The degree of vascularity of the capillary network between skeletal muscle fibers and in associated tissues depends greatly upon the type of training. The quantity of interstitial fat, most marked in atrophied muscle, is also determined by the degree of training. Lymph vessels are not found within voluntary muscle. A muscle caused to be in traumatic or reflex spasm will become modestly inflamed. There may result some transudation precipitation of fibrin, collagen, and mineral salt deposition, and, if extended, may result in a chronic myositis and myofibrosis. In addition, the myofascial planes of the erectors will become inflamed at the points of major stress. Transudation and fibrin formation result to produce myofascial plane adhesions.

Muscle Soreness and Stiffness

Muscle soreness may occur shortly after activity and pass quickly, or it may not appear until up to 48 hr after exercise and persist for several days. Stiffness, a sign of poor physical fitness in the weekend athlete or unusual stress in the trained athlete, may be confused with minor strain as both stiffness and strain produce pain due to increased intramuscular pressure. The stiffness syndrome features gradually increasing pain, swelling, and restricted motion.

Most authorities today feel that the disorder is not involved with the local accumulation of lactic acid: stiffness results from the accumulation of extracellular muscle fluid due to increased capillary-filtration pressure in an unconditioned muscle where the vascular bed is unable to keep up with the necessary vascular return. The disperal of the accumulating extracellular fluid is also delayed because of the lack of lymphatics within voluntary muscle.

Muscle Cramps and Spasms

Cramps are characterized by spontaneous, prolonged, painful muscle contraction, usually occurring in the voluntary weight-bearing muscles. They often develop during sleep or soon after violent exertion, and may vary from slight contractions to violent spasms. Cramps frequently follow drinking ice water or other cold drinks too quickly or in too large a quantity after exercise. Normally, many motor units rest while others are firing; but in the cramp phenomenon, all motor units fire and cause the spasm. Why this happens is not clear, but impaired fluid intake, electrolytic balance, and blood flow are often involved.

Background.   Heat cramps are often caused by excessive salt loss. However, other factors may be involved such as muscle anoxia, cold, a blow or strain, or for some yet undetermined reason. Cramps are differentiated from heat stroke and heat exhaustion in that the mental state is clear, the temperature is normal, and blood pressure and ECG are normal. Swimming too soon after a meal increases the danger of active-extremity cramps because much of the general circulation is diverted to the abdomen for absorption purposes. Hormonal factors may be involved in the female athlete, especially during the menstrual period.

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

Management.   Relief can be provided by stretching the affected muscle within its normal range after intermittent cold applications, then applying firm pressure kneading. Relaxation and warmth of the affected muscles usually offers further relief, and it sometimes helps to massage the spastic area toward the periphery.

In severe muscle tightness, cold is often effective when combined with exercise: Have the patient flex or extend the limb against manual resistance in the direction of tightness and in the range where limitation occurs, followed by voluntary relaxation. This should be done while cold applications are being applied. As the part begins to relax, the joint should be passively put through its normal range of motion. Probably one of the most effective techniques is that of "spray and stretch" discussed later in this chapter with trigger areas.

The incidence of cramps can be reduced by adequate warmup, salt, water, and protective equipment which will prevent contusion. Muscle fatigue is frequently averted by sympathetic stimulation effecting an adrenalin reaction, as well as correcting postural faults, endocrine imbalances, neural and circulatory impairment, and actions which enhance respiratory efficiency. If salt loss is the cause, therapy consists of salt tablets (1 g every 1-3 hr) until symptoms subside.

Muscle Contusion

Muscular contusion is a disturbance of muscle tissue in the nature of a bruise resulting from a direct force over the muscle. Usually, there is no or little accompanying disturbance to the skin or subcutaneous tissues. However, muscles may be lacerated by sharp or pointed objects. A compound wound has the added problem of infection and must be treated by surgical methods.

Background.   After contusion, there is local swelling, tenderness, pain on motion, and mild function impairment. Muscle fibers have no break in their surrounding sheath. Following repeated intermittent trauma to a muscle, the normal resolution is interrupted, fibrous scarring occurs in the hemorrhagic area, and this is frequently followed by calcification (myositis ossificans).

Management.   Ice, compression, elevation, and rest of the part is necessary in the acute stage to minimize bleeding. Heat and exercise are indicated after 2 hr. The initial pain of traumatic bruises, contusions, abrasions, swelling, and minor strains may be controlled with a vapocoolant such as ethyl chloride. The affected area is sprayed until the tissue just begins to frost and turn white. Further spraying is contraindicated because excessive spraying is likely to intensify pain from muscle spasm and increase motion limitation. Rapid evaporation of the coolant absorbs heat and causes cooling depending on the dosage. The smallest dosage needed to produce the desired effect should be used because the anesthetic time interval (10-60 sec) is often sufficient to help relieve the initial pain from trauma.

Muscle Ruptures

A muscle action not balanced by reciprocal inhibition of the antagonistic muscle (eg, blow, unexpected force) may result in its rupture by sudden contraction or a less common injury to its antagonist by overstretching. Muscles previously weakened by fatigue or disease are more apt to rupture.

Rupture 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 tendinous attachment to the muscle belly. Normal continuity is broken and quite obvious on palpation until 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 considered an effect of banding of the overlying fascia.

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. Such rupture is characterized by painful voluntary contraction, ecchymosis at an area of local tenderness, swelling, edema, and hemorrhage. 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.

Management.   Treatment for hemorrhage must be provided in the early stage. Support, progressive exercises, heat, ultrasound, and massage are indicated in the later stage. Surgical approximation of the torn ends may be necessary.

