Myofascial Pain in Athletes

Background

Voluntary, or skeletal, muscle is the largest single organ of the human body and accounts for nearly 50% of the body's weight. The number of muscles in the body depends on the degree of subdivision that is considered and on the number of variable muscles that are included. Not counting heads, bellies, and other divisions of muscles, the Nomina Anatomica reported by the International Anatomical Nomenclature Committee under the Berne Convention lists 200 paired muscles, or a total of 400 muscles. Any one of these muscles can develop myofascial trigger points (MTrPs).[1] MTrPs are hyperirritable tender spots in palpable tense bands of skeletal muscle that refer pain and motor dysfunction, often to another location.[2, 3]

The myofascial pain syndromes (MPS) owe their ever-widening acceptance to the pioneering work of Travell and her later collaboration with Simons.[2, 3] In 1983, they combined their clinical experience in a detailed description of the multiple pain syndromes attributed to this disorder. In doing so, they further defined the major clinical components that are characteristic of myofascial pain, the most important being the TrP, the taut band, and the local twitch response. See the image below.

Myofascial pain in athletes. Cross-sectional drawing shows flat palpation of a taut band and its trigger point.Left: Skin pushed to one side to begin palpation (A). The fingertip slides across muscle fibers to feel the cord-line texture of the taut band rolling beneath it (B). The skin is pushed to other side at completion of movement. This same movement performed vigorously is snapping palpation (C).Right: Muscle fibers surrounded by the thumb and fingers in a pincer grip (A). The hardness of the taut band is felt clearly as it is rolled between the digits (B). The palpable edge of the taut band is sharply defined as it escapes from between the fingertips, often with a local twitch response (C). NextEpidemiologyFrequencyUnited States

MTrPs are extremely common and become a painful part of nearly everyone's life at one time or another. Latent TrPs, which often cause motor dysfunction (eg, stiffness, restricted range of motion) without pain, are far more common than active TrPs that cause pain.

Active TrPs are commonly found in postural muscles of the neck, shoulder, and pelvic girdles and in the masticatory muscles. In addition, the upper trapezius, scalene, sternocleidomastoid, levator scapulae, and quadratus lumborum muscles are commonly involved.

Reports of the prevalence of MTrPs in specific patient populations are available. The data indicate a high prevalence of this condition among individuals with a regional pain complaint, as shown in Table 1.

Table 1. Prevalence of Myofascial Pain (Open Table in a new window)

RegionPracticeNumber StudiedPrevalence of Myofascial Pain, %GeneralMedical17230GeneralPain medical center9693GeneralComprehensive pain center28385CraniofacialHead and neck pain clinic16455LumboglutealOrthopedic clinic9721

The wide range in the prevalences of myofascial pain caused by TrPs is likely due to differences in the patient populations examined and in the degree of chronicity, at least in part. Probably even more important are differences in the criteria used to diagnose MTrPs and, most important, differences in the training and skill of the examiners.

PreviousNextFunctional Anatomy

Some isolated large round muscle fibers and some groups of these darkly staining, enlarged, round muscle fibers appear in cross-sections. In longitudinal sections, the corresponding feature is a number of contraction knots. An individual knot appears as a segment of muscle fiber with extremely contracted sarcomeres. This contractured segment has a corresponding increase in diameter of the muscle fiber.

The structural features of contraction knots presents a likely explanation for the palpable nodules and the taut bands associated with TrPs. Three single contraction knots can be seen scattered among normal muscle fibers. Beyond the thickened segment of the contractured muscle fiber at the contraction knot, the muscle fiber becomes markedly thinned and consists of stretched sarcomeres to compensate for the contractured ones in the knot segment. In addition, a pair of contraction knots separated by empty sarcolemma may represent one of the first irreversible complications that result from the continued presence of the contraction knot.

PreviousNextSport Specific Biomechanics

The activation of a TrP is usually associated with some degree of mechanical abuse of the muscle in the form of muscle overload, which may be acute, sustained, and/or repetitive. In addition, leaving the muscle in a shortened position can convert a latent TrP to an active TrP; this process is greatly aggravated if the muscle is contracted while in the shortened position.

In paraspinal muscles (and likely other muscles, too), a degree of nerve compression that causes identifiable neuropathic electromyographic (EMG) changes is associated with an increase in the numbers of active TrPs. These TrPs may be activated by disturbed microtubular communication between the neuron and the endplate because the motor endplate is involved in the pathophysiologic process of the peripheral core TrP.

The histopathologic complications that could contribute to the chronicity of the condition and make treatment more difficult include the following:

Distortion of the striations (sarcomere arrangement) in adjacent muscle fibers for some distance beyond the contraction knot (see the image below). This produces unnatural shear forces between fibers that could seriously and chronically stress the sarcolemma of the adjacent muscle fibers. If the membrane were stressed to the point at which it became pervious to the relatively high concentration of calcium in the extracellular space, it could induce massive contracture that could compound the shear forces. Myofascial pain in athletes. Schematic of a trigger point complex of a muscle in longitudinal section.A: The central trigger point (CTrP) in the endplate zone contains numerous electrically active loci and numerous contraction knots. A taut band of muscle fibers extends from the trigger point to the attachment at each end of the involved fibers. The sustained tension that the taut band exerts on the attachment tissues can induce a localized enthesopathy that is identified as an attachment trigger point (ATrP).B: Enlarged view of part of the CTrP shows the distribution of 5 contraction knots. The vertical lines in each muscle fiber identify the relative spacing of its striations. The space between 2 striations corresponds to the length of one sarcomere. The sarcomeres within one of these enlarged segments (ie, contraction knot) of a muscle fiber are markedly shorter and wider than the sarcomeres in the neighboring normal muscle fibers, which are free of contraction knots. The occasional finding of a segment of an empty sarcolemmal tube between 2 contractions knots may represent an additional irreversible complication of a contraction knot.

Latent TrPs can produce other effects characteristic of a TrP, including increased muscle tension and muscle shortening; but these do not produce spontaneous pain. Both active and latent TrPs can cause significant motor dysfunction. The same factors that are responsible for the development of an active TrP can, to a lesser extent, cause a latent TrP. An active key TrP in one muscle can induce an active satellite TrP in another. Inactivation of the key TrP often inactivates its satellite TrP without treatment of the satellite TrP itself.

The intensity and extent of the pattern of referred pain depends on the degree of irritability in the TrP, not on the size of the muscle. MTrPs in small, obscure, or variable muscles can be as troublesome to the patient as TrPs in large familiar muscles.

TrPs are activated directly by acute overload, overwork fatigue, direct impact trauma, and radiculopathy. TrPs can be activated indirectly by other existing TrPs, visceral disease, arthritic joints, joint dysfunctions, and emotional distress. Satellite TrPs are prone to develop in muscles that lie within the pain reference zone of key MTrPs or within the zone of pain referred from a diseased viscus, such as the pain due to myocardial infarction, gastric ulcer, cholelithiasis, or renal colic. A perpetuating factor increases the likelihood of overload stress that can convert a latent TrP to an active TrP.

With adequate rest and in the absence of perpetuating factors, an active TrP may spontaneously revert to a latent state. Pain symptoms disappear; however, occasional reactivation of the TrP by exceeding that muscle’s stress tolerance can account for a history of recurrent episodes of the same pain over a period of years.

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Snapping Hip Syndrome

Background

Snapping hip syndrome is characterized by an audible snap or click that occurs in or around the hip. This syndrome is well recognized but poorly understood. Snapping hip syndrome may be due to an external cause (eg, snapping of the iliotibial band or gluteus maximus over the greater trochanter) or an internal cause (eg, snapping of the iliopsoas tendon over the iliopectineal eminence, acetabular labral tear, intra-articular loose body). Acetabular labral tears and intra-articular loose bodies are relatively uncommon causes of internal snapping hip syndrome and are not discussed in detail. Snapping hip syndrome may be painful or painless. While some athletes may seek attention for a painless audible snap, most do not seek medical attention unless the snapping hip is painful.

NextEpidemiologyFrequencyUnited States

No data are available on the prevalence or incidence of snapping hip syndrome. The syndrome occurs most often in individuals aged 15-40 years and affects females slightly more often than males. In one clinic, the rate of some form of snapping hip syndrome in female ballet dancers with hip complaints was 43.8%, and approximately 30% noted pain with this condition.

PreviousNextFunctional Anatomy

The pelvis is the link between the trunk and the lower extremities. The ball-and-socket joint of the hip allows for 3° of freedom, approximately 120° of flexion, 20° of extension, 40° of abduction, 25° of adduction, and 45° each of internal and external rotation. The iliotibial band, or tensor fascia lata, is a ligament that originates from the iliac crest and inserts on the lateral proximal tibia. Crossing 2 joints, this ligament functions to flex and rotate the thigh medially.

The most common cause of a snapping hip is the iliotibial band snapping over the greater trochanter. This may be associated with trochanteric bursitis or with increased varus of the hip. The finding of a tight iliotibial band is common. Sudden loading of the hip (eg, landing after a jump) may reproduce this sensation of the iliotibial band subluxing over the greater trochanter. With sudden loading, the hip typically is flexed, causing the iliotibial band to move anteriorly followed by the tendon snapping backward as the individual recovers and extends the hip.

The gluteus maximus is the largest of the gluteal muscles and functions as an extensor and external rotator of the hip. Originating along the posterior ilium, dorsal surface of the sacrum, and gluteal aponeurosis, the gluteus maximus inserts on the iliotibial tract and gluteal tuberosity of the femur. During extension of the hip, the distal border may snap over the greater trochanter of the femur.

The psoas and iliacus muscles originate from the lumbar spine and pelvis, respectively, and are innervated by the L1, L2, and L3 nerve roots. These muscles converge to form the iliopsoas muscle and insert onto the lesser trochanter of the proximal femur as the iliopsoas tendon. The psoas major tendon exhibits a characteristic rotation through its course, transforming its ventral surface into a medial surface and its dorsal surface into a lateral surface. The iliac portion of this tendon has a more lateral position and the most lateral muscle fibers of the iliacus muscle insert onto the lesser trochanter of the femur without joining the main tendon. The iliopsoas muscle passes anterior to the pelvic brim and hip capsule in a groove between the anterior inferior iliac spine laterally and the iliopectineal eminence medially. The musculotendinous junction is consistently found at the level of this groove.

