Bicycle Seat Neuropathy

Background

Bicycle seat neuropathy is one of the more common injuries reported by cyclists.[1, 2, 3, 4, 5] The injuries and symptoms are due to the cyclist supporting his or her body weight on a narrow seat, and they are believed to be related to either vascular or neurologic injury to the pudendal nerve.[2, 5, 6, 7, 8, 9, 10]

For excellent patient education resources, visit eMedicineHealth's Men's Health Center and First Aid and Injuries Center. Also, see eMedicineHealth's patient education articles, Impotence/Erectile Dysfunction, Erectile Dysfunction FAQs, and Bicycle Safety.

NextEpidemiologyFrequencyUnited States

A wide frequency range has been reported for bicycle seat neuropathy, but it is believed to be underreported. The medical literature contains several case reports of reversible neuropathy[5, 9] and several retrospective studies surveying participants in long-distance cycling races and tours.[8, 11, 12]

Andersen and Bovim surveyed 260 cyclists participating in a long-distance bike tour that was 335.54 miles (540 km) in length.[8] Of responding males, 35 (22%) reported symptoms of either numbness or pain in the pudendal area. Thirty-three (21%) males reported penile numbness, with 10 (6%) male cyclists reporting symptoms that lasted longer than 1 week. In addition, 21 males (13%) reported symptoms of impotence, 11 of whom experienced symptoms for longer than 1 week, and 3 of whom reported impotence lasting longer than 1 month.[8]

Kuland and Brubaker reported that during the 1976 Bikecentennial tour, there was a 7% incidence of pudendal and/or penile numbness, but this study only surveyed 89 of 1200 participating cyclists.[11]

Weiss studied symptoms of cyclists participating in a 500-mile (804.97 km) bicycle tour.[12] Of the participating cyclists, 45% reported at least mild and transient perineal numbness; 10% reported the symptoms as severe, and 2% of the cyclists had to temporarily stop riding. Perineal numbness has also been documented in women cyclists. LaSalle et al surveyed 282 female members of a Dallas cycling club.[13] In this group, 34% of the women reported perineal numbness.

Potter et al assessed the differences between men and women with regard to bicycle saddle pressure distribution during seated cycling.[14] The authors noted that there were significant differences between the sexes in saddle loading, and these differences were especially relevant with regard to the position of the bicycle handlebar positions. In particular, the drops hand position shifted the rider's weight, such that more weight was supported on the anterior pelvic structures.[14]

PreviousNextSport-Specific Biomechanics

The cause of bicycle seat neuropathy has been attributed to several different ischemic events. Amarenco et al and Oberpenning et al hypothesized that compression of the pudendal nerve as it passes through the Alcock canal causes the condition.[9, 15] The Alcock canal is enclosed laterally by the ischial bone and medially by the fascial layer of the obturator internus muscle. The pudendal nerve exits the canal ventrally, below the symphysis pubis, and innervates the genital and perineal regions.

Oberpenning et al postulated that long-distance cycling results in the indirect transmission of pressure onto the perineal nerve within the Alcock canal.[9] Weiss and Bond separately proposed that bicycle seat neuropathy is due to temporary and transient ischemic injury to the dorsal branch of the pudendal nerve secondary to compression of the nerve between the bicycle seat and the symphysis pubis.[12, 16] Weiss also theorized that the genital branch of the genital-femoral nerve could be involved in cases in which scrotal paresthesia is reported.[12]

Bicycle seat design (eg, shape) may be the major extrinsic factor for the development of bicycle seat neuropathy.[1, 4, 6, 17, 18, 19, 20, 21] Results of computer modeling reported by Spears et al showed that wider bicycle seats that support the ischial tuberosities decrease pressure on the perineal area.[19] Other studies have also demonstrated the effect bicycle seat design has on penile blood flow[20] and penile oxygen pressure.[21]

PreviousProceed to Clinical Presentation , Bicycle Seat Neuropathy

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Patellofemoral Joint Syndromes

Background

Patellofemoral joint complaints are one of the most common musculoskeletal complaints in all age groups. Complaints vary from anterior knee pain to peripatellar knee pain to retropatellar knee pain.[1, 2, 3, 4, 5, 6, 7] Nonspecific complaints may include global or generalized knee pain, joint line pain, or posterior knee pain. Often, there is a paucity of objective findings despite subjective complaints. The problem may vary from one of short duration to one of a recurrent or chronic nature.

The etiology of patellofemoral joint syndrome is multifactorial and results from a combination of intrinsic and extrinsic factors.[1, 2, 3, 4, 5, 6, 7, 8] Treatment is often conservative in nature. Because of the variable nature of the complaints and an often lack of objective identifiable pathologic cause of patellofemoral joint complaints, this condition can be difficult to evaluate, diagnose, and treat, which may cause great frustration for the physician and patient alike.[5]

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

Related Medscape Reference topics:

Patellofemoral Arthritis

Plica Syndrome

NextEpidemiologyFrequencyUnited States

Patellofemoral joint syndrome may affect as many as 25% of all athletes.

PreviousNextFunctional Anatomy

The patellofemoral joint is composed of the articulation of the patella with the femoral condyles of the femur. The patella has a configuration of a triangle with its apex directed inferiorly. Superiorly, it articulates with the trochlea, the distal articulating surface of the femur.

The patella is the largest sesamoid bone in the body and protects the knee from direct trauma. Localized within the quadriceps tendon, the patella also acts as a fulcrum for extension of the quadriceps.

Medial movement of the patella is controlled by the vastus medialis oblique (VMO) muscle. Lateral tracking is guided by both the vastus lateralis and the iliotibial band. Patellar motion is further constrained by the patellofemoral ligament, the patellotibial ligament, and the retinaculum.

The patella is engaged with the trochlea at 20-30 º of knee flexion. At 90 º, the patella contacts the lateral and medial femoral facets within the condylar fossa. At 130-135 º of knee flexion, the medial facets of the patella contact the articulating surface of the femoral condyles. In knee extension, the patella abuts the suprapatellar fat pad.

PreviousNextSport-Specific Biomechanics

The patella lies within the quadriceps tendon and thereby increases the mechanical advantage of the quadriceps mechanism. Not only does the patella increase the force of knee extension by 50%, but it also provides stability to the patellar tendon and minimizes the forces placed on the femoral condyles.

Tracking of the patella begins with the lower patellar border lying in contact with the suprapatellar fat pad when the knee is fully extended. With knee flexion, the patella moves proximally with a lateral shift, which is limited in excursion by the lateral retinaculum. As the knee continues to flex, the tibia internally rotates and the patella moves upward. The amount of force placed on the patellofemoral joint increases with increasing knee flexion. On the other hand, knee hyperflexion increases patellofemoral stress, as does extreme extension.

The vector force placed on the patella may be affected by the Q-angle.[9] The Q-angle is a line created from the anterior superior iliac spine (ASIS) to the mid patella, which intersects with a line from the mid patella to the tibial tubercle when the knee is in full extension. An average Q-angle for a male is 14 º, whereas that for a female is 17 º. Q-angles larger than average can indicate abnormal patellar tracking.

