebrae of the cervical spine, characterized by a short neck, low hair line, 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) paraoccipital process, a bony connection between the occiput and the first transverse process, lying close to the condyle.

j.   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.

k.   Spondylolysis:   congenital defect in the pars interarticularis which usually leads to anterior displacement of the vertebral body (spondylolisthesis) later in life.

l.   Ossiculum terminale:   non-union of the secondary ossification center at the tip of the dens.

m.   Os odontoideum:   congenital non-union of the odontoid with the body of the axis.

n.   Ponticulus posticus:   ossification of the posterior portion of the atlanto-occipital ligament.

o.   Ponticulus lateralis:   a bony arch extending from the superior articulating surface of the atlas to its transverse process.

p.   Occipital vertebra:   a morphological structure resembling a vertebral segment which surrounds the foramen magnum.

q.   Third condyle:   an arch on the anterior margin of the foramen magnum which articulates with the odontoid in cases of occipital vertebrae.

r.   Paramastoid process:   bony column arising from the transverse process of the atlas which articulates with the base of the skull at the jugular process.

s.   Sagittal cleft vertebrae:   bifid vertebrae; failure of unification of the laterally placed primary ossification centers of the vertebral bodies.

t.   Supernumerary vertebral segments:   congenital development of additional vertebral segments.

      Common Extraspinal Malformations

a.   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.

b.   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.

c.   Cervical rib:   rib or portion of rib from C7.

d.   Sprengel's deformity:   congenital elevation of the scapula with adduction and downward rotation of the scapula attended by kyphoscoliosis of the brachi-ocervical spine.

      Arthritis

1. Osteoarthritis and spondylosis:   Osteoarthritis (degenerative joint disease, hypertrophic arthritis, arthrosis) is a noninfectious degeneration of freely movable joints with loss of integrity of the cartilage and proliferative bony changes (exostosis, spurring, lipping, osteophytes). Spondylosis is a degeneration of the IVD with attendant proliferative changes of the margins of the body of the vertebrae. In hypertrophic arthritis, several joints may be affected, and there may result much pain because nerves pass through or over the new-formed bone and become compressed. This form is most often seen in the spine as spondylitis deformans where a portion of the front and side of the vertebral column is "plastered over" with new-formed bone which later invades the intervertebral cartilage and produces finally either a straight "ramrod" spine or a forward-curved spine. In the early stages, the disease is recognized by: (a) Nerve pain, running around the body or down the legs as the intercostal and spinal nerves are compressed --in fact, many neuralgias and sciaticas are due to this disease. (b) Limitation of motion, where the process is usually unilateral, wholly or predominantly, hence the patient can usually bend much better to one side than to the other. Motion is also more or less limited in other directions, but forward bending is fairly well-performed as a rule, in sharp contrast with "lumbago" which renders forward bending almost impossible. (c) Coughing or sneezing often gives great pain, probably because the costovertebral joints are involved in the new growth. If ankylosis of these joints occurs later, the respiratory movements of the chest are interferred with.

2. Rheumatoid arthritis:   (atrophic arthritis) is a degeneration of joints of unknown etiology characterized by inflammation, proliferation of synovial membrane followed by necrosis, fibrosis, and loss of bone substance. The disorder may take one of several forms in the spine and pelvis; eg,

   (1) ankylosing, characterized by an eventual ossification of the spinal ligaments,
   (2) Marie Strumpell spondylitis, where ankylosing usually begins at the sacroiliac ligaments and ascends the spine; the ligaments are involved, but not the discs,
   (3) Von-Bechterew's spondylitis, where ankylosing usually begins at the costovertebral ligaments, descends the spine, and the discs begin to ossify, and
   (4) Still's disease, which is an acute rheumatoid arthritis in children.

   Marie-Strumpell's disease:   (spondylitis ossificans ligamentosa) refers to a chronic form of arthritis characterized by a primary ossification of the ligaments of the spine which begins in the sacroiliac or lumbar area and extends upward to include the thoracic and cervical vertebrae resulting is a "poker" spine. The disorder begins with pain and stiffness or marked rigidity in the lower spine without pain, although the hips and sacroiliac joints are tender and often ache. Later stages present a dorsal kyphosis and flattened chest associated with shoulder inversion. Hip rigidity results in a waddling gait.
   
   Von Bechterew's arthritis:   (spondylitis muscularis) is a slow, progressive, degenerative arthritis that begins in the cervical area and progresses into the dorsal spine. Features include stiffness, ankylosis, dorsal kyphosis, and nerve involvement resulting in hypotonia and muscular atrophy but no true paralysis develops. There is usually diminished cutaneous sensation with some nerve root pain, especially in the intercostal region.
   
   

3. Rheumatic arthritis:   a possible feature of rheumatic fever.

4. Specific infectious arthritis due to known infectious agents; for example, gonorrheal arthritis, tuberculosis arthritis, syphilitic arthritis, and other types of infectious arthritis.

5. Miscellaneous forms such as gouty arthritis, traumatic arthritis, tumors of joints, and other miscellaneous forms.

      Infections of the Spine and Pelvis

1. Tuberculosis of the body of a vertebra (Pott's disease) may lead to pathological compression fracture, thus the formation of a sharp angulation (gibbus).
   
   In spinal tuberculosis, Pott's disease, the distortion of the bones with formation of a knuckle in the back is often obvious and practically diagnostic. In other cases, the examiner must depend on muscular spasm or abscess formation. The muscular spasm gives a stiff back and often psoas contaction. The abscess is peculiar in that it usually works along in the sheath of the psoas and points in the groin below Poupart's ligament; less often, it appears in the back or in the gluteal region; and rarely, it may invade almost any part of the body (lung, gullet, gut, peritoneum, rectum, hip joint, etc).
   
   Psoas spasm, which is common in both hip and spinal tuberculosis, is by no means peculiar to these diseases, and it is worth remembering that it may be due to various lesions such as (a) spinal dysarthrias, (b) hypertrophic arthritis of the spine, (c) appendix abscess, and (d) perinephritic abscess.

2. Osteomyelitis, syphilis of bone, fungus infections of bone, and other infections.

      Avascular Necrosis, Osteochrondritis, and Osteochondrosis

These conditions present a loss of bone substance thought to be due to loss of blood supply, and they may affect any bone. More common forms and similar conditions are:

1. Spine and pelvis:  

   (1) osteochondritis deformans juvenilis (Scheuermann's disease, adolescent kyphosis) is a vertebral epiphysitis characterized by disturbance of ossification of the epiphysis,
   (2) vertebral osteochondritis (vertebra plana, Calve's disease) is localized to one vertebra,
   (3) osteochondritis deformans (coxa plana, Legg-Perthes disease) is an avascular necrosis of the head of the femur.

2. Avascular necrosis of other joints:  

   (1) Osgood-Schlatter's disease, of the tuberosity of the tibia,
   (2) Kienbock's disease, of the lunate,
   (3) Preiser's disease, of the carpal scaphoid,
   (4) Kohler's disease, of the tarsal scaphoid,
   (5) Freiberg's disease, of the head of the second metatarsal.

3. Osteochondritis dissecans:   may occur in any bone and is characterized by ischemic necrosis and partial detachment of cartilage and bone from the articular surface. It is usually seen in the femoral condyles.

4. Kummel's disease:   (post-traumatic kyphosis) is a degeneration and collapse of a vertebral body following injury.

      Tumors of the Back

1. Aneurism of the descending aorta may point in the back near the angle of the left scapula. It is the only pulsating tumor of this region.

2. Perinephritic abscess usually points between the crest of the ilium and the 12th rib, a few inches from the spine.

3. Tuberculosis abscess, originating in vertebral tuberculosis, may point in the same region, though more often it follows down the sheath of the psoas and points near Poupart's ligament. A "cold abscess" starting from a necrosed rib is sometimes seen in the back. A probe leads to dead bone at the end of the sinus. Microscopic examination of excised pieces is one of the best ways of excluding actinomycosis, though this disease is less apt to form sinuses.

4. Sarcoma of the scapula, the only tumor of the scapula that is often seen, occurs in children and rarely after the second decade. With a solid, nearly painless tumor of this bone in a child, sarcoma should always be suspected. Benign exostoses are possible, but usually occur later in life. Histological examination arrives at the decision.

5. Epithelioma, arising from the skin of the back, presents the ordinary evidences of this form of cancer.

6. The multiple subcutaneous abscesses due to glanders are more common on the extremities, but they may be found on the trunk as well. Flattened, oval, fluctuating nodes with slight tenderness are suggestive. Bacteriological examination of the purulent contents settles the diagnosis.

      Miscellaneous Diseases

1. Osteitis deformans (Paget's disease of bone) is characterized by bone absorption and irregular new bone formation which fails to calcify properly, may remain soft (some cases show an increased hardness), and leads to an eventual marked thickening.

2. Infantile cortical hyperostosis (Caffey's disease) is characterized by deposition of subperiosteal bone, particularly in the mandible, clavicle, and shafts of long bones with accompanying inflammation.

3. Sudeck's atrophy (post-traumatic osteoporosis) is an atrophy of bone following trauma thought to be due to a neurodystrophic process vasospasm.

4. Schmorl's disease is an erosion of the spongiosum of the body of the vertebrae by the intervertebral disc due to repeated trauma and degeneration of the epiphyseal plate.

5. Metabolic disorders affecting bone, endocrine disorders of bone, and congenital development errors of bone --all may affect the spine.

      Spinal Curvatures

Diagnosis is not difficult upon examination:

1. KYPHOSIS or backward convexity of the spine, if sharply angular, suggests Pott's disease. If the curve is gentle and gradual, it may be due to postural "round shoulders", to hypertrophic arthritis, to emphysema, Paget's disease, or rickets. The rachitic curve is flaccid, simply from muscle weakness, and is associated with other evidences of rickets.
   
   In emphysema and Paget's disease, the kyphosis goes with the other signs of these diseases. In hypertrophic arthritis, the curve is rigid, irreducible, and usually painless. "Round shoulders" can be straightened by muscular effort and represent a postural habit.

2. LORDOSIS, an exaggeration of the normal forward convexity of the lumbar spine is seen in tuberculosis of the hip or spine, in paralysis of the dorsal or abdominal muscles (especially muscular dystrophy), and in abdominal tumors or pregnancy, which need to be counterbalanced by backward bending.

3. SCOLIOSIS is a combination of lateral curvature with twisting of the spine. In slight or doubtful cases, the tips of the spinous processes should be marked with a marking pencil which makes the deviation easily visible.

      Prominent Scapulae

This condition is usually due to:

(1) lateral curvature of the spine or
(2) serratus paralysis, recognized by the startling prominence of the scapula if the patient pushes forward with both hands against resistance such as a wall resulting in a condition called "angel-wing" scapula.