The iliopsoas muscle functions as a hip flexor and external rotator of the thigh. Furthermore, an iliopsoas-infratrochanteric muscular bundle has been described, which likely relates to the iliopsoas tendon. This muscular bundle arises from the anterior inferior iliac spine (above the origin of the rectus femoris muscle), courses along the anterolateral aspect of the iliacus muscle, and inserts without a tendon onto the anterior surface of the lesser trochanter of the femur. The iliopsoas bursa lies between the musculotendinous junction and the pelvic brim. An internal cause of snapping hip has been described as the iliopsoas tendon snapping over the iliopectineal eminence, hip capsule itself, or lesser trochanter (less likely). The motion of extending a flexed, abducted, and externally rotated hip reproduces the snapping phenomenon.

Among ballet dancers, those with snapping hip have a narrow bi-iliac width, greater range of movement in hip abduction, decreased range of motion in external rotation, and greater strength in the external rotators of the hip. These findings suggest that skeletal or biomechanical conditions may predispose an individual to the development of a snapping hip.

PreviousNextSport-Specific Biomechanics

In snapping hip syndrome, slightly different biomechanics are involved with the iliotibial band than with the iliopsoas musculotendinous unit. This condition may develop as the result of an acute injury leading to subsequent bursitis, tendinitis, or biomechanical changes. More commonly, snapping hip syndrome is the result of repetitive overuse.

External snapping hip syndrome may be caused by either the iliotibial band or gluteus maximus snapping over the greater trochanter. Subluxation of the iliotibial band over the greater trochanter may occur while the hip extends from a flexed position (in which the iliotibial band moves from a position anterior to the greater trochanter to a position posterior to the greater trochanter). This action is most pronounced with sudden loading of the hip joint into a flexed position, such as occurs when landing a jump (eg, dismounting from an apparatus in gymnastics, rebounding in basketball, long jumping in track-and-field competitions).

The gluteus maximus is a powerful extensor of the thigh and trunk when the lower extremities are fixed. However, it is posturally unimportant, relaxed with standing, and used little in walking. The gluteus maximus is used in activities such as running, climbing, and rising from a seated or stooped position. It also regulates flexion at the hip (a paradoxical action).

Internal snapping hip syndrome is most commonly caused by a snapping of the iliopsoas tendon over the iliopectineal eminence. As an overuse phenomenon, this condition may occur in any activity resulting in repeated hip flexion or external rotation of the femur. Activities that may predispose to iliopsoas tendinitis include dancing, ballet, resistance training (eg, squats), rowing, running (particularly uphill), track and field, soccer, and gymnastics.

During the adolescent growth spurt, a tendency exists for the hip flexors to become relatively inflexible. For younger athletes, this can lead to problems as increased stress is placed on the iliopsoas musculotendinous unit and general biomechanics are altered. Tightness of the iliopsoas, tensor fascia lata, or rectus femoris can lead to inhibition of the gluteus maximus, allowing for an anterior pelvic tilt, which can lead to adverse affects on the kinetic chain.

Excessive anterior tilt due to a tight iliopsoas muscle, tight hip adductors, and a relatively weak rectus abdominis can lead to increased lumbar lordosis with subsequent increased stress on the lower lumbar disks, facet joints, and sacroiliac joints. This also may result in increased knee flexion during gait at the heel-strike and midstance phases. The increase in eccentric load across the knee extensor mechanism may result in patellar tendon injuries (eg, patellar tendinitis, Osgood-Schlatter disease). With increased knee flexion, compressive forces at the patellofemoral articulation increase and may predispose to patellofemoral problems.

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Femur Injuries and Fractures

Background

The spectrum of femoral shaft fractures is wide and ranges from nondisplaced femoral stress fractures to fractures associated with severe comminution and significant soft-tissue injury. Femoral shaft (see image below) fractures are generally caused by high-energy forces and are often associated with multisystem trauma. Isolated injuries can occur with repetitive stress and may occur in the presence metabolic bone diseases, metastatic disease, or primary bone tumors.[1, 2]

An example of an isolated, short, oblique midshaft femoral fracture, which is very amenable to intramedullary nailing. Although not seen in this x-ray film, radiographic visualization of both the proximal and distal joints should be performed for all diaphyseal fractures.

Most femoral diaphyseal fractures are treated surgically with intramedullary nails or plate fixation. The goal of treatment is reliable anatomic stabilization, allowing mobilization as soon as possible. Surgical stabilization is also important for early extremity function, allowing both hip and knee motion and strengthening. Injuries and fractures of the femoral shaft may have significant short- and long-term effects on the hip and knee joints if alignment is not restored.

Treatment of femoral shaft fractures has undergone significant evolution over the past century. Until the recent past, the definitive method for treating femoral shaft fractures was traction or splinting. Before the evolution of modern aggressive fracture treatment and techniques, these injuries were often disabling or fatal. Traction as a treatment option has many drawbacks, including poor control of the length and alignment of the fractured bone, development of pulmonary insufficiency, deep vein thrombosis, and joint stiffness due to supine positioning.

The femur is very vascular and fractures can result in significant blood loss into the thigh. Up to 40% of isolated fractures may require transfusion, as such injuries can result in loss of up to 3 units of blood.[3] This factor is significant, especially in elderly patients who have less cardiac reserve.

Femoral fracture patterns vary according to the direction of the force applied and the quantity of force absorbed. A perpendicular force results in a transverse fracture pattern, an axial force may injure the hip or knee, and rotational forces may cause spiral or oblique fracture patterns. The amount of comminution present increases with the amount of energy absorbed by the femur at the time of fracture.[1, 2, 4, 5]

For excellent patient education resources, visit eMedicineHealth's First Aid and Injuries Center. Also, see eMedicineHealth's patient education article Broken Leg.

Related Medscape Reference topics:

Femoral Neck Stress and Insufficiency Fractures [in the Orthopedic Surgery section]

Femoral Neck Stress Fracture

Femur Fracture [in the Emergency Medicine section]

Related Medscape resources:

Resource Center Exercise and Sports Medicine

Specialty Site Emergency Medicine

Specialty Site Orthopaedics

CME A 49-Year-Old Man With a Femur Fracture and Hyperdense Bones

CME Vitamin D and Musculoskeletal Health

NextEpidemiologyFrequencyUnited StatesThe incidence of femoral fractures is reported as 1-1.33 fractures per 10,000 population per year (1 case per 10,000 population). In individuals younger than 25 years and those older than 65 years, the rate of femoral fractures is 3 fractures per 10,000 population annually. These injuries are most common in males younger than 30 years. Causes may include automobile, motorcycle, or recreational vehicle accidents or gunshot wounds. The average number of days lost from work or school from femoral fractures is 30.The average number of days of restricted activity due to femoral fractures is 107.The incidence of femoral injuries and fractures increases in elderly patients.PreviousNextFunctional Anatomy

The femur is the strongest, longest, and heaviest bone in the body and is essential for normal ambulation. It consists of 3 parts (ie, femoral shaft or diaphysis, proximal metaphysis, distal metaphysis). The femoral shaft is tubular with a slight anterior bow, extending from the lesser trochanter to the flare of the femoral condyles. During weight bearing, the anterior bow produces compression forces on the medial side and tensile forces on the lateral side. The femur is a structure for standing and walking, and it is subject to many forces during walking, including axial loading, bending, and torsional forces. During contraction, the large muscles surrounding the femur account for most of the applied forces.[1, 2, 4, 5]

Several large muscles attach to the femur. Proximally, the gluteus medius and minimus attach to the greater trochanter, resulting in abduction of the femur with fracture. The iliopsoas attaches to the lesser trochanter, resulting in internal rotation and external rotation with fractures. The linea aspera (rough line on the posterior shaft of the femur) reinforces the strength and is an attachment for the gluteus maximus, adductor magnus, adductor brevis, vastus lateralis, vastus medialis, vastus intermedius, and short head of the biceps. Distally, the large adductor muscle mass attaches medially, resulting in an apex lateral deformity with fractures. The medial and lateral heads of the gastrocnemius attach over the posterior femoral condyles, resulting in flexion deformity in distal-third fractures.

The blood supply enters the femur through metaphyseal arteries and branches of the profunda femoris artery, penetrating the diaphysis and forming medullary arteries extending proximally and distally. With intramedullary nailing, the blood supply is disrupted and progressively reestablishes itself over 6-8 weeks. Healing of the fracture is enhanced by the surrounding soft tissue and local recruitment of blood supply around the callus. The femoral artery courses down the medial aspect of the thigh to the adductor hiatus, at which time it becomes the popliteal artery. Injuries to the artery occur at the level of the adductor hiatus, where soft-tissue attachments may cause tethering. Uncommonly, the sciatic nerve is injured in femoral shaft fractures; however, it may become injured in proximal or distal femoral injuries.

Related Medscape Reference topics:

Nerve Entrapment Syndromes [in the Neurosurgery section]

Nerve Entrapment Syndromes of the Lower Extremity [in the Orthopedic Surgery section]

PreviousNextSport-Specific Biomechanics

Trauma-induced fractures of the femur occur with contact and during high-speed sports. A significant amount of energy is transferred to the limb in a femur fracture, such as might be generated in skiing, football, hockey, rodeo, and motor sports.

Stress fracture

A femoral stress fracture is the result of cyclic overloading of the bone or a dramatic increase in the muscular forces across their insertion, causing microfracture. These repetitive stresses overcome the ability of the bone to heal the microtrauma. The area most susceptible to stress fracture is the medial junction of the proximal and middle third of the femur, which occurs as a result of the compression forces on the medial femur.

Stress fractures can also occur on the lateral aspect of the femoral neck in areas of distraction and are less likely to heal nonoperatively than compression-side stress fractures. Stress fractures occur most often in repetitive overload sports such as in runners and in baseball and basketball players. For more information, refer to the Medscape Reference article Femoral Neck Stress Fracture.

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Patellar Injury and Dislocation

Background

Patellar pain is common in both athletic and nonathletic individuals. Among athletes, men tend to present with more patellofemoral injuries, including traumatic dislocations, than women. In the nonathletic population, women present more commonly with patellar disorders.