Other factors that may affect the vector force on the patella include the following:

Femoral anteversionTibial torsionHyperpronation of the footAtrophy of the VMO muscleA tight lateral retinaculumPatella position (patella alta/baja or subluxation)Inflexibility of the quadriceps, hamstring, iliotibial, and calf muscle-tendon unitsGeneral ligamentous laxityPreviousProceed to Clinical Presentation , Patellofemoral Joint Syndromes

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Concussion

Practice Essentials

Concussion, or mild traumatic brain injury (MTBI), is common among contact and collision sports participants.[1, 2, 3, 4, 5, 6, 7] One definition of concussion is a condition in which there is a traumatically induced alteration in mental status, with or without an associated loss of consciousness (LOC).[1] A broader definition is a traumatically induced physiologic disruption in brain function that is manifested by LOC, memory loss, alteration of mental state or personality, or focal neurologic deficits.

Essential update: Repeat concussions in children and teens may lead to prolonged recovery

In a prospective cohort study of 280 patients aged 11 to 22 years who presented to an emergency department with acute concussion, repeat concussions increased the risk for prolonged recovery.[8, 9] Patients with a history of previous concussions had symptoms that lasted twice as long (24 d) as those who did not have such a history (12 d). Moreover, symptoms lasted a median of 28 days for patients who had had more than 1 previous concussion and 35 days for those who had had a concussion within the previous year. Significant predictors of prolonged recovery following subsequent concussions included previous concussion, age 13 years or older, no loss of consciousness, and an initial Rivermead Post-Concussion Symptoms Questionnaire score exceeding 18.[8, 9]

Signs and symptoms

An athlete suffering from an MTBI may demonstrate the following:

Confusion: Athletes with an MTBI often appear acutely with a confused or blank expression or blunted affectDelayed responses and emotional changes: Delayed response to simple questioning may be demonstrated, along with emotional lability; the emotional lability may become more evident as the athlete attempts to cope with his or her confusion Pain/dizziness: Many athletes report an associated headache and dizzinessVisual disturbances: Visual complaints may include seeing stars, blurry vision, or double visionAmnesia: Pretraumatic (retrograde) and posttraumatic (antegrade) amnesia may be present; usually, the duration of retrograde amnesia is quite brief, while the duration of posttraumatic amnesia is more variable (lasting seconds to minutes), depending upon the injury Signs of increased intracranial pressure: A history of persistent vomiting may suggest a significant brain injury with associated elevated intracranial pressure; other signs of increased intracranial pressure include worsening headache, increasing disorientation, and a changing level of consciousness

Physical examination

The physical examination should include assessment of the following:

Appearance: The initial clinical examination should include a careful inspection of the athlete's general appearanceHead and neck: Palpating the head and neck is important when looking for an associated skull or cervical injuryFacial bones: Palpate the facial bones and the periorbital, mandibular, and maxillary areas after any head traumaJaws: Open and close the mouth to help in the evaluation of possible temporomandibular joint (TMJ) pain, malocclusion, or mandibular fracture Nose: Inspect the nose for deformity and tenderness, which may indicate a possible nasal fracturePresence of discharge: Persistent rhinorrhea or otorrhea (clear) indicates a possible associated skull fracture.Vision: Perform a careful, detailed neurologic examination that includes evaluation of the visual fields, extraocular movements, pupillary reflexes, and level of the eyes Strength and sensation: Assess upper-extremity and lower-extremity strength and sensationCoordination and balance: Concussed patients often have difficulty with the finger-nose-finger test and will use slow, purposeful movements to complete the task

Postconcussive syndrome

Postconcussive syndrome consists of prolonged symptoms that are related to the initial head injury. Symptoms usually consist of the following:

Persistent, recurrent headachesDizzinessMemory impairmentLoss of libidoAtaxiaSensitivity to light and noiseConcentration and attention problemsDepressionAnxiety

See Clinical Presentation for more detail.

Diagnosis

Imaging

The following imaging studies can be used in the examination of head injury:

Computed tomography scanning: CT scanning continues to be the imaging study of choice for evaluating acute head injuryMagnetic resonance imaging: MRI is the imaging study of choice for patients who have prolonged symptoms (>7 days) or when a late change occurs in an individual's neurologic signs or symptoms

Although positron emission tomography (PET) scanning and functional MRI (fMRI) may be used in evaluating patients with concussion, their clinical application in most cases of MTBI is uncertain.[10, 11, 12]

Neuropsychological testing

Detailed neuropsychologic testing is employed more often at the professional level and in research in athletes with MTBI.

See Workup for more detail.

Management

Most patients with MTBI recover in 48-72 hours, even with detailed neuropsychological testing, and are headache free within 2-4 weeks of the injury.

A clinical report by the American Academy of Pediatrics (AAP) on the diagnosis and management of sports-related concussions in adolescents and children noted the following[13] :

Cognitive and physical rest is the mainstay of management of patients with concussionOngoing neuropsychological testing is a helpful tool during management

Although several different guidelines regarding return to play have been established, the main criteria for an athlete's return to play after a concussion include the following:

Complete clearing of all symptomsComplete return of all memory and concentrationNo symptoms after provocative testing: Provocative testing includes jogging, sprinting, sit-ups, or pushups (ie, exercise that raises the athlete's blood pressure and heart rate)

Davis and Purcell have released an assessment of the evaluation and management of acute concussion in young children.[14]

In 2013, the American Academy of Neurology issued updated guidelines for the evaluation and management of sports concussion.[15]

See Treatment and Medication for more detail.

NextBackground

Concussion has many different meanings to patients, families, and physicians.[1, 16, 17, 18] One definition of concussion is a condition in which there is a traumatically induced alteration in mental status, with or without an associated loss of consciousness (LOC).[1] A broader definition for concussion is a traumatically induced physiologic disruption in brain function that is manifested by LOC, memory loss, alteration of mental state or personality, or focal neurologic deficits.[1] Concussions usually result in relatively temporary impairment of neurologic function.[10, 18, 19]

Concussion or mild traumatic brain injury (MTBI) is common among most contact and collision sports participants.[1, 2, 3, 4, 5, 6, 7] For many physicians, even those who specialize in MTBI, this area is confusing due to the paucity of scientific evidence to support much of the clinical decision making that is faced in the office.[4, 11, 16, 17, 20] The inconsiderable amount of good scientific research in the area of MTBI is due to problems with ambiguous definitions of concussion, inconsistent criteria when selecting patients to study, variability of injury mechanisms and locations, and differing means of measuring cognitive function.[21, 22] The purpose of this article is to review the epidemiology and diagnosis (but not necessarily the classification) of MTBI, as well as the role of imaging studies, issues regarding return to play, and complications surrounding MTBI.

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

PreviousNextEpidemiologyFrequency

United States

The incidence of head injury varies with the sport and the age of the participants; many head injuries are likely unreported due to their supposed mild nature; mild concussions may go unnoticed by teammates, coaches, and even the athletes themselves.[1] An athlete's fear of medical disqualification may also lead to underreporting. Studies of high school athletes show the rate of concussions per 1000 exposures as follows: 0.59 for football (boys), 0.25 for wrestling (boys), 0.18 for soccer (boys; 0.23 for girls), 0.09 for field hockey (girls), and 0.11 for basketball (boys; 0.16 for girls). The data from one study noted that concussions account for nearly 15% of all sport-related injuries in high school athletes.[23]

Among National Collegiate Athletic Association (NCAA) soccer players, the rate of injury has been reported as 0.4-0.6 per 1000 athlete exposures[6] ; 72% of these injuries were described as mild and were almost always secondary to direct contact with an opponent. None of the injuries in this group of Atlantic Coast Conference (ACC) soccer players was noted to be a direct result of heading the ball. In contrast, boxing is the sport with the highest rate of head injuries and has more deaths than any other organized athletic activity. At the professional level, many of the boxing bouts end with a technical knockout (ie, brain injury).

