Posttraumatic Subluxation-Fixation Implications
Etiology, Effects, and Common Coincidental Factors
Posttraumatic Subluxation-Fixation Implications
Etiology, Effects, and Common Coincidental Factors
Clinical Monograph 5
By R. C. Schafer, DC, PhD, FICC
The kinetic aspects of spinal biomechanics are an important consideration in traumatology since the totality of function is essentially the sum of its individual components. However, although reminders are frequently given, the multitude of causes and effects of an articular subluxation complex (spinal or extraspinal) will not be detailed here that is primarily directed to chiropractic clinicians and advanced students who are well acquainted with standard hypotheses. For a detailed description, the reader is referred to:
Basic Principles of Chiropractic:
The Neuroscience Foundation of Clinical Practice
Arlington, Virginia, American Chiropractic Association, 1990.
The biomechanical efficiency of any one of the 25 vertebral motor units, from atlas to sacrum, can be described as that condition (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. The degree of fixed derangement (subluxation-fixation) of a bony segment within its articular bed and normal range of motion may be an effect in the range of microtrauma to macroscopic damage. Regardless, it is always attended by some degree of mobility dysfunction; neurologic insult; and overstress of the muscles, tendons, and ligaments involved and their respective mechanoreceptors.
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Once produced, the lesion becomes a focus of sustained pathologic irritation in which a barrage of impulses streams into the spinal cord where internuncial neurons receive and relay them to motor pathways. The contraction that provoked the subluxation initially is thereby reinforced, thus perpetuating both the subluxation and the pathologic process engendered. Sensory reflex phenomena can also be involved, and they frequently are. The nerve impulse creates a multitude of cellular reactions and responses besides those of even the most intricate, subtle, and variable sensations and motor activities. Once this is appreciated, we must add the complexities of trophic effects, neuroendocrine interrelations, biochemical affinities, proprioceptive buildup, summation increments, facilitation patterns, the input of the ascending and descending reticular activating mechanisms, genetic neurologic diatheses, synaptic overlaps, demoralization and disintegration of synaptic thresholds, the neurologic spread and buildup, reflex instability, predisposition to sensorial aberrations, undue cerebrovisceral or viscerocerebral interactions, psychosomatic overtones, and those many phenomena that science is only beginning to understand or are beyond our present understanding. This underscores that the quality and sometimes quantity of nerve function relates directly or indirectly to practically every bodily function and contributes significantly to the beginning of physiologic dysfunction and the development of pathologic processes.
Inequality in muscle balance leading to a subluxation complex may be initiated by trauma, postural distortion phenomena, biochemical reactions, psychomotor responses, paralytic effects, somatic and visceral reflexes.
Trauma. Frank trauma may cause inflammation, degeneration, etc, and particularly the muscular splinting reaction that muscles make when their surrounding tissues are injured or overstressed. This alters the position and motion of the structural tissues involved. Sustained microtrauma, though of a less acute nature, may produce a slow continual irritation and eventually create degenerative pathologic changes that similarly alter muscular reaction. The obvious trauma of a fall or blow that surprises a joint with the intrinsic muscles unprepared will cause a sprain with all its normal effects. A sudden slip during a lift is equally damaging to an unprepared or weak joint.
Indirect Stress. Depending on the degree of stress produced, any internal or external overstress factor involves the nervous system directly or indirectly, resulting in decreased mobility of the vertebra of the involved neuromere. This decreased mobility may be the result of
- muscle splinting, especially on the side of greatest stimulation according to Fluger’s Law or
- from abnormal weight distribution to the superior facets and other structures of the vertebrae involved.
Fluger’s Law states that if a stimulus received by a sensory nerve extends to a motor nerve of the opposite side, contraction occurs only from corresponding muscles; and, if contraction is unequal bilaterally, the stronger contraction always occurs on the side stimulated. When involving one or more vertebrae, this state of decreased mobility of the motor unit encourages neurodysfunction leading to pathologic processes in the areas supplied by the affected nerve root or neuromere, depending on the degree and chronicity of involvement.
Psychomotor Responses. These responses refer to the reaction of musculature to emotional effects on the nervous system as the body depicts a state of psychologic stress. They may be environmentally, socially, or intrinsically initiated. Psychosomatic, psychovisceral, somatopsychic, or visceropsychic reflexes may be involved singularly or in combination.
The phrase “ligament sprain” is redundant. A sprain is joint injury in which the ligaments or capsule are partially torn or severely stretched without dislocation being fixed; ie, there may have been a partial dislocation that spontaneously reduced itself. O’Donoghue defines a sprain as any overstress ligament injury that produces some degree of damage to ligament fibers or their attachment. If an attachment is involved, the status may be called a sprain-fracture for some degree of periosteal avulsion has occurred.
The extent of damage depends on the amount, direction, and duration of the force and the strength of the tissues involved. Keep in mind that joint ligaments are designed as reinforcing straps that permit normal ranges of motion but restrict abnormal motion. Thus, a sprain cannot exist without some degree of instability, pain, swelling, or limitation of movement. The patient may recall hearing a pop or snap during a severe sprain.
Sprains are classed by severity as acute, subacute, or chronic, or by the area of involvement such as cervical, thoracic, thoracocervical, brachiocervical, thoracocostal, thoracolumbar, lumbar, lumbosacral, sacroiliac, iliofemoral, knee, ankle, shoulder, elbow, wrist, etc. Although the terms subacute and chronic may refer to diagnostic entities, they are confusing. An explanation of the specific subacute or chronic joint instability is more descriptive and desirable. Grading according to the extent to which the integrity of the involved ligaments have been compromised is favored by Garrick/Webb and many other authorities.
In differentiating sprain and strain, the examiner must keep in mind that sprain involves the ligaments and capsule of a joint and strain involves muscles and tendons. However, any tissue may be strained in injury if the word “strain” is being used as a verb. When used as a noun or state of being, sprain refers solely to ligament and/or capsule injury and strain solely to muscle or tendon injury. Sprain usually elicits pain on movement of the affecte joint even without muscular effort. In contrast, strain produces pain on muscle effort even without joint movement (eg, in resisted contraction).
Periarticular and intraarticular ligaments can normally be stretched by passive movements of the related joint to the limit of their range of motion without inducing pain. Irritated or hardened ligaments become painful by stretching and deep pressure. When palpable, an irritated ligament will be tender; and if it can be squeezed, pain will be evoked.
Ligaments are generally much stronger than necessary to resist normal forces. If overstress is chronic or occurs at an unguarded moment, the ligaments are so overstretched to allow the articulating bones to slide (subluxate) out of their normal positions for a given motion.
Ligaments play a much greater part in supporting loads than are generally thought. Electromyographic studies involving fatigue from forces acting across a joint prove that muscles play only a secondary role. Such fatigue is basically a form of pain originating in the ligaments rather than muscle. Thus, some researchers feel that if the muscles involved in a problem are weak to begin with, there is a more immediate ligament action that produces the characteristic fatigue syndrome.