Anatomic morphology of patellar insertion into the intercondylar notch. Muscles influencing patellar biomechanics.

Patellofemoral problems are mainly diagnosed by obtaining a thorough history and performing a physical examination. Imaging studies help confirm the diagnosis. Plain radiography is not as sensitive as magnetic resonance imaging (MRI), but it is the least expensive and most readily available modality.

Patellofemoral syndromes are usually the result of biomechanical imbalances of the kinetic chain, with each individual having an optimal joint-loading limit that is dependent on his or her unique skeletal and muscular anatomy, combined with his or her unique neuromuscular patterning. As this limit is surpassed, the patient is at risk for either acute injury, such as patella dislocation, or chronic injury, such as patellofemoral pain syndrome. Therefore, the goal of a rehabilitative treatment program must be to guide the patient toward performing functional activities without surpassing his or her optimal joint-loading limit. Therapy techniques need to be designed around this principle.

In general, surgery is more effective in preventing recurrences of dislocation because skeletal and muscular components of the patellofemoral joint and extensor mechanism are realigned; however, surgery also has risks. In a patient with normal anatomy, surgery should be considered an option after all conservative treatment modalities are unsuccessful. Patients with anatomic abnormalities may benefit from earlier surgical consideration.

Traditionally, several different systems have been used to classify patellofemoral dysfunction. Some were developed from a functional perspective, whereas others were developed from an anatomic viewpoint. This latter perspective was held by Insall and Merchant, who classified patellofemoral dysfunction according to anatomy.

In 1972, Insall proposed a method of classification based on cartilage damage. The 3 categories in his system are normal, damaged, and variably damaged cartilage. In 1986, Fulkerson and Schutzer developed a system based on measuring arthralgias against joint instability to determine the necessity for surgical intervention. In 1988, Merchant created a system of 5 categories for patellofemoral dysfunction, which included acute trauma, dysplasia, idiopathic chondromalacia, osteochondritis dissecans, and synovial plicae.

No standardized and widely accepted method of patellofemoral dysfunction classification applicable for all specialties has been developed. However, for the purposes of rehabilitation medicine, patellofemoral disorders may be loosely divided into 3 categories. These are soft-tissue abnormalities, patellar instability due to subluxation and dislocation, and patellofemoral arthritis.

For excellent patient education resources, visit eMedicineHealth's First Aid and Injuries Center. Also, see eMedicineHealth's patient education articles Knee Pain and Knee Injury.

NextEpidemiologyFrequencyUnited States

Pain of the patellofemoral joint secondary to patellofemoral dysfunction is the most common disorder of the knee. A 5-year study published in 1984 revealed that 25% of all knee issues in a sports injury clinic were of patellofemoral origin. Another study similarly revealed that 1 in 4 runners is afflicted by patellofemoral pain. Whether related to sports or not, 1 of every 4 painful knees has been reported to be the result of patellofemoral dysfunction.

Patellar injury and dislocation are more prevalent in individuals who participate in certain sports and activities. Anterior knee pain is the most common initial manifestation. In order of descending prevalence, soccer players, weight lifters, runners, and shooters regularly report acute knee pain. In addition, studies show soccer players and weight lifters have the most potential for long-term knee pain.

One study reported 52% of 31 soccer players, 31% of 29 weightlifters, 21% of 28 long-distance runners, and 17% of 29 shooters reported knee pain at least once per month.[1] Thijs et al evaluated gait-related intrinsic risk factors for patellofemoral pain in 102 novice recreational runners.[2] The authors findings suggested an increased risk for patellofemoral pain may be due to excessive impact shock during heel strike and at the propulsion phase of running. In addition, Thijs et al believe their results do not support the theory that those at risk for this condition show an altered static foot posture relative to those who are unaffected.[2]

Swimming also places the athlete at risk for knee pain.[3] On the other hand, sports such as tennis are not associated with knee pain. In summary, factors that cause knee pain include the type, amount, and duration of sports activity.

In addition to activity-specific variance, patellofemoral pain displays some variation between the sexes. A study revealed that in the general population, the female-to-male ratio for patellofemoral dysfunction is 2:1. However, in the athletic population, more men than women experience such syndromes. Further, the study revealed acute dislocation occurred more frequently in males and that recurrent dislocation may be more common in individuals whose initial dislocation occurred when they were younger than 15 years.

Patellofemoral disorders are more likely the result of inappropriate activity duration and type as opposed to genetic factors. Aoyagi et al examined the higher prevalence of joint pain of female Japanese individuals living in rural Japan versus female Americans of Japanese descent living in Hawaii.[4] Despite the similar genetic stock, significant differences in prevalence of joint pain were noted. The researchers postulated that environmental factors influencing activity levels and types were responsible.

Similarly, Zhang et al found that Chinese women in Beijing have a higher prevalence of knee osteoarthritis versus American women in Framingham, Massachusetts.[5] Again, this was thought to be the result of the lower activity levels of women living in the United States. In the same study, men from Beijing were found to have a similar incidence of knee osteoarthritis compared with their Framingham counterparts.

International

Nietosvaara et al studied the annual incidence of acute patellar dislocations in Finnish children younger than 16 years.[6] They found an annual incidence of 43 cases per 100,000 children. Over a 2-year period, 72 children revealed patellar dislocations. Of these, 28 (39%) of the knees had associated osteochondral fractures. Of the 28 osteochondral fractures, 15 had capsular avulsions of the medial patellar margin, and another 15 had intra-articular fragments from the patella and/or lateral femoral condyle.[6]

PreviousNextFunctional Anatomy

Soft-tissue elements that affect the patella are the stabilizing capsular and ligamentous structures within which the patella lies. Some ligaments of the knee are continuous with the fibrous capsule surrounding the patella. When injuries occur, all structures are simultaneously affected. These ligaments hold the patella in place during static and dynamic phases.

The synovial capsule, a separate structure, lies deep to the fibrous capsule and may often be damaged.

The regional anatomy of the knee soft tissues is as follows:

Anteriorly: The synovial capsule forms attachments around the peripheral margins of the patella.Laterally: The lateral or fibular collateral ligament is a tough, round cord that attaches proximally at the lateral epicondyle of the femur and distally at the head of the fibula. This ligament transects the tendon of the biceps femoris, and the popliteus tendon runs medial to it. The biceps femoris tendon is very strong, rarely tears, and protects the joint against varus forces. If torn, the biceps femoris tendon usually tears at the distal end, and the peroneal nerve may be injured, resulting in foot drop. In such cases, the head of the fibula is often fractured because the ligament is stronger than the bone. Increased tension from these lateral structures predisposes individuals for lateral patellar tracking and dislocation. Medially The medial or tibial collateral ligament is a flat band extending from the medial epicondyle of the femur to the medial condyle of the tibia. The medial collateral ligament is continuous with the medial meniscus and the capsule of the knee joint. Three medial ligamentous structures provide static restraint to lateral movement of the patella. These were further defined by a cadaveric study conducted by Andrikoula et al.[7] The medial patellofemoral ligament (MPFL) is a band of retinacular tissue that originates at the medial femoral condyle and attaches to the proximal two thirds of the medial border of the patella. This ligament is overlaid by the distal fibers of the vastus medialis obliquus (VMO) muscle, and the authors found that to a variable extent, its fibers merge into the deep aspect of this muscle. The medial patellomeniscal ligament (MPML) attaches the anterior horn of the medial meniscus to the inferior border of the medial patella. The medial patellotibial ligament (MPTL) connects the distal patella to the tibia.The MPFL has been found to be the major medial soft-tissue restraint to patellar lateral displacement. Studies indicate that up to 97% of acute lateral patella dislocations result in disruption of the MPFL. In studies examining in vitro patella subluxation, an isolated release of the MPTL resulted in a 50% increase in lateral displacement. The results of one study on pediatric patients noted that the zone of MPFL injury after primary patellar dislocation was predominantly isolated to the patellar attachment, which is in contrast to previously published literature. MRI findings showed that the anatomic insertion of the MPFL is distal to the physis in 93% of patients and that the MPFL is more likely to be injured at the patellar attachment. These data provide important evidence to assist in surgical reconstruction of the MPFL in pediatric or adolescent patients.[8] Finally, the 2 more distal structures, the MPML and MPTL, provide important secondary restraints.Posteriorly: The oblique popliteal ligament is broad and strengthens the synovial capsule posteriorly. The oblique popliteal ligament originates inferiorly from the medial condyle of the tibia, and it inserts superiorly and laterally to the posterior aspect of the capsule. The posterior capsule is supplemented by the arcuate popliteal ligament, which stretches from the fibular head and splits. Some fibers run medially to insert into the tibial intercondylar area, and other fibers run superiorly and medially to the posterior lateral epicondyle of the femur. Superiorly: The knee joint capsule inserts into the femur proximal to the condylar margins anteriorly and intercondylar line posteriorly. Inferiorly: The knee joint capsule attaches to the articular margin of the tibia and to the fibular head. The capsule opening for the popliteus is located here. The capsule has openings to the bursae and to the popliteus muscle and tendon.

Pain may develop in these periarticular soft-tissue structures as a result of patellofemoral dysfunction, or vice versa. All these structures operate as a functional unit to optimize weight-bearing capacity. These structures decrease joint-reaction forces (JRFs) and form a base of support for the upper body. If one of these structures is altered, a greater risk of patellar injury and dislocation can develop.

The patellofemoral mechanism is very complicated. Patellofemoral malalignment, abnormal patellar configuration, and a previous history of instability increase the risk for anterior knee pain, patellar dislocation, and recurrent dislocations. The risk for symptoms increases when a combination of factors exists.

PreviousNextSport-Specific Biomechanics

Excluding acute patellar trauma, patellar injury and dislocation are the end result of patellofemoral force imbalances. These force imbalances may also result in less dramatic presentations of patellofemoral pain. Deformities of cartilage resulting from arthritis; congenital variants of the patellofemoral joint; imbalances in lower extremity muscular strength and/or firing pattern; skeletal imbalances at the hip, knee, ankle, or foot; and changes of the patellar stabilizing capsular and ligamentous elements may also contribute to the development of patellofemoral pain and/or dislocations.