In congenital syphilis, the median or vertebral border of the scapula is sometimes markedly concave and called a scaphoid scapula.


Clinical Significance of Bipedism

Bipedism, the structural imperative of our species, compels certain anatomical considerations to appreciate the fact that the spine is of commanding clinical importance because of its intimate involvement with the neurological element. The human biped profiles a unique and singular relationship between the musculoskeletal mechanism and the neurological bed. The neurological factors that relate to bipedism represent the rationale of chiropractic science and art.

Derangements in the musculoskeletal system in the human are much more common than in the quadriped. Consequently, man as a biped is heir to those elements that are the consequence of disturbed body mechanics. In this regard, Janse has listed the following points in his writings:

JOINT CHANGES.   The sacroiliac articulations at the time of birth are of the amphiarthrodial disposition. But as standing and locomotion are acquired, the joints are induced to assume diarthodial motorcity and come to possess encompassing ligaments, articulating cartilages, and bed of proprioceptors.

PROPRIOCEPTIVE STIMULATION.   Anatomists and neurologists no longer question the significance of the entire proprioceptive bed disposition in the ligamentous and myological elements of the spine and pelvis. No anatomist would deny the augment of the fasciculi gracilis and cuneatus of the spinocerebellar system, the righting and postural pathways of the tectospinal extensions, or the ascending and descending components of the reticular activating mechanism. The proprioceptive bed of the spine has ascending and descending connections with the thalamencephalon and the alerting center of the reticular formations of the mesencephalon, known as the ascending and descending retricular activating mechanisms. Spinal and pelvic derangements inimically excite this mechanism to a point of undue wakefulness (insomnia). Clinicians are definitely beginning to acknowledge that a disturbance of these neurological elements will result in varying syndromes.

STRUCTURAL STRESS.   Bipedism augments the concern of gravity and weight bearing, postural faults, strains and stresses of occupation, play, and trauma. Because of such stress, the articular, syndesmotic, and myological proprioceptive complex is often disturbed which results in the development of many common spinosomatic and spinovisceral syndromes. The intervertebral disc, especially in certain areas of the spine, becomes a most vulnerable unit of disturbance, discogenic extension and resultant disc syndromes. A deranged spinal or pelvic segment within its motor bed will always result in disturbance of the proprioceptive bed with facilitation of the discomfort and pain phenomenon.

DEVELOPMENTAL DEFECTS.   Nature, via genetic factors and it's difficulty with phylogenetic increments, commonly leaves the spine in defect and instability. The incidence of neck and low back involvements of a protracted and recurring nature is much higher in those patients (especially younger people) whose spines show evidence of development defects and anomalies. Bipedism greatly augments the mechanical and neurological complications of the lumbosacral complex. As the low back and sciatic syndromes are evaluated, no clinician can be disrespectful of this fact. Furthermore, such lumbosacral defects and complications as asymmetrical facet facing, imbrication, sacralization (especially the pseudo type), lumbarization, pars defect, discopathy, iliotransverse ligament sclerosing, retrolisthesis and L5-S1 reverse rotation become priorities of clinical importance.

FATIGUE SPASM.   In the human biped, a great deal more neuromuscular energy is expended in postural, locomotive, occupational, and recreational efforts than in any other vertebrate. Fatigue, therefore, intrudes itself upon the foregoing clinical profiles. A characteristic of all erector muscles of the head, neck, back, and pelvis is that when they experience postural and stress fatigue, they go into a splinting-type painful spasm. Thus, according to Janse, when a provoked postural, erector, or cantilever muscle tires and goes into fatigue spasm as a compensatory necessity, the muscle becomes painful because the spasm impinges upon the neurotendinous and neuromuscular spindles and trigger mechanisms are created. This pain is most commonly asymmetrical and the result of a distorting, compressing nature. If there is a pre-existing derangement (pathology or defect), the asymmetrical fatigue spasm may be the "extra straw that breaks the camel's back" which triggers a subliminal accumulation into a full-blown acute symptom expression or becomes the provocative factor in a nagging chronic discomfort that will not abate.

On the other hand, Nelson feels this concept is conjecture as "muscles get stronger with use. The only time a used muscle gets weaker is when its nutrition is absent or reduced. This is the result of neurological reflexes." Removing the 'triggering' mechanism is not enough, the whole load must be removed for proper repair.

PATHOLOGICAL SPASM.   The primary causes of pathological muscle spasm are strain, stress, trauma, sprain derangement, postural and occupational fatigue, emotional torpor, psychic stress, referred irritation from visceral involvements, and nerve root irritations associated with interosseous derangements. When a synovial articulation is subjected to such stress as named above or to toxic insult, the muscles that move the joint are reflexly provoked into spasm because of the irritation of the articular sensory bed. This spasm, so often asymmetrical, will not infrequently force the joint into greater derangement or compression and thus set up the inimical phenomenon of circulus vitiosus. In cases of pathologic spasm, the patient's history may show that muscles in painful pathological spasm may be caused to relax at times if the muscles had been provided a position of physiological rest and an appropriate therapy had been applied.

INTRAFASICULAR GLUEING.   A muscle in spasm or under strain from any cause (or a stressed tendon or ligament) will become congested. This congestion always results in some degree of transudation and the conversion of fibrinogen into fibrin which acts as a cobweb-like adhesion or interfascicular glueing which impedes fascicular glide. As a result in muscles, tendons, and ligaments under strain, there occurs interfascicular, painful constrictions leading to the common algias of these structures. If permitted to continue, callogen infiltration and even calcific deposition may take place. When a tendon is similarly involved or when a ligament is subject to strain, similar changes take place with callogen and calcium invasion resulting in possible fibrosis and calcific tendonitis or syndesmitis.

TRIGGER POINTS.   Concurrently, similar events occur in the myofascial planes at a point of major tensil stress leading to the development of "trigger points" and the resulting delta or spread effect. All muscles have their fascial encasements (epimesium, perimesium, endomesium); and, as muscles lie and move one upon the other, the myofacial planes are described. The amount of fasciculii involved in the all-or-none contraction effort determines the tone or strength of muscle contraction. Furthermore, a muscle usually does more work at one point of its composite than at another.

The torso of man the biped is much like a "skyscraper" wherein strain and stress is greater at certain points than at others. Within the zone of these points of primary function and stress, there is a relatively heavy deposition of sensory nerve endings and motor end plates. When these areas, heavily populated with neurological elements and vascular ramifications, are subject to trauma, occupational stress, the strains of postural fatigue, and viscerospinal inimical reflexes, the process of transudation, fibrin precipitation, glueing and adhesion formation ensues to establish an intramuscular and myofascial plane trigger point. To this must be added the neurological principle of fascilitation and spread. Not uncommonly, there is a musculoskeletal syndrome complex that challenges the clinical capacity of the best.

SOFT TISSUE MICROTRAUMA.   Muscles, tendons, ligaments, fascies, and aponeuroses are comprised of bundles of fibers called fasciculi. In the event of trauma, the entire muscle, tendon, ligament, etc, may not tear loose or rupture. Most commonly, only a limited number of fasciculi are involved. This is known as "fascicular separation" and commonly associated with "whiplash" cervical sprains, the low back sprain of athletics, and so forth. In frequent sequelae, the structure is repaired with low grade replacement tissue (fibrosis) and invaded by mineral salt deposition (calcification infiltration).

PSYCHIC TENSION.   None deny the hazardous effects of emotional torpor and negative affectations on the cardiovascular, gastrointestinal, and respiratory systems. The term psychosomatic has become a household inference. More commonly, the reference is actually to a psychovisceral effect. A most common psychosomatic reflection is the tension and stress spasms of the spinal musculature contributing to the build-up and triggering phenomena of occipital and cervical migraines, recurring torticollis, shoulder-hand syndromes, psoas and femoral algias, as well as low back and sciatic problems. Emotional-mental tension and stress almost invariably refer themselves into the spinal musculature to augment or trigger syndromes of possible manifold quality and quantity.

THE INTERVERTEBRAL DISC.   Uniquely, the IVD or at least the nucleus pulposus is primitive mesenchymal tissue. Only during intrauterine life and infancy does it have a blood supply, namely a branch of 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 infancy, it involutes and atrophies. Thereafter, the disc obtains nutrition by means of canaliculus seepage. The degenerative process usually begins in the nuclear substance and then extends into the annulus and the cartilaginous apophyseal plate of the vertebral body. This weakening process eventually involves the retaining fibers of Sharpey, the interbody articulations of Luschka, and the crisscrossing interwining fibroelastic fasciculli comprising the laminae of the annulus fibrosus. From here, the process extends into the periosteal articular margins resulting in proliferative changes that end in aburnation, lipping, and even osteophytosis. This entire conglomerate of events may be referred to as degenerative proliferative arthrosis of the spine or discogenic spondylosis. As a consequence to this process, we may list the following:

l.   A weakening of the annulus fibrosis, most frequently at one of the other posterolateral aspects with possible prolapsus and even frank rupture with nuclear herniation.

2.   Loosening of the retaining mechanism of the IVD as well as the entire motor unit resulting in disc prolapsus and hyperkinesis of the vertebral segment of an undue gravitational weight-bearing pathologic interosseous disrelation (subluxation).

3.   Undue traumatic stress upon the ligamentous retaining mechanism with traumatic insult inflicted upon the proprioceptive bed. Such insult results in nagging persistent pain and asymmetrical reflex spasm of those msucles that relate to the vertebral segment of the motor bed involved.

THE INTERVERTEBRAL FORAMEN.   When the zygapophysial articular complex of a vertebral motor bed is subjected to the strain and stress of "off centering", the IVF area becomes congested, fibrinogen is precipitated into fibrin, and the capsular ligament becomes thickened by infiltrated callogenous substances. These factors place the spinal nerve trunk under compression by the likely undue pressure of congestion, thickening of the capsular ligament, or the binding by adhesions between the dural root sleeve and the nerve root or trunk or between the sheath and the adjoining ligaments.

All this causes the nerve root to snag as it attempts to glide back and forth within the IVF during normal spinal movements.

THE GANGLION.   The dorsal root ganglion occupies a precarious position within the vicinity of the IVF. This is especially true at the cervical level where it tends to occupy the medial limits of the IVF and is thus vulnerable to and most likely to become involved in any changes of the IVF diameters on any event of trauma or the manifold tissue processes of discogenic spondylosis as described previously.

THE NERVE ROOT.   The position and course direction of the nerve root within and through the IVF is significant. When either position or direction of entrance or exit is modified, the nerve root becomes vulnerable to encroachment. This is due to the fact that whenever the normal curves of the spine are modified such as in 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 undue approximation to one or the other walls of the IVF. Thereafter, the least additional deviation may precipitate a nerve root irritation syndrome.