Chronic ligament pain usually develops when a joint is under strong prolonged tension, and a hypomobile joint should be the first suspicion in such cases. Generally, chronic pain arising from ligaments comes on slowly after assuming some posture in which the involved joint(s) is held at a limit of motion. The ache arises from the stimulation of ligament, capsule, and periosteal mechanoreceptors.
In chronic conditions, the stretching of fibrous bands under continuous overtension is due partly to fiber elongation. However, most of the stretch is a product of proliferative fibroblastic activity where more collagenous tissue is produced to increase the length of the structure. This phenomenon is often seen in subluxations of postural or occupational origin where unilateral stress results in stretching of some tissues and laxity of other supporting and check ligaments. It is for this reason, among others, that chronic subluxations are often difficult to hold in normal alignment. The site must be periodically aligned and supported until ligament laxity is corrected.
When ligaments are subjected to continuous stress, they becomes chronically inflamed and invaded by collagen substance and mineral salts. This results in sclerosis and varying degrees of calcification. In addition, when ligaments and capsules are subjected to acute traumatic overstress, they may be rupture of some of the comprising fasciculi with attended minute hemorrhages. If the involved ligaments possessed elastic fibers, there will be a definite shortening as an after-effect.
Just as unnecessary bone is resorbed, a ligament will not retain an unnecessary lengthened state. This process is demonstrated in acquired flatfoot where weight is constantly applied on the medial aspect of the foot leading to stretching of supporting ligaments and a flattening of the arch.
Acute Sprain Added to Chronic Sprain
An examiner must keep in mind that when connective tissue is subjected to continuous pull, it becomes chronically inflamed and invaded by collagen substance and mineral salts. This results in sclerosis and varying degrees of calcification. In addition, when these altered tissues are subjected to acute traumatic stress, some of the constituent fasciculi rupture. This is attended by an array of minute hemorrhages. Further attempts at repair result in collagen tissue deposition and mineral invasion that also produce sclerosis and calcification. If the involved ligament possessed elastic fibers, there will be a definite shortening. This knowledge is at the core of all rational rehabilitation programs involving sprain.
Classes of Acute Sprain
Sprains can be classed by severity, stage, or the area of involvement. In differentiating sprain and strain, textbooks frequently remind the examiner to keep in mind that sprain involves the ligaments of a joint and strain involves the muscular and tendinous structures. Sprain usually elicits pain on passive movement of the affected joint when the joint’s muscles are relaxed; strain elicits pain on active motion even without joint motion (eg, resisted movement). However, this author has rarely found the need to differentiate joint strain from sprain in posttraumatic joint injury because they inevitably coincide in variable degrees and their management, with exceptions to be explained, is generally the same. Thus, the term sprain/strain will be frequently used in this manual.
First-Degree Sprain. In a mild sprain, there is a small amount of internal bleeding in a localized area of the affected ligaments with only a few fibers separated. No actual loss of function or reduced strength is found. The involved ligaments generally require no protection and are not weakened. Mild sprain is characterized by tenderness on palpation that is not marked at the bony insertion by swelling or other features of overt inflammation. Joint instability is negligible.
Second-Degree Sprain. This is a moderate sprain with a partial tear, characterized by increased severity of first-degree symptoms. A tendency to recurrence is a complication, as is the potentiality of traumatic arthritis and permanent instability if improperly treated. A moderate sprain results from severe tearing of many fibers with at least half remaining undamaged. This type of sprain shows some loss of function in the injured area even if the torn ligaments are not widely separated. These fibers rejoin during the natural healing process unless the damage is great or treatment is inadequate. If damage is great, considerable scar tissue may form, and a permanent weakness of this section of the ligament may result is appropriate actions are not taken. Moderate sprain is characterized by a greater degree of symptoms than exhibited in a mild sprain, lack of normal ligamentous resistance on digital pressure, and increased joint movement on tension from movement or manipulation.
Third-Degree Sprain. This is a severe sprain with complete ligament tears, characterized by severe swelling, hemorrhage, tenderness, complete loss of function, abnormal motion, and possible deformity. When a sprain is classed 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 has a greater degree of symptoms than presented by a moderate sprain plus marked excessive joint motion indicating definite separation on tension or motion. Severe pain may or may not be present. Abnormal motion may be exhibited with series of bilateral stress radiographs or cineroentgenography. Persistent instability and traumatic arthritis are common complications. If seen soon after injury before swelling occurs, a palpable gap may be felt at the site of tear. Surgical joining is usually necessary, but this should not be the basis for dismissal. Postsurgical chiropractic rehabilitative procedures are far more beneficial long-term than those provided by most orthopedic surgeons.
Garrick/Webb believe that rigid immobilization for a sprain much beyond 48 hours is counterproductive because of the invitation for disuse atrophy, taut capsule, and adhesion formation. A torn ligament is no stronger after immobilization than before and assisting joint muscle stabilizers have weakened proportionately. Sprains producing complete rupture requiring surgical repair may be an exception to this 48-hour rule, but the nefarious effects of immobilization remain.
Ligaments are stabilizers, not motor elements. Muscle-tendon units are motor units. While the term sprain is limited to ligament and capsule injury, strain is confined to injuries of the muscle-tendon unit. The phrase “muscle strain” is redundant.
Injuries to muscles and tendons are difficult to differentiate and need not be from a clinical standpoint. Rarely will surgery reveal a tendon injury with completely uninvolved muscle fibers, or vice versa. Another misconception is that strains are always the result of overstretching a muscle. More common, report Garrick/Webb, the injury occurs because tension within the musculotendinous unit is actively increased abruptly. This intensified tension may be the result of a sharp antagonistic contraction where the agonist tears before it can lengthen. A third misunderstanding is that a weak muscle is taut not flaccid. A very weak muscle fatigues easily, and a muscle forced beyond its capacity in strength or endurance will tighten defensively. Taut braiding spinal erectors are classic examples of this. They will not be found in the well-conditioned athlete.
Tendon attachments are contiguous with periosteum, with some fibers entering the bony cortex. Tendons have great intrinsic strength capable of withstanding the action of strong muscle contraction yet are often incapable of withstanding a sudden unexpected stretching force (eg, misstep). For protection, the Golgi tendon-stretch receptors (when healthy) signal a safety collapse reflex on excessive muscle contraction. This tends to ounterbalance the stretch receptors in muscle that excite contraction on stretching.
Lymph vessels are not found in voluntary muscle. The degree of vascularity in the capillary network between skeletal muscle fibers and associated tissues depends greatly on physical conditioning. The quantity of interstitial fat, most marked in atrophied muscle, is also determined by the muscle’s degree of conditioning (eg, physical training).
A muscle in traumatic or reflex spasm becomes somewhat inflamed. Some transudation precipitation of fibrin, collagen, and mineral salt deposition may result and, if extended, produce chronic myositis and myofibrosis. Myofascial planes (especially of erectors) also may become inflamed at points of overstress. Myofascial transudation and fibrin formation commonly result in potentially disabling myofascial adhesions if not properly treated.