The patella is the largest sesamoid bone in the body, and it resides within the complex of the quadriceps and patellar tendons, superiorly and inferiorly, respectively. The patella assists in coordinating the forces of these tendons and functions as both a lever and a pulley. As a lever, the patella magnifies the force exerted by the quadriceps during knee extension. As a pulley, the patella redirects the quadriceps force as it undergoes normal lateral tracking during flexion.

The greater the anteroposterior length of the patella, the greater the angle between the quadriceps and patellar tendons, thus decreasing the force generation needed by the quadriceps to support the upper body at any particular angle of knee flexion. One study demonstrated that the patella most significantly increases the moment arm of the quadriceps at 20° of knee flexion. After patellectomy, the moment arm of the quadriceps is obliterated. After patellectomy, one study demonstrated the effectiveness of the quadriceps-patellar moment arm to be reduced by 31% at 0° of flexion, 22% at 30°, 13% at 60°, 12% at 90°, and 10% at 120°.

The quadriceps tendon and the patellar tendon are continuous with each other and work in cooperation. Muscular forces are transmitted in differing proportions to each tendon over the changing angle of the knee as it flexes and extends. At different angles of knee flexion, the quadriceps and the patellar tendons appear to alternate the role of being the primary force transmitter. From 0-20° of knee flexion, the consensus among researchers is that tension in the patellar tendon is greater than in the quadriceps tendon. From 20-50° of flexion, which tendon has more tension is controversial among research findings. From 50° to full flexion, tension in the quadriceps tendon is greater than in the patellar tendon. Theoretically, isolated development of either the quadriceps tendon or the patellar tendon is accomplished by appropriately limiting knee flexion in exercise programs.

The chondral surface of the patella articulates with the trochlear surface of the distal femur, which forms a groove between the medial and lateral femoral condyles anteriorly. The trochlear surface is continuous with the intercondyloid fossa as it extends inferiorly and posteriorly. The lateral aspect of the trochlear surface is more prominent than the medial aspect, and it extends further anteriorly.

The chondral surface of the patella has several divisions. The 3 transverse ridges create 3 roughly equal-sized upper, middle, and lower groups. Two vertical ridges are found on the chondral surface of the patella. The prominent median vertical ridge separates the medial and lateral facets. The facets are at an acute angle to each other, with the prominent ridge acting as their adjoining corner.

These structures form a V-shaped wedge along the transverse plane for the purpose of better insertion into the depression formed by the trochlear groove. The lateral facet is larger in most individuals. The medial facet is further separated into medial and lateral surfaces by a less prominent vertical ridge. The medial surface of the medial facet is sagittally oriented and only makes contact with the femur when the knee is flexed past 90°. Pain at this range of motion (ROM) that is associated with a compressive mechanism, such as increased JRFs, is suggestive of lesions on the chondral surface.

In full extension, the patella does not fit into the trochlear groove but lies over the smooth synovial tissue that overlies the supratrochlear tubercle. The lateral aspect of the tubercle has a smooth, continuous transition with the trochlear groove. The medial aspect of the tubercle is sharply elevated in regard to the trochlear groove. In normal motion, the patella moves superolaterally, riding the lateral aspect of the supratrochlear tubercle so that it makes a smooth translation from the groove to the tubercle.

The cartilage of the patella contacts the trochlear cartilage of the femur to reduce friction during motion of the patellofemoral joint. Gross normal joint motion is along a sagittal plane. This is why examination of the joint at the transverse plane reveals a congruent articulation, whereas the joint along the sagittal plane is incongruent. Good contact at the transverse plane promotes medial/lateral stability, whereas the incongruent sagittal articulation provides more free space for superior/inferior movement.

Compared with the femoral cartilage, the patellar cartilage is thicker, more pliant, and more permeable. In fact, the cartilage of the inner patella at the prominent median vertical ridge is normally the thickest cartilaginous structure in the body, suggesting its role in counteracting tremendous JRFs. These characteristics of the patellar cartilage allow it to sit deeper in the trochlear groove and conform to its shape, allowing for better articulation and distribution of JRFs. However, these actions place a burden on the collagen-proteoglycan matrix of the patellar cartilage and may be the reason for the higher prevalence of patellar cartilaginous lesions compared with femoral trochlear cartilaginous lesions.

JRFs at the patellofemoral joint are directly related to the contraction of the quadriceps.

The stress at the patellofemoral joint can be mathematically defined as the sum JRF divided over the surface area of force distribution. From 0-60°, the surface area of the patella contacting the femur enlarges with increased knee flexion. This provides a larger contact surface area over which to distribute the load as the load is increasing. Beyond 60° of flexion, anatomic studies regarding the contact area have been inconclusive.

The location of contact for the patella and femur vary with different degrees of flexion and joint load. At 0°, no contact occurs; in early flexion, the distal patella contacts the proximal trochlea; at 90° of flexion, the superior aspect of the patella contacts the femur; when flexion is greater than 90°, the contact area returns to the center of the patella; and when the knee is fully flexed, the inner border of the medial femoral condyle is in contact with the small vertical ridge of the medial facet.

Lateral tracking of the patella leads to decreased efficiency of the quadriceps extensor mechanism and increased patellofemoral joint stress. A lateral patellar subluxation of only a few millimeters results in a decreased contact surface area between the patellar and trochlear surfaces as the lateral facet moves closer to the lateral side of the trochlear groove and the distance between the medial facet and the medial side of the trochlear groove increases. The total JRF, initially distributed over both patellar facets, is now completely transmitted to the lateral patellar facet. This increases lateral facet stress and may result in pain, chondromalacia, and the development of arthritic changes.

A summary of forces on the patellofemoral joint follows. They maintain the physiologic positioning of the patella dynamically within the trochlea and extensor mechanism and provide for patella stability and proper tracking.

Static stabilizers: These provide fixed inhibition to lateral translation of the patella and most notably include the MPFL but also include the MPML and MPTL. These 3 structures play a primary role in stabilization during the first 20-30° of knee flexion when the patella has not fully engaged the trochlea. At knee flexion greater than 30°, the geometry of the patella-trochlea interface combined with posteriorly directed force vectors provide most of the stabilization for the joint. Dynamic stabilizers: These are muscular structures and are primarily the quadriceps group. The VMO muscle has been noted to provide a medially directed dynamic stabilizing force on the patella during knee extension. Andrikoula et al's cadaveric study demonstrated that the VMO fibers are at approximately a 40° medially directed angle to the rectus tendon.[7] Weakness of the quadriceps in general, and specifically of the VMO, allows lateral tracking and deviation of the patella. With persistent lateral patellar deviation, lateral structures (eg, distal fibers of the iliotibial band) contract, resulting in further lateral deviation and greater lateral subluxation. Lateral deviation of the patella also results in altered VMO length and/or tension, which may diminish the medially directed force generation of the VMO muscle. The adductor magnus should also be noted with this group because the distal fibers of the VMO often attach to the adductor magnus tendon and strengthening of the adductor group may contribute to the ability of the VMO to provide active, dynamic restraint.

A summary of risk factors for patella subluxation and dislocation is as follows:

Disruption of either of the 2 groups of stabilizers noted abovePatella alta: This is an abnormally high-riding patella and is associated with a long patella tendon. In a healthy knee, the patella is roughly equal in length to the patella tendon. In patella alta, the ratio of the tendon length to the patella body length is increased, placing the patella in an elevated position that delays patella engagement of the trochlea until an increased angle of flexion. This greatly increases the risk for dislocation. Several different methods can be used to measure patellar instability on a true lateral radiograph of the knee. One such method is the Insall-Salvati index. Patella alta is defined as a ratio of patella tendon length divided by the greatest diagonal length of the patella equal to greater than 1.2. Escala et al found 78% sensitivity and 68% specificity for objective patella instability (OPI) for this parameter.[9] Patella tilt: This parameter may be measured on various axial views of the knee. For patella tilt greater than 11°, Escala et al found 93% sensitivity and an odds ratio of 8.7 for OPI.[9] They found this single parameter to be of the highest combined sensitivity and specificity for identifying patients with OPI. Hypoplastic trochlea: This may also be evaluated on a true lateral radiograph. A classification system was designed by Dejour et al and defined 4 grades of dysplasia.[10] Dejour et al also suggested that the so-called crossing sign they introduced was present on 96% of their patients with patella instability. Using a measurement of trochlear groove depth at the Roman arch level, Escala et al found 85% sensitivity and an odds ratio of 7.7 for OPI.[9] Elevated Q-angle: This represents an estimate of potential lateralizing forces on the patella and is affected by several skeletal features. It is the intersection of 2 lines on the anterior aspect of the lower extremity of a standing patient. One line is from the anterior superior iliac spine to the middle of the patella, and the second line is from the tibial tubercle to the middle of the patella; the Q-angle is the angle between these lines. A Q-angle greater than 15° may predispose an individual to lateral patellar tracking and possible dislocations, although some authors report as high as 20° within a patient’s normal range. This topic is explored in more detail in Physical. Genu valgum: This medially directed knee joint may be the result of a valgus femur, valgus tibia, or intra-articular height loss within the lateral compartment of the knee. Genu valgum may be evaluated on an anteroposterior radiograph. Increased valgum increases the tendency for valgus motion of the knee joint with loading and, as such, increases the potential for lateral motion of the patella. Increased femoral anteversion: This increases the internal rotation of the femur and increases the lateral displacement force vector affecting the patella. According to Post et al, this factor is additive when associated with concurrent genu valgum.[11] This factor may be clinically estimated by evaluating relative internal versus external rotation at the hip. However, accurate measurement is best obtained with computed tomography (CT) scanning of the hips. Coxa valga: This also increases the lateral displacement force vector acting on the patella. This skeletal factor increases valgus stress at the knee. Foot pronation: When present, this contributes to the lateral forces on the patella. It can be easily managed with in-shoe orthotics. Lateral tibial tubercle: This moves the pull of the extensor mechanism laterally and thus increases laterally directed forces on the patella. External tibial torsion: This contributes to the lateral placement of the tibial tubercle, thus increasing the effective Q-angle and increasing the lateral displacement vector acting on the patella. Family history of dislocation: This is reported in the literature and may represent a correlation with an underlying biomechanical anomaly preserved among family members. Other: Escala et al identified other radiographic measurements that are indicators of OPI. These include short patella nose ([9] Kinetic chain models

JRFs of the patellofemoral joint are different when studied under closed and open kinetic chain models. When the kinetic chain is closed (eg, leg press, squats), the JRF increases when the knee is flexed 0-90°. To counteract this load, a greater surface area of the patella comes into contact with the femur, effectively dissipating the forces. However, the contact area does not increase as much as the reaction force. Therefore, forces on the contact areas increase during flexion to 90°. Further flexion greater than 90° causes a leveling off or a decrease in the JRFs. After 90° of flexion, the contact of the quadriceps tendon with the trochlear groove further diffuses the load. Irrespective of the cause, JRFs decrease when the knee is flexed 90-120°.