Sports activities that place the athlete at high risk for a head injury include boxing, football, ice hockey, wrestling, rugby, and soccer. Physicians and other allied health providers who are responsible for the medical care of such contact or collision sports participants should be adept at evaluating, treating, and making playability decisions related to the short- and long-term consequences of an injury to the brain.

PreviousNextSport-Specific Biomechanics

The mechanisms of brain injury may differ among sports activities. Possible mechanisms of injury include compressive forces, which may directly injure the brain at the point of contact (coup); tensile forces produce injury at the point opposite the injury (contrecoup) because the axons and nerves are stretched; finally, rotational forces may result in a shearing of axons. Therefore, the direct force at the point of contact may not be solely responsible for the severity of an injury if a high rotational component with a significant shear effect occurs.

All of the different mechanisms may result in biochemical changes related to perfusion, energy demand, and utilization at the site of injury that are not well understood. At this time, it is unclear whether any experimental animal model or human studies on more severe brain-injured patients accurately reflect the pathophysiology of the typical mild traumatic alteration in brain function.

PreviousProceed to Clinical Presentation , Concussion

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Shoulder Impingement Syndrome

Background

In 1972, Neer first introduced the concept of rotator cuff impingement to the literature, stating that it results from mechanical impingement of the rotator cuff tendon beneath the anteroinferior portion of the acromion, especially when the shoulder is placed in the forward-flexed and internally rotated position.[1]

Neer describes the following 3 stages in the spectrum of rotator cuff impingement:

Stage 1, commonly affecting patients younger than 25 years, is depicted by acute inflammation, edema, and hemorrhage in the rotator cuff. This stage usually is reversible with nonoperative treatment. Stage 2 usually affects patients aged 25-40 years, resulting as a continuum of stage 1. The rotator cuff tendon progresses to fibrosis and tendonitis, which commonly does not respond to conservative treatment and requires operative intervention. Stage 3 commonly affects patients older than 40 years. As this condition progresses, it may lead to mechanical disruption of the rotator cuff tendon and to changes in the coracoacromial arch with osteophytosis along the anterior acromion. Surgical l anterior acromioplasty and rotator cuff repair is commonly required.

In all Neer stages, etiology is impingement of the rotator cuff tendons under the acromion and a rigid coracoacromial arch, eventually leading to degeneration and tearing of the rotator cuff tendon.

Although rotator cuff tears are more common in the older population, impingement and rotator cuff disease are frequently seen in the repetitive overhead athlete. The increased forces and repetitive overhead motions can cause attritional changes in the distal part of the rotator cuff tendon, which is at risk due to poor blood supply. Impingement syndrome and rotator cuff disease affect athletes at a younger age compared with the general population.

NextEpidemiologyFrequencyUnited States

No documented information on the occurrence of shoulder impingement syndrome exists.

PreviousNextFunctional Anatomy

The shoulder consists of 2 bones (humerus, scapula), 2 joints (glenohumeral, acromioclavicular), and 2 articulations (scapulothoracic, acromiohumeral) that are joined by several interconnecting ligaments and layers of muscles. Minimal bony stability in the shoulder permits a wide range of motion (ROM). Soft tissue structures are the major glenohumeral stabilizers. Static stabilizers consist of the articular anatomy, glenoid labrum, joint capsule, glenohumeral ligaments, and inherent negative pressure in the joint. Dynamic stabilizers include the rotator cuff muscles, long head of the biceps tendon, scapulothoracic motion, and other shoulder girdle muscles (eg, pectoralis major, latissimus dorsi, serratus anterior).

The rotator cuff consists of 4 muscles that control 3 basic motions, abduction, internal rotation, and external rotation. The supraspinatus muscle is responsible for initiating abduction, the infraspinatus and teres minor muscles control external rotation, and the subscapularis muscle controls internal rotation. The rotator cuff muscles provide dynamic stabilization to the humeral head on the glenoid fossa, forming a force couple with the deltoid to allow elevation of the arm. This force couple is responsible for 45% of abduction strength and 90% of external rotation strength.

The supraspinatus outlet is a space formed on the upper rim, humeral head, and glenoid by the acromion, coracoacromial arch, and acromioclavicular joint. This outlet accommodates passage and excursion of the supraspinatus tendon. Abnormalities of the supraspinatus outlet have been attributed as a cause of impingement syndrome and rotator cuff disease, though other causes have been discovered. Impingement implies extrinsic compression of the rotator cuff in the supraspinatus outlet space. Bigliani and associates discovered and described how variations in acromial size and shape can contribute to impingement.[2]

Cadaveric studies show 3 variations in acromion morphology, as follows: type 1 is flat, type 2 is curved, and type 3 is hooked anteriorly. Although the curved configuration was the most common (43% prevalence, compared to 17% flat and 40% hooked), the hooked configuration most strongly was associated with full-thickness rotator cuff tears. Other sites of impingement in the supraspinatus outlet space include the coracoacromial ligament (where thickening can occur) and the undersurface of the acromioclavicular joint (where osteophytes can form). The medial coracoid rarely is involved. These impingement sites in the supraspinatus outlet are compressed further when the humerus is placed in the forward-flexed and internally rotated position, forcing the greater tuberosity of the humerus into the undersurface of the acromion and coracoacromial arch.

Nonoutlet impingement also can occur. Causes may be loss of normal humeral head depression from either a large rotator cuff tear or weakness in the rotator cuff muscles from a C5/C6 neural segmental lesion or a suprascapular mononeuropathy. This condition also may occur because of thickening or hypertrophy of the subacromial bursa and rotator cuff tendons.

PreviousNextSport-Specific Biomechanics

Overuse or repetitive microtrauma sustained in the overhead position may contribute to impingement and rotator cuff pathology. Shoulder pain and rotator cuff disease are common in athletes involved in sports requiring repetitive overhead arm motion (eg, swimming, baseball, volleyball, tennis).

Secondary impingement often is attributed to impingement, which seldom is mechanical in nature in young athletes. Rotator cuff disease in this population may be related to subtle instability, and, therefore, may be secondary to such factors as eccentric overload, muscle imbalance, glenohumeral instability, or labral lesions. This has led to the concept of secondary impingement, which is defined as rotator cuff impingement that occurs secondary to a functional decrease in the supraspinatus outlet space due to underlying instability of the glenohumeral joint.

Secondary impingement may be the most common cause in young athletes who frequently place large, repetitive overhead stresses on the static and dynamic glenohumeral stabilizers, resulting in microtrauma and attenuation of the glenohumeral ligamentous structures, which leads to subclinical glenohumeral instability. Such instability places increased stress on the dynamic stabilizers of the glenohumeral joint, including the rotator cuff tendons.