Pain from a damaged tendon usually arises when attached muscle fibers contract. Torn tendon fibers will usually not cause pain when the muscle is relaxed but will with the least muscle shortening. The pain of tendinitis is uperficial, essentially resulting from associated tenosynovitis. t can be evoked by passively rolling the tendon back and forth within its sheath.
Tendon sheaths (synovium) are lined with specialized connective tissue cells similar to those lining bursae and the synovial membrane of joints. Thus, inflammatory reactions within tendon sheaths to traumatic influences (strains) are akin to those seen in bursae and joint-cavity disorders. The term tenosynovitis generally includes all inflammatory disorders involving tendons and their enveloping sheaths. The cause may be either trauma (direct blow, overuse) or infection (sterile or unsterile).
Etiology. Tenosynovitis is usually acute, relieved by rest, but may become chronic and resemble rheumatoid arthritis. The normally avascular synovium reacts with an increased blood volume, inflammatory cells invade, synovial fluid is oversecreted with an increased fibrin content. This results in the formation of “sticky” adhesions between tendons and adjacent tissue. These adhesions produce palpable “snowball crepitation” as the tendon moves within its sheath. Chronic inflammation of the sheath always holds the danger of stenosis, especially at sites where tendons cross (eg, De Quervain’s disease, snap finger).
Types. Traumatic tenosynovitis (peritendinitis crepitans) has two types. The common form is due to repeated overuse of a musculotendinous unit to a point of fatigue where the tissues cannot functionally adapt. Vigorous exercise in a habitually sedentary weekend athlete is an example of overactivity that may bring on characteristic symptoms. Within a few hours after a hard session of unaccustomed effort, the involved tendon sheath becomes edematous.
Pathology. Adjacent muscle fibers show degenerative changes, lose glycogen content, and accumulate lactic acid, which spreads over the tendon. This acidity causes the edematous swelling. Pathologic changes are particularly evident at the musculotendinous junction and in the peritendinous areolar tissue. Thrombosis of the venules occurs, and fibrin is thrown out into the aveolar tissue and between muscle fibers. A sticky fibrinous exudate is thus produced that may be accompanied by a serous effusion within the tendon sheath. It is proper treatment especially at this stage of injury that is so important toward ideal rehabilitation.
Clinical Features. Symptoms peak in 24-28 hours after injury. There is a gradual onset of pain radiating along the involved tendon on active contraction or passive stretching. There is a soft, warm, frequently red, localized swelling at the musculotendinous junction that usually renders an audible silky or leathery crepitus whenever the tendon is moved.
A less frequently seen form of tenosynovitis is an acute hemorrhagic type resulting from direct contusion or a puncture wound that does not introduce infection. A bloody and serous sterile fluid forms within the tendon sheath. In the hemorrhagic type, the pain is dull and aching, a feeling of fullness is perceived at the site of the affected tendon sheath, and crepitation is not usually prominent.
The differentiation of joint swelling between hemarthrosis and synovitis is an important part of any joint examination following trauma. This is important because joint aspiration is usually contraindicated in simple synovitis but early aspiration is almost mandatory in hemarthrosis. Blood within a joint is an irritant, easily becomes a site of infection, and may resolve into iron deposits, fibroblastic proliferation, and severely restricting adhesions. Synovial fluid is normal within a joint, and excessive amounts will be readily absorbed with rest and applications of elevation, cold, and pressure unless the cause of the swelling remains (eg, repeated trauma).
Inflammation of areolar tissue around a tendon (peritendinitis) is a common result of sudden increases in physical work or training. It features swelling, pain which is relieved by activity, tenderness, and palpable crepitus.
Fascial hernias develop from contusions or small puncture wounds producing a weakness in the fascial sheath that envelops all muscles. They may also develop in weakened aponeuroses in patients with chronic compartment syndromes because of the increased pressure. Such hernias are sometimes found after injury where a muscle’s nerves emerge from its fascia. Palpation then reveals a tumor-like mass when the muscle is relaxed, which may disappear when the muscle is activated. This is the opposite finding of a hidden lipoma.
Etiology. Muscle action not balanced by reciprocal inhibition of the antagonistic muscle (eg, a blow, an unexpected force) may result in its rupture through its sheath by violent sudden contraction or a less common injury to its antagonist by overstretching. Muscles previously weakened by fatigue or disease are more apt to rupture. While complete muscle rupture is rare, a split in a muscle sheath due to weakness or a break may allow some muscle tissue to herniate during contraction. This may follow injury or be a postsurgical complication. The sheath opening may be large or small.
Muscle ruptures associated with nonpenetrating 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. In the elderly, muscle rupture can occur under minimal loads as a result of degeneration within the muscle’s tendon.
Clinical Features. A soft mass is noted at the site of the opening during palpation. As with fascial hernia, it disappears when the muscle is contracted and reappears on relaxation. Weakness may be a complaint. In true cases, permanent correction can only be made by surgery. The syndrome is characterized by knife-like pain, followed by a sensation of extreme local weakness. If a complete tear occurs, the lesion is usually at the tendon’s attachment to the muscle belly. Normal continuity is broken and obvious on palpation unless obliterated by hemorrhage and swelling. Function is lost in proportion to the degree of tear. Direct evidence is gained by testing function with gravity eliminated.
The asymptomatic ripple-pattern (ladder muscle) seen in some athletes on passive stretch is not of traumatic origin but believed to be an effect of banding of overlying fascia. Rupture in youth features painful voluntary contraction, ecchymosis at an area of local tenderness, swelling, edema, and hemorrhage. Palpation often reveals the defect. After the acute stage, persistent weakness remains and there is an increase in muscle bulk proximal to the rupture site on contraction. In the elderly, muscle ruptures feature considerably less pain, swelling, tenderness, and ecchymosis; however, they do present with late persistent weakness and increased bulk on contraction.
Tendon rupture is rare in people under the age of 40 years. Both complete and partial ruptures are most often seen of the Achilles tendon of middle-aged athletes. The cause is usually traced to overuse, direct violence during stretch, or a poorly placed injection. Its site is usually found just proximal from the point of insertion into bone. The rare event of spontaneous tendon rupture occurs only when the tendon is weakened by advanced degenerative processes.
Rupture at the Musculotendinous Junction. This injury features a sudden stabbing pain followed by swelling and sometimes hematoma. Pain is increased when the affected muscle contracts. A gap may be noted when swelling subsides that gives a clue to the extent of muscle tear. Surgical correction is not usually necessary unless the separation is severe, but alert rehabilitation measures is always necessary to restore full function.
Rupture Near Insertion into Bone. Tendon rupture near its bony insertion features sharp pain often accompanied by perception of an abrupt dull snap at the site. The sharp pain soon subsides, but joint weakness does not. Partial rupture is characterized by acute pain during activity that persists until stress can be avoided. When activity is resumed, severe pain returns. A tender swelling is inevitably noted on palpation.