Soft-tissue damage is usually more painful and can be more serious than bone injury. Bone heals with calcium, 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 also takes longer to heal than bone tissue. Bone tissue may actually be stronger after the healing process has taken effect, whereas soft tissue is usually weaker after repair.

The most common muscle injury is strain of a few muscle fibers and associated connective tissue. Players refer to it as a muscle pull or tear. In strain, both intrinsic or extrinsic muscle stress can produce torn muscle fibers, connective tissues, and vessels within a muscle belly or at its points of origin or insertion. A strain cannot affect a muscle and not the tendon or vice versa; if it affects one part of the unit, it affects the other. Thus, the musculotendinous unit must be considered as a whole in cases of strain.

Chronic strain is the result of prolonged overuse which produces an inflammation at the tendinous attachment, musculotendinous junction, or within the tendon itself. As activity continues, the inflammatory reaction progresses to calcification at the muscle origin or tendon insertion with possible spur development. Intramuscular hemorrhage is not uncommon in conditions of chronic strain. Tendons with sheaths are more likely to become inflamed, with the inflammation spreading between the tendon proper and the sheath.

Background

A strain is damage to a muscle or tendon resulting from overuse or excessive stretching, direct trauma, and/or overcontraction against resistance. It can involve anything from a minor irritation of muscle fibers to an actual separation of the tendon from the bone structure.

The incidence in the upper extremities is highest in the biceps and triceps (eg, glass arm), and in the elbow, wrist, and fingers in tennis players. Incidence is highest in the lower extremities in the quadriceps, hamstrings (eg, sprinting), anterior tibial, adductors (eg, horseback riding), triceps surae (eg, tennis), and Achilles tendon (eg, older runners). Pulled spinal muscles are often seen in weight lifting, gymnastics, and rowing. Pectonius and psoas muscle strain is often seen in ballet dancers and athletes who do considerable kicking.

The exact cause of muscle tears in unknown. Some feel they are the result of technical error, some unknown circulating toxin, or a postural fault where an activator muscle is jerked into action before the prime fixers are ready. Regardless, the mechanism appears to be a breakdown in coordination of the reflex inhibition necessary for synchronous contraction of antagonistic muscle groups; eg, fatigue, weakness, and straining are known to cause a cortical bombardment of the spinal centers, manifested in overstriding.

Hematoma Formation

Interstitial hematomas are usually the result of contusion, while intramuscular hematomas are the result of intrinsic tears. Both contractile and noncontractile elements are damaged during muscle strain, but the greatest injury is suffered by the capillary network between skeletal muscle fibers. The effect is seepage of blood and tissue fluid into interstitial and extracellular muscle spaces which are already engored by activity hyperemia. A degree of hematoma is the result, and it may protude within the potential space between muscles. When extrinsic stress is severe, bleeding may also result within the deep and subcutaneous connective tissues to compound the problem.

Hematoma development is smaller and localized in open wounds because the open surface relieves pressure, restricting tracking into deeper tissues. When intramuscular tension returns after injury, intramuscular bleeding points tend to become compressed. Clotting occurs within a few hours, but slight trauma (eg, massage) may cause further hemorrhage even after 2-3 days. Resolution follows with a degree of absorption and fibrosis as previously described.

Symptoms

The onset is acute with searing pain which rapidly fades into a dull ache. Pain is increased on movement, especially against gravity. Weakness is not commonly associated. Examination presents a locally spastic and tender muscle with swelling. If rupture is severe, a gap may be palpated. A bulge in the long axis (eg, thigh) on vigorous contraction points to hernia. Contraction against resistance and passive stretching produces pain relative to the degree of hematoma. In the late stage, extensive skin discoloration is common and often appears some distance from the site of injury. Subacute and/or chronic strains may result in a myofascitis and/or myofibrositis.

Classes of Muscle and Tendon Strains

Strains are classified by either severity or by area. When classified by severity, the terms mild, moderate, and severe are generally applied. 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-T9.

Muscle strains can be classified into three degrees of injury:

1. First-Degree Strain.   This is a mild muscle pull caused by trauma to a part of the musculoskeletal unit from forceful stretch that results in a lowgrade inflammation and some muscle-tendon disruption. Hemorrhage, disability, and strength or function loss are mild. It 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 complication is recurring strain; tendinitis and periostitis at the site of attachment may develop.
   
   

2. Second-Dreee Strain.   This is a moderately pulled muscle caused by trauma to the musculoskeletal unit from excessive stretch or violent contraction that results in torn fibers without complete disruption. It is characterized by increased first-degree strain symptoms. There is moderate hemorrhage and swelling. Muscle spasm and function loss are especially greater. The complications are similar to those seen in first-degree strain.
   
   

3. Third-Degree Strain.   This is a severely strained muscle. The trauma results in a ruptured muscle or torn tendon which may be represented as a musclemuscle, muscle-tendon, or tendon-bone separation. A palpable defect is often present. It 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, roentgenograms exhibit softtissue swelling and an avulsion fracture at the tendinous attachment.

It is typical of muscle injuries that the pain is out of proportion to the extent of damage. This pain is the result of hematoma pressure which stretches adjacent muscle fibers and connective tissues, as well as the result of irritation from extravasated blood. As complete muscle rupture is rare, loss of functional ability is usually a secondary concern.

Emergency Care

Immediately after injury, a cold pressure pad should be applied to inhibit bleeding. If occurring on a limb, elevation should also be applied to the limb which has been elastic bandaged (distal to proximal) up the limb. In minor tears, gentle active movement should be encouraged to reduce the pain, in spite of the discomfort, but this is inadvisable when swelling is rapid.