These increased demands may lead to rotator cuff pathology (eg, partial tearing, tendonitis). Furthermore, as the rotator cuff muscles fatigue, the humeral head translates anteriorly and superiorly, impinging upon the coracoacromial arch. This leads to rotator cuff inflammation. In these patients, treatment should address underlying instability.

The concept of glenoid impingement has been advanced as an explanation for partial-thickness tears in throwing athletes, particularly those involving the articular surface of the rotator cuff tendon. Such tears may occur in the presence of instability due to increased tensile stresses on the rotator cuff tendon from abnormal motion of the glenohumeral joint or increased forces on the rotator cuff necessary to stabilize the shoulder.

Arthroscopic studies of these patients note impingement between the posterior superior edge of the glenoid and the insertion of the rotator cuff tendon with the arm placed in the throwing position (abducted and externally rotated). Lesions were noted along the area of impingement at the posterior aspect of the glenoid labrum and articular surface of the rotator cuff. This concept is believed to occur most commonly in throwing athletes and must be considered when assessing for impingement.

PreviousProceed to Clinical Presentation , Shoulder Impingement Syndrome

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Clavicular Injuries

Practice Essentials

Although clavicle fractures are common and usually heal regardless of the selected treatment, complications are possible, warranting careful attention to these injuries. Multiple attempts have been made to devise a classification scheme for clavicle fractures. The most common system is the following one, created by Allman, in which the clavicle is divided into thirds[1] :

Group I fractures: Middle third injuriesGroup II fractures: Distal third injuriesGroup III fractures: Medial (proximal) third injuriesSigns and symptoms

Clinical signs and symptoms of clavicle fracture include the following:

The patient may cradle the injured extremity with the uninjured armThe shoulder may appear shortened relative to the opposite side and may droopSwelling, ecchymosis, and tenderness may be noted over the clavicleAbrasion over the clavicle may be noted, suggesting that the fracture was from a direct mechanismCrepitus from the fracture ends rubbing against each other may be noted with gentle manipulationDifficulty breathing or diminished breath sounds on the affected side may indicate a pulmonary injury, such as a pneumothoraxPalpation of the scapula and ribs may reveal a concomitant injuryTenting and blanching of the skin at the fracture site may indicate an impending open fracture, which most often requires surgical stabilization Nonuse of the arm on the affected side is a neonatal presentationAssociated distal nerve dysfunction indicates a brachial plexus injuryDecreased pulses may indicate a subclavian artery injuryVenous stasis, discoloration, and swelling indicate a subclavian venous injury[2, 3]

See Clinical Presentation for more detail.

Diagnosis

Laboratory studies

Complete blood count (CBC): If a vascular injury is suspected, to check the hemoglobin and hematocrit valuesArterial blood gas (ABG): If a pulmonary injury is suspected or identified

Imaging studies

Chest radiography: Obtain an expiration posteroanterior (PA) chest film (along with the above-mentioned ABG test) if a pulmonary injury is suspected or identified Radiography of the clavicle and shoulderComputed tomography (CT) scanning with 3-dimensional (3-D) reconstruction: To help evaluate displaced fracturesArteriography: If a vascular injury is suspectedUltrasonography

See Workup for more detail.

Management

The vast majority of clavicle fractures heal with nonoperative management, which includes the use of a figure-of-eight brace or a simple shoulder sling.

Surgical indications include the following:

Complete fracture displacement[4] Severe displacement causing tenting of the skin with the risk of punctureFractures with 2 cm of shorteningComminuted fractures with a displaced transverse "zed" (or Z-shaped) fragment[4] Neurovascular compromiseDisplaced medial clavicular fractures with mediastinal structures at risk[5] Polytrauma (with multiple fractures): To expedite rehabilitationOpen fracturesAn inability to tolerate closed treatmentFractures with interposed muscleEstablished, symptomatic nonunionConcomitant glenoid neck fracture (floating shoulder)

When a midshaft clavicle fracture requires surgical fixation, the commonly performed procedure involves open reduction of the fracture, followed by either insertion of an intramedullary device or fixation with a plate and screws.[6, 7, 8, 9]

In a distal clavicle fracture, stable fixation can be achieved in many ways, including through combinations of a coracoclavicular screw, Dacron or Mersilene tape, tension banding, a Kirschner wire (K-wire), and clavicular plates. Regardless of the exact technique used, the general principles of fracture reduction and fixation and stabilization of the coracoclavicular interval apply.

See Treatment and Medication for more detail.

Image libraryA posterior view demonstrating a closed clavicle fracture tenting the skin (arrow), which can potentially lead to an open fracture. NextBackground

Clavicle fractures are common and easily recognized because of their subcutaneous position, as shown in the images below. Fracture union usually progresses regardless of the treatment initiated. Despite the innocuous appearance of clavicle fractures, however, potential treatment difficulties and possible complications warrant careful attention to these injuries. (See Prognosis, Treatment, and Medication.)

A posterior view demonstrating a closed clavicle fracture tenting the skin (arrow), which can potentially lead to an open fracture. Comparison of both clavicles, with the left tenting the skin (wide arrow). Close-up view of clavicle tenting the skin (arrow).

The clavicle is the first bone in the body to ossify, beginning at the fifth week of gestation.[2] Through age 5 years, the growth is primarily through intramembranous ossification. The medial epiphysis ossifies late, beginning at age 12-19 years, and may not completely fuse until age 22-25 years. Physial injuries around this area may be mistaken for fractures, and care should be taken in evaluating injuries. (For patients aged 22-25 years, the Salter-Harris classification for physial injuries can be used, and nonoperative treatment can often be initiated.) (See Anatomy, Clinical Presentation, DDx, and Workup.)

Historically, clavicle fractures have been considered best treated nonoperatively, with good outcomes. Management typically included the use of either a shoulder sling or a figure-of-eight brace. The vast majority of these fractures healed, with variable amounts of cosmetic deformity.

Studies have examined the different patterns of displacement and clinical outcomes of clavicle fractures according to their location. The medical literature has focused predominantly on fractures of the middle and distal clavicle but is still lacking concerning the management of medial clavicle fractures; the literature does, however, indicate that medial clavicle fractures respond well to nonoperative management. Controversy remains concerning operative versus nonoperative treatment of middle and distal clavicle fractures.[10, 11, 12, 13] (See Treatment and Medication.)