Classification of Acute Strain
Strains, as sprains, are classed by either severity or area. When classified by area, names of specific muscles are used such as gluteal, intercostal, abdominal, and perivertebral strain. 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, or right thoracocostal strain of T6-T11. When classified by severity as well, the terms first degree (mild), second degree (moderate), and third degree (severe) are generally applied according to the following descriptions.
First-Degree Strain. This is a mild muscle overstress causing trauma to a part of the musculoskeletal unit from forceful stretch resulting in a low-grade inflammation and some muscle- and/or tendon-fiber disruption. Hemorrhage and disability are mild. The injury is characterized by local pain aggravated by movement or muscle tension. Physical signs include local tenderness, swelling, mild spasm, ecchymosis, and minor strength and function loss. The common complications in recurring strain are tendinitis and periostitis at the site of attachment.
Second-Degree Strain. This is a moderately overstressed muscle caused by trauma to the musculoskeletal unit from excessive stretch or violent contraction resulting in torn fibers without complete disruption. It is characterized by increased first-degree-strain symptoms. There are moderate hemorrhage and swelling. Muscle spasm and function loss, especially, are greater. Complications are similar to those seen in first-degree train.
Third-Degree Strain. This is a severely strained muscle. The trauma results in a ruptured muscle or torn tendon that may be represented as a muscle-muscle, muscle-tendon, or tendon-bone separation. A palpable defect is usually felt at the site. The injury is characterized by severe pain, tenderness, swelling, spasm, disability, ecchymosis, hematoma, and muscle function loss. Prolonged disability is the major complication. After the acute stage, x-ray films exhibit soft tissue swelling and an avulsion fracture at the tendon’s attachment to periosteum. Surgical joining is usually necessary, and postoperative chiropractic rehabilitation measures are recommended.
The tendons of the rotator cuff and the origin of the elbow extensors are common sites of calcium deposits. Deposition is usually abrupt and associated with a subdued inflammation of the joint capsule and its lining. Major characteristics are pain and muscle spasm limiting movement. Relief may occur suddenly as a deposit is spontaneously ruptured into a bursa or joint cavity. Occasionally, deposition is a slow asymptomatic manifestation of tendon degeneration.
Due to chronic overstress at points of tendon insertion, fatigue fractures may appear in the cortex of the bone, causing the area to be invaded by bone cells. In late stages, compact bone may be found on roentgenography to extend well over an inch into the tendon and very frequently mistaken for a bone spur. Such extensions are subject to fracture; but unless exposed to direct trauma or undue intrinsic overstress, they are usually asymptomatic.
Traumatic Myositis Ossificans
Myositis ossificans is heterotopic bone formation occurring after contusion and hematoma near bone in collagenous supportive tissues such as skeletal muscles, ligaments, tendons, and fascia. It is commonly the effect of direct muscle bruising, especially repeated contusions (as seen in contact sports and certain occupations), on the anterior aspects of thighs and arms. True myositis need not be part of its cause. Ossification of infiltrated blood along the muscle origin on bone is all that is necessary.
Background. Connective tissue surrounding muscle rapidly invades a traumatized area, and this tissue retains its embryonal ability to be transformed into more differentiated tissue. Following primary interstitial myositis, there is a transformation of the connective tissue into bone. A fluffy calcification shows on roentgenography in 2-4 weeks after injury. The calcification matures in 3 months; and in 5 months, ossification appears. The lesion is characterized by an indurated, tender, indistinct mass of a single muscle group that exhibits local heat. It is common in teenagers and young adult males, and occurs 80% of the time in the biceps brachialis after dislocations. It is also frequently seen in the thigh (quadriceps). Periosteal tears undoubtedly encourage ossification.
Management. Early cold, rest, and compression to the injured muscle help to reduce potential ossification. Immobilization is usually required for about 2 weeks after injury, followed by progressive active range-of-motion exercises. Exercise should not begin early as it provokes extension of the calcareous deposits. Heat is helpful in the later stages. Extremely large and painful lesions may require surgery after ossification is mature and when the site is near a joint and disturbing function. Protection of the part is the best preventive measure.
Absorption is inhibited after injury if bleeding is excessive or if a hematoma forms within lax tissues. When the clot retracts, a serum-filled cavity (presenting a fluctuant swelling) remains that is lined with organizing fibrin deposits. Referral for aspiration is seldom successful; surgical drainage is indicated. Progressive exercises may begin gently even when the pressure bandage is still applied because an inserted drain is rarely necessary.
Localized cystic swelling is sometimes applied is the result of mucinous degeneration of connective tissue occurring near a tendon sheath or joint capsule. The cause is unclear, but trauma or degeneration is thought to be a factor. A defect in the fibrous sheath of a joint or tendon permitting a segment of underlying synovium to herniate should always be a suspicion. The initial irritation accompanying the herniation stimulates further fluid accumulation so that the sac or encapsulation enlarges, sometimes to a large degree. In the late stages, the synovial hernia firms and sometimes hardens. Early transillumination and palpation will reveal a translucent fluctuant mass.
Findings. One large cyst may be felt, or several small cysts may coalesce to form a multilocular lesion. Its walls are composed of dense fibrous tissue. Bundles of nerve fibers are often seen microscopically in the areas of mucinous degeneration. Ganglions are usually obvious when on the dorsum of the wrist or foot. They give rise to a localized swelling, gradual or sudden in onset, that may vary in size from time to time. Associated weakness and mild neuralgia may be reported, but most complaints will be of a cosmetic nature. When connected to a tendon sheath, the ganglion becomes prominent when the tendon is stretched.
Management. Small ganglia can be therapeutically ruptured by pressure or a sudden blow, but they frequently recur. After disruption of the gelatinous material into the tissues, the area should be firmly compressed for a few days. The classic practice of smashing a ganglion with Gray’s Anatomy, however, is not successful if the ganglion is attached to a joint capsule. Aspiration followed by corticotherapy is often recommended by allopaths. Surgical incision may be necessary and is a far more appropriate solution.
The osteocytes forming 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.
Many fracture and dislocation complications such as nerve and vessel injury occur not from the trauma itself but from poor first aid that does not provide adequate splinting before movement. Traumatic bone injury rarely occurs without significant soft-tissue damage. Physical examination must be gentle but thorough because deep soft-tissue trauma is poorly visible on radiographs until many days after injury.
Healthy bone has an excellent blood supply with some exceptions in the metaphyseal area; but tendons, ligaments, discs, and cartilage are poorly vascularized. Yet, both bone and joints challenge the host’s reparative and defensive mechanisms. The pressure of pus under hard bone blocks circulation, and emboli, thrombosis, and vasospasm can cause additional devascularization. When circulation is deficient, local phagocytic function and nutrition go begging. Healing is therefore inhibited.
When subjected to prolonged weight-bearing or traumatic overstress, bone demineralizes and undergoes degenerative changes, resulting in deformity of the articulating surfaces. Concurrently, the attending excoriation of the periosteal articular margins results in proliferative changes such as lipping, spur formations. or eburnation. These facts must be balanced with the fact that diminished physical activity encourages osteoporosis and, conversely, exercise encourages the development of healthy bone structure. Common radiologic patterns of bone destruction are shown in Table 1.