Case Management

Treatment should be designed to inhibit hematoma development and promote rapid resolution. Such care reduces pain (the chief complaint) and inhibits excessive adhesions and scar tissue (the disability factor). In cases of intrinsic injury, the cause of injury must be determined and preventive measures instigated.

The pressure pad should remain in place 2-3 days, with tightening when necessary. Gentle, active unresisted exercise should be encouraged. Bed rest may be required if bruising is severe, but rest has no place in treatment after the first 48-72 hr unless complete rupture or myositis ossificans is knowingly in progress. Rest after the acute stage promotes atrophy, adhesion formation, and scarring.

Appropriate physiotherapeutic measures (eg, diathermy) may be started in 2-3 days after injury to promote vasodilation and reduce spasm. Later, ultrasound, massage, and progressive resistance exercises may be instigated to encourage dispersal. As improvement continues, exercises are increased in variety and vigor to tolerance until they meet activity needs. Local anesthetic injections to diminish pain are dangerous because they deaden natural protective mechanisms and increase the size of the space-occupying lesion. Jaskoviak has found acupuncture to be an effective adjunct.

Rehabilitation

During strain recovery, full exercise of the unaffected parts, depending upon the site and scope of injury, may be carried out to maintain general fitness. Faradism has been found useful in stimulating inhibited muscles, but it is contraindicated if there is any suspicion of myositis ossificans. When a case is first presented long after injury, a program of progressive mobilization is necessary due to the probable marked fibrosis. Rehabilitation is not complete until the player is physically capable of returning to competition, knows that he/she is capable, and full muscle extensibility is demonstrated.

Determining the Anatomical Movers of Human Movement

Training a person to properly analyze the anatomical movers at the point of performance has been a difficult task until recently. Chun has developed a method that depends on the principle that a body moves along the direction of the resultant of the applied separate forces. A body segment must move along the direction of the resultant of muscular tension, tissue passive resistances, and external forces applied on the segment such as gravity, elasticity of the equipment used, friction, muscular tension of opponents, etc. Generally, the direction of the segmental motion and the external forces would be known. The direction of the muscular tension could therefore be determined, as well as the principle muscles responsible for the movement.

To develop analytical capabilities, Chun states that the examiner should be aware that there are usually three types of situations in which the determination of the principle movers of human motion are possible:

1. First, the direction of segmental motion would be classified as opposite to the direction of the external forces (ie, gravity, etc). This would indicate that the movers are located on the same anatomical side as that of the segmental motion.
   
   

2. Second, slow moving segmental actions would occur in the same direction as that of the external forces. As a consequence, the movers would be located on the opposite side of the segmental motion.
   
   

3. Third, rapid segmental movements would also occur in the same direction as that of the external forces. The movers would now represent muscles lying on the same side of the segmental motion.

Infection, myositis ossificans, and cyst formation are typical complications of muscle strain. Other complications such as aneurysm, arteriovascular fistulae, phlebitis, and phlebothrombosis will be discussed in Part 4 on a regional basis.

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 a serious neurologic deficit. A complicated strain is accompanied by mild autonomic disturbances and may be associated with preexisting 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 preexisting pathology or injury to the spinal column contents. A complicated sprain is accompanied by preexisting pathology or injury to the spinal column contents. In general, 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 damaged cells and the accumulation of exudate may provide fertile soil for the invasion of inflammatory processes and delayed repair.

Acute and Chronic Spasticity

When muscles become acutely spastic or chronically indurated, normal movement is impaired and foci for referred pain are established. Even with proper conditioning and warmup procedures, myalgic syndromes are commonly seen when treating athletes because they habitually ignore the warning signals of pain. The degree of impairment is essentially determined by the severity of spasm, the amount of induration, and the extent of functional disability.

Both spastic and indurated muscles are characterized by circulatory stasis, which is essentially the effect of compressed vessels. This leads to the poor nutrition and the accumulation of metabolic debris. Palpation will often reveal tender areas that feel taut, gristly, ropy, or nodular.

An area of chronically indurated muscle tissue is often adjacent to an area of muscle that has entered into a state of fatty degeneration. When found through palpation, this area should not be confused with that of a lipoma (adipoma). These soft benign fatty tumors are frequently multiple but not metastatic, varying in size from a pea to a large egg. While most lipomata are located subcutaneously, those imbedded deep within skeletal muscle tend to rise to the surface when the involved muscle is exercised and to recede during rest.

      MANAGEMENT

Treatment should be directed to normalize the continuous motor firing, dislodge collections of metabolic debris, and improve circulation and drainage. Regardless of the modality used, intensity should be maintained below the threshold of pain to prevent a protective contraction of the involved musculature. Heat (superficial or deep), sine-wave muscle stimulation, negative galvanism, and massage have all proved themselves effective. When deep mechanical vibration is used, several clinicians believe that pressure across muscle fibers tends to release accumulated metabolic by-products, while pressure parallel to muscles fibers (directed to the heart) enhances drainage.

Lowe points out 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.

Infection

Infection is rare except in open wounds or aspirated hematomas. Especially if a bacteremia exists, a hematoma may become infected and produce suppuration. This is a greater possibility if the hematoma is sited in a relatively poorly vasculated area. Rest and referral for antibiotics and surgical drainage is usually indicated. Progressive exercises may begin as soon as drainage stops, with normal training after healing is complete.