IMMEDIATE COMPLICATIONS.   When for any reason a vertebral segment or segments are embarrassed by abnormal motoricity, added articular and proprioceptive responsibility is imposed upon segments above and below the involved area. Thus there is an extension of inimical effect that may have noticeable complications. In addition, the phenomenon of bipedism neurologically necessitated the development of an ascending and descending reticular activating mechanism. This is a rather protopathically comprehended neurological mechanism associating the proprioceptive patterns with the mesencephalic, and thalamencephalic alert, righting and wakefulness centers. It can be assumed that spinal and pelvic interocceous disrelation may over excite the ascending portion of this mechanism and thus unduly excite alertness and wakefulness to the extent of insomnia. On the otherhand, undue attention-stress may, by means of the descending portion, provoke undue stimulation of the cellular elements in the anterior and latera horns and provoke inimical somatic and autonomic reactions.

FAULTY COLON HYGIENE.   This leads to an overload of toxic elements in the blood which always aggravates local or systemic involvements. A history of belated elimination can be assured to worsen, for example, the neuralgias, myalgias, arthridites, asthma, eczema, etc.

Hildebrandt and Howe describe normal and abnormal spinal biomechanics similar to the following adaptation of their papers:

Normal Spinal Biomechanics   As the "axial organ" of the body, the erect spinal column is a primary concern in static postural equilibrium. However, since the body is never actually in a static state in life, but exists in a state of "quiescent dynamics" in the static postural attitude and a state of "active dynamics" in movement, the kinetic aspects of normal spinal biomechanics are an important consideration. In this regard as an "organ entity", the total of spinal function is the sum of its individual component parts, described as follows:

The Vertebral Motor Unit   The individual components of the spinal column are the vertebral motor units which are described here as "a biomechanical concept which confers a quality and quantity of intellectual motoricity to the relationship of two vertebrae, firmly interconnected by the intervertebral disc and restraining ligaments, which are activated to controlled, purposeful function by muscles which are respondent to a sensory and motor nerve supply".

Functional Efficiency of the Spinal Column   The spinal column as a total unit consists of 25 vertebral motor units. The functional efficiency of the total unit is described as "that condition of the vertebral motor units (individually and collectively) in which each gravitationally dependent segment above is free to seek its normal resting position in relation to its supporting structure below, is free to move efficiently through its normal ranges of motion, and is free to return to its normal resting position after movement".

Normal Vertebral Movements   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. To some extent, all vertebrae are able to function in all three dimensions; however, it is generally accepted that the magnitude of such movements varies to some degree in the lumbar, thoracic, and cervical spinal regions as well as in the lumbosacral, thoracolumbar, thoracocervical, and cervico-occipital transitional areas. Although there is some difference of opinion regarding specificity of such movements in the various spinal areas, the following is given as approximate:

a.   Normal Movements of the Spinal Regions

LUMBAR SPINE.   In the lumbar spine as a whole, lateral flexion is relatively free, followed in order of mobility by extension, flexion, and rotation. Most significant to movements in the lumbar spine is the fact that all movements are to some degree "three dimensional"; ie, when the lumbar spine bends laterally, it tends to also rotate posteriorly on the side of convexity and assume a hyperlordotic tendency.

THORACIC SPINE.   In the thoracic spine, all movements are relatively limited, especially in the upper regions, due to the restriction imposed by the costovertebral and costotransverse articulations. Rotation of the thoracic spine is somewhat greater than flexion and extension which are approximately equal. As in the lumbar spine, all three movements are somewhat three-dimensional with rotation and lateral flexion being most evident. In view of the rather limited normal movement of the thoracic spine, the gross idiopathic type scolioses in this area are difficult to comprehend.

CERVICAL SPINE.   In the cervical spine, all movements are relatively free. The cervical spine is most flexible in flexion and rotation, the latter occurring most freely in the upper cervical area and progressively restricted downward. When the cervical spine bends laterally, it tends to rotate anteriorly on the side of the convexity; ie, opposite to the lumbar spine.

b.   Normal Movements of the Transitional Areas

LUMBOSACRAL AREA.   The lumbosacral area of L5-S1 constitutes a rather unique "universal joint"; eg, when the sacrum rotates anterior-inferior (downgrade) on one side within the ilia, L5 tends to rotate in the opposite direction, thus effecting a "mechanical" postural accommodation with the lumbar spine above assuming a posterior rotation on the side of the unilateral anterior-inferiority. It also tends to assume an anteroflexion position, thus effecting the three-dimentional movements of the lumbar spine as previously described. In view of the intricacy of the lumbosacral junction, anomalies such as asymmetrical facets have a strong influence on normal movements in this area.

THORACOLUMBAR AREA.   Due to restriction of normal movement in the thoracic spine and the relatively mobile lumbar spine below, the thoracolumbar area undergoes some degree of hypermobility in all three body planes. Because of this, as is true to some extent in all spinal transitional areas, the thoracolumbar junction is more prone to stress both above and below.

THORACOCERVICAL AREA.   In the thoracocervical area, normal movement is somewhat similar to that in the lumbosacral area insofar as the stress to which both areas are subjected is similar. As L5 is relatively immobile on the sacrum, C7 is relatively immobile on T1, with the major amount of movement in the thoracocervical junction being at C6-7 and primarily that of rotation.

Abnormal Spinal Biomechanics

Abnormal spinal biomechanics primarily relates to the intervertebral subluxation and other spinal "dysarthrias" which result in structural and functional inadequacies of the spinal column, thus constituting a factor in the production of disease states of the body. With respect to the preceding discussion of normal spinal biomechanics, the intervertebral "dysarthric subluxation" is described as "the condition of a vertebral motor unit which has lost its normal structural and/or functional integrity and is, therefore, unable to move from its normal resting position, unable to move properly through its normal ranges of motion, or unable to return to its normal resting position after movement".

1. Precipitating Factors of Spinal Subluxations
   
   Although the spinal dysarthric subluxation may be either a cause or an effect, it is considered here as an etiologic finding. As a primary etiology, the following precipitating factors may be described:

   a.   Direct Spinal Dysarthric Subluxation.   This direct subluxation of a spinal vertebral motor unit is that event which results from local trauma, postural stress, abnormal development, or pathology, with such conditions leading to structural and functional impropriety of the articulations.
   
   b.   Indirect Spinal Dysarthric Subluxation.   The indirect subluxation of a spinal vertebral motor unit is that event which results from muscular imbalances, with such conditions also leading to structural and functional impropriety of the articulations.

2. Effects of Spinal Subluxations
   
   As a primary concept of chiropractic clinical science, spinal dysarthric subluxations may result in the development of disease states locally within the vertebral motor unit itself or throughout the body. These primary and secondary effects are described as follows:

   a.   The primary effects are localized conditions occurring within the articulations due to interarticular stress and trauma (often microtrauma) such as irritation, inflammation, swelling, necrosis, and degenerative changes.
   
   b.   The secondary effects are those extensions of the primary effects which may be disseminated throughout the body as a result of neurovascular insult within the confines of the intervertebral foramina, traumatic insult to the rami communicantes or sympathetic ganglia, proprioceptive alterations, etc.

In consideration of the spinal dysarthric subluxation as a cause-effect interrelationship, it is hypothesized that, once initiated, this biomechanical impropriety becomes an etiologic "vicious cycle" from cause to effect and from effect back to cause which, if not interrupted by corrective effort, will carry on to an ultimate and perhaps fatal conclusion.


The Spinal Subluxation

      Subluxation: A Clinical Entity

The concept that an "off centered" vertebral or pelvic segment is attended by an inimical effect upon the neuromuscular bed which may eventuate in the cause of, aggravation of, or "triggering" of certain syndromes is a biological classic and a major contribution to the field of functional pathology and clinical biology by the chiropractic profession.

The degree of derangement of an osseous segment within its articular bed may vary from a microtrauma to one that is macroscopic and quite readily discernable. It is always attended to some degree by articular dysfunction, neurological insult, strained muscles, tendons, and ligaments. Once produced, the lesion becomes a focus of sustained pathological irritation. A barrage of impulses streams into the spinal cord where internuncial neurons receive them and relay them to motor pathways for conduction to muscles. The contraction that provoked the subluxation initially is thereby reinforced, thus perpetuating both the subluxation and the pathological process engendered.

      Clinical Types 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. Pathological subluxation: a pathological "off centering" derangement in an articular bed that has become deformed as the result of degenerative change.

3. Traumatic subluxation: traumatic in consequence to an extraneous force and the associated muscle spasm.

4. Reflex subluxation: reflex "off centering" induced by asymmetrical muscle contraction from aberrant visceral reflexes.

5. Defect subluxation: subluxation of an anomalous or developmentally defected 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 motoricity effort.

7. Hypermobile subluxation: pathological segmental hypermotoricity in consequence to the loss of integrity of the retaining mechanism caused by trauma or degenerative pathology.

      Causes of Subluxation

The immediate causes of subluxation 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, intervertebral disc, ligaments, etc. Nelson asks, "The abnormal spinal mechanics cause the subluxation, but what causes the abnormal spinal mechanics?"

1. Inequality of Muscle Balance
   
   Inequality in muscular balance may be initiated by trauma, postural distortion phenomena, biochemical reactions, psychomotor responses, paralytic affects, and somatic and visceral responses.
   
   TRAUMA.   Acute frank trauma may cause inflammation, degeneration, etc, and particularly the muscular splinting reaction that the muscles make when their surrounding tissues are injured, and thus alter the position and motion of the structural tissues that are related. Sustained microtrauma, though of a less acute nature, may cause a slow continual irritation and may eventually create degenerative pathologic changes which similarly alter muscular reaction.
   
   POSTURAL DISTORTION PHENOMENA.   Postural compensations for either mechanical activity or for structural changes in the skeleton itself are referred to as postural distortion phenomena. These changes, as well as other causes of subluxation, often result in a series or combinations of minor mechanical errors which together may be termed scoliosis, kyphosis, lordosis, distortion, or similar terms. Such distortion phenomenon is dependent upon the ability of the spine to adjust to any interference in the body's vestibular, visual, or proprioceptive adaptation which is incompatible with the normal balance of the musculoskeletal system to gravity. Whether this structural imbalance creates disturbances or appears asymptomatic is dependent upon the neurological irritation developing from the tissues affected. They may not elicit apparent disturbance at a given time; but, rather, at a later date when they overcome the adaptation and resistance of the individual.
   