The open-chain model encompasses lower extremity non – weight-bearing exercises such as leg curls and extensions. When the leg is at 0° flexion, the reaction forces of the patellofemoral joint are low because the patella does not contact the femur when the leg is in full extension. Studies have shown widely varying results from 5-25° of flexion. With the knee flexed to 90°, the JRFs increase and the contact area decreases, resulting in very high patellofemoral stress. A study of knee flexion-extension with a 0.9-kg ankle weight showed JRFs are greatest at 36° of flexion. JRFs are lowest at 90° of flexion.

Closed-chain exercises are most protective for the patellofemoral joint when performed at 0-45° of flexion. Open-chain exercises should be performed from 0-5° of flexion and from 90° to full flexion. JRFs should be limited as much as possible during repetitive motion to avoid chondrosis and chondromalacia. In strengthening or rehabilitative exercises for the quadriceps, programs should be designed with open and closed kinetic chain models in mind.

Anatomic variants

When evaluating patients with patellofemoral disorders, the physician needs to consider anatomic variants, which often manifest as bone deformities and would include bipartite patellae. Additionally, the knee joint may be affected by congenital anomalies. Many genetic syndromes involve the knee joint, including congenital patellar aplasia, nail patella syndrome, small patella syndrome, Meir-Gorlin syndrome, RAPADILINO syndrome (RA for radial, PA for absent/hypoplastic patellas and cleft/high-arched palate, DI for diarrhea/dislocated joints, LI for little size/limb malformations, NO for long, slender nose/normal intelligence), and genitopatellar syndrome. A 2005 article by Bongers et al reviews genetic anomalies in greater depth.[12]

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Posterior Cruciate Ligament Injury

Background

The posterior cruciate ligament (PCL) is described as the primary stabilizer of the knee by many authors. PCL injuries are less common than anterior cruciate ligament (ACL) injuries, and they often go unrecognized. The PCL is broader and stronger than the ACL and has a tensile strength of 2000 N. Injury most often occurs when a force is applied to the anterior aspect of the proximal tibia when the knee is flexed. Hyperextension and rotational or varus/valgus stress mechanisms also may be responsible for PCL tears. Injuries may be isolated or combined with other ligamentous injuries. A PCL tear can result in varying degrees of disability, from no impairment to severe impairment. PCL injury has been overly simplified, and the functional disability of PCL injury may be underestimated.[1] The radiographs belowdemonstrate the results of suchinjuries, comparing a normal knee with one that has a damaged PCL.

A normal lateral radiograph of a knee. In a normal knee, a line drawn along the posterior femoral condyle will not intersect the posterior tibial condyle. A lateral radiograph of a knee with a posterior cruciate ligament injury. Note that the same line as in the above image will bisect the posterior tibial condyle due to a posterior sag and an incompetent posterior cruciate ligament.

The primary function of the PCL is to prevent posterior translation of the tibia on the femur. The PCL also plays a role as a central axis controlling and imparting rotational stability to the knee. This injury has received little attention in the past, compared with the ACL; however, this emphasis on the ACL has stimulated increased interest in the treatment of PCL injuries. Controversy regarding treatment of isolated PCL injuries exists in the literature, with recommendations supporting both operative and nonoperative therapy. Current management of PCL injuries unfortunately can yield relatively poor clinical outcomes, whether surgically or conservatively treated.[2]

NextEpidemiologyFrequencyUnited States

True incidence in the United States is unknown. In National Football League predraft physical examinations, a 2% incidence of isolated, asymptomatic, and unknown PCL injuries was found; operated, isolated, and combined PCL injuries were reported at an incidence of 3.5-20%. On the KT-1000 stress test examination, a 7% incidence of PCL injuries was found, of which 40% were isolated and unidirectional and 60% were multidirectional.

PreviousNextFunctional Anatomy

As demonstrated in the images below, the PCL originates from the intercondylar notch of the femur on the roof of the medial femoral condyle. The insertion is central on the posterior aspect of the tibial plateau, on a depression between the tibial plateaus, extending 1 cm below the articular surface.[3] The ligament is composed of a larger anterolateral bundle and a smaller posteromedial bundle. The anterior component is tightest in the midarc of flexion and the posterior fibers are tight in extension and deep flexion.

A view of the broad origin of the posterior cruciate ligament (PCL) on the medial femoral condyle of a left knee. The anterior cruciate ligament has been removed for surgical reconstruction. An additional view of the posterior cruciate ligament broad origin and insertion in a knee pending anterior cruciate ligament reconstruction.

In addition, variable anterior and posterior meniscofemoral ligaments of Humphrey and Wrisberg attach distally and proximally to the PCL, respectively. The meniscofemoral ligaments attach distally to the posterior horn of the lateral meniscus, in a slanting orientation, providing resistance to the tibial posterior drawer.[4] The PCL is an extrasynovial structure that lies behind the intra-articular portion of the knee. The primary function of the PCL is to resist posterior displacement of the tibia in relation to the femur; its secondary function is to prevent hyperextension and limit internal and varus/valgus rotation.

PreviousNextSport Specific Biomechanics

Disruption may occur with forced hyperextension while the foot is planted in dorsiflexion. A force applied to the anteromedial aspect of the knee, as during a football tackle, results in a posteriorly directed force and a varus hyperextension force, leading to PCL and posterolateral capsular ruptures.

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Iliopsoas Tendinitis

Background

Hip and pelvis injuries represent 2-5% of all sports injuries. Among these injuries, groin pain is the most common finding. The most common sports-related injuries in the hip, pelvis, and thigh area are musculotendinous, (eg, quadriceps strain, adductor tendinitis) and, less commonly, iliopsoas tendinitis. Iliopsoas tendinitis and iliopsoas bursitis are closely interrelated because inflammation of one inevitably causes inflammation of the other, due to their close proximity. Therefore, these 2 conditions are essentially identical in terms of presentation and management.

In basic terms, iliopsoas tendonitis is an inflammation of the tendon or area surrounding the tendon. Major causes of iliopsoas tendinitis are acute trauma and overuse resulting from repetitive hip flexion. See the image below.

Iliopsoas stretch. NextEpidemiologyFrequencyUnited States

No data on prevalence of iliopsoas tendinitis exists. Despite this, it is a relatively uncommon and poorly recognized cause of anterior hip or groin pain. Iliopsoas tendinitis is noted to affect young adults more commonly, with a slight female predominance.

PreviousNextFunctional Anatomy

The pelvis links the trunk and lower extremities. The hip, a ball and socket joint, allows for 3 degrees of freedom. Range of motion (ROM) of the hip includes approximately 120° of flexion, 20° of extension, 40° of abduction, 25° of adduction, and 45° each of internal rotation and external rotation. The resting position of the hip is considered to be 30° of flexion and 30° of abduction.

The psoas and iliacus muscles originate from the lumbar spine and pelvis, respectively, and are innervated by the upper lumbar nerve roots (ie, L1, L2, L3). These muscles converge to form the iliopsoas muscle, which inserts onto the lesser trochanter of the proximal femur as the iliopsoas tendon. The psoas major tendon exhibits a characteristic rotation through its course, transforming its ventral surface into a medial surface. The iliac portion of this tendon has a more lateral position, and the most lateral muscle fibers of the iliacus muscle insert onto the lesser trochanter without joining the main tendon.

The iliopsoas muscle passes anterior to the pelvic brim and hip capsule in a groove between the anterior inferior iliac spine laterally and iliopectineal eminence medially. The musculotendinous junction is consistently found at the level of this groove. The iliopsoas muscle functions as a hip flexor and external rotator of the femur.

An ilio-infratrochanteric muscular bundle has been described, which likely relates to the iliopsoas tendon. This muscular bundle arises from the interspinous incisure and anterior inferior iliac spine (above the origin of the rectus femoris muscle), courses along the anterolateral edge of the iliacus muscle, and inserts without a tendon onto the anterior surface of the lesser trochanter. The iliopsoas bursa lies between the musculotendinous junction and the pelvic brim. This bursa is the largest in the body and may extend proximally into the iliac fossa or distally to the lesser trochanter. Communication between this bursa and the hip joint occurs in approximately 15% of all adults.

A variety of terms have been used to describe and classify tendon injuries. Tendonitis is typically associated with an acute injury through which failure of the tendon fibers and disruption of the vascularized peritendinous connective tissue produces an acute inflammatory response within the tendon. Tendinitis may be acute, subacute, or chronic, depending on the duration of symptoms.

Peritendinitis is a condition in which an acute injury produces an inflammatory response in only the soft tissue surrounding a tendon, without disruption of the tendon fibers. On the other hand, tendinosis is often associated with chronic microtrauma to the tendon, such as repetitive overload. In the case of tendinosis, fiber failure tends to be characterized by intrasubstance failure, compared with peritendinous disruption, which occurs in tendinitis. Microscopic findings in tendinosis include fibrillar degeneration, angiofibroblastic proliferation, myxoid degeneration, fibrosis, and, occasionally, chronic inflammation.

PreviousNextSport-Specific Biomechanics

Acute injury and overuse injury are the 2 main causes of iliopsoas tendinitis. The acute injury typically involves an eccentric contraction of the iliopsoas muscle, but also may be due to direct trauma. Overuse injury may occur in activities involving repeated hip flexion or external rotation of the thigh. Activities that may predispose to iliopsoas tendinitis include dancing, ballet, resistance training, rowing, running (particularly uphill), track and field, soccer, and gymnastics.