Traumatic Myositis

Myositis is an inflammation of muscle tissue, usually involving only the skeletal muscles. Contusion and trauma may cause an inflammation of muscles wherein the involved muscles become red, swollen, tender, painful, and almost of wooden hardness. This type of myositis usually subsides without any suppuration.

Background.   Disease of muscle tissue is often mistaken for disease of the adjacent joint, tendon sheath, or some type of neuralgia. Muscle pain is not localized subjectively with the same accuracy as is pain in the more superficial structures, thus such vague localization requires a most careful examination. Functional use of a muscle is painless if the inflammatory process lies entirely within the muscle sheath, but perimyositis may cause pain during function. Myositis causes pain only when the muscle is palpated or stretched. Whenever stretching a muscle causes pain, that muscle should be carefully palpated for sensitive areas and palpable swelling or induration. Points of sharply defined tenderness can usually be found. In testing muscle tenderness, portions of the muscle should be pressed between two fingers rather than by pressing the muscle upon underlying bone to avoid mistaking a periostitis for a myositis.

Management.   Rest, local heat, and acupuncture may be helpful. Massage is beneficial if applied in the later stages.

Traumatic Myositis Ossificans

Myositis ossificans is a condition of heterotopic bone formation which can occur in collagenous supportive tissues such as skeletal muscles, ligaments, tendons, and fascia following hematoma. It is commonly the effect of direct muscle bruising, especially repeated contusions as seen in contact sports, on the anterior aspects of thighs and arms.

Background.   Connective tissue which surrounds the muscle rapidly invades the traumatized area, and connective tissue retains its embryonal ability to be transformed into more differentiated tissue. Following the 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 presents local heat. It is common in teenagers and young adult males, and occurs 80% of the time in the biceps brachialis after dislocations but is frequently seen in the thigh (quadriceps). Periosteal tears undoubtedly encourage ossification.

Management.   Early cold, rest, and compression to the injured muscle helps 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 be begun 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 disturbing function. Protection of the part is the best preventive measure.

Myalgia or muscular rheumatism is a generalized term referring to aching muscles associated with stiffness, tenderness, and varying degrees of disability increased by active motion. Rare is the person who has not suffered some form of stiff neck, pleurodynia, scapulodynia, dorsodynia, lumbago, or sore leg muscles after unusual exertion or chilling. It appears to be the commonest form of persistently recurring pain other than headaches.

Background

Fibrositis is a better term than myalgia since the changes occur chiefly in the white fibrous connective tissue of tendons, muscles, nerve sheaths, fascia, periosteum, joint capsule, and ligaments. These changes are a hypothermic edema and proliferation of white fibrous connective tissue as a result of chilling, toxic influences, acute trauma, chronic strain, or physical fatigue.

Thermal and barometric changes, Vitamin B deficiency, chemical intoxication, metabolic imbalances, as well as dampness and respiratory infection are important precipitating factors. Focal infection is often an important factor as is a malfunctioning colon. Regardless, the mode factor is via the capillary circulation and the nervous system.

The early state is one of effusion with a localized inflammatory serofibrinous exudate causing puffy swelling. The exudate may be absorbed or organized by fibroblast invasion and proliferation of fibrous tissue. In the latter stage of fibrous thickening, fibrous bands and nodules sometimes form in the muscles and fascia as adhesions and press on arterioles and nerve filaments producing contracture and atrophy.

Such a condition is undoubtedly a part of the arthritic syndrome which has a wide variety of manifestations:

1. ntramuscular fibrositis (myositis, myofascitis, muscular rheumatism)
   
   

2. Bursal fibrositis (bursitis)
   
   

3. Perineural fibrositis or interstitial neuritis (eg, brachial neuralgia, sciatica)
   
   

4. Periarticular fibrositis (capsulitis, capsular rheumatism)
   
   

5. Tendinous fibrositis (palmar or Dupuytren's fibrositis)
   
   

6. Subcutaneous fibrositis (panniculitis)

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.

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. Some investigators, 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 may become painful without trauma, 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 where remissions can be associated with not taking the drug. Physical findings are usually negative, but there may be some pulmonary involvement.

Other causes rarely seen in athletics include rheumatoid arthritis, polymyalgia rheumatica, dermatomyositis, scleroderma, systemic Lupus erythematosus, and various connective-tissue diseases.

Muscles are enclosed and supported by strong fascial compartments. A compartment syndrome is any condition that increases pressure within an anatomic space which results in circulatory embarrassment to the contents of the space. Any muscle crush or interference with circulation may result in muscle swelling restricted by the fascial sheath which leads to extreme pressure and cellular death.

Background

The syndromes are seen in both the upper and lower extremities, especially in the forearm and leg. Typical locations in the upper extremities include the volar and dorsal comparts of the forearm and the intrinsic compartments of the hand. Lower extremity locations are found at the anterior, lateral, and posterior superficial and deep compartments of the leg. The disorder is often seen in football where a limb is stepped on by a studded shoe.

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 some factor(s). Hemorrhage, increased capillary permeability or capillary 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 (eg, a tight dressing).

Examination

During the neurologic examination, be sure to test light touch and two-point discrimination. Laboratory data are of little help. Grade muscle strength of potentially involved muscles, and palpate for tenseness. Passive muscle stretch will increase pain in ischemic muscles. Each syndrome has its individual clinical picture of pain, tenseness, weakened muscles, and sensory changes. See Table 17.1.

A diminished peripheral pulse may point to either a compartment syndrome or arterial occlusion. Hot red skin overlying an affected compartment suggests a complication of thrombophlebitis or cellulitis. Kidney failure or myoglobinuria may add to and complicate the picture. A poorly responding case of shin splints with pain even on rest suggests a compartment syndrome.