   BIOCHEMICAL REACTIONS.   The acute or chronic hypotonicity or hypertonicity of musculature may be due to various biochemical changes within the above mentioned tissues. This may be brought about by either local or general pathologies which may cause anoxia, ischemia, toxicity, etc, or by systemic nutritional deficiencies or chemical exposures that would affect the chemical environment of cells histologically.
   
   PSYCHOMOTOR RESPONSES.   These responses refer to the reaction of the musculature to emotional effects on the nervous system as the body depicts its psychological stresses.
   
   PARALYTIC EFFECTS.   Primary disease of the neuromuscular system itself such as in poliomyelitis or other paralytic diseases affect musculoskeletal tone or strength and, therefore, affect position and quality of motion.
   
   SOMATIC AND VISCERAL RESPONSES.   These responses refer to the secondary reactions of the muscular system to somatic or visceral sensory irritation which may develop elsewhere in a given neurological segment. We are constructed from an embryological nature in such a manner that the various components of a given vertebral segment and its ramifications or neuromere may be influenced by sensory stimuli that arise from any of the tissues supplied by these components. The somatic or visceral sensory neurons that enter into a given neurological segment and cause somatic or visceral motor response may cause a similar response throughout the various ramifications of that segment. This of course is dependent upon certain states of sensitivity or facilitation, certain convergencies or divergencies within the nervous system, and particularly upon the intensity and duration of the initiating stimulation. Therefore, we could have a visceral sensory irritation in the intestinal tract or other viscus that is causing motor changes not only in the internal organs, but also in the vascularity and the musculature of the body. These changes may result in motor alterations in the tone of muscles, consequently resulting in a spasm or splinting action. If long standing, degenerative changes, atonicities brought about by atrophy, contractures, or other pathologic changes within the musculature may develop which may influence the mechanics of the segments involved.

2. Abnormal Structural Support
   
   Mechanical errors in position or motion may also be brought about by structural alterations in the supporting tissues of the joint itself. These in turn may be brought about by:

   a.   Developmental abnormalities causing asymmetry of the vertebrae, cartilage, muscular structure, and so forth.
   
   b.   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.
   
   c.   The resolution of macro- or micro-traumas or of other primary pathology may cause fibrosis, degeneration, or other retrograde changes of a structural nature within the joints themselves.

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.

      Local Effects of General Mechanical Stress

Mechanical disturbances can adversely affect the body in a number of ways such as:

1. Compression stress or irritation of NERVES leads to increase or decrease of conduction with consequent trophic changes.

2. Load stress on MUSCLES lead to hypertrophy or atrophy.

3. Compression stress on BONE leads to sclerosis or alteration of its normal shape and internal architecture.

4. Leverage stress at JOINTS leads to weakness or sprain of ligaments, articular and intra-articular cartilage damage, and synovitis.

5. Blocking stress or irritation of BLOOD VESSELS leads to ischemia or congestion.

6. Pressure stress on SKIN and CONNECTIVE TISSUES leads to thickening or thinning.

7. Pressure or stretching stress of VISCERA leads to disturbed visceral function and abnormal reflexes. Abnormal body mechanics affecting the thoracic and abdominal cavities interfere with normal function (a) by abnormal efferent visceral stimuli reaching organs from the faciliated segment, (b) by abnormal tensions and stretching of the visceral supports, nerves, blood and lymph vessels which supply the viscera, (c) by abnormal vasomotor impulses to these blood vessels, (d) by venous pooling as the result of inactivity, diaphragm dysfunction, organ displacement, and sustained postural stress.

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 CNS with consequent hormonal reactions that are systemic in character. Also considered must be the associated emotional stress as the result of the local stress which contributes to the clinical picture.

      Local, Mechanical, and Neurologic Effects of Spinal Subluxation

The effects of subluxations may be divided into three major categories:

1. The immediate local effect of any tissue irritation, degeneration, or the changes of disease.

2. The mechanical effect, motion, and balance of the local segment, or the effect upon the skeleton elsewhere, due to compensatory distortions and alterations as the proprioceptive mechanism would correct its mechanics to the presence of structural imbalance.

3. More importantly, the neurologic effects of subluxation: These neurologic effects may be differentiated as direct physical nerve pressure, circulatory changes, meningeal irritations, cerebral spinal fluid flow alterations, and proprioceptive responses and reflexes.
   
   DIRECT PHYSICAL NERVE PRESSURE.   This may come from the misaligned osseous segment itself or from the various soft tissue pathologies that are causing or affected by the mechanical fault such as contractures, adhesions, inflammatory residues, and atrophies 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 ramifying reflexes.
   
   CIRCULATORY CHANGES.   The lymphatic or vascular system may be influenced by mechanical pressure therefore causing chemical or physical changes within tissues such as anoxia, toxicity, swelling, edema, etc, and the consequent derangement of normal function brought about by these metabolic disorders.
   
   MENINGEAL IRRITATIONS.   The mechanical errors in motion and position may cause tractional effects upon the meningeal coverings of the cord or dural-root sleeves which may produce mechanical pressure upon the neurons emitting from the cord itself. These may, therefore, cause the elicitation of abnormal neurologic motor effects or sensory interpretations.
   
   CEREBRAL SPINAL FLUID FLOW ALTERATIONS.   These refer to the mechanical effect upon the flow of cerebral spinal fluid within the central nervous system and perhaps within the peripheral nerves themselves. According to some researchers, minute pressure on meninges may alter the mechanics or flow of cerebral spinal fluid and interfere 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 necessary for proper inflow and outflow of this nutrient material.
   
   PROPRIOCEPTIVE RESPONSES AND REFLEXES.   Perhaps the most significant effect is that of proprioceptive irritation. The musculoskeletal tissues and particularly the ligaments and paravertebral or intervertebral musculature of the spine are endowed with proprioceptive neurons. First, when overly stimulated by stretching, these neurons interpret the stimuli as somatic sensory stimulation which may be perceived as pain. Second, they may also send reflexes to their motor components and cause muscular changes within the paravertebral muscles or elsewhere in the somatic musculature supplied by the segment. Third, they may be interpreted as visceral sensory stimuli, whose visceral motor response is now altering circulatory changes, smooth muscle activity, glandular secretions, or trophic activity in the musculoskeletal tissues or visceral organs supplied by a given neurologic segment or within the cord itself. It is this vast ability of the proprioceptive sensory beds to influence motor changes, both of a somatic-motor or visceral-motor nature, that is perhaps the most universal effect of the vertebral subluxation.

Many spinal subluxations have more than one immediate cause and effect. Abnormality of development may be complicated by degenerative joint disease, retrograde changes, inflammation, muscle splinting, etc. 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.

      Criteria Indicative of Subluxation

The importance of a subluxation is dependent upon its clinical features and whether the lesion and its neurogenic responses are affecting the total health of the individual to a significant degree. Minor mechanical errors in positions and motion occur in all of us as do consequent neurologic irritations from their effects. We are all subject to environmental irritations and respond to them in a manner that creates errors in musculoskeletal symmetry in the body.

Therefore, errors in position and mechanics of our related anatomical structures occur. These in turn cause or perpetuate neurologic aberrations of motor reflexes. However, these motor responses may be of a temporary nature for the body is capable of correcting mechanical faults within its structure provided they are of a minimal nature.

On the otherhand, certain forms of lesions cannot be corrected without proper professional attention. It is not so much the presence of a subluxation that is significant but how it is affecting the total economy of the body and how involved it is in the production of aberrant neurologic responses and the creation of a state of disease. These effects may be determined by a proper diagnosis and spinal analysis. In order to evaluate this condition, there are various criteria that indicate a subluxation of clinical significance.

These criteria may be divided into two divisions: the neurophysiological and the structural.

      Neurologic Manifestations

The neurologic manifestations of a subluxation are indicated by the response the nervous system makes to irritation that is not external to it, and as such discernable in its immediate environment, but rather from within the body. Thus, it is an intrinsic source of neurologic irritation. This neuropathy may produce somatic sensory responses, somatic motor responses, and/or visceral motor responses.

Examples of somatic sensory responses are pain, paresthesias, hyperesthesia, hypoesthesia, or some other abnormal sensation.

Somatic motor responses may include abnormal muscular tone or contraction such as hypotonicity to spasm and even atrophy, weakness, or degeneration in long-standing cases. The above findings are indicated by objective examination, palpation, muscle testing, measurements, electromyography, alterations in mechanical balance and movement, and other standard diagnostic procedures.

Visceral motor responses of the nervous system may be evidenced as:

1. Changes in the circulation of the skin which can be measured by various heat sensitive devices, galvanometers or infrared photography. This change is often analogous to circulatory changes in the deeper tissues, as they too are affected by similar vasomotor responses.

2. 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 dryness, as well as hyperesthesia or hypoesthesia, in a local area of the spine implies altered vasomotor activity in the subsequent spinal segment. Hyperesthesia and hyperhidrosis are usually associated with an increased "red response" to scratching and a decrease in electrical skin resistance.

3. Changes in the quality of tissue from trophic disturbances such as atrophies, degenerations, thinning or discoloration of the skin, or other changes that reflect visceral trophic abnormalities.

Thus, the presence of a subluxation influences its neurologic ramifications. When these neurologic processes are of clinical significance and without cause from other environmental irritations (or emotional etiologies) that the body is adapting to, this form of intrinsic error should be considered. If it is the source, its diagnosis and correction are necessary to the dimunition of the neuropathic reflexes initiated from its immediate tissues.

      Structural Alterations

In addition to its neurologic manifestations, a subluxation may also be determined by its structural alterations. These structural alterations may be:

1. Objectively visualized or palpable as alterations in the normal anatomic relationships of one joint to another. 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 positions of motion.

2. Evident by the presence of certain objective or subjective signs and symptoms when the joint and tissues are put through certain kinetic or orthopedic tests.

3. Visualized on x-ray films and exist as disrelationships in the normal anatomical structural relationship of one joint to another. This may not be evident in a given view, but in the view best depicting the mechanical fault. In addition, they may only be evident on views showing an area when it is put through various positions of motion.

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 structural faults and diminish their influences upon it. Consequently, the signs and symptoms of neuropathic processes are more significant than the structural alterations. The major importance is not the positional relationship of the osseous segments, but the significance of the soft tissue changes that are causing or are affected by this such as the neuropathic reflexes arising from the soft tissues, tendons, ligaments, muscles, etc.

The structural presence of a subluxation is important because of these reflexes, and the position of the segment is important because it mirrors the changes in the musculoskeletal system.

All subluxations do not show all the neurological and structural features that have been discussed.

In evaluating cartilaginous alterations in any joint, keep in mind that several factors influence cartilage degeneration:

(a) severe isolated or repeated minor trauma,
(b) chronic mechanical stress or tension,
(c) local circulatory excesses or deficiencies,
(d) idiopathic biochemical factors,
(e) developmental anomalies or malformations, and
(f) the inherited cellular quality of the cartilage.