During the adolescent growth spurt, the hip flexors tend to become relatively inflexible. This inflexibility can lead to problems in younger athletes because stress placed on the iliopsoas musculotendinous unit increases and general biomechanics are altered. Tightness of the iliopsoas, tensor fascia lata, or rectus femoris can lead to inhibition of the gluteus maximus, allowing for an anterior pelvic tilt. This in turn leads to adverse affects on the kinetic chain. Excessive anterior tilt can lead to increased lumbar lordosis with resultant stress on the lower lumbar discs, facet joints, and sacroiliac joints and may result in increased knee flexion at heel strike and during midstance phases of the gait cycle. The subsequent increase in eccentric load across the knee extensor mechanism may result in patellar tendon injuries. With increased knee flexion, compressive forces at the patellofemoral contact surface increase and may predispose to patellofemoral problems.

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Medial Gastrocnemius Strain

Background

A medial calf injury is a musculotendinous disruption of varying degrees in the medial head of the gastrocnemius muscle that results from an acute, forceful push-off with the foot.[1, 2, 3, 4, 5, 6] This injury occurs commonly in sports activities (eg, hill running, jumping, tennis), but it can occur in any activity. A medial calf injury is often seen in the intermittently active athlete, often referred to as the "weekend warrior.

This condition has been termed "tennis leg" because of its prevalence in this particular sport, but medial calf injury can happen in a variety of sports or other activities. One mechanism that occurs is on the back leg during a lunging shot, in which the knee is extended while the foot is dorsiflexed. This action puts maximal tension on the gastrocnemius muscle as the lengthened muscle is contracted at the "push off," resulting in a medial calf injury. (See also the Medscape Reference article Calf Augmentation.)

An unusual presentation of a medial gastrocnemius injury during namaz praying was reported by Yilmaz et al, who performed a retrospective study of the sonographic and magnetic resonance image (MRI) findings of patients referred over 7 years with leg pain and swelling.[7] Of 543 patients, 14 had a final diagnosis of medial gastrocnemius rupture that occurred during namaz praying. Nine of 14 (64.2%) patients had incomplete tears at the musculotendinous junction, and 5 of 14 (35.8%) patients had partial tears.

The diagnosis in 4 of 14 (28.6%) patients was misattributed to deep vein thrombosis due to clinical findings and presentation, associated fluid collection between the gastrocnemius and soleus muscles was found in 11 of 14 (78.5%) patients, and isolated fluid collection between the gastrocnemius and soleus muscles was seen in 1 patient.[7] The investigators suggested ultrasonography and MRI can be used to correctly diagnose patients with medial gastrocnemius injuries.

For excellent patient education resources, visit eMedicineHealth's First Aid and Injuries Center. Also, see eMedicineHealth's patient education articles Muscle Strain and Sprains and Strains.

NextEpidemiologyFrequencyInternational

Medial calf injuries occur more commonly in men than in women, and these injuries usually afflict athletes and others in the fourth to sixth decade of life. Medial calf injuries are most commonly seen acutely, but up to 20% of affected patients report a prodrome of calf tightness several days before the injury, thus suggesting a potential chronic predisposition.

PreviousNextFunctional Anatomy

The medial head of the gastrocnemius muscle originates from the posterior aspect of the medial femoral condyle, and as it courses distally, the medial head merges with the lateral head of the gastrocnemius. Further distally, the joined heads of the gastrocnemius merge with the soleus muscle-tendon complex to form the Achilles tendon. The main function of the gastrocnemius muscle is to plantar flex the ankle, but it also provides some knee flexion, as well as contributes to the posterior stability of the knee and partially to the motion of the menisci with flexion/extension of the knee. Throughout the belly of the muscle, the medial gastrocnemius has several origins of tendinous formation. Most strains occur at this musculotendinous junction.

PreviousNextSport-Specific Biomechanics

The medial calf injury usually occurs when an eccentric force is applied to the gastrocnemius muscle, which usually happens when the knee is extended, the ankle is dorsiflexed, and the gastrocnemius attempts to contract in the already lengthened state.[1, 2, 3, 4, 5, 6] This is the common position of the back leg in a tennis stroke, and it results in the greatest force to the muscle unit; but medial calf injuries can also occur during a typical contraction of ankle plantar flexion, especially if the athlete is pushing or lifting a large weight or force.

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Brachial Plexus Injury in Sports Medicine

Background

Peripheral nerve injuries are not common in noncontact sports. However, in contact and collision sports such as football and rugby, brachial plexus injuries occur often. The greater incidence of brachial plexus injuries has been suggested to be the result of direct trauma from participation in contact sports.[1, 2, 3, 4, 5]

The result of trauma to the brachial plexus can lead to the cervical "stinger" or "burner" syndrome, which is classically characterized by unilateral weakness and a burning sensation that radiates down an upper extremity. The condition may last less than a minute or as long as 2 weeks, with the latter duration described as a chronic burner syndrome.

Recent studies

Bertelli et al reviewed the sensory losses and pain symptoms of 150 patients with brachial plexus lesions that were evaluated and operated on. Sensory losses were believed to be documented on the basis of dermatomal root distribution and pain symptoms were believed to be attributed to lower root avulsion. Prior to surgery, patients underwent clinical evaluation and CT myelo scanning with intradural contrast. Hand and finger sensation were evaluated preoperatively; upper root lesions showed hand sensation was preserved. In C8-T1 root injuries, diminished protective sensation was observed on the ulnar aspect of the hand. C8 and T1 injuries always were avulsed from the cord. This indicated an overlapping of the dermatomes, which was not as widely reported. Hand sensation was largely preserved in patients with partial injuries particularly on the brachial side.[6]

Sulaiman et al reviewed the clinical outcomes in patients who underwent nerve transfer operations for brachial plexus reconstruction at Louisiana State University over a 10-year period, evaluating recovery of elbow flexion and shoulder abduction. The authors found that nerve transfers for repair of brachial plexus injuries resulted in excellent recovery of both elbow and shoulder functions. They also noted that patients who had direct repair of brachial plexus elements in addition to nerve transfers tended to do better than those who had only nerve transfer operations.[7]

Terzis and Barmpitsioti studied the use of wrist fusion in patients with brachial plexus injuries with multiple root avulsions resulting in wrist instability, imbalance, and inability to control the placement of the hand in space. Of 35 patients who underwent wrist fusion and answered questionnaires about their overall perceptions, 97.14% were satisfied with wrist stability and 88.57% reported that the procedure enhanced the overall upper limb function. The Disabilities of the Arm, Shoulder and Hand score was 59.14 +/- 12.9, reflecting moderate ability in daily activities. According to the authors, wrist fusion in patients with brachial plexus palsy is recommended as a complementary procedure, offering a stable, painless carpus, with improvement of overall upper limb function and appearance.7

NextEpidemiologyFrequencyUnited States

Brachial plexus injuries are the most common peripheral nerve injuries seen in athletes. True rate of brachial plexus injuries is difficult to determine due to significant underreporting. Many stingers last briefly, and players do not seek medical attention. Clancy et al reported that 33 of 67 college football players (49%) sustained at least 1 burner during collegiate play.[8] Sallis et al surveyed Division III college football players and reported that 65% experienced brachial plexus injuries.[9] In addition, Sallis reported an 87% recurrence rate in these individuals. Meeuwisse reported that 7.2% of all football injuries were brachial plexus injuries.[10] Traumatic brachial plexus injuries can occur in 0.1% of pediatric patients who have experienced multitrauma.[11]

International

True measure of international occurrence of brachial plexus injuries is undetermined due to significant underreporting in athletes and lack of studies in rugby and hockey involving brachial plexus injuries.

PreviousNextFunctional Anatomy

Injuries to the cervical spine are common. The common level of injury is at C5-C6. Damage to other areas of the spinal area can lead to an array of motor and sensory deficits. The following is a list of cervical nerve roots with the associated area of potential motor and sensory deficits:

C4 - Trapezius; shoulder; top of shouldersC5 - Deltoid, rotator cuff; shoulder abduction; lateral upper arm or distal radiusC6 - Biceps, rotator cuff; elbow flexion; lateral forearm and thumbC7 - Triceps; elbow extension; index and middle finger tipsC8 - Extension of fingers; distal thumb; fourth and fifth fingersPreviousNextSport Specific Biomechanics

The following 3 mechanisms are common to brachial plexus injury:

Traction caused by lateral flexion of the neck away from the involved side (similar to the mechanism in birth trauma)Direct impact to the Erb point causing compression to the brachial plexus (often associated with poor-fitting shoulder pads)Nerve compression caused by neck hyperextension and ipsilateral rotation (The neural foramen narrows in this mechanism.)PreviousProceed to Clinical Presentation , Brachial Plexus Injury in Sports Medicine

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Peroneal Tendon Syndromes

Background

Injuries to the peroneal tendons are common but not always clinically significant.[1] They are misdiagnosed as a lateral ankle sprain most of the time, because isolated injury to the peroneal tendons is rare.[2, 3] Injury can occur in one or both peroneus longus and brevis tendons and is typically classified as acute or chronic. Function can be severely compromised by any tendon disruption; conversely, complete tendon rupture can be asymptomatic. Lesions have been seen in symptomatic patients, as well as in cadaver studies of patients who were presumably asymptomatic.[4] The reason for this variation is not known.

The image below depicts the anatomy of the lateral ankle.

Lateral ankle anatomy demonstrates the peroneal tendons as they course beneath the superior retinaculum. The anterior talofibular, calcaneofibular, and posterior talofibular ligaments are also shown.

Acute injuries of the peroneal tendons include tendinitis, tear/rupture, laceration, and dislocation/subluxation. Acute injuries typically have 1 of 2 mechanisms as the cause: (1) inversion ankle injury, which is often seen with associated anterior talofibular ligament and/or calcaneofibular ligament disruption, and (2) a powerful contraction of the peroneal muscles with a forcefully dorsiflexed foot.

Chronic injuries include longitudinal tears[5, 6, 7, 8, 9] and recurrent subluxation[10, 11, 12] of the peroneus brevis tendon.[13] These chronic injuries are usually associated with ankle or subtalar arthritis and ankle instability. People with "bad" or "weak" ankles may have peroneal tendon pathology. Core and lower extremity biomechanics must be evaluated in any chronic atraumatic peroneal tendinopathy, as flaws in those mechanics are usually the culprit.