                                        Compartment                          

                                                            Posterior        

Sign         Anterior         Lateral          Superficial       Deep         
Pain on      Toe flexion      Foot inversion   Foot dorsi-       Toe extension
passive                                        flexion
movement

Site of      Between fibula   Lateral fibula   Bulk of calf      Between tibia
 tissue      and tibia,       area                               and Achilles 
 tenseness   anteriorly                                          in posterior-
                                                                 medial lower
                                                                 leg

Weakened     Tibialis         Peronei          Gastrocnemius     Tibialis  
muscles      anterior,                         Soleus            anterior
             toe extensors                                       toe flexors

Sensory      1st web space    Dorsum of foot   No signs          Plantar 
change       (deep peroneal)  (deep and                          surface
distribution                  superficial                        (poster tibial)
                              peroneal)

Tendons 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 an unexpected stretching force (eg, misstep). For protection, the Golgi tendon-stretch receptors have an inhibitory effect on muscle contraction. This tends to counterbalance the stretch receptors within muscle which excite contraction upon stretch.

Tenosynovitis

Tendon sheaths are lined with specialized connective tissue cells similar to cells lining bursae and the synovial membrane of joints. Thus, reactions within tendon sheaths to external influences are akin to those seen in bursae and joint cavity affections. The term tenosynovitis generally includes all affections of the tendons and their enveloping sheaths.

Background.   Continual pain at a tendinous insertion can usually be traced to a sudden unexpected strain, to chronic stress, and rarely to contusion. Nerve entrapment, epicondylitis, soft-tissue nipping, and osteoarthritis may be confused or superimposed within the clinical picture. The two most common sites are at the origin of the extensor tendon at the lateral epicondyle (tennis elbow) and the origin of the adductor longus at the pubis.

Tenosynovitis is usually the result of overuse or compression of a tendon possessing a synovial sheath or secondary to systemic infection. The disorder is usually acute, relieved by rest, but may become chronic and resemble rheumatoid arthritis. 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) is divided into 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 sedentary weekend athlete is an example of overactivity which may bring on the characteristic symptoms. Within a few hours after a hard session of unaccustomed effort, the involved tendon sheath becomes edematous. Pathologic changes are particulary 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 which may be accompanied by a serous effusion within the tendon sheath. The adjacent muscle fibers show degenerative changes, lose glycogen content, and accumulate lactic acid, which spreads over the tendon. This acidity causes the edematous swelling. The second form is an acute hemorrhagic type resulting from direct contusion or a puncture wound which does not introduce infection. A sterile outpouring of bloody and serous fluid occurs within the tendon sheath.

Symptoms develop in 24-28 hr after injury. There is a gradual onset of pain radiating along the involved tendon upon active contractive or passive stretching. There is a soft, hot, frequently red, localized swelling at the musculotendinous junction which usually renders an audible silky or leathery crepitus whenever the tendon is moved. 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.

Inflammation of the areolar tissue around a tendon (peritendonitis) is a common result of sudden training increases. It features swelling, pain which is relieved by activity, tenderness, and palpable crepitus.

Management.   Rest and support are necessary from 1 to 2 weeks, followed by massage, progressive exercises, and therapeutic heat.

Tendon Rupture

Rupture is exceedingly rare in players under the age of 40 years. Both complete and partial ruptures are most commonly seen of the Achilles tendon of middle-aged athletes. Tendinitis with healing and repair might precede an episode of complete rupture requiring prolonged casting or surgical repair. The cause is usually traced to overuse, direct violence during stretch, or a poorly placed injection. Its site is commonly found just away from the point of insertion into bone. The rare event of spontaneous tendon rupture occurs only when the tendon is weakened by degenerative processes.

Rupture Near Insertion.   Rupture here is characterized by sharp pain, often accompanied by perception of an abrupt "thud" at the site. The sharp pain soon subsides, but joint weakness does not. Partial rupture is characterized by acute pain during activity which persists until stress can be avoided. When activity is resumed, severe pain returns. A tender swelling is inevitably noted on palpation. Surgery presents the risks of complications but usually leads to a quicker return to activity (within 3-4 months) than conservative measures.

Rupture at the Musculotendinous Junction.   This features a sudden stabbing pain followed by swelling and sometimes hematoma. Pain is increased when the affected muscle is contracted. A gap may be noted when swelling subsides to indicate a degree of muscle tear, but surgery is rarely necessary.

Ganglion

The localized cystic swelling to which the term "weeping sinew" is applied is the result of a mucinous degeneration of connective tissue occurring near a tendon sheath or joint capsule. The cause is unclear, but trauma is thought to be a factor.

Background.   One large cyst may be felt, or several small cysts may coalesce to form a multilocular cyst. The walls are composed of dense fibrous tissue. Bundles of nerve fibers are often seen in the areas of mucinous degeneration. Ganglions are usually seen on the dorsum of the wrist or foot. They give rise to a localized swelling, gradual or sudden in onset, which may vary in size from time to time. Weakness and mild neuralgia may be perceived. If connected to a tendon sheath, the ganglion becomes prominent when the tendon is stretched.

Management.   Small ganglia may be ruptured by pressure or a sudden blow. After disruption of the gelatinous material into the tissues, the area should be firmly compressed for a few days. However, this method is not successful if the ganglion is attached to the joint capsule; surgical incision may be necessary.