Fracture classification

Multiple attempts have been made to devise a classification scheme for clavicle fractures. The most common system is the following one, created by Allman, in which the clavicle is divided into thirds[1] :

Group I fractures: Middle third injuriesGroup II fractures: Distal third injuriesGroup III fractures: Medial (proximal) third injuries

Neer made a significant revision to the Allman classification scheme. Group II (distal clavicle) fractures were further divided into 3 types, based on the location of the clavicle fracture in relation to the coracoclavicular ligaments. The reason for this modification was that distal clavicle fractures behave differently depending on the exact location of the injury. The designations are as follows (see Clinical Presentation and Workup)[14] :

Type I fractures: Minimally displaced and occur lateral to an intact coracoclavicular ligament complex; these fractures may be treated nonoperatively and symptomatically (see the image below) Type II fractures: Occur when the medial fragment is separated from the coracoclavicular ligament complex; the medial fragment is displaced cephalad by the pull of the sternocleidomastoid muscle, and the distal fragment is displaced caudally by the weight of the upper extremity, with the intact coracoclavicular ligament complex; the resulting deformity leads to marked displacement of the fracture ends, predisposing this fracture type to a higher prevalence (up to 30%) of nonunion Type III injuries: Minimally displaced or nondisplaced and extend into the acromioclavicular (AC) joint; as with type I fractures, these injuries can be treated symptomatically; the development of late AC degenerative changes can be treated with distal clavicular excision Type I fracture of the distal clavicle (group II). The intact ligaments hold the fragments in place. A type II distal clavicle fracture. In type IIA, both conoid and trapezoid ligaments are on the distal segment, while the proximal segment, without ligamentous attachments, is displaced. A type IIB fracture of the distal clavicle. The conoid ligament is ruptured, while the trapezoid ligament remains attached to the distal segment. The proximal fragment is displaced.

The Neer type II fracture was later divided into types IIA and IIB, as follows (see the images below):

Type IIA - Displaced due to fracture medial to the coracoclavicular ligaments; the conoid and trapezoid remain attached to the distal fragment Type IIB - Displaced due to fracture medial to the coracoclavicular ligaments; either the conoid is torn or, more rarely, both the conoid and trapezoid are torn Anatomy of the clavicle indicating potential fracture sites. PreviousNextAnatomy

The clavicle is an S-shaped bone that acts as a strut between the sternum and the glenohumeral joint. Another function of the clavicle is to help protect the neurovascular bundle that runs behind it. The junction of the middle and distal thirds of the clavicle is a common site of fracture because this is the thinnest part of the bone, and there is relatively little protection by muscular attachments.

Numerous muscular and ligamentous forces act on the clavicle, and knowledge of these differing forces is necessary to understand the nature of displacement of clavicle fractures and why certain fracture patterns tend to cause problems if not reduced and surgically stabilized. (See the image below.)

Anatomy of the clavicle indicating potential fracture sites.

The clavicle articulates with the sternum at the sternoclavicular (SC) joint and with the acromion at the AC joint. Many ligamentous structures attach to the clavicle and provide stability for the articulations with the sternum and the acromion. The primary stabilizers of the SC joint are the anterior and posterior capsules. Other ligamentous structures attaching here are the interclavicular ligament and the costoclavicular ligament. Stability of the SC joint in the anterior-posterior plane is derived predominantly from the posterior capsule, with additional stability conferred by the anterior capsule. The interclavicular and costoclavicular ligaments have little effect on stability of the joint.

At the level of the AC joint, the coracoclavicular and AC ligaments provide stability for the joint. The coracoclavicular ligament is actually 2 separate ligaments, the conoid and the trapezoid, which both attach from the coracoid to the inferior surface of the distal clavicle. Debski et al have delineated the different functions of the conoid and trapezoid in resistance to applied loads to the AC joint.[15] The conoid is the predominant restraint to anterior and superior loading, while the trapezoid is the major restraint to posterior loading at the AC joint. The AC ligament is at the superior-lateral aspect of the clavicle and overlies the AC joint.

Three muscles originate on the clavicle, and 3 muscles insert on it. The muscles that take their origin from the clavicle are as follows:

SternohyoidPectoralis majorDeltoid

The muscles that insert on the clavicle are as follows:

SternocleidomastoidSubclaviusTrapezius

These 6 muscles may become deforming forces on the clavicle in the presence of a fracture, with the displacement of fracture fragments depending on the location of the fracture in relation to the muscular and ligamentous attachments.

Many other important structures are in extremely close contact with the clavicle and are thus subject to injury in the context of clavicle fractures. The subclavian artery (which becomes the axillary artery as it passes anteriorly to the first rib) and vein are both in close proximity to the middle portion of the clavicle. Additionally, the brachial plexus also passes behind the clavicle posterolateral to the subclavian vessels and is at risk with displaced fractures of the middle clavicle.

The subclavius muscle lies between the clavicle and these neurovascular structures, and, though small, it is believed to prevent more frequent damage to these structures. Reports also exist of injuries to the apices of the lung, most commonly with displaced middle third clavicle fractures.

PreviousNextPathophysiology

Because of its subcutaneous position, the clavicle may be fractured easily, with the fracture often being an isolated injury. However, clavicle fractures are also common in the context of high-energy injury or multiple traumatic injuries. In these situations, it is important to examine the patient for other associated injuries, such as rib fractures, scapula fractures, other fractures about the shoulder girdle, pulmonary contusion, pneumothorax, hemothorax, and closed head injuries. (See the image below.)

Clavicle fracture with rib fractures. Remember to look for associated injuries.

The frequency with which the 3 groups of fractures occur is as follows:

Group I (middle third) - Approximately 80%Group II (distal third) - 12-15%Group III (medial third) - Less than 5%Group I fractures

Most group I fractures occur medial to the coracoclavicular ligament, at the junction of the middle and outer third of the clavicle. The proximal fragment is typically displaced upward because of the pull of the sternocleidomastoid muscle. The usual mechanism of injury involves a direct force applied to the lateral aspect of the shoulder as a result of a fall, sporting injury, or motor vehicle accident. Group I fractures are shown in the images below

Nondisplaced middle clavicle fracture. Displaced fracture of middle clavicle. Displaced middle clavicle fracture. Group II fractures

Fractures of the distal third of the clavicle result from a direct blow to the top of the shoulder. They occur distal to the coracoclavicular ligament.[16]

Group III fractures

Fractures of the medial third of the clavicle occur as a result of a direct blow to the anterior chest. A diligent search for associated injuries should accompany group III fractures because considerably strong forces are required to fracture this area of the clavicle.

Greenstick or buckle-type fractures are common in children. Most of these fractures are nondisplaced and heal uneventfully.

PreviousNextEtiology

Clavicle fractures may be caused by direct or indirect trauma. The most common mechanism is an indirect one, involving a fall directly onto the lateral shoulder.[17, 18, 19] Examples of a direct mechanism would be a blow from a hockey stick or a direct fall onto the clavicle. At-risk athletes include those in football, hockey, and soccer and those at risk for falling during roller skating, skiing, bicycling, or horseback riding.

A less common mechanism for clavicle fractures is a fall onto an outstretched hand (ie, a FOOSH injury). The radiographs below depict clavicle fracture in a hockey player.

Comminuted fracture in a hockey player. Note the medial fragment tenting the skin. Additional view of fracture displacement and comminution in a hockey player. The sternocleidomastoid is the deforming force of the medial fragment. Radiographs after open reduction and internal fixation of a comminuted fracture in a hockey player. PreviousNextEpidemiologyOccurrence in the United States

The clavicle is the most frequently fractured bone in the body in childhood, accounting for 10-16% of all fractures in this age group.

In adults, clavicle fractures account for 2.6-5% of all fractures and 44% of all shoulder girdle injuries.[20, 21, 22] Middle third (group I) fractures account for 69-82% of all fractures of the clavicle, whereas distal third (group II) fractures account for 12%, and medial third (group III) fractures occur in 6% of cases.[20, 21]

Clavicular injuries affect 1 in 1000 people per year. Bimodal incidence occurs in men younger than 25 years and older than 55 years. Pneumothorax occurs in 3% of patients.

