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
counterbalance 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
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
superficial, essentially resulting from associated tenosynovitis.
It 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
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
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
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.
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
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
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
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
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
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
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
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
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
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
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