Table 1. Common Radiologic Patterns of Bone Destruction
|Type of Destruction||Major Features||Examples|
|Moth-eaten||Multiple, coalescing holes, moderate size, similar to an aggressive process.||Osteomyelitis|
|Permeative||Multiple, small holes that tend to become smaller and fewer near the periphery of the from normal to abnormal bone.||Unlocalized infection|
|Geographic||Single or multiple, sharply marginated, relatively large, punched-out holes.||Multiple myeloma|
When considering bone-originating pain, recall whether the structure involved is compact or cancellous and whether or not any increased pressure is involved. Compact bone is relatively insensitive to painful stimuli. Most of the pain sensitive fibers within the medullary portion of bone are those few located within vascular walls. The periosteum, however, is richly supplied with nociceptors. Radiologic reaction types of periosteal disorders are shown in Table 2.
Table 2. Radiologic Reaction Types of Periosteal Disorders
|Reaction Type Interrupted||Examples|
|Lamellated (onion skin)||Infection, Ewing’s sarcoma, osteosarcoma|
|Perpendicular (spiculated or sunburst||Infection, Ewing’s sarcoma,osteosarcoma|
|Codman’s triangle||Infection, hemorrhage, malignancy|
|Solid Reaction Type||Examples|
|Cloaking||Chronic infection or advanced malignancy|
|Dense undulating||Vascular disorders|
|Dense and elliptical with destruction||Osteoid osteoma|
|Thin||Osteoid osteoma, eosinophilic granuloma|
|Thin and undulating||Hypertrophic pulmonary osteoarthropathy|
Simple contusions involving subcutaneous tissues overlying periosteum are called “bone bruises” and frequently occur at or near a joint. Because periosteum is richly endowed with nerves and innervated vessels, severe bruises and fatigue fractures are quite painful despite the lack of roentgenographic evidence. Bone tenderness remains long after soft-tissue tenderness has eased when periosteum is affected -sometimes for several months. Wherever the site, the patient is disabled or considerably hampered as long as tenderness and pain exist.
Bone Inflammation and Infection
The early symptoms and signs of acute bone or joint infection are periarticular pain and tenderness. The patient has extreme difficulty or refuses to move the joint. The cardinal signs of infection (heat, redness, swelling) may appear much later than pain and tenderness, and sometimes they never appear. Radiographs are of little help in arriving at an early diagnosis. When radiographic evidence is obvious, the disease is chronic. Sometimes comparative bilateral films exhibit slight soft-tissue-shadow evidence.
Orthopedists generally favor immobilizing an infected area, but many disagree about casting or splinting. Casting is usually used when bone damage is significant and to prevent a pathologic fracture. Mild continuous traction is used to allow some joint mobility without further damage to articular cartilage.
Periostitis. Periostitis is usually associated with joint injury, especially that of the knee and elbow. It results from violent muscle strain that damages periosteum. If severe enough to detach the periosteum, a degree of hematoma develops. The bruised joint is swollen, extremely tender, and movements are restricted. Physical examination may spur suspicions of fracture, but early roentgenographic findings are negative. Later, ossification of the hematoma is shown by induration of the swelling and new bone formation. If severe hematoma is associated, aspiration may be necessary. In milder cases, firm support and physical therapy are appropriate. Periostitis is slow to heal and usually requires at least several months restriction from forceful activity or contact sports.
Osteomyelitis. With the exception of infested compound fractures, repeated injuries, surgery, and piercing wounds, the incidence of osteomyelitis is low. When diagnosed, antibiotics are invariably required for control. Staphylococcus aureus is the common agent in all ages, and over 50% of the strains are penicillin resistant. Blacks are prone to develop a subacute form of osteomyelitis, especially if there is an indication of sickle cell anemia. The time between initial infection and circulatory troubles is often rather short. If effective treatment is delayed and partial circulatory embarrassment is allowed for more than just 72 hours after the infection begins, surgery may be the only alternative and loss of joint function may be the result.
Intra-articular fractures are not uncommon. They involve articular surfaces and associated cartilage. Osteoarthrosis results if reduction is not accurate. However, a displaced fragment need not be removed if it does not interfere with function. Dislocations with complicating fractures often involve joint impaction and fragmentation. They usually present great instability and require operative repair.
Clinical Features. A working diagnosis of fracture may be based on any combination of signs and symptoms. Additional assistance in diagnosis may be obtained from the history and confirmed by roentgenography. For instance, a history of falling, receiving a blow, or having felt or heard a bone snap may help in the discovery of more evidence such as:
Swelling and discoloration at the site of injury that increase with time may indicate fracture. With fracture, the swelling is due to the accumulation of tissue fluid and blood. When blood collects near the surface of the skin, a bluish discoloration may be seen. Protrusion of a bone segment, unnatural depression, or abnormal flexion may also indicate fracture.
Tenderness or pain on slight pressure on the injured part may indicate a fracture. Deep, sharp pain on an attempt to move the involved bone is presumptive evidence of fracture. Grating of bone ends against each other during movement indicates fracture. Movement, however, should rarely be attempted to see if crepitation is present as it causes further damage to the surrounding tissues and promotes shock.
Some diagnostic pitfalls in orthopedics are pointed out by Iversen/Clawson. They include:
- considering accessory ossicles as fractures;
- overlooking an osteochondral, a tibial-spine, or a stress fracture;
- forgetting that an upper-tibial fracture might progress into valgus;
- failing to realize the instability of an apparently undisplaced lateral condyle fracture of the humerus; and
- not appreciating the frequency of distal forearm fractures that slip.
The Repair Process. Although bone is noted for its hardness and supportive characteristics, bone is similar to soft tissue in that it is resilient, highly vascular, and constantly changing. It adapts to disease and heals itself when fractured. Bone growth and repair are most efficient during youth and adolescence in which fractures heal rapidly. Abnormally slow healing can almost always be contributed to a deficiency in minerals and vitamins, rarely to endocrine or metabolic etiologies. However, if control is poor for site motion, joint distraction, and infection, complications can cause delayed union or nonunion.
Fractures repair, as do all living tissues, by cellular growth, yet there are some unique characteristics due to bone’s high mineral content. Nevertheless, many similarities exist in the healing of connective tissue that can be generalized to direct proper treatment. That is, if the healing of a fracture is understood, the healing of any connective tissue can be understood and enhanced.
After fracture, a hematoma develops between the split ends. This space becomes invaded within a few days by granulation tissue, which in time becomes converted into fibrocartilage. This fibrocartilage is an osteoid tissue where new bone is laid down for union. After this stage, resorption and remodeling occur to reduce the initial callus formation in an attempt to restore the bone to its original size and shape.