International occurrence

The annual incidence rate of clavicular fractures is estimated to be between 30 and 60 cases per 100,000 population.[12]

Sex- and age-related demographics

Clavicular injuries occur 2.5 times more commonly in males than in females, reflecting a greater involvement of males in contact and violent sports and motor vehicle accidents (MVAs).

Clavicle fractures, the most common of all pediatric fractures, can present even in the newborn period, especially following a difficult delivery. A large peak incidence occurs in males younger than 30 years due to sports injuries. A smaller peak occurs in elderly patients, who tend to sustain clavicle fractures (in association with osteoporosis) during low-energy falls.[12]

PreviousNextPrognosis

Most clavicle fractures treated nonoperatively heal, although with variable amounts of cosmetic deformity. Younger children generally require shorter periods of immobilization (2-4 wk) than do adolescents and adults (4-8 wk).

Complications

Nonunion

Nonunion is a failure to show clinical or radiographic progression of healing after 4-6 months. The following are risk factors for nonunion:

Fracture comminutionSignificant fracture displacement or shorteningType 2 fractures of the distal third of the clavicleRefractureFemale sexAdvanced ageFractures with more than 2 cm of shortening

The nonunion rate for all midclavicle fractures treated nonoperatively is 6%; the rate is 15% for displaced midclavicle fractures treated nonoperatively.[23] Symptoms of nonunion can be pain, motion, or loss of function. Note, however, that many nonunions are asymptomatic and require no treatment. Refer patients with symptomatic nonunion to an orthopedic surgeon to discuss surgical options. In some situations, a bone stimulator to help promote bone healing can be tried before surgery.

Murray et al reported that smoking was the greatest risk factor for nonunion among patients treated nonoperatively for diaphysial clavicle fractures. In a study, the investigators followed the healing course of 941 patients with such fractures and, using multivariate analysis, found that, along with smoking, both comminution and fracture displacement were particularly significant factors in nonunion.

The investigators determined that by using known risk factors, a statistical model can be used to estimate the probability of nonunion in a specific patient and can therefore help to determine whether he or she should be treated surgically. The investigators also concluded that smoking cessation needs to be included in the treatment of diaphysial clavicle fractures.[24]

Malunion

Malunion is when the fracture heals with significant angulation, shortening, and a poor appearance. Mild malunion is common after clavicle fractures, but it is usually not clinically significant. Occasionally, the patient can have pain or a mild limitation in motion or strength. Symptoms from nerve impingement may occur but are uncommon. Surgeries for malunion attempt to restore the clavicular length and correct any angular deformity of the clavicle.

Neurovascular injuries

Group I fractures (middle third of the clavicle) have been associated with injuries to the neurovascular bundle and the pleural dome.

Neurovascular compromise can develop from exuberant callus formation or from malunion. The medial cord and ulnar nerve are affected most often; treatment is surgical in nature. Brachial plexus compression resulting from hypertrophic callus formation may cause peripheral neuropathy.

Intrathoracic injuries

These include the following:

PneumothoraxSubclavian artery and vein injuryInternal jugular vein injuryAxillary artery injury

Other

A spike of bone can form subcutaneously after angulated fractures heal. This can be symptomatic for athletes who wear shoulder pads or for backpackers. If a donut pad is not sufficient to relieve symptoms, surgical excision can be considered. Posttraumatic arthritis can develop if a clavicle fracture enters the AC or SC joints.

Complications after group III fractures (medial third of the clavicle) resemble those associated with posterior sternoclavicular dislocations, including pneumothorax and compression or laceration of the great vessels, trachea, or esophagus.

Mortality

While the overwhelming majority of clavicle fractures are benign, there is a possibility of associated, life-threatening intrathoracic injuries.

Kendall et al reported a fatality from an isolated clavicle fracture from transection of the subclavian artery,[25] the first such report in the literature. The fatality may have been due to the fact that the fall was not witnessed and the patient lay unassisted for an unknown period of time. The patient never regained spontaneous circulation, and the injury to the subclavian artery was diagnosed at autopsy. The postmortem examination revealed a midclavicular fracture with transection of the subclavian artery. A 2.6-L hemothorax and damage to parietal and apical pleura were noted, but no other injuries were present.

Although this case is unique, it does emphasize the need to be aware of the potentially catastrophic complications of damage to the vascular structures in close proximity to the clavicle.

PreviousNextPatient Education

At the initial visit, discuss the following with the patient who has a clavicular injury:

A visible prominence may remain at the fracture site after it heals; this may be more evident in thin individualsFracture nonunion is possible, and surgery may be necessaryRefracture is a possibility if the patient engages in contact sports, particularly if he or she returns to play before the bone healing is solid

Educate patients about proper placement and adjustment techniques for a figure-of-eight bandage (clavicle strap) and inform them that paresthesias or edema in the hands or fingers indicate that the strap is too tight and should be removed.

Neonatal clavicle fracture

Advise parents to minimize pressure and movement of the ipsilateral arm during handling of a neonate with a clavicle fracture. The parent may try to pin the shirt sleeve of the affected arm to the front of the child’s shirt to minimize movement.

For patient education information, see the First Aid and Injuries Center, as well as Broken Collarbone (Broken Clavicle) and Shoulder Dislocation.

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Cervical Spine Acute Bony Injuries in Sports Medicine

Background

Cervical spine fractures lead to substantial morbidity and mortality. Neck injury in athletes can quickly end or change the future of an athlete. Failure to properly recognize and provide early care in cervical spine fracture cases may lead to devastating complications.[1, 2, 3, 4]

A C3 spinous fracture is depicted in the image below.

Lateral view of a C3 spinous fracture.

For patient education resources, see the Back, Ribs, Neck, and Head Center, as well as Neck Strain, Vertebral Compression Fracture, and Whiplash.

NextEpidemiologyFrequencyUnited States

The incidence of all spinal injuries in the United States has been reported at approximately 10,000 cases per year. Nearly 200,000 people in the United States have a history of spinal injuries. These statistics do not differentiate between injuries with fracture and injuries without fracture.[5, 6, 7]

Sports-related activities represent 10-15% of these injuries, and spinal injuries represent 2-3% of all sports-related injuries. Certain sports (eg, American football, diving, gymnastics, skiing, wrestling, rugby, hang gliding, surfing, equestrian events) are more frequently associated with the risk of spinal trauma.[2, 3, 4, 6, 7, 8, 9, 10, 11, 12]

The most common spinal injuries cited in the literature are injuries secondary to contact sports such as football. Nearly 1.2 million high school athletes and 200,000 college and professional athletes participate in football. The National Football Head and Neck Injury Registry contains data on cervical spine injuries as a result of participation in football. A trend can be seen over time, as equipment and helmets improved. The incidence of cervical spine injuries increased until 1976. In that year, antispearing rules were established to prevent the athlete from using the helmet as driving force in tackles. Direct collision created higher axial loads than the neck could withstand, leading to high injury rates. This rule, along with better coaching of blocking and tackling techniques, has resulted in a significant decrease in the number of spinal injuries.[10]

Diving is often cited as another significant cause of cervical spine injuries. Injuries resulting from diving are often associated with devastating outcomes. Diving rules (eg, depth of starting areas) and proper technique have lowered the probability of injury during supervised athletic events. However, unsupervised swimming and diving into shallow water present significant risks. Public awareness of this problem has led to the development of special awareness programs, but the risk of injury remains high.