      Clinical Approach

Disease is a byproduct of the interaction of irritants, forces, and processes both within and without the patient, and all these factors have their influence of the patient's total adaptation. However, these factors are not all equal in their importance in a given patient, and a differential diagnosis is necessary to qualify which are of paramount importance in an individual case.

The profession has found that all the causes and effects of a subluxation syndrome are also not of equal significance. Structural alterations and neurologic effects may arise from specific segments and/or musculoskeletal lesions that are, in turn, mechanically altered by errors in position or motion elsewhere in the musculoskeletal system.

The discerning examiner attempts to separate the more acute, but compensatory, adaptation from the more chronic, but major, lesions. These major subluxations are often found to be specific positional errors which have as their origin alterations in the integrity of the structural supporting tissues of the joint itself. As such, they are beyond the capacities of the muscular system to correct by its own functional adaptations.

      Events at the Intervertebral Foramen

There are 115 diarthroses within the spine and pelvis that are vulnerable to the "off centering fixation" of subluxation. Each of these articulations is an organ of proprioceptive sensitivity which under articular strain is insulted and provoked to express pain. Near these articulations are the intervertebral foramina which transmit the spinal nerve trunk, the spinal blood vessels, and the small spinal recurrent nerve. The foramina are dynamic: widening and expanding with spinal motion, serving as a channel for nerve egress and ingress, and allowing compression and expansion of the lipoareolar bed.

In review, the factors that modify the diameters of the IVF are:

(1) the disrelation of subluxation,
(2) changes in the normal curves of the spine,
(3) the presence of induced abnormal curves 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.

These factors mitigate the viable contents of the IVF and subject its contents to physiologic compromise which 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 as:

1. Induced disrelation between level and direction of nerve root origin (spinal cord) and nerve root exit (IVF) is an important factor. Whenever there is subluxation, change in normal curves (reduced or kyphotic cervical curve), or presence of abnormal curves (scoliosis), the relative levels of points of nerve root origin and exit are altered, and hence the position, direction, and course of the nerve roots and trunk within the IVF become abnormal. Compression or irritations are thus more likely.

2. Paraforaminal adhesions in consequence to stress and traumatic edema often result in a painful restriction of the normal back-and-forth glide (1/4 to 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 placing the involved part in extension.

3. Irritation/compression of the dorsal root ganglion may be a factor. The general sensory dorsal root ganglion of each spinal nerve lies within the upper medial aspect of the IVF. Whenever its position is altered or the diameters of positions of the IVF are modified, the ganglion may be subject to compression and irritation.

Initially, subluxation is always attended by the following aspects of micro-trauma:

(1) minute hemorrhage and transudation,
(2) para-articular and paraforminal 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 annulus, 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 irritation, and
(7) minute tearing of the attachments of the dural root sleeves as they attach to the lining periosteum of the IVF.

In consequence, the following pathological changes occur:

(1) The presence of extravasation and edema along with the precipitation of fibrinogen into fibrin result in interfascicular, forminal, and articular adhesions that restrict fascicular glide, ingress and egress of the foraminal contents, and the competent motoricity of the vertebral segment within its articular bed.
(2) Whenever there is extravasation, mineral salts are precipitated and infiltration and sclerosing result.
(3) Binding adhesions may develop between the dural root sleeves and the nerve roots within the inter-radicular foramen and between the spinal nerve root sheath and the inner margins of the IVF. And
(4) when subjected to microtrauma, mesenchymal connective tissue undergoes a relative rapid and extensive degenerative change with loss of functional integrity and substance.

Because of the effects of the subluxation's microtrauma and the consequent pathological changes involved, the neurologic insult may result in:

(1) modification of the basic chronaxie,
(2) alteration of normal impulse amplitude, wave length, force intensity, and/or
(3) extension of the refractory period.

This altered status of the nerve-fiber threshold and the impulse proper leads to dysfunctions in the sensory, motor, vasomotor, and spinovisceral fields.

1. Dysfunctions in the sensory field include varying degrees of discomfort and pain, tension, superficial and deep tenderness, muscular tone, periosteal tenderness, hyperesthesia and hypoesthesia, haptic sensations, acroparesthesia, formications, flushing, numbness, coldness, and postural fatigue.

2. Dysfunction in the motor field include painful and especially proximal muscle spasms, sluggish and incoordinated movements and gait, paralyses, fasiculations, tics and tremors.

3. Dysfunction in the vasomotor field include local swellings, angioneurotic edema, flushing, blanching, mucous membrane congestion, urticaria and dermatographia.

4. Dysfunction in the spinovisceral field include visceral musculature abnormalities, glandular and mucous membrane secretory malfunctions, sphincter spasms of the detrusor muscles and myocardium.

In addition, certain spinosomatic and spinovisceral syndromes may result.

For example, if the involvement is in the area of C1-C4, cervical portion of the sympathetic gangliated chain, or the 9th-12th cranial nerves as they exit from the base of the skull and pass into their compartments within the deep cervical fascia, such syndromes may include:

(1) suboccipital or postocular migraine,
(2) greater occipital nerve extension neuralgia,
(3) mandibular, cervical, auricular, pectoral, or precordial neuralgia,
(4) paroxysmal torticollis,
(5) congestion of the upper respiratory mucosa, paranasal sinuses, or eustachian tube with hearing loss,
(6) cardiorespiratory attacks,
(7) ocular muscle malfunction,
(8) pathological hiccups,
(9) scalenus anticus syndrome, and
(10) painful spasms in the suboccipital area.

Pain can be perceived in the vicinity of the spinal column by a number of factors such as:

(1) mechanical irritation of the nerve roots,
(2) mechanical irritation of any of the involved pain-sensitive soft tissues,
(3) edema and vascular distension,
(4) reflex spasm of the paravertebral muscles,
(5) chemical irritation of any of the involved pain-sensitive tissues by the effect of inflammatory exudates,
(6) by referred pain from viscera or distant structures, and
(7) psychic mechanisms.

Classification of Subluxations

Through the years, there have been numerous concepts within the profession of what constitutes a vertebral subluxation. Each of these has had its own rationale and each has had certain validity that has been a contribution to our understanding of this complex phenomenon. The basis of classifying the manifestations of subluxations herein is based upon the concept of the intervertebral motor unit.

      The Intervertebral Motor Unit

An intervertebral motor unit is comprised of two vertebrae and their contiguous structures forming a complete set of articulations at one intervertebral level. For this reason, a subluxation is often defined as "the alteration of the normal dynamics, anatomical or physiological relationships of contiguous articular structures".

The motor unit has an anterior and a posterior portion, and each has peculiar and special characteristics. The articulations are actually the mobile or motor portion of the unit. This is stressed because of the tendency to speak of a subluxated vertebrae when in fact it is solely the articulations that subluxate.

1. The anterior portion of the motor unit includes the vertebral bodies, the intervertebral disc, the anterior and posterior longitudinal ligaments, and the other associated soft tissues. This anterior portion is weight bearing and supportive. It has very little sensory innervation. Changes or pathology affecting these structures, though they may be quite spectacular in appearance on a x-ray film and alter biomechanics and spinal mobility significantly, are seldom accompanied by much pain or other subjective discomfort in the local area.

2. The posterior motor unit comprises the pedicles, neural foramina, articular processes and apophyseal articulations, the ligamenta flava and those which encapsulate the articulation, the interspinous and supraspinous ligaments, and all the muscles and other attached soft tissue structures. The posterior portions of the motor units are richly endowed with sensory and proprioceptive innervation. Thus problems, pathologies, stresses, and distortions that affect these structures are usually painful.

In this regard, after Hildebrandt and Howe, the biomechanical element of the vertebral motor unit subluxation is classified in accordance with its static or kinetic aspects and in accordance with the number of vertebral motor units involved as follows.

Biomechanical Classification of Spinal Subluxations

STATIC INTERSEGMENTAL SUBLUXATIONS

1. Flexion
   

2. Extension
   

3. Lateral Flexion (left or right)
   

4. Rotation (left or right)
   

5. Anterolisthesis and/or Spondylolisthesis
   

6. Retrolisthesis
   

7. Lateralisthesis (left or right)
   

8. Altered Interosseous Spacing (increased or decreased)
   

9. Osseous Foraminal Encroachment.

KINETIC INTERSEGMENTAL SUBLUXATIONS

1. Hypomobility and/or Fixation
   

2. Hypermobility or Loosened Motor Unit
   

3. Aberrant Motion.

SECTIONAL SUBLUXATIONS

1. Alterations of Curves Secondary to Muscular Imbalance
   

2. Alterations of Curves Secondary to Structural Asymmetries
   

3. Decompensation of Adaptational Curves
   

4. Abnormalities of Motion.

PARAVERTEBRAL SUBLUXATIONS

1. Costovertebral-Costotransverse (primary or secondary)
   

2. Sacroiliac (primary or secondary).

The characteristics and significance of the various subluxation classifications are given primarily for explanatory purposes and are not intended to be absolute or all inclusive. The presence of structural or functional subluxations as represented by this classification does not imply clinical significance; ie, they must be corrrelated with other clinical findings for confirmation such as the patient's history and physical examination findings, roentgenology, etc.

General Description of Various Types of Classified Spinal Subluxation-Fixations

Following are the generally accepted characteristics and significance of the classified vertebral motor-unit subluxation-fixations:

Refer to Chapter 6:   Radiologic Manifestations of Spinal Subluxations for a more thorough review of the following Subluxation-Fixations.

FLEXION SUBLUXATION:   Characterized by approximation of the vertebral bodies at the anterior and 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 nucleous pulposis and buldging of annular 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 vertebral motor unit.

EXTENSION SUBLUXATION:   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 excusion of the nucleous pulposis and buldging of the annular fibers, 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 motor unit.

LATERAL FLEXION SUBLUXATION:   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 of subluxation is suspicious of 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 nucleous pulposis with buldging of the annular fibers, stretching of the anterior longitudinal ligament at its lateral aspect, and biomechanical impropriety of the vertebral motor unit.

ROTATIONAL SUBLUXATION:   Featured by rotatory displacement 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 is significant of torsion binding of the annular fibers of the IVD, decreased resiliency of the IVD due to torque compression of the annular 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 motor unit.

ANTEROLISTHESIS SUBLUXATION WITHOUT SPONDYLOLYSIS:   Characterized by an anterior-inferior excursion of the vertebral body at the anterior and anteriorsuperior excursion of the vertebral body and facets at the posterior. This type subluxation points toward irritative microtrauma at the anterior IVD, forward shearing stress to the annular fibers of the IVD, stretching of the anterior and posterior longitudinal ligaments, imbrication of the facets with forward shearing stress to the synovia, and biomechanical impropriety of the vertebral motor unit.