Sola believes that myofascial pain may be the most common pain problem faced by most physicians. It may present as a primary complaint or as a crippling adjunct to any number of other problems (eg, unequal leg lengths, disuse, immobilization, chronic strains, poor posture, gait disturbances, connective-tissue diseases, arthritides). Trigger point syndromes often appear related to a lack of appropriate exercise; thus, they are less common (but not absent) in athletes and laborers than they are in sedentary workers.

A trigger point can be demonstrated much easier than it can be defined. Clinicians for many years have found highly localized, exquisitely sensitive areas within or near a painful region. When pressure is placed on the sensitive spot (trigger point), local pain, referred pain, or both may be initiated. Besides deep pressure, an application of heat, cold, electrical stimulation, needling, or some other stimulus may evoke a painful trigger-point reaction. The power of such a reaction appears to be moderated by a number of general factors (eg, conditioning, genetic predisposition, hormonal balance, personality, previous injury (scar tissue), and emotions).

Trigger points are foci of stress inflammation which result in binding cobweb adhesions that incarcerate sensory nerve endings to produce sharp demarcation of referred pain especially upon pressure. A trigger point itself, or myodysneuria, is a small, deep, hypersensitive area in a myofascial structure from which high-intensity impulses bombard the central nervous system and give rise to deep-aching referred pain --as contrasted with the ischemic-compression nerve pain of prickling, tingling, and numbing which follows the segmental distribution of an entrapped peripheral nerve.

An irritable trigger point in or near a muscle is often a little-recognized cause of spasm and myofascial pain. Many cases of torticollis, shoulder pain, tennis elbow, substernal aches, lumbago, sciatica, hip pain, knee pain, and ankle pain can be traced to trigger-point mechanisms. Such conditions are frequently misdiagnosed as myalgia, myofascitis, nonarticular rheumatism, and sometimes as muscle strain or joint sprain. This is especially true when symptoms persist long after precipitating events.

Etiology

Myofascial trigger areas, as pointed out by Johnson and others, may be produced by direct trauma to muscle or joint, chronic muscular stress, chilling of fatigued muscles, acute myositis, nerve root trauma, visceral ischemia or dyskinesia, arthritis, and hysteria. Long-term myofascial pain following activation of a trigger area is believed to be a reflex pain cycle sustained by the trigger area. Predisposing influences may be any factor which leads to chronic stress (physical or emotional) and fatigue. Nerve root compression, chronic visceral dysfunction, remote joint lesions, chronic infection, heavy alcohol consumption, a low metabolic rate with creatinuria, diminished serum potassium or calcium levels, diminished Vitamin C or B levels, estrogen deficiency, and hypothyroidism are frequent factors in contributing to noxious feedback which perpetuate trigger points. The opposite is also true; ie, somatovisceral reflexes from trigger points may reinforce and perpetuate a visceral disorder such as ectopic cardiac rhythm, for one example.

Impulse discharges from a trigger area may be related to vasoconstriction and other autonomic effects which are limited to a more or less predictable reference zone of pain. This is true for both visceral disease and the myofascial structures. One must distinguish between the site of pain (the reference zone) and the source of pain (the trigger area). Thus, it is important to differentiate true somatic pain from the somatic pain component of visceral pain. Although the somatic component of such pain syndromes may be relieved and indicated for this use, the visceral cause of the pain complex must never be overlooked by casual therapy for temporary relief of a trigger area.

Causes of Trigger Point Pain

Trigger points are generally considered to be "weak" points within myofas- cial tissue that are particularly sensitive to stress-induced change. That is, they may remain quiescent until a certain stress triggers a syndrome that involves a number of positive feedback cycles such as sensory and motor reflexes, sympathicotonia, vascular responses, and, possibly, extracellular fluid changes, which eventually lead to hypertonia, fatigue, and endogenous pain or the intensification of traumatic pain.

Although the exact physiologic mechanisms of trigger point pain are unknown, Sola offers a rational neurophysiologic explanation. He feels that, because of physiologic defense mechanisms such as splinting and bracing of muscles, vasomotor changes, increased sympathetic discharge, and hormonal and other humoral changes in plasma and extracellular fluids, the spastic muscle or fascia (which is probably more sensitive than surrounding tissue due to previous injury or a genetic weakness) fatigues and signals its distress to the central nervous system. A number of responses may result. For example, various muscles associated with the trigger point may become more tense and begin to fatigue because of motor reflexes. Sympathetic responses lead to vasomotor changes within and around the trigger point. Zimmermann reports that local ischemia following vasoconstriction or increased vascular permeability following vasodilation may lead to changes in the extracellular environment of the cells involved, release of algesic agents (eg, bradykinins, prostaglandins), osmotic changes, and pH changes -- all of which may increase the sensitivity or activity of nociceptors in the area. The sympathetic hyperactivity may also cause smooth muscle contraction in the vicinity of nociceptors, thus increasing their activity. This increased nociceptor input may then contribute to the cycle by increasing motor and sympathetic activity, which, in turn, leads to increased pain. This pain may be shadowed by growing fatigue that adds an overall mood of distress to the patient's status and feeds back to the cycle. Sola believes that, as tense muscles in the affected area begin to fatigue in an environment of sympathico- tonia and local biochemical change, latent trigger points within the involved muscles may also begin to fire --thus adding to the positive feedback cycle and spreading the pain to these muscles or muscle groups. Finally, the stress of pain and fatigue, coupled with both increased muscle tension and sympathicotonia throughout the body (conceivably with ipsilateral emphasis through the sympathetic chain), may lead to focal exacerbations or trigger points in other muscles that are far remote from the initial area of pain.