For excellent patient education resources, visit eMedicineHealth's First Aid and Injuries Center. Also, see eMedicineHealth's patient education article Ankle Sprain.

NextEpidemiologyFrequencyUnited States

The occurrence of injuries to the peroneal tendons is not actually known. DiGiovanni et al found that 25-77% of patients with chronic lateral ankle instability had some type of injury to the peroneal tendons.[14] Over 33 months, Fallat et al noted that of 638 acute ankle "sprains" seen at the Oakwood Hospital Downriver Center Emergency Room and Occupational Medicine Clinic in Dearborn, Michigan, only 83 involved damage to the peroneal tendons, whereas more than 450 involved the anterior talofibular ligament.[1]

PreviousNextFunctional Anatomy

The peroneal tendons originate in the lateral compartment of the leg. The peroneus longus originates from the head and proximal two thirds of the fibula, whereas the peroneus brevis originates from the distal two thirds of the fibula. Both tendons have a musculotendinous portion that courses just below the lateral malleolus.

At the posterior aspect of the lateral malleolus, the peroneal tendons lie within the fibular groove, with the peroneus brevis medial and anterior to the peroneus longus. The fibular groove forms the anterior border of the fibro-osseous tunnel that the peroneal tendons course through. The inferior retinaculum and the calcaneofibular ligament form the posterior border.

The posterior talofibular and the calcaneofibular ligaments form the medial border. The superior retinaculum forms the lateral border. Just inferior to the lateral malleolus, the peroneus brevis courses anteriorly, crossing over the cuboid to insert on the fifth metatarsal styloid. (See the following image.)

Lateral ankle anatomy demonstrates the peroneal tendons as they course beneath the superior retinaculum. The anterior talofibular, calcaneofibular, and posterior talofibular ligaments are also shown.

Inferior to the peroneus brevis, the peroneus longus turns beneath the cuboid in a tunnel formed by the long plantar ligament and the groove of the cuboid. It then courses to insert onto the first metatarsal and medial cuneiform. In 20% of the population, an os peroneum may be present within the peroneus longus tendon as it turns under the cuboid bone. In 0.1% of the population, a structure known as the os vesalianum—a sesamoid bone—is found at the insertion of the peroneus brevis tendon.

PreviousNextSport-Specific Biomechanics

Most sports have elements of running and lateral movement. Sports such as soccer, basketball, and football can be highly demanding on the lower extremity.

The role of the peroneus muscles is to evert the ankle and stabilize its subtalar motion. In balancing the foot, they play off the posterior tibialis muscle on the opposite side of the tibia. Maximal exertion occurs with side-to-side movement and jumping.

The importance of the peroneus muscles is most obvious after lateral ankle sprains. Trauma to the lateral ankle distorts the proprioceptive sense and stretches the connective tissues. The peroneus muscles are often stretched and injured from traction when the foot inverts.

Ankle instability ensues and continues until the lateral retinaculum heals, the peroneal muscles recover, and proprioception returns. If the retinaculum does not heal properly and cannot retain its tension to stabilize the peroneal tendons, symptoms of instability may not resolve without further intervention.

An analysis of overall biomechanics is essential in finding out the factors involved with peroneal tendon damage, especially when there is no traumatic insult. Leg-length discrepancies, femoroacetabular impingement, core instability, and low back pain are some of the correlated factors involved with lower extremity repetitive injuries, but little research has cemented the relationship. However, the core is the powerhouse of the body, and if foot planting is not well controlled by the hip and thigh, then extraneous forces run through the lower leg, ankle, and foot. This can only be controlled by increasing the activity of the supporting muscles, of which the peroneal tendons belong.

PreviousProceed to Clinical Presentation , Peroneal Tendon Syndromes

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Repetitive Head Injury Syndrome

Background

Primary head injury can be catastrophic, but the effects of repetitive head injuries must also be considered. Second-impact syndrome (SIS), a term coined in 1984, describes the situation in which an individual sustains a second head injury before the symptoms from the first head injury have resolved.

The second injury may occur from days to weeks following the first. Loss of consciousness is not a requirement of this condition, the impact may seem relatively mild, and the athlete may appear only dazed initially. However, this second impact causes cerebral edema and herniation, leading to collapse and death within minutes. Only 17 cases of confirmed SIS have been reported in the medical literature. Thus, the true risk and pathophysiology of SIS has not been clearly established.

Importantly, even if the effects of the initial brain injury have already resolved (6-18 mo post injury), the effect of multiple concussions over time remains significant and can result in long-term neurologic and functional deficits. These multiple brain insults can still be termed repetitive head injury syndrome, but they do not fit the classification of SIS. True SIS would most likely have a devastating outcome.

A study of American high school and college football players demonstrated 94 catastrophic head injuries (significant intracranial bleeding or edema) over a 13-year period.[1] Of these, only 2 occurred at the college level. Seventy-one percent of high school players suffering such injuries had a previous concussion in the same season, with 39% playing with residual symptoms. On the other hand, results from a study of concussion by the National Football League demonstrated no cases of SIS or catastrophic head injury in players returning to play in the same game after resolution of symptoms.[2]

The outcome of multiple minor head injuries over a prolonged period has not been well studied and is not well understood. The preponderance of data assessing the impact of repetitive head injuries on short- and long-term neurologic (cognitive) performance has been focused on the sports of boxing and American football.[1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15]

Numerous studies of professional boxers have shown that repeated brain injury can lead to chronic encephalopathy, termed dementia pugilistica.[12, 13, 14, 15] Likewise, the autopsies of 2 former professional football players with a history multiple concussions demonstrated changes that were consistent with chronic encephalopathy.[5, 6] Another investigation of retired professional football players showed a 3-fold increase of depression in players with a history of 3 or more concussions.[3] Older studies of American and Australian rules football showed no effect from repetitive mild head injuries.[11] However, more recent studies of collegiate football players showed an association between multiple concussions and reduced cognitive performance, prolonged recovery, and the increased likelihood of subsequent concussions.

Evidence has also been gleaned from other sports that involve head impact. Nonrandomized studies of soccer players who have had multiple minor concussions have demonstrated that these individuals performed worse on neuropsychologic tests compared with a control group.[16, 17, 18, 19]

Neuropsychologic testing is the standard for monitoring cognitive recovery after concussion. However, 2 studies suggest that abnormalities in visual motor and motor cortex function persist after neuropsychologic testing has normalized.[8, 20] Slower recovery in patients with a second concussion was also seen.

Basic science research is also ongoing. Experiments in concussed rats demonstrated prolonged abnormalities in metabolic markers of brain activity when a second impact was administered at 3 days[21, 22] This implies there may be a metabolic window of vulnerability to a second impact that leads to chronic or prolonged symptoms. Clinically useful biomarkers for brain injury are also being investigated.

Update on chronic traumatic encephalopathy

The effects of single or multiple TBIs in later-life are poorly understood, particularly in mild TBI (mTBI). Recent studies suggest that even mTBI can lead to an increased risk of later-life cognitive impairment and neurodegenerative disease, especially when repeated injuries are involved.[23, 24, 25] TBIs of mixed severity have been associated with an elevated incidence of Alzheimer disease (AD) and other dementias[26, 27, 28] and a reduced age of onset for AD,[29] although not in all studies.[30]

It has long been suspected that repeated concussions can result in dementialike symptoms many years after injury, a condition labeled chronic traumatic encephalopathy (CTE). The brain structures damaged in CTE are critical for memory and executive function.[31, 32]

CTE has been studied in boxing, wherein retired boxers developed dementia at a higher rate and a younger age compared with the general population.[33] More recently, brain autopsies of athletes in various sports with confirmed CTE have demonstrated tau-immunoreactive neurofibrillary tangles and neuropil threads,[25, 34] suggesting that pathological processes similar to AD may be involved.

A critical gap in the literature exists with respect to later-life neuropsychological functioning after TBI. In a study of individuals with TBI of varying initial severity, researchers found later-life cognitive impairments when compared with a control group in the areas of episodic memory, short-term memory, visuospatial processing, object naming, and semantic processing.[35] Regarding CTE specifically, neuropsychological deficits have been observed but appropriate norms do not exist.[36]

A meta-analysis found no cognitive effects in 289 amateur boxers[37] ; however, a large survey study suggested that multiple concussions increase the risk of later-life cognitive dysfunction. Recently, the diagnosis of mild cognitive impairment (MCI, also known as insipient dementia) and self-reported memory problems were more common among football players who reported 3 or more concussions than those who reported none.[23, 24] Although several cross-sectional studies in sports injury populations have been performed later in life, the long-term effects of TBI in nonsports populations (military, civilian) remain poorly defined.

The possibility of a link between mTBI and CTE or early dementia has widespread implications for military service members and veterans. TBI is an important source of morbidity in the ongoing global war on terrorism (GWOT).[38] TBI has been called the "signature injury" of Operation Iraqi Freedom (OIF), Operation Enduring Freedom (OEF), and Operation New Dawn (OND), affecting up to 20% of all service members deployed in theatre. More than 233,000 TBIs have been officially reported in OIF/OEF/OND between 2000 and 2012 (www.dvbic.org/tbi-numbers.aspx), nearly 80% of which are mild.[39] Explosive munitions in the form of improvised explosive devices (IEDs) have caused the overwhelming majority of these identified cases. The prevalence is likely higher than the above-reported numbers, given the frequency of blast exposure in the GWOT and the fact that mTBI may go unrecognized during and even after deployment.

Missed or delayed diagnosis of mTBI is attributed to the subtlety of symptoms, the overlap of clinical signs and the common effects of heightened arousal and activity in times of combat, a lack of knowledge as to the specifics of diagnosis and detection, greater attention paid to more visible concomitant injuries, and a reduced subjective awareness related to cognitive deficits in the acute period on behalf of the injured service member.[40]

At present, a definitive diagnosis of CTE is made on postmortem examination, using a battery of immunohistochemical markers to define pathognomonic histopathologic features of this disease process, such as tau-immunoreactive neurofibrillary tangles and neuropil threads. There are no clear in vivo diagnostic tools to diagnose CTE. Identification of such a tool or set of tools would provide key data to clinicians caring for this patient population, aid in conducting epidemiological studies to explore the natural history of CTE, and provide objective diagnostic endpoints to support clinical trials to explore therapies for this disease process. Much more attention in recent years has been put towards the early detection of dementia than that of CTE.