While healthy bone is highly vascular, readily repairs itself, and resists infection, avascular bone is defenseless in participating in the reparative process. Thus, after injury, treatment must be directed to prevent further devascularization and to encourage improved vascularity. Intra-articular and metaphyseal fractures enjoy an abundant blood supply, thus early and active movement of the joint should be encouraged. However, proper stabilization of distal and proximal joints must be maintained in diaphyseal fractures because of the relatively poor blood supply. Thus, special concern must be given to increasing circulation and preventing stiffness.
Emergency Care. The first step is to make a brief but thorough examination to determine the extent of injuries. Treatment of any life-endangering condition such as respiratory failure, cardiac arrest, or hemorrhage takes precedence over that for fracture. The care applied directly to the fracture is a part of the prevention or lessening of shock because pain is lessened and the likelihood of further trauma is reduced. In the initial treatment for fractures, the rule, “Splint them where they lie”, applies. Open fractures are dressed before splints are applied.
Special care must be taken to avoid moving the fractured part because the razor-sharp ends of fractured bone can easily cut through vessels, nerves, muscles, and skin. Such additional damage would, of course, increase the possibility of hemorrhage, shock, and loss of limb or life. If movement of the patient is unavoidable or is essential in treatment, the fractured part must be supported if further damage is to be avoided. Slight traction distal to the part may be necessary to restore circulation, the lack of which is shown by absence of the pulse distal to the fracture. Circulatory impairment is especially common after elbow fracture.
With the individual suffering multiple injuries, the most commonly overlooked injuries are fractures of the basilar skull, C7 vertebra, femoral neck, orbit, pelvis, radial head, talus, tibial plateau, T12 and L1 vertebrae, and zygomatic arch. Associated dislocations of the lunate, perilunate, posterior femoral head, posterior shoulder, and scaphoid are common.
Stress (Fatigue) Fracture. Bone-fatigue fractures may be the effect of an improper relation between overstress and adaptability of bone. They indicate a reaction to stress in an unconditioned person. The most common example of this is the so-called “march foot” of infantrymen, mailmen, and new track recruits. It’s commonly the result of being overstressed in running practice or forced marching without adequate preliminary conditioning.
Hairline fractures, where a true fracture line is not clear, may develop in almost every bone of the body after trauma. These will not usually be evident in films taken immediately after injury. Often, 7-10 days must elapse before they can be visualized on film. On occasion, they are seen only by overlying periosteal elevation and callus formation, and not by a readily detected fracture line. If symptoms persist without change for 7-10 days after trauma despite negative films taken immediately after the injury, new films should be ordered to rule out fracture.
Because of the associated weakness, swelling, and tenderness, differentiation from strain/sprain is difficult by physical examination. Protection and rest until the callus matures to bone is all the treatment usually necessary. However, stress fractures of the neck of the femur, anterior midthird of the tibia, tarsal navicular, and base of the fifth metatarsal deserve orthopedic consultation.
Chondral Fracture. Until recent years, chondral and osteochondral fractures have been overlooked. O’Donoghue reports that they are especially common in the knee and ankle. Early diagnosis is difficult because symptoms in the acute stage are obscure and disability is slight. A misdiagnosis of chronic sprain, idiopathic synovitis with effusion, or chondromalacia (especially patellar) is often made. At the knee, a joint mouse and/or osteochondritis dissecans may be an effect.
MYALGIA, MYOSITIS, AND RELATED CONDITIONS
Muscle pain is not localized subjectively with the same accuracy as is pain in more superficial structures, thus such vague localization requires a most careful examination. Muscle inflammation is often mistaken for disease of the adjacent joint, tendon sheath, or some type of neuralgia. The examiner should keep in mind that any type of excessive motor fiber stimulation results in pathologic, involuntary, and painful muscle spasm. Severe spasm places considerable tension on highly sensitive periosteum via its tendon attachment. It is one thing to find muscle spasm and another to determine if it is protective, compensatory, hysterical, or a causative factor.
Motion limitations due to spasm are seen frequently in joint pathology and subluxation syndromes, but they may occur in almost any form of joint trouble, particularly in the larger joints. Spasm may be due to direct irritation or trauma; stretching or pressure on a nerve trunk, plexus, or peripheral nerve branches; secondary to trauma of an adjacent structure; toxic irritation of the anterior horn cells; or psychogenic origins.
Peripheral spasm may be the result of encroachment irritation of a nerve root. It is for this reason that chiropractic spinal adjustments have corrected many cases of chronic shoulder, arm, and knee pain that have been previously treated medically or surgically only at the site of pain.
Pain arising from an injury to muscle tissue may be provoked by making the muscle contract against resistance without allowing it to shorten; ie, preventing movement of adjacent joints. This test, although possibly helpful in differentiating myalgia from the pain of other etiologies, is not absolute because it is not always possible, even with great care, to avoid some indirect pressure or tension on adjacent structures. Another factor is that pain arising from a chronic contraction of an involved muscle is not increased by contracting the muscle further.
Although skeletal muscle tissue lacks an intrinsic lymph supply, a muscle’s connective-tissue sheath and tendons are richly endowed with lymphatic vessels. During the normal physiologic exchange of fluids through capillary walls, the quantity of fluid leaving the capillary is usually greater than that entering the venule. The related lymphatic network takes up the excess and eventually delivers it to the venous system. This process allows a continuous exchange of tissue fluids and maintains a constant pressure of interstitial fluid.
The flow of lymph increases during activity as does capillary circulation, but the flow can be impeded by excessive pressure exerted by a constantly hypertonic or phasically contracted muscle. De Sterno shows that inhibited lymph drainage contributes to muscle pain during prolonged activity by
- causing a build-up of interstitial fluids that increases hydrostatic pressure and
- encouraging the accumulation of metabolic waste products that would normally be drained by the lymphatics and venules.
It is the author’s belief that much of the success of chiropractic treatment of traumatized tissues is from the special concern given to normalizing lymphatic and venous homeostasis as soon as possible. The effect is minimization of fibrosis when coupled with early articular mobility.
Myositis is an inflammation of muscle tissue, usually involving only the skeletal muscles. Contusion and trauma may cause an inflammation of muscles in which the involved muscles become red, swollen, tender, painful, and almost of woody hardness. This type of myositis usually subsides without suppuration.
Muscle function remains painless if an inflammatory process lies entirely within the muscle sheath, but perimyositis may cause pain during function. Myositis produces pain only when the muscle is palpated or stretched. Whenever stretching a muscle causes pain, that muscle should be carefully palpated for sensitive areas, swelling, or induration. Points of sharply defined tenderness can usually be found. In seeking muscle tenderness, portions of the muscle should be pressed between two fingers rather than pressing the muscle on underlying bone to avoid mistaking periostitis for myositis.
This disorder is characterized by chronic joint inflammation producing stiffness and deep aching. It’s of unknown etiology but often precipitates in the underconditioned or those past middle age following overstress. Attacks usually involve the shoulder and hip areas. Aching is perceived in the joints, and paresthesias are felt in the fingers. The proximal muscles, which are painfully stiff but not weak or atrophic, are chiefly involved, and their tendon insertions and associated joint capsules may become thick and tender. However, persistent synovitis or bony erosions are not characteristic of polymalgia rheumatica (PMR).