On the other hand, Simons offers a neurochemical explanation of trigger point development that deserves consideration. He feels that a traumatically induced tear in the sarcoplasmic reticulum initially causes the release of calcium that acts in conjunction with adenosine triphosphate (ATP) to continuously stimulate local contractile activity. This uncontrolled contraction shortens and tenses fibers within the involved muscle bundle(s). Such increased physiologic activity can initiate a subsequent increase in sustained, uncontrolled, localized metabolic activity by the muscles that is capable of producing substances that cause a hypersensitivity of involved sensory nerve fibers and, possibly, stimulate localized reflex vasoconstriction to help control what otherwise might be a rapidly increasing metabolic activity. The result is local tenderness, referred pain, and decreased blood flow within the involved muscle area. Once the local energy and nutrient supply becomes restricted in this manner, ATP stores become depleted. When this occurs, the local physiologic contracture of muscle fibers is converted to an energy- deficient contraction. Thus, the sarcoplasmic reticulum of the muscle must be repaired. If sufficient energy is not available, the calcium pump (which is the most energy-sensitive step in the contractile mechanism) will respond with continued muscle contraction, creating an even greater energy depletion. It is hypothesized that normal function may be restored by stretching the locked actin and myosin filaments far enough apart to eliminate contraction. Simons believes that enough ATP will then accumulate to restore a normal sacroplasmic reticulum, which would allow the inhibited circulation to slowly remove the accumulation of metabolic by-products. In this context, Sandman feels that the amount of degen- eration or pathologic alteration created may relate directly to the length of time these conditions are allowed to exist within a muscle.

Reference Zones

Muscle pain exists in recognizable patterns in correspondence to a trigger point, but these pain patterns are often obscure or distant from the trigger point itself. That is, the site where the patient feels pain and the place where the pain originates are not usually the same. Not all trigger areas, however, are widely removed from their reference zones; the reference of pain may at times even circumscribe the trigger area. They may or may not follow the distribution of dermatomes, sclerotomes, peripheral nerves, or acupuncture meridians.

The referred pain is initiated or the site is found whenever the trigger site is stimulated by deep pressure, a small-blunt probe, ultrasound, needling, extreme heat or cold, or stretching motions of the structure containing the trigger area. The resistance to stretching produces shortening of the affected muscle which limits motion and causes some weakness without atrophy. 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.

Common Sites

Although one or more trigger points may occur in any muscle, they usually form in clusters and certain muscles and muscle groups (eg, antigravity muscles) appear to be more liable than others. Common trigger point syndromes are described in Table 16.2. It should be noted that reference patterns vary considerably according to the severity and chronicity of the trigger point phenomenon involved.

Trigger points are primarily found in the "stress sites" of the myofascial planes of the erector muscles of the back, pelvis, neck, and shoulder girdle. A trigger area at a particular site gives rise to a consistent distribution of referred pain which varys only slightly from person to person, indicating that the impulses follow fixed pathways. These pathways are similar to those of visceral pain which is referred in predictable patterns that do not follow a simple segmental distribution. Once the pain reference pattern of a trigger point is known, it can be used to locate the muscle that is the source of the pain.

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.

The effects may be widespread. For example, a trigger point in or near the quadratus lumborum can be responsible for low back pain, sacroiliac pain, or pain referred to the buttock, hip, calf, anterior thigh, abdomen, or groin. A trigger point in the vastus lateralis muscle is a common source of referred pain to the knee.

In time, a chain reaction is often seen where satellite trigger points eventually develop. Travell gives the example of trigger points in the sternal division of the sternocleidomastoid muscle which refer pain to the sternum are often associated with satellites in the sternalis muscle on the anterior sternum which refer pain deep under the sternum, across the upper pectoral region, and sometimes down the arm --often leading to a misdiagnosis of angina or mastalgia.

Secondary Sites

Trigger point 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. Thus, while a trigger points in the neck and upper thoracic muscles may be found to be responsible for tension headaches, a group of "mother" trigger points should be sought on the dorsal aspect of the ilia.

UPPER BODY
Location                  Primary Reference Zone or Symptoms                 
Infraspinatus             Posterior and lateral aspects of the shoulder. 

Intercostal mm.           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 abdominus          Anterior abdominal wall. 

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.
 
LOWER BODY
Location                  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 fasciae latae, gluteus
                          maximus and minimus, sacroiliac joints, hip,
                          groin, posterior thigh and calf, cervical extensors,
                          upper thoracic muscles. 

Tensor fasciae latae      Lateral aspect of the thigh, from ilium to the knee.

Cycles of physiologic responses arising from trigger points typically involve

(1) well-defined pathways (eg, motor reflexes, sensory changes),

(2) anticipated autonomic feedback reflexes, and

(3) hypothesized microscopic tissue changes. Motor and sensory reactions are usually exhibited in local and general muscle fatigue, hypertonia, weakness, possibly a fine tremor, hyperirritability, pain, and hypoesthesia. The autonomic concomitants are similar to those seen with Meridian acupoints. Travell believes that these are frequently expressed as decreased skin resistance, increased pilomotor reaction in the reference area, vasodilation (possibly with dermatographia), and skin temperature changes (coolness).

In the typical myofascial syndrome, standard physical diagnostic procedures, laboratory analyses, and roentgenography fail to show significant bone, joint, or metabolic changes. According to Sandman and others, the focus of pain appears to be from exercise of an ischemic muscle and/or chemoreceptor and mechanoreceptor stimulation from pressure by accumulated metabolic debris or irritation by released acetylcholine, blood serum, bradykinin, histamine, inflammatory exudates, substance P, and 5-hydroxytryptamine.