ANTEROLISTHESIS SUBLUXATION WITH SPONDYLOLYSIS:   Featured by anterior excursion of the vertebral body independent of the posterior division of the vertebral motor unit. The posterior division of the motor 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 nucleous pulposis with buldging of the annular fibers, forward shearing stress to the annular fibers, stretching of the anterior longitudinal ligament, and biomechanical insult of the vertebral motor unit.

RETROLISTHESIS SUBLUXATION:   Featured by posterior-inferior excursion of the vertebral body and posterior-inferior excursion of the facets. This subluxation signifies irritative microtrauma to the posterior IVD, posterior shearing stress of the annular fibers, 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 motor unit.

LATEROLISTHESIS SUBLUXATION:   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. This situation points toward irritative microtrauma to the IVD on the side opposite deviation, lateral and posterior shearing stress to the annular fibers 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 motor unit.

DECREASED INTEROSSEOUS SPACE SUBLUXATION:   Featured by narrowing of the intervertebral disc space and inferior excursion of the facets. This situation is characterized by degeneration of the IVD with approximation of the vertebral bodies, traumatic compression of the IVD with possible herniation of the nucleous pulposis through the 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 motor unit.

INCREASED INTEROSSEOUS SPACE SUBLUXATION:   Characterized by superior excursion of the vertebral body and superior excursion of the facets. This type of subluxation results in inflammatory swelling or pathologic enlargement of the IVD, traction shearing stress to the annular fibers of the IVD and the synovia of the facet articulations, stretching of the anterior and posterior longitudinal ligaments, and biomechanical insult to the vertebral motor unit.

BONY FORAMINAL ENCROACHMENT SUBLUXATION:   Featured by potential concomittant finding of other types of subluxations with possible relationship to osteophytic interforaminal spurs in conjunction with other types of subluxations. It is featured by associated microtraumas and macrotraumas to the vertebral motor unit; compression, irritation, and swelling of the foraminal contents; osseous and soft tissue primary degenerative processes of the vertebral motor-unit structures; and interforaminal neurovascular insult effecting possible disseminated secondary pathophysiologic processes.

HYPOMOBILITY AND/OR FIXATION SUBLUXATION:   Characterized by fixation of the vertebral motor unit in relation to the supporting structure below and compensatory hypermobility of the vertebral motor unit above the level of fixation. It is associated with irritative excessive function of a hypermobile vertebral motor unit resulting in microtrauma or macrotrauma 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 motor units involved.

HYPERMOBILITY SUBLUXATION:   Featured by a hypermobile vertebral motor unit in relation to a normally functioning or hypomobile motor unit below. This situation has the same features as that of a hypomobile and/or fixation subluxation except for a possible traumatically loosened vertebral motor unit as opposed to compensatory hypermobility of a vertebral motor unit within its normal range of motion.

ABERRANT MOVEMENT SUBLUXATION:   Characterized by movement of a vertebra "out of phase" with the segment above and below wherein two motor units are involved. This type subluxation points toward microtrauma to both of the vertebral motor units involved, occlusion of the IVFs above and below the aberrant segment, shearing stress to the IVDs and synovia of both vertebral motor units, restriction of the neural canal, and biomechanical impropriety of both vertebral motor units.

COSTOVERTEBRAL-COSTOTRANSVERSE SUBLUXATION:   Featured by misalignment of the costal processes in relation to the vertebral bodies and transverse processes independent of vertebral motor unit subluxation (ie, primary) or misalignment of the costal processes in relation to the vertebral bodies and transverse processes as a result of vertebral motor unit 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 motor unit subluxation and/or are contributory to the chronicity of a subluxation, induction of spinal curvatures and/or are contributory to the chronicity of curvatures present, and irritations to the sympathetic ganglia and rami communicantes.

SACROILIAC SUBLUXATION:   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 point toward irritative microtrauma to the interarticular structures, induction of a vertebral motor unit subluxation and/or are contributory to chronicity of subluxations, induction of spinal curvatures and/or are contributory to the chronicity of curvatures present, and biomechanical impropriety of the pelvis in static postural accommodation and in locomotion.

During spinal analysis, the major spinal motions evaluated are flexion, extension, right and left lateral flexion, and right and left rotation. Motion of a superior segment is described in terms of the segment beneath it.

      Spinal Motions

When the spine is in a neutral standing or sitting position, the anterior surface of a vertebral body will rotate to the side opposite the lateroflexion with the vertebral bodies tending to crawl out from under the load. This pattern of function takes place usually within multiple spinal segments, but dysfunction will occur when ligaments and muscles attached to and affecting the vertebral articulations are shortened or lengthened to effect restricted or excessive otion of one or more segments.

The articular facets open during flexion, close during extension, and individual segments rotate and side bend to the same side. When the neutral position is resumed, the spinal joints should return to their "normal" position.

The direction of vertebral rotation is determined by inspection and dynamic palpation of the transverse processes, with the process being more posterior on the side toward which the vertebrae has rotated. If one or more segments are rotated to one side in the neutral position, lateroflexion will usually be noted to the side opposite the rotation. In spinal flexion, the segment that is rotated will be side bent to the same side with a loss in its ability to bend forward. Likewise, during spinal extension, the rotated segment is rotated to the same side and is unable to bend backward.

      Motion Barriers

To keep measurements standardized, 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 uncomfortable to the patient. This point is referred to as the anatomic motion barrier. In evaluating the degrees of passive motion, the joints should be moved up to but not through the anatomic motion barrier. Thus, joint motion is accomplished by passively carrying the joint(s) through a range of motion until the motion barrier is encountered and recording the degrees of movement allowed.

      Evaluating Joint Motion

The range of motions 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 muscle or group of muscles is made by carrying the joint to the extreme of allowed movement permitted by the antagonist muscles afterwhich the examiner resists an active maximum effort by the patient to contract the muscles being tested. Strength is recorded bilaterally according to the method previously explained; ie, Grade 5 to Grade 0.


Multipositional Spinal Inspection and Palpation

At this point, it would be well to review the earlier sections on Antero-Posterior Balance, Lateral Balance, Rotational Balance, Body Type and Balance Defects, and Symptomatology of Balance Defects.

      Approximate Topographical Landmarks in Relation to the Anatomy of the Vertebral Column (After States)

External occipital protuberance (EOP): Prominence, midline of occipital base.

C1    1cm inferior and slightly anterior of the mastoid process.

C2    First prominent spinous process below the EOP.

C4    Hyoid bone.

C6    Cricoid cartilage.

C7    Second prominent spinous process below the EOP.

T1    Most prominent spinous process in the region.

T2    Jugular notch.

T5    Angle of Louis.

T7    Inferior angle of the scapula.

T10    Xiphoid process.

L1    Transpyloric plane.

L3    Umbilicus.

L4    Iliac crests.

L5    Transtubular plane.

S2    Level with PSISs.

Sciatic notch:    2" inferior and 1" lateral to PSIS.

Ischial tuberosity:   2" inferior to apex of coccyx and on a vertical line through the PSIS.

The art and science of spinal examination, diagnosis, and analysis demands 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 following descriptions of positions, adapted from papers by the LACC Technic Department and NCC, are suggested for a complete spinal analysis:

(1) Adams' position,
(2) the anatomic position,
(3) the prone position, and
(4) the dorsal recumbent position.

      The Adams' Position

The patient assumes the Adams' position by standing erect, with the heels together, then bending forward with the fingers as near the floor as possible without straining. For an indication of spinal flexibility, the distance between the fingertips and the floor should be measured. In bending, the knees should not be flexed.

This is possibly the best position in which to detect any vertebral rotation. As the patient goes into and out of the Adams' position, the vertebral column should be examined for any areas that may be flattened or do not move evenly. With the patient in the Adams' position, finger palpation should be done with the fingertips upon the tips of the spinous processes. With motion by the patient, the various segments of the spine can be seen to glide closer together or further apart. Should an area be observed that remains rather immobile or without the normal gliding action, further tests and x-ray studies should be made of this section of the spine.

While the patient remains in the Adams' position, note the following points:

(1) Is flexion unrestricted?
(2) Is flexion straight forward or deviated laterally?
(3) Do the spinous processes line up straight? This is more easily determined by dotting the spinous processes with a skin pencil. And
(4) are there abnormal prominences of the angles of the ribs?

As the patient advances in age and the spine settles, there will of course be less flexibility, as will be the case in a contractured condition of the paravertebral musculature.

Where the spine does not bend straight forward, but deviates to one side, even ever so slightly, a search should be instituted for contractured, thickened, or shortened muscles, tendons, and/or ligaments of the column existing on one side and not on the other. When one or more spinous processes are out of alignment, either spinal lesions, subluxations, or an abnormality of the spinous process is indicated. Frequently, two or more spinous processes that are out of alignment will indicate multiple subluxations in portions of the vertebral column, perhaps with the exception of the middle thoracic column from about the 4th through the 9th thoracic vertebrae. But even these may sometimes be involved.

Discovery of elevation or prominence of the ribs on either side may denote a rotation of the vertebrae upon their axis.

Shortening of the ligaments with contracture of the musculature of the spine will be evidenced by abnormal stiffness or hardness of the muscles on the side of the spine that is contractured.

In pelvic mechanical pathologies on the side of involvement, there is an observable slanting and anteriority of the pelvis in the forward bending position. The sacral dimple, as compared to that of the opposite side, is prominent and inferior. There is a noticeable lumbar scoliosis to the side of involvement.

      The Anatomical Position

Have the patient stand with his heels together, with his hands hanging normally at his sides. Encourage the patient to stand normally and not try to assume "good posture" or the "military stance". Note the following:

1.   Compare the dots over the spinous processes positionally with their appearance when the patient was in the Adams' postion.

2.   Note the angles of the ribs. In pelvic mechanical pathologies on the side of involvement, there is a reduction in the height and depth of the body angle as observed from the posterior. A low and less prominent iliac crest will be best observed from the front.

3.   Check the curvatures of the spine. Evaluate as normal or abnormal; lordotic, kyphotic, or scoliotic.

4.   Check for winged scapulae or for scapulae failing to lie smoothly upon the chest wall. The midthoracic spine is always scoliotic towards the side that the vertebral margin of the scapula is more prominent and flaring. If the shoulder is high on the right and the scapula flares on the right, the entire cervicobrachial and thoracic spine is scoliotic toward the right. If the shoulder is high on the right yet the left scapula flares, it indicates that the cervicobrachial spine is scoliotic to the right and the midthoracic spine is scoliotic to the left.