A mild form of giant cell arteritis is related in 16% of PMR patients. Unlike patients with fibrositis, patients with polymyalgia express such systemic symptoms and signs as a constantly elevated erythrocyte sedimentation rate, weight loss, malaise, headache, anorexia, fever, and mild anemia. Diagnosis is difficult to arrive at except by exclusion.
Striated muscles, especially the erectors, become painfully splinted (intrinsically immobilized) by involuntary spasm when fatigued. In time, trophic changes occur and tone is lost. In ordinary spasm, relaxation of affected muscles occurs at rest. This is not so for splinted muscles. If there is spasm present after trauma, the irritating focus can usually be attributed to irritating ischemia initially and blood debris later. For some unknown reason, prolonged states often establish a self-sustaining reflex spasm that continues long after the initial cause has been erased.
Splinting is explained by understanding the stretch reflex. This reflex is not normally initiated by voluntary contraction. The myotatic stretch reflex uses a single sensory neuron and is initiated by stretching the muscle spindle’s annulospiral receptors. The effect is a protective contraction, designed to protect against further stretch so that the muscle may maintain a constant length. This reflex action is several times more severe if initiated by a sudden stretch than by a slow stretch. It is also well to remember that inhibitory impulses are transmitted to the motor neurons of the antagonists (reciprocal inhibition) and facilitating impulses are transmitted to the synergists both of which enhance the response.
Prolonged pain from bone, muscle, tendon, and joint lesions with resultant long-term splinting or pseudoparalysis leads to eventual osteoporosis in involved and possibly adjacent bones. Joint contractures may also develop. This is an example, similar to a psychic conversion symptom, where a sensory symptom may lead to definite structural changes.
When muscles become acutely spastic or chronically indurated, normal movement is impaired and the foci for referred pain are established. Both spastic and indurated muscles are characterized by circulatory stasis that is essentially the effect of compressed vessels. This leads to cellular nutrition impairment and the accumulation of metabolic debris. Palpation often reveals tender areas that feel taut, gristly, ropy, or nodular. The degree of impairment is essentially determined by the severity of spasm, the amount of induration, and the extent of functional disability. Even with proper conditioning and warm-up procedures, myalgic syndromes are commonly seen when treating athletes or stoic individuals because they habitually ignore the warning signals of pain.
Treatment is commonly aimed at normalizing the continuous motor firing, dislodging collections of metabolic debris, and improving circulation and drainage. Despite the modality or manual procedure used, its intensity should be maintained below the threshold of pain to prevent a protective contraction of the involved muscles. Stretching, heat, sine-wave muscle stimulation, negative galvanism, vibromassage, and goading have all been effective, separately and in combination. When deep mechanical vibration is used, several clinicians report that pressure across muscle fibers tends to release accumulated metabolic by-products, while pressure parallel to muscle fibers (directed to the heart) enhances drainage. Lowe recommends that when spastic areas do not release adequately or conventional methods only offer temporary relief, a nutritional evaluation should be made. A calcium, Vitamin D, and/or magnesium deficiency may be a contributing cause.
On examination, spasticity and stiffness have similar physical findings, but the causes are different. As described above, spasticity is the result of contracted muscles. Stiffness is caused by taut connective tissues that have lost their normal elasticity, plasticity, and/or pliability -indicating the initiation of fibrosis. In chronic states, low-grade spasticity and progressing stiffness are often superimposed.
The relief of stiffness is one of the first goals of rehabilitation after the control of pain. Common techniques include continuous passive manual stretch, spray and stretch, continuous traction, and prolonged stretch with weights. Middleton also includes the use of walk-away casts and dynasplints. However, proprioceptive neuromuscular facilitation (PNF) techniques increase joint flexibility more efficiently than static or dynamic stretching procedures.
A large number of localized tender sites, widely dispersed and symmetrical, suggests fibrositis. In contrast to fibrositis, a small number of points clustered in a single region and unassociated with diffuse aching stiffness and fatigue suggests a referred pain syndrome. Smythe defines primary fibrositis (fibromyalgia) as a syndrome of pain and stiffness lasting at least 3 months that is confined chiefly to tendon insertions, areas of bony prominences, and periarticular areas. His studies found that it is common in women of the 25-35 age group and frequently seen in broad muscles of both genders following prolonged overstress. Signs of joint involvement and muscle wasting are minimal or absent. Roentgenographic signs and laboratory data are indefinite. Common sites of fibrositis are shown in Table 3.
Table 3. Common Sites of Fibrositis
|1. Low cervical||Anterior surface of intertransverse spaces C5-C7.|
|2. Trapezius||Center of upper fold.|
|3. Costochondral||Just lateral and cephalad to 2nd costochondral junction.|
|4. Supraspinatus||Near the scapula’s medial border, above the scapular spine.|
|5. Lateral elbow||About 11/2 inches distal to the lateral epicondyle, in the lateral intermuscular space (“tennis elbow” point).|
|6. Low lumbar||L4-S1 interspinous ligaments.|
|7. Gluteus medius||Superior-lateral aspect of buttocks (deep).|
|8. Medial fat pad||Over superomedial knee ligaments, cephalad to joint line.|
Associated muscle stiffness is aggravated by chilling, fatigue, immobility, anxiety, and insomnia, and relieved by heat, massage, and moderate exercise. Tension headaches and irritable bowel syndrome are frequently associated, suggesting sympathetic involvement. Exacerbations are commonly modulated by changes in weather, physical activity, and emotional stress. When generalized, at least five specific points of tenderness will be found such as at the lateral area of the elbows, in the upper border of the trapezius muscles, along the posterior iliac crests, in the perivertebral lumbar region, and at the medial aspect of the knees.
Cramps are defined as powerful involuntary muscular contractions shortening the flexor muscles that result in extreme, often incapacitating, pains stimulated by ischemia and hypoxia of muscle. There are two types of extremity muscle cramps:
- cramps associated with prolonged exercise and
- nocturnal cramps. The exact cause in either case is unknown.
Fascitis near a joint is an arthritis-mimicking disorder sometimes seen following prolonged microtrauma that features pain, swelling, warmth, and stiffness of an extremity. Palmar fascitis, which leads to Dupuytren’s contracture, frequently mimics synovitis and polyarthritis. A systemic form of fascitis is associated with liver disorders, thyroid disease, and malignant ovarian neoplasms.
Trigger Point Development
A trigger point essentially is a small hypersensitive area in a myofascial structure from which impulses bombard the CNS and give rise to referred pain. Like a subluxation complex, points 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 sustains it. The focal sites are usually unknown to the patient until revealed by palpation.
Trigger-point pain may present as a primary complaint or a crippling adjunct to many other problems; eg, unequal leg lengths, disuse, immobilization, chronic strains, poor posture, gait disturbances, connective-tissue diseases, arthritides, etc. Trigger point syndromes often appear related to a lack of appropriate exercise; thus, they are less common but not absent in the large muscles of athletes and manual laborers than they are in sedentary workers.