PreviousNextFunctional Anatomy

The human spine serves to provide structural support and bony protection of the spinal cord. The cervical spine consists of 7 bony vertebrae separated by flexible intervertebral discs. They are joined together by an intricate network of ligaments, which helps form the normal lordotic curve of the cervical neck.[13]

The spinal column can be divided into 2 separate columns based on function and injury patterns. The anterior column consists of the bodies of the vertebrae, intervertebral discs, and the anterior and posterior longitudinal ligaments. The function of the vertebral body is to support weight. The posterior column contains the spinal canal and consists of the pedicles, laminae, articulating facets, and transverse and spinous processes. These structures form the vertebral arch, which encloses the vertebral foramen and protects the neural tissues.

The arch is formed by bilateral pedicles that are oriented posteriorly and join 2 laminae. The spinous process arises posteriorly from the vertebral arch. The cervical transverse processes and 4 articular processes also arise from the arch. The cervical transverse processes are unique to the vertebral column with an oval foramen transversarium. The vertebral arteries pass through these foramina. The posterior column also includes a group of ligaments including the supraspinous, infraspinous, interspinous, and nuchal ligaments.

The first 2 cervical vertebrae are atypical in form and function. The next 5 vertebrae are all similar in structure and function. The atlas, C1, is a ring-shaped bone that supports the skull. Two concave, superior articular facets articulate with the occipital condyles. The atlas does not have a body or spinous process. The atlas has an anterior and posterior arch, each with a tubercle and lateral mass. The axis, C2, is the strongest cervical vertebrae. The atlas rotates on 2 large articulating surfaces. The odontoid process (dens) projects superiorly from the C2 body and is the bony structure that the atlas rotates on. The odontoid process is held in place by the transverse ligament of the atlas.

PreviousNextSport-Specific Biomechanics

Contact sports, falls, and diving in sports may lead to vertebral stress and fractures. Sports that involving tackling can increase exposure to mechanisms causing fractures.

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Cervical Spine Sprain/Strain Injuries

Background

The most frequent cervical injuries in athletes are probably acute strains and sprains of the musculature of the neck, as well as soft-tissue contusions.

A strain refers to an injury to a muscle, occurring when a muscle-tendon unit is stretched or overloaded. Cervical muscles that are commonly strained include the sternocleidomastoid (SCM), the trapezius, the rhomboids, the erector spinae, the scalenes, and the levator scapulae.

A sprain refers to a ligamentous injury, and the diagnosis of cervical sprain implies that the ligamentous and capsular structures connecting the cervical facet joints and vertebrae have been damaged. Practically, a cervical sprain may be difficult to differentiate from a strain, and the 2 injuries often occur simultaneously. Pain referred to the muscle can arise from any source that is modulated by the dorsal rami.

Numerous epidemiologic studies have been completed in the hopes of identifying the injury risk patterns that are associated with specific sports. Many athletes are reluctant to report minor injuries, and because the overwhelming numbers of sports-related spinal injuries are self-limited and resolve before being reported, the accuracy of these studies has been challenged. The mainstay of prevention and treatment of cervical spine injuries is maintaining good strength and flexibility through conditioning.

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

Related Medscape Reference topics include the following:

Atlantoaxial Injury and DysfunctionCervical Disc DiseaseCervical Spine Injuries in SportsNextEpidemiologyFrequencyUnited States

Cervical spine injuries occur in an estimated 10-15% of football players, most commonly in defensive ends, linemen, and linebackers.[1, 2] The reinjury rate in high school football players following all cervical spine injuries is reported at 17.2%. Football players with 2 previous injuries are reported as having an 87% risk of reinjury. Wrestlers with no history of injuries to the neck have a 20% chance of sustaining a neck injury in a given year[3] ; however, wrestlers who have had a previous neck injury have an approximate 50% chance of recurrence.

Sporting accidents are second only to motor vehicle accidents as the leading cause of emergency department visits involving neck injuries, and as more people participate in athletic activity, the incidence of cervical injuries can be expected to rise as well.[4, 5]

PreviousNextFunctional Anatomy

The spinal cord is protected by the cervical spine, which provides support for the head and allows for a significant amount of range of motion (ROM).[6, 7] Seven cervical vertebrae, stacked vertically, comprise the skeletal portion of the spine. Each vertebra (except C1 and C2) has a common body anteriorly and a ring of bone formed by the laminae and pedicles posteriorly. This protective ring of bone forms the spinal canal, which surrounds and protects the spinal cord. The tissues that surround the cord and the spinal fluid fill the remaining space. The C1 vertebra, or atlas, is ring-shaped, has large lateral masses, and attaches to the occipital condyles of the skull, providing support. See the images below.

Bony framework of head and neck. Cervical vertebrae, the atlas and the axis. Cervical vertebrae. Atlantooccipital junction.

The transverse ligament lies anteriorly between the 2 lateral masses of C1 and just posteriorly to the odontoid process of the C2 vertebra, or axis (see the image below). Projecting upward from the body of C2, the odontoid process is contained between the anterior arch of C1 and the transverse ligament. Displacement of C1 and C2 may be associated with rupture of this ligament, which may result in a spinal cord injury.

Internal craniocervical ligaments.

The remaining cervical vertebrae (C3-C7) are similar in function and appearance. The ovoid vertebral bodies are wider than they are tall. The bilateral raised uncinate processes located posterolaterally correspond to similar beveled surfaces on the inferior aspect of the superior vertebral body. These joints of Luschka, also known as uncovertebral joints, are not present in the embryologic development of the cervical spine but arise as a result of the degenerative and adaptive changes of annular tissue to stresses and loads.

The cervical zygapophyseal joints are synovial in nature. Their articular surfaces are covered with hyaline cartilage, and their fibrous capsules are lined with synovium. The orientation of the cervical zygapophyseal joints allows them to play a weight-bearing role and to provide resistance to anterior translation. Because the C2-C3 facet sits between the upper and lower parts of the cervical spine that move differently, it is considered transitional anatomically and biomechanically.[7]

The lower cervical spine flexes and extends, and the atlantoaxial joint moves in rotation. During lateral bending, the spinous processes move to the convexity of the curve (spinous processes move to the right during left lateral bending) in the middle and lower cervical regions. Coupled lateral bending occurs in the opposite direction to the applied axial rotation above the C2-C3 level. Lateral bending from C2-C3 distally is always coupled with rotation in the same direction because of the approximate 45° inclination of the cervical zygapophyseal joints. The obliquity of the articular surfaces in the frontal plane determines the relative amount of side bending or rotation that occurs. The more vertical the joint surface, the more side bending is coupled; the more horizontal the joint surface, the more rotation is coupled.

Regressive changes occur in cervical zygapophyseal menisci with age. The meniscus retracts and narrows between childhood and the fourth decade of life. The meniscus helps increase the contact surface area when articular facets come together, thus helping to transmit some of the load.