5.   Observe the comparative height of the scapulae, one compared to the other. The cervicobrachial spine is always scoliotic toward the side of the high shoulder.

6.   Digitally explore the contours of the trapezius muscles for normal development or for abnormal tightness or tenderness.

7.   Note the position or tilt of the patient's head.

8.   Digitally explore the sternocleidomastoideus and suboccipital muscles. Asymmetrical fullness of the suboccipital musculature indicates upper cervical rotation.

9.   Note the comparative height of the iliac crests. If chronic sciatic neuralgia is on the high iliac crest side, degenerative disc weakening with posterolateral protrusion should be suspected. If occuring on the side of the low iliac crest, one must consider the possibility of a sacroiliac slip and lumbosacral torsion as being the causative factor.

10.   Sitting behind the patient, reach around the crests and place a finger of each hand upon the ASISs, having the patient lean slightly forward without bending at the waist. Determine if there is abnormal pressure on your finger on one iliac spine as against the other.

11.   Check the transverse processes of the lumbar vertebrae.

12.   Check the position of the gluteal cleft. A line passed through the gluteal cleft should demonstrate its lower end equally between the feet and its upper end, and over the 7C and the occipital protuberance.

13.   Note tension of the gluteals.

14.   Note the comparative height and depth of the sacral dimples.

Next, have the patient seat himself on the examining stool, thus immobilizing the pelvis. Have him rotate his body first to the right and then to the left. Then have him laterally bend first to the right and then to the left. Finally, have him flex and then extend the spine while you observe the integrity of the column during these movements.

A difference in the height of the scapula and the iliac crests usually indicates a scoliosis. Lateral positions of the spinous processes and anterior or posterior positions of the transverse processes together with an elevation of the angles of the ribs would indicate a rotation of vertebrae. Bear in mind the possibility of a spinous process being asymmetrical, deviated to the right or left, without the body of the vertebra being involved.

      Segment Deviation in Distortion Patterns

The part or segment always rotates or deviates into the distortion pattern with greater ease than out of the distortion pattern, For example:

l.   If the upper cervical segments indicate body rotation to the right, the head and neck rotate to the right with greater ease than to the left.

2.   If the atlas shows a left lateral shift, right lateral flexion of the head is more readily and completely realized than the same effort to the left.

3.   If there is a right (convexity to the right) cervicoscoliosis, the patient can laterally flex the head to the left much more readily than to the right.

4.   If the thoracic spine shows vertebral body rotation to the right, the patient in a forward bent position swings his torso into right rotation much more readily than to the left.

5.   If there is a right structural scoliotic deviation of the lumbar area, the patient sitting straddle on a bench to fix the pelvis will find it easier to rotate the torso to the right than to the left.

6.   If the right innominate is in posterior rotation subluxation, with the patient standing supporting himself with hands on the back of a chair, he carries his thigh forward, flexes his knee and carries it upward against his abdomen (and thus rotates the innominate further posteriorly) much more readily than extending the thigh backward and thus rotating the innominate anteriorly.

      Anatomical Short Leg

Evidence of an anatomic short leg or an anterior-inferior sacral subluxation, or both, also show that:

(a) in standing, a person seeking postural comfort will always support himself by standing on the short leg and on the side to which the sacrum has slipped anteriorly and inferiorly, (b) with the patient in the Adams' position, the pelvis slants anteriorly and inferiorly, and (c) using the double weight scales, the patient usually carries the most weight on the side of the short leg and anterior-inferior sacrum.

      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.

As far back as D.D. Palmer, digital examination of the spinal column has been conducted within the profession 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 spinal dysarthrias by the findings of variations in muscular tonus and local sensitivity.

Since pain from nerve roots or nerve 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.

      Dynamic Bony Palpation

Motion palpation and range of motion analyses are often utilized as standard examining procedures for spinal evaluation. These studies, however, along with static palpation, muscle strength, and postural studies either require a considerable degree of intuitive judgment or have not been adequately investigated to rule out possible interpretive ambiguities.

Motion palpation is described by Shepherd as starting with the atlanto-occipital joint: The head is moved in lateral flexion. The atlas is palpated moving downward and backward on the side opposite flexion. In rotation, the transverse is felt to move less than the mastoid on the side opposite rotation. In extension, the atlas projects forward; and in flexion, the atlas projects backward. In gliding the atlas anterior without flexion or extension, there is separation between the jaw and the transverse.

The axis is palpated in lateral flexion as moving opposite flexion. In flexion and extension, the spinous is felt to open and close on C3. The third cervical may be palpated in lateral flexion, flexion, and extension much like the axis, noting the separation and closure of the spinous. Rotation reveals minimum motion and is difficult to palpate. The same procedure is applied to the rest of the cervical spine.

Motion palpation in the thoracic spine must of necessity encompass the vertebral joints, the costovertebral joints, and the sternocostal joints. The vertebral joints are palpated in lateral flexion of the head; ie, it is demonstrated that lateral flexion of the head of approximately 30° will yield palpable motion in the lumbar spine. The costovertebral joints are palpated by placing the thumbs on the ribs and asking the patient to take a deep breath. If the rib rises, it is considered normal; if it remains down or down to some extent in relation to the opposite side, it is considered "locked". The sternocostal joints are palpated by placing thumbs on opposite ribs and asking the patient to take a deep breath. This may reveal one side rising markedly less than a normal opponent, indicative of a fixation.

The lumbar spine can be palpated in lateral flexion as are the cervicals and dorsals. Flexion and extension motion are difficult to feel and are useful only in classic retrolisthesis and anteriolisthesis.

The sacroiliac and the lumbosacral joints may be palpated in the standing position. The thumbs are placed on the PSISs and the patient is asked to raise the right leg, for example, up and down, bending the knee as if in taking a step. The right sacroiliac will be observed to go posterior and inferior. After about 20° of leg raise, the left sacroiliac spine also drops posterior and inferior. This is normal sacroiliac motion. Any other motion than the one described indicates a problem in this joint.

The sacrum is palpated by placing the thumbs on the PSISs and asking the patient to bend both knees and dip approximately 6 inches. The PSISs will be observed to spread if the sacrum is in normal articulation. The L4-L5 joint is palpated by observing lateral flexion with the thumbs in the same position. If the PSIS opposite flexion goes inferior, this is normal motion. Any other motion indicates a fixation of the L4-L5 joints.

      Muscle Palpation

With practice, it is possible to palpate the comparative tone of the spinal intrinsic muscles. The rotatores or deepest 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 very helpful indicators.

Muscle tone evaluation requires precise knowledge of anatomy and much practice 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.

Also located here will often be hyperesthesia or 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 muscle tone which feel softer to the touch than like areas. These areas are often found at or near the level of involvement.

      Muscle Weakness Associated with Spinal Subluxations

The following listing, adapted from the works of Goodheart, indicates the muscle weaknesses which are apparent when either subluxation or compensation occur at a specific level in the spine. This listing may prove useful in identifying the spinal segment causing the weakness, and these levels will often be close to the areas identified by other procedures. It should be noted that not all the muscles associated with a specific level will be of equal weakness, and the weakness observed will not improve until both the secondary compensation and the primary subluxation are cleared.

In the below listing, the spinal nerves are not necessarily the spinal nerves that innervate these muscles but are the findings of applied kinesiology.

Atlas	Supraspinatus
Axis	Anterior neck muscles
C7–T1	Levator scapulae
T2	Teres minor Subscapularis Upper trapezius Anterior neck muscles Teres major
T3	Teres minor Subscapularis Deltoids Anterior serratus Coracobrachialis Anterior deltoid Upper trapezius Anterior neck muscles Teres major
T4	Deltoids Anterior serratus Coracobrachialis Anterior deltoid
T5	Deltoids Anterior serratus Pectoralis major Rhomboids Anterior deltoids Popliteus
T6	Pectoralis major Pectoralis minor Rhomboids Popliteus
T7	Latissmus dorsi Triceps Trapezius
T8	Latissmus dorsi Triceps Trapezius Adductors Quadriceps
T9	Adductors Quadriceps
T10	Sartorius Quadriceps Gracilis Soleus Gastrocnemius
T11	Sartorius Quadriceps Gracilis Soleus Gastrocnemius Quadratus lumborum
T12	Quadratus lumborum Psoas Sartorius Gracilis Soleus Gastrocnemius
L1	Psoas
L2	Tensor fasciae latae Anterior tibial Sacrospinalis
L3	Tensor fasciae latae
L4	Tensor fasciae latae
L5	Abdominal muscles Gluteus medius Piriformis Peroneus Gluteus maximus Hamstrings
Sacrum	Piriformis Abdominals Peroneus Gluteus maximus Hamstrings.

      Percussion of the Spine

The percussion hammer is helpful during analysis. The hammer is held between the thumb and forefinger and used to percuss the spinous processes with a lancing blow: similar to a slow pendulous swing rather than a heavy-handed blow. The examiner feels the blow as well as hears a variance in the sounds produced from the individual spinous processes.

Normal sounds vary for different regions of the spine because of the heavy musculature associated with the lumbar area and the lungs anterior to the thoracic spine. Age (unossified cartilage in the young, osteoporosis in the elderly) and muscle wasting also have an effect upon percussion sound and vibration quality.

Spinal percussion should be elicited when the spine is flexed. When a subluxated vertebra is percussed, the patient may report pain and tenderness. Hyperemia may appear over the spinous process of a subluxated segment when percussed.

Lingering pain after percussion is suspicious of an underlying pathology. Pain that immediately disappears suggests the presence of a traumatic joint pathology because the percussive force jars the joint. A dull pain of a throbbing nature which slowly disappears is suggestive of a fracture, bone disease, or neoplasm, as it does in any other part of the skeleton.

      Skin Temperature Analysis

Instruments such as the nervoscope, thermoscribe, dermathermograph, etc., are often used in the field to elicit heat patterns along the vertebral column. It is theorized that when a subluxation exists, it will produce an infintesimal amount of heat over the involved nerve area which can be detected. It is usually conducted by using a double thermocouple galvanometer device that is glided up or down each side of the spinal column to register minute temperature differentials which allegedly are related in some manner to a spinal subluxation.

Hildebrandt recalls that this procedure at one time was a popular procedure to evaluate spinal subluxations. In recent years, however, it has lost considerable support for lack of an appropriate clinical hypothesis on which to base its interpretation. Nevertheless, as neurologically controlled vasoconstriction/vasodilation of subcutaneous blood vessels results in some degree of skin surface temperature differential, future research may offer a more justified basis for use.