Primary points can be localized through electric stimulation, blunt mechanical probing, or ultrasonic searches. With practice, digital pressure may localize a deep tender point of taut muscle tissue. At this point, a positive "jump sign", with referred pain, is often associated. This sign is the result of a visible shortening of the muscle which contains the trigger point by placing the muscle in a relaxed position, applying moderate passive stretch, and snapping the trigger site briskly with a finger or probe. Chronic trigger points are often "latent"; ie, they are less apt to produce pain (except on needling) and are less irritable on deep palpation. But, they frequently produce a reflex jerk of the part (jump sign) as do active trigger points.

Deep direct digital pressure for 5-10 sec, pulsating ultrasound, nonsurging sinusoidal currents to tolerance, ice massage, acupuncture, acupressure, and nonfrosting sweeping sprays of a surface coolant across the site and zone with passive stretching of the affected muscle have been reported beneficial. Of the noninvasive techniques, the intermittent application of intense cold by the "spray and stretch" method is considered the most simple and most effective. Keep in mind, however, that trigger points themselves are frequently secondary to another condition (eg, strain, subluxation, stasis, visceral disorder) which must be diagnosed and treated.

Any trigger point therapy is generally considered more effective if the involved area in placed in a position of relaxed passive stretch during treatment. In addition, regardless of the type of procedure utilized to treat trigger points, the intensity of the therapy must be kept just below the threshold of pain because pain will initiate a defensive reflex contraction, which would aggravate the disorder rather than alleviate it. Most authorities feel that, regardless of the therapy utilized, it should be concluded with some form of therapeutic heat that is followed by passive stretching movements in all ranges of motion that is conducted within patient tolerance.

      SPRAY AND STRETCH TECHNIQUE

Fluori-methane and ethyl chloride may be used as a counterirritant in the management of myofascial pain, restricted motion, and muscle spasm with or without related trigger points. Fluori-methane is preferred to ethyl chloride in that it is less cold to the patient, noninflammable, not explosive, not a general anesthetic, and nontoxic when used correctly.

The vapocoolant is applied in one direction, never back and forth, at a distance of 18-24 inches and at the rate of 4 inches per second. A fine stream is used, not a mist. The rhythm should be a few seconds on and a few seconds off. If spraying near the face, take precautions to cover the patient's eyes, nose, and mouth. The degree of cooling with from two to four unhurried, even, parallel, nonoverlaping sweeps with the spray, about -inch apart, does not result in local anesthesia, but it is often enough to cause immediate and sometimes lasting disappearance of pain in acute joint sprain or muscle spasm precipitated by trauma.

If an irritative trigger point is involved, spray from the active trigger point to the referred pain zone. Continue the therapy until all trigger points found (several are common) have been sprayed.

To be effective, passive movement must be used while spraying to gently stretch the muscle containing the trigger area. Spray and stretch until the muscle reaches its maximum or normal resting length. The stretch of the muscle should begin as you start spraying the affected area. It should be gentle but firmly applied by a sustaining passive stretch to the muscle while the patient remains relaxed. Overchilling muscle tissue or overstretching will set up painful spasms which defeat the purpose of the therapy. During stretching, you should feel a gradual increase in range of motion of the affected muscle. Active motion in the direction of restriction should be tested after every one or two sweeps. The spraying and stretching may require from two to four applications to achieve the results desired. Stop the treatment if there is no positive effect in 5 min. A few sweeps are usually sufficient to cover the skin representation of the affected muscle and extinguish the pain. Avoid skin frosting. The benefits may last several hours, days, or be permanent.

It takes about 5 min for skin and subcutaneous tissues to rewarm. During this time, moist hot packs can be applied to the area while the procedure is being conducted in another region. Following treatment, the patient should be given some simple exercises to be carried out a few times each day. It is not uncommon to find on a follow-up visit that the original trigger points have vanished and the remaining discomfort can be traced to secondary trigger points missed on the first treatment.

The relief of pain facilitates early mobilization in restoration of muscle function. The benefits are apparently derived from the spray producing nociceptive impulses that propel faster from skin receptors along afferent nerves to higher centers than do noxious impulses from the muscle spindles which travel along smaller afferents. The nociceptive impulses seem to set up a refractory state that blocks the slower muscle-pain impulses. Thus, the muscle is allowed to relax and be stretched to its normal resting length and pain-free state.

While vapocoolant sprays are quite beneficial in acute cases, chronic cases sometimes show better results with acupuncture. This is probably due to an acute case being a purely neurophysiologic disorder at the onset which in time develops organic changes that are benefited by the mechanical effects of the needling of the trigger areas but not by the cooling effect. Nevertheless, dramatic relief of painful motion of many years standing without structural deformity has been reported with only a few sparyings.

A vapocoolant spray may also be used as a clinical aid in diagnosis in differentiating trigger-point disorders from other conditions. For example, if muscle spasm is secondary to some other active cause of musculoskeletal pain or to a neurogenic cause, the relief of the spasm may make the patient's pain worse, pointing the way to a correct diagnosis.

      ACUPUNCTURE

In some cases, trigger sites are more associated with acupuncture points than they are with established trigger-point pathways. It appears that the introduction of impulses by any means at a rate more rapid than pain overloads the dorsal horn of the spinal cord to such an extent that the transmission of pain impulses is not perceived by the patient (gate theory). At least one study has indicated that the results of ultrasonic "acupuncture" are equivalent to that of needle acupuncture, as well as to afford benefits in patient receptiveness, less exactness necessary in site location, and its noninvasiveness.