In recent years, significant effort has been devoted to the creation of imaging agents that selectively accumulate at sites of interest and emit a signal that can be detected by either positron emission tomography (PET) or single-photon emission computed tomography (SPECT). In contrast to CT and MRI sequences, PET and SPECT have the significant advantage of providing information on changes occurring at the cellular or molecular level. To date, a number of targeted imaging agents have been cataloged at the NIH MICAD Web site: http://www.ncbi.nlm.nih.gov/books/bookres.fcgi/micad/home.html.

In studies of aging, sensory and motor changes have been observed that precede dementia in the domains of olfaction, eye movement, and balance. Olfactory impairment has been identified as a preclinical marker of AD.[41] Olfactory function is also reduced after brain injury.[42, 43]

Researchers have recently demonstrated that early neuromotor impairments are predictive of late global outcome after TBI.[44] Using video-oculography, saccadic eye movement abnormalities have been described in patients with cortical neurodegeneration (AD) and/or nigrostriatal neurodegeneration (Parkinson disease).[45] Furthermore, eye movement abnormalities have been identified in adults with postconcussive syndrome.[46] Research has also demonstrated the utility of a mobile video-oculography device.[47, 48]

Finally, balance impairments (as measured by computerized posturography (CPT) are more common in dementias of all types compared with controls[49] and have been demonstrated acutely after mild TBI.[50] CPT score is predictive of recurrent falls in persons with balance and vestibular disorders.[51]

Tau proteins (collectively termed "total-tau") are a logical indicator of CTE and, more broadly, TBI-onset neurodegeneration. Total-tau in cerebrospinal fluid (CSF) is one of the most predictive biomarkers for clinical use in neurodegenerative disorders associated with cognitive impairment.[52] While serum total-tau has been less predictive than CSF for age-onset neurodegenerative disease (eg, AD), it has been demonstrated to be discriminative in other pathologic causes of brain dysfunction, including higher-risk mTBI patients.[53]

Given the unique pathology associated with CTE and tau accumulation more broadly and around blood vessels, it is entirely plausible that long-term neurodegeneration following trauma may selectively present elevated serum-tau levels. It is further postulated that long-term serum-tau levels in posttraumatic subjects will be less age-dependent than CSF-tau levels in age-onset neurodegeneration. The authors’ contention is entirely consistent with the known pathobiology of CTE, specifically the excessive tau accumulations seen across broad cortical areas with a focus around blood vessels in regions of geometric inflection that are most stressed by the deformation forces of brain trauma.

CTE has also been characterized by widespread TDP-43 proteinopathy.[54] TDP-43 is involved in regulating translation in mitochondrial RNA in the brain. It has been associated with the physiological response to traumatic axotomy.[55] Blood levels of TDP-43 are elevated in association with a variety of neurodegenerative conditions, to include frontotemporal lobar degenerations, amyotrophic lateral sclerosis (ALS), and AD.[56, 57] However, no publication to date has examined it as a biofluid marker for CTE. As in the case of tau, TDP-43 fibrillaries accumulate at anatomical points of geometric inflection in the brains of CTE subjects. Given that trauma focuses deformation forces in these areas, it is highly plausible that TDP-43 accumulation is in contact with the compromised microvasculature and, as such, would be present in the blood of trauma patients with latent CTE.

Beta-amyloid (Ab) peptides are yet other biomarkers with diagnostic and prognostic utility for a broad number of neurodegenerative disorders.[52] Ab plaques are common immediately after TBI,[58] and Ab continues to accumulate in traumatized axons that survive.[59] Recently, it has been reported that Ab plaques are diffusely yet widely present throughout the brains of moderate-to-severe TBI subjects at 1 year or longer following injury.[58] Plaques were also found to be predominantly in a fibrillary form that resembled AD pathology more than acute TBI. Importantly, diffuse, widespread fibrillary Ab accumulation resembles CTE pathology.[60] Until recently, CSF has been the only biofluid found to provide reliable Ab measures. However, the latest blood Ab assays are providing predictive and prognostic performance in MCI and AD that is considered particularly useful for longitudinal monitoring and so it holds relevance to the present application.[61]

While blood assays are most often developed for disease biomarkers, urine provides certain distinct advantages. Precedence exists in the form of a urine assay for neural thread protein (NTP), which is already available as a clinical test for neurodegenerative disorders.[62] Recently NTP has shown particular promise for the early prediction of AD.[63] Importantly, NTP is related to tau pathobiology in connection with neurodegeneration,[62] and is thus likely to correlate with other tauopathies such as CTE. In addition to NTP, urine may also provide ready access for Ab measures. Complicating blood Ab assays is the interaction with predominant protein. However, normal renal filtration removes this confound, allowing smaller metabolites, possibly Ab peptides, to be detected more easily. The authors further suspect that smaller breakdown products of tau protein may be accessible in urine for the same reasons, which are readily detected by total-tau antibody.[64]

Possession of the APoE-ε4 allele is a risk factor for dementia.[33] Carriers may have altered brain activity, even at a young age.[65] Long-term, but not short-term, effects of TBI may be influenced by APOE. APOE was not associated with poorer neuropsychological performance 1 month after mild or moderate TBI.[66] However, TBI was found to increase AD risk of APOE 10-fold[67] and cognitive decline after 30 years was greater in TBI patients with the APoE-ε4 allele compared with those without.[68] Environmental factors, in particular multiple concussions, may influence the effects of APOE. Boxers with the APoE-ε4 allele who had participated in many bouts were more likely to have CTE, while the allele was not a risk factor in boxers who had only experienced a few fights.[58]

Certainly, more research is needed to better understand the chronic and catastrophic effects of repetitive head injuries.

For patient education resources, see the Back, Ribs, Neck, and Head Center and Dementia Center, as well as Concussion and Dementia in Head Injury.

NextEpidemiologyFrequencyUnited States

The National Center for Catastrophic Sports Injury Research in Chapel Hill, NC, reported 35 cases of SIS among American football players from 1980-1993. Seventeen were confirmed by necropsy, surgery, or magnetic resonance imaging (MRI) findings. Eighteen were probable cases of SIS, despite inconclusive necropsy findings.

The number of reported SIS cases increased from 1992-1998, but this increase is thought to be due to more frequent recognition and reporting. Some clinicians believe that SIS is overreported. Boden et al reported an average of 7.08 catastrophic head injuries per year in high school football, compared with 0.15 for college football from 1989-2002.[1] The incidence was 0.67/100,000 for high school players and 0.21/100,000 for college players. Thirty-nine percent of the affected athletes reported playing with residual symptoms.[1] There were 8 fatalities, of which 1 individual had cerebral edema as the only radiographic finding. It was unclear as to whether a second impact occurred in this case.

With the advent and improvement of the helmet in American football and with the introduction of new rules that make spearing illegal, the incidence of head-injury fatalities has decreased from 2.64 cases per 100,000 persons in 1968 to 0.20 cases per 100,000 persons since 1977. The US Centers for Disease Control and Prevention estimates a 20% rate of concussion from football brain injuries (predominantly high-school and college level), which equates to an estimated 300,000 concussions per year.

Collins et al showed that 20% of the college football players they studied had 2 or more concussions during their career.[7] Furthermore, a study by Daniel et al found that the symptoms of an estimated 60,000 football players who suffer concussion may persist for 4 or more months in up to 24% of these individuals.[20]

The US Consumer Product Safety Commission tracks product-related injuries through its National Injury Information Clearinghouse. According to the Consumer Product Safety Commission, an estimated 311,766 sports-related head injuries were treated at US hospital emergency departments in 2004.

Schulz et al reported on a prospective cohort study of North Carolina high-school athletes followed from 1996–1999.[69] Subjects were clustered by school and sport, and the sample included 15,802 athletes, with 1–8 seasons of follow-up per athlete. Concussion rates ranged from 9.36 concussions per 100,000 athlete-exposures in cheerleading to 33.09 concussions per 100,000 athlete-exposures in football, where "athlete-exposure" is 1 athlete participating in 1 practice or game. The overall rate of concussion was 17.15 concussions per 100,000 athlete-exposures.

Cheerleading was the only sport for which the practice rate of concussions was greater than the game rate.[69] Almost two thirds of cheerleading concussions involved 2-level pyramids. Concussion rates were elevated for athletes with a history of concussion, and they increased with the increasing level of body contact permitted in the sport.

Powell and Barber-Foss reported a 2-year review of 235 US certified athletic high-school training records. The authors estimated a total of 62,816 cases of mild traumatic brain injury (TBI) annually among high-school varsity athletes, with football accounting for approximately 63% of these cases and a varied incidence among 10 other popular sports.[70]

Matser et al showed that 23% of the amateur soccer players they studied had 2-5 concussions during their career.[16] Boden et al found that the overall prevalence of college soccer-related concussions was 0.6 cases per 1000 athlete-exposures for men and 0.4 cases per 1000 athlete-exposures for women.[17] The authors reported that the vast majority (72%) of these concussions were grade 1, and none were grade 3.[17]

The actual number of athletes who may be affected by repeated minor head injuries is largely unknown.

PreviousNextFunctional Anatomy

SIS is thought to occur because of a loss of autoregulation of the cerebral blood flow, which leads to vascular engorgement, increased intracranial pressure (ICP), and eventual herniation. This herniation may involve the medial temporal lobe and may occur medially across the falx cerebri or inferiorly through the tentorium. Herniation can also force the cerebellar tonsils to move inferiorly through the foramen magnum. The athlete's condition rapidly worsens, and brainstem failure occurs in 2-5 minutes.

PreviousNextSport-Specific Biomechanics

The brain is protected by bone and is cushioned by tough meninges and cerebrospinal fluid. Despite these protective surroundings, blunt-force trauma to the head can cause injury to the site of impact (coup injury) and the site immediately opposite of the impact (contrecoup injury). Factors that dissipate the force (eg, equipment, neck muscle strength) can minimize this trauma.

PreviousProceed to Clinical Presentation , Repetitive Head Injury Syndrome

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