      Spinography

Roentgenology of the spinal column, in whole or in part, in either a standing or sitting weight-bearing position to determine the possible existence and nature of spinal subluxations and distortions is a common clinical practice. When properly conducted and interpreted, much useful information can be obtained. However, many authorities within the profession feel that some interpretive procedures utilized need re-evaluation through controlled clinical studies in light of today's technological concepts.

A number of other roentgenological examination procedures are being investigated such as cineroentgenography and orthogonal (3-dimentional static x rays) roentgenography which may prove to offer meaningful procedural advancements.

      Orthopedic, Neurologic, and Other Clinical-Tests

Standard or modified orthopedic and neurologic testing procedures are commonly used in the field during the physical examination and spinal analysis to determine possible subluxation characteristics and effects and differentiate them from gross trauma or pathology.

In addition to these standard procedures, other procedures are being investigated such as electromyography, contourography, thermography, and applied kinesiology. Although the value of any one procedure is limited, the experienced examiner gains considerable insight into the status of the spinal column when a number of approaches are coordinated.


Postural Considerations

It has long been felt clinically that spinal subluxations will be reflected in the erect posture and that spinal distortions result in the development of subluxation syndromes. Consequently, an array of different methods and instrumentation have been developed for this type of analytical approach such as plumblines with foot positioning plates to allow for visual evaluation relative to gravitational norms, posturometer devices to measure specific degrees in attitude, multiple scale units to measure weight of each vertical half or quadrant of the body, and contourography. Such procedures yield useful information; however, as with other methods, there is a great deal of possible ambiguity in the interpretation of findings.

      General Points of Eye Dominance in Posture Analysis

It is important to realize that the examiner's peripheral vision is used for judging the body bilaterally and simultaneously. This is true in posture analysis as well as in the physical examination when, for instance, bilateral motion of the rib cage is assessed. If the examiner has a dominant eye, the reclining patient should be observed with the dominant eye over the midline of the patient's body.

An examiner may determine eye dominance by:

(1) holding the index finger of the right hand at arm's length directly in front of the nose at the level of the eyes,
(2) approximating the tips of the left index finger and thumb as if to form a circle,
(3) placing this circle directly in front of the nose about elbow distance away,
(4) sighting in the tip of the right index finger in the middle of the circle using both eyes,
(5) closing the left eye to see if the right index finger stays in the middle of the circle; if it does, the right eye is dominant, and
(6) closing the right eye and seeing if the right index finger stays in the middle of the circle; if it does, the left eye is dominant.

      Influence of Subluxations on Posture

Posture, as defined by Rich and Dukett, is a relationship of each body structure to the entire structure.

A few influences on spinal and pelvic posture are:

(1) gravity,
(2) environment; eg, occupation, weather,
(3) architecture of the vertebral column, upper and lower appendages, organs and tissues that attach to or are suspended from the spinal column,
(4) physiology, normal and abnormal,
(5) pathology,
(6) mental health, emotions, stress, etc, and
(7) pain.

Vertebrae move in the planes of their articulations. It is at the level of the posterior intervertebral articulations along with their facets that most subluxations occur and influence the IVF far more than any other articulations of the spinal column. Changes in the diameter of normal IVFs result in an abnormal joint formation which predisposes subluxation as well as to begin a direct factor in altering the AP curve of the particular region of the spine that this structural defect is found.

Another influence on the 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 vertebral column.

The articular variances of the articular process 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 sclerosis. This hardening process is usually followed by hypertrophy or overgrowth, often referred to as exostosis, and produces an appearance of an irregular articular surface when the facet is viewed in profile in roentgenology. Coexistent with this finding, the interarticular spaces gradually become narrowed, hazy, obscured, and even obliterated on film.

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 which seems a more reasonable descriptor because of the implications of the suffix "itis". Though there may not be evidence of direct bony encroachment from the process of arthrosis directly into the IVFs, one must consider that the process of arthrosis does produce a general narrowing of the diameters of the IVFs and hence produces an interference with the expression of nerve transmission.

The vertebral body deserves consideration because, even though we usually think of its function as forming the anterior boundary of the neural canal and a slight contribution to the boundry of the foramen, almost any change in its size, shape, or position will alter these boundries. 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 IVF. In some instances, it is difficult to separate the change of the vertebral bodies and the IVDs.

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 of the medullary substance which influences spinal posture include:

(1) loss of substance,
(2) collapse,
(3) comminuted fragmentation,
(4) scalloping of margins,
(5) wedging that may be triangular, quadrangular, or trapezoid in shape,
(6) biconcave deformity (cupping),
(7) serrated formations,
(8) irregular cartilagnious plates such as in osteochrondrosis or underdevelopment of the secondary ossification centers, (9) Schmorl's nodes, and
(10) osteophytes.

Changes in the vertebral body that do not appreciably alter the AP curve, neural canal, or foramina, but do denote limitation of movement or fixation, include marginal sclerosis or cartilage 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 same fashion as that which develops on the margin of the articular facet. These procsses of overgrowth may or may not produce encroachment of the neural 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.

The dynamic functions of the spine are dependent upon seven articulations:

(1) posterior intervertebral (synovial),
(2) vertebral bodies and IVDs (nonsynovial),
(3) costovertebral (synovial),
(4) joints of Luschka (synovial),
(5) sacroiliac (nonsynovial),
(6) symphysis pubis (nonsynovial), and
(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 absence of pain in the nonsynovial types of articulation. The other contributing factor of pain illicitation is found in the sensory nerves of the periosteum or perichondrium. May it be remembered that the posterior intervertebral articulation contains both synovial and perichondrium while the anterior vertebral articulation contains neither of these two connective tissues.


General Description of Various Types of Spinal Curvatures

Following are the generally accepted characteristics and significance of the various classified spinal distortions:

ALTERATION OF CURVES SECONDARY TO MUSCULAR IMBALANCE: Featured by scoliosis and/or alteration of the normal anterior-posterior curves wherein there is no apparent structural basis. This type of distortion is associated with muscular weakness or spasticity such as of the psoas in the lumbar spine or the sternocleidomastoidious in the cervical spine; postural imbalance and interference to normal locomotive effort; muscular soreness and fatigue; irritative microtrauma to all involved vertebral motor units; compensatory curvatures; and biomechanic impropriety transmitted throughout the entire spinal column.

ALTERATION OF CURVES SECONDARY TO STRUCTURAL ASYMMETRIES: Characterized by unleveling of spinal support due to anomaly, trauma, or pathology wherein structural unleveling of the spine above will tend to portray a normal compensatory response if the motor units are functional. This situation signifies general postural imcompetence and interference to the normal locomotive effort; muscular tension, soreness, and fatigue; irritative microtrauma to all the involved motor units; compensatory curvatures; and a biomechanical insult transmitted throughout the entire spinal column.

DECOMPENSATION OF ADAPTATIONAL CURVES: Featured by absence or reversal of compensatory curvatures that should be present because of structural unleveling and a tendency for the vertebral bodies to rotate in a direction opposite to that which would normally occur. This situation points toward acute muscular contractions, pain associated with movement, a frequently associated acute disc syndrome, strained effort in the erect posture with compensatory voluntary torsion of the spine above, radicular neurological involvements, and biomechanical impropriety transmitted throughout the entire spinal column.

ABNORMAL MOTION OF A SPINAL SECTION: Characterized by restriction of movement of two or more vertebral motor units wherein the regions above or below may exhibit excessive compensatory movement. This type of distortion is associated with muscular soreness, fatigue, and other muscle dysfunctions, possible ossification of the longitudinal ligaments, possible degenerative joint disease with concomittant ankylosis, microtrauma to all involved vertebral motor units, and biomechanical insult to all associated motor units.

1.   SUBLUXATION AS A PRIMARY FACTOR: A subluxation may exist as a primary and perpetuating cause of disease. Its initiation may be considered the most recent condition, or most important, and other qualifying complications may derive from it. Examples of diagnostic descriptions would be

(a) extension subluxation of L5 with facet syndrome and periarticular and paravertebral myofibrosis,
(b) right lateral flexion subluxation of T7 with upper thoracic scoliosis and a right scapulocostal syndrome,
(c) right rotational subluxation of C6 with hypomobility, hypermobile subluxation of C5, and attendant paravertebral muscular spasms,
(d) extension subluxation of C1 with suboccipital myofibrositis and attendant radiculitis of the C2 nerve,
(e) right lateral flexion subluxation of L5 with attendant lumbar scoliosis, spondylosis, and extension sciatic neuralgia.

2.   SUBLUXATION COMPLICATING SPRAIN OR STRAIN: A subluxation may arise from and complicate a recent sprain or strain injury. Its involvement may be explained as in

(a) cervical sprain with concomitant paravertebral myofascitis and consequent flexion subluxation of C5 and attendant radiculitis,
(b) thoracocostal strain with consequent left rotational subluxation of T6 and attendant intercostal muscle spasm and extension neuralgia,
(c) right gluteal strain with consequent hypomobile subluxation of the sacroiliac articulation,
(d) lumbosacral sprain with consequent flexion subluxation of L5 and attendant periarticular capsulitis and radiculitis of L5.

3.   SUBLUXATION COMPLICATING STRUCTURAL FAULTS: A subluxation may arise and complicate structural asymmetrics, developmental anomalies, or other chronic musculoskeletal lesions. Descriptive examples are

(a) right scoliosis sectional subluxation of the lumbar spine with predisposing right leg deficiency, attendant lumbar paravertebral myofibrositis, and reflex sciatic neuralgia,
(b) extension subluxation of L4 with consequent facet syndrome and predisposing spondylolisthesis of L5 with separation of the pars interarticularis,
(c) extension subluxation of C1 and suboccipital neuralgia with underlying sectional lordosis of the cervical spine and kyphosis of the thoracic spine with predisposing spondylosis,
(d) chronic strain and myofibrositis of the cervical paravertebral muscles with predisposing left lateral flexion subluxation of T2 and consequent cervical scoliosis,
(e) lumbar spondylosis and degenerative joint disease with predisposing right rotational subluxation of L5 and attendant developmental tropism.

4.   SUBLUXATION WITH RELATING VISCERAL COMPLICATIONS: Since the internal visceral complications, as ramifications of a subluxation syndrome, are difficult to always prove, this aspect of the patient's condition must be qualified. If the examinations show that the internal signs and symptoms are a direct consequence of the subluxation, this condition should be mentioned in the diagnosis. If they exist, but are not related, they should be mentioned as associated findings. However, under present Medicare regulations, it should be made clear in written reports that it is the subluxation syndrome that is being treated and that other disease conditions are being given whatever the condition requires according to clinical judgment or have been referred.


5.   MULTIPLE DIAGNOSTIC ENTITIES: When more than one specific and unrelated diagnostic entity is present, each should be separated and identified by numbering.