Travell calls trigger points foci of stress inflammation that result in binding cobweb adhesions that entrap sensory nerve endings to produce sharp demarcation of pain especially upon pressure. In the typical myofascial syndrome, laboratory analyses and roentgenography fail to show significant bone, joint, or soft-tissue changes. Common upper and lower body trigger point syndromes and their primary reference zone or symptoms are shown in Table 4.
Table 4. Common Trigger Point Syndromes
|Location: Upper Body||Primary Reference Zone or Symptoms*|
|Infraspinatus||Posterior and lateral aspects of the shoulder.|
|Intercostal muscles||Thoracodynia, especially during inspiration.|
|Levator scapulae||Posterior neck, scalp, around the ear.|
|Pectoralis major||Anteromedial shoulder, arm.|
|Pectoralis minor||Muscle origin or insertion.|
|Quadratus lumborum||Anterior abdominal wall, 12th rib, iliac crest.|
|Rectus abdominis||Anterior abdominalwall.|
|Semispinalis capitis||Headache, facial pain, dizziness.|
|Splenius cervicis||Headache, facial pain, dizziness.|
|Sternocleidomastoideus||Headache, dizziness, neck pain, ipsilateral ptosis, lacrimation, conjunctival reddening, earache, facial and forehead pain.|
|Trapezius||Lower neck and upper thoracic pain, headache.|
|Location: Lower Body||Primary Reference Zone or Symptoms*|
|Anterior tibialis||Anterior leg and posterior ankle.|
|Gastrocnemius/soleus||Posterior leg, from popliteal space to heel. These trigger points may be involved in intermittent claudication.|
|Gluteus medius||Quadratus lumborum, tensor fascia lata, gluteus maximus and minimus, sacroiliac joints, hip, groin, posterior thigh and calf, cervical extensors, upper thoracic muscles.|
|Tensor fascia lata||Lateral aspect of the thigh, from ilium to the knee.|
* Reference patterns vary considerably according to the severity and chronicity of the trigger-point phenomenon involved.
The power of a reaction appears to be moderated by several general factors. Examples include conditioning, genetic predisposition, hormonal balance, scar tissue from previous injury, malnutrition, or prolonged emotional stress. The 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, or hysteria. Pain also occurs whenever the trigger 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 shortening of the affected muscle with limitation of motion and weakness. Certain muscles and muscle groups such as the antigravity muscles appear to be affected more than others. The pain may be localized in one muscle or group, or it may also involve remote muscles or groups. Primary trigger points in the gluteus medius, for example, are commonly related to secondary trigger points in the neck and shoulder girdle.
Cycles of physiologic responses arising from trigger points typically involve:
- well-defined pathways (eg, motor reflexes, sensory changes),
- anticipated autonomic feedback reflexes, and
- microscopic tissue changes. Motor and sensory reactions usually manifest in local and general muscle fatigue, hypertonia, weakness, possibly a fine tremor, hyperirritability, pain, and hypesthesia.
The high-intensity discharges from a trigger area may be accompanied by vasoconstriction and other autonomic effects limited to the reference zone of pain. Although one or more trigger points may occur in any muscle, they usually form in clusters. These autonomic concomitants are similar to those seen with acupoint meridians. Travell believes that these are frequently expressed as decreased skin resistance, increased pilomotor reaction in the reference area, vasodilatation (possibly with dermatographia), and skin temperature changes (coolness).
Muscles enclosed and supported by strong fascial compartments may become involved in a muscle-fascia interface syndrome. It may be caused by intrinsic or extrinsic overstress or some type of circulatory obstruction in which pressure within a restricted anatomical space increases enough to produce circulatory embarrassment to the contents of the space. Compartment syndromes manifest in both the upper and lower extremities, but they commonly occur in the forearm and leg. Typical locations in the upper extremity include the volar and dorsal compartments of the forearm and the intrinsic compartments of the hand. Lower extremity locations are found at the anterior, lateral, posterior superficial, and deep compartments of the leg.
The Pathophysiologic Process. Any muscle crush or interference with circulation (eg, arteriosclerosis) may result in muscle swelling restricted by the fascial sheath, leading to extreme pressure producing cellular death. Arteriosclerosis should not be thought of as strictly a disease of the elderly. Autopsies of young soldiers in the Vietnam War showed findings of extensive arteriosclerosis. Increased pressure within a compartment may effect vascular closure, a reflex vasospasm, and/or decreased perfusion pressure. The cause for the increased pressure may be traced to either an increase in compartment content or a decrease in compartment size by one or several factors.
Hemorrhage, increased capillary permeability or pressure, infusion, and hypertrophy are common causes of an increased compartment content. A decrease in compartment size is usually the effect of localized external pressure. Each syndrome has its individual clinical picture of pain, tenseness, weakened muscles, and sensory changes.
Clinical Features. A diminished peripheral pulse may point to either a compartment syndrome or arterial occlusion. Hot red skin over an affected compartment suggests a complication of thrombophlebitis or cellulitis -both of which can lead to serious extension and systemic invasion. Kidney failure or myoglobinuria may add to and complicate the picture. A poorly responding case of shin splints with pain even on rest suggests some degree of compartment syndrome. Because people appear to have a predisposition toward compartment syndromes, they should be identified as early as possible and examined frequently because the syndrome is usually progressive. In severe cases, referral for early decompression may be indicated, based on especially detailed records.
In athletes and physical laborers, secondary local phlebitis often accompanies contusions, sprains, strains, and varicose veins. Its effects can be minimized by rest and enhancing posttraumatic circulation; eg, early mild muscle activity after injury. It is important to differentiate simple inflammation from clot formation that may lead to a dangerous embolism. If a febrile reaction occurs, hospitalization should be considered.
An area of chronically indurated or weakened muscle is often next to an area of muscle that has entered a state of fatty degeneration. When found through palpation, this area should not be confused with a lipoma (adipoma). Lipomata are soft benign fatty tumors, frequently multiple but not metastatic, that vary in size from a pea to a large egg. While most lipomata are located subcutaneously, those embedded deep within skeletal muscle tend to rise to the surface when the involved muscle is exercised and to recede during rest.
Common posttraumatic stasis is well known. Posttraumatic lymphadenitis and lymphangitis, exhibited by warm red tender streaks extending toward neighboring tender swollen lymph nodes accompany infection. These potentially serious inflammatory infections are usually complications to hand and foot abrasions and fungal infections. Rarely does suppuration arise. If signs are not quickly abated by elevation and indirect warmth, referral should be made without delay for culture and appropriate antibiotic therapy.
Psychogenic rheumatism is a common example of psychic conversion. It is characterized by variable symptoms that include fleeting joint pains that shift from site to site and typically worsen under times of emotional stress rather than physical activity or changes in weather. The patient reports “good days” interposed between “bad days” that are unrelated to a common factor. There is an overreaction to gentle palpation such as facial grimaces and rapid “touch me not” withdrawal. It is sometimes seen in unmotivated youngsters that are coerced into athletic or certain work activity by parents or peers.
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