The many articulations between the cervical vertebrae make the extensive ROM in the cervical spine possible. However, this large ROM comes at the cost of stability. Cervical spine stability is provided by a combination of the zygapophyseal joints and numerous ligaments and muscles. Extension, flexion, lateral bending, and rotation are permitted by the orientation of the zygapophyseal joints and ligaments. Positioning of the head makes combinations of these motions necessary. In a young person, cervical flexion and extension is about 100°. Bilateral rotation is about 80°, with approximately 50% of this range occurring between C1 and C2. The range of lateral bending is about 30-50°. Older individuals usually have reduced end ROMs because cervical mobility usually decreases with age.

Intervertebral discs are located in between each of the cervical vertebrae from C2-C7. These discs consist of a water-containing central portion, the nucleus pulposus, and a tough fibrous outer ring, the annulus fibrosis. The discs are subject to prolonged and repetitive loading from muscle forces acting across them and from the weight of the head. With their viscous central portion, the intervertebral discs are able to transmit these forces between the end plates of adjacent vertebral bodies. These biconvex discs conform to the concavity of the vertebral bodies, and they also contribute to normal cervical lordosis because they are thicker anteriorly. Only the outer one third to one half of the annulus fibrosis in adults receives a vascular supply. The rest of the annulus and the whole nucleus pulposus are avascular.

The annular fibers consist of 10-20 circumferential collagenous lamellae. The fibers within each lamella are oriented 35° from the horizontal, although the direction of inclination alternates with each lamella. As a result, rotation and translation are more likely to damage the annulus because resistance can be offered only by half of the lamellae whose fibers are oriented in the direction of motion.

The functions of a ligament are: (1) to provide stability to the joint, (2) to absorb energy during trauma, and (3) to act as a joint position transducer during physiologic motions. Ligaments, along with the paracervical muscles in the cervical spine, prevent motion between vertebrae that might injure the spinal cord or nerve roots. The cervical spine ligaments have numerous and complex interrelationships (see the images below).

External craniocervical ligaments. Internal craniocervical ligaments.

Running vertically along the anterior and posterior aspects of the vertebral bodies, the anterior and posterior longitudinal ligaments attach to the discs as well. The tightly attached posterior longitudinal ligament is thick in its central portion, which helps prevent a disc herniation from pressing directly on the cord posteriorly. The interspinous ligaments are also located posteriorly but are not as well developed in the cervical region.

The ligamentum flavum, a yellowish elastic membrane, overlies the space between the laminae of adjacent vertebrae and the neural arches. The posterior location of the ligamentum flavum helps to restrain hyperflexion. The ligamentum flavum becomes shortened and thicker in hyperextension and elongated and thinner in hyperflexion. During hyperextension, it may protrude into the cervical canal as much as 3.5 mm. Impingement on the spinal cord during extension is normally prevented by the elastic properties of the ligament; however, hypertrophy of the ligamentum flavum or loss of elasticity through degeneration may lead to canal narrowing or cord impingement.

The capsular ligaments, oriented approximately orthogonal to the articular facets, provide maximal mechanical efficiency in resisting distraction of the facets but relatively poor resistance to shear. The posterior longitudinal ligament limits flexion and distraction, the tectorial membrane limits flexion and extension, and the supraspinous and interspinous ligaments limit flexion and anterior horizontal displacement.

The main function of the alar ligaments is to restrain rotation. The alar ligaments originate from the posterolateral aspect of the dens of C2 and insert on the medial surfaces of the occipital condyles. When a single alar ligament is cut, axial rotation increases significantly to both sides; thus, both ligaments are required to be intact for restraining motion. Alar ligaments are stretched the most when the head is rotated and flexed together, and the ligaments are relaxed during extension. The anterior aspect of the transverse ligament acts as the pivot about which C1 (ie, the atlas) rotates.

Holding the odontoid process of C2 against the anterior ring of the atlas, the transverse ligament functions as a restraining band on the dens. Flexion and anterior displacement of the atlas is restrained by its orientation. The facet joint capsules are strong fibrous structures that contribute to posterior stability.

A muscle injury or reaction of some degree is associated with almost every cervical injury. The musculature of the neck is vulnerable to the same types of injuries that affect muscles elsewhere in the body. The role of the muscles is to stabilize the spine, carry loads, and produce motion. The action of the intervertebral muscle forces is to restore the intervertebral motions of an injured spine to its intact values.

The capital flexor muscles include the following:

Longus capitisRectus capitis anterior and lateralSuprahyoid and hyoid muscles

The capital extensor muscles include the following:

Splenius capitisSemispinalis capitisLongissimus capitisObliquus capitis inferior and superiorRectus capitis posterior major and minor

The cervical flexor muscles include the following:

Anterior scaleneMiddle scaleneSCM

The cervical extensor muscles include the following:

Semispinalis cervicisLongissimus cervicisSplenius cervicis

Because the bulk of the flexor muscle groups are at the C4-C5 level and the main mass of the extensor muscle groups overlies the C6-T1 levels as well as the atlantoaxial area, these muscle groups are likely sites of major stresses. The muscle groups that laterally flex and rotate the cervical spine include the following:

Rectus capitis lateralisObliquus capitis inferior and superiorIntertransversariiMultifidiIliocostalis cervicisLongus colliLevator scapulaeLongissimus capitisSplenius cervicisSplenius capitisSCMScalene muscles

The images below illustrate several views of muscles of the neck.

Lateral view of the muscles of the neck. Anterior view of the muscles of the neck. Infrahyoid and suprahyoid muscles. Scalene and prevertebral muscles.

Related Medscape Reference topics include the following:

Cervical Spine Injuries in SportsCervical Sprain and StrainDisk Herniation ImagingPreviousNextSport-Specific Biomechanics

When contact is made with the head or body, deceleration injuries occur, and sudden flexion and extension of the neck can result. This type of injury is likely to occur in contact or collision sports such as football, soccer, rugby, or lacrosse.

The posterior neck muscles may be strained when resisting flexion forces, and/or the anterior neck muscles may be strained when resisting hyperextension. Microtears or strains in these muscles are caused by the sudden muscular contractions that try to decelerate the applied force. Forced twisting, which is common in wrestling, can also cause a cervical strain. The twisting injury usually happens in the wrestler who is pinned on the mat, and a flexion-extension injury is more likely to happen during the takedown. Deceleration and rotational forces can also cause microtears or stretching of the small intertransverse and interspinous ligaments as well as the joint capsules.

In cervical sprains, the immediate soft-tissue trauma occurs in the structures in and around the facet joints. This trauma occurs with varying severity, including multiple tears in ligamentous tissue with focal hematomas and hemorrhages. A fibrous tissue contraction is the net final effect of the repair of these strained capsular and ligamentous tissues so that restriction of motion and stiffening of the neck may eventually result. The short capsular ligaments of the Luschka interbody joints lack the normal laxity of the capsular structures surrounding the facet joints. Because of their anatomic position, the articulating surfaces of these vertebral body joints are particularly susceptible to injury from axial compression when the head is in a laterally tilted or neutral position.

The cervical spine can absorb much of the imparted energy of collisions by dissipation through the normal lordotic curve of the cervical spine, the paravertebral musculature, and the intervertebral discs. However, when the neck is flexed about 30°, the forces applied to the top of the head are directed to a straight-segmented column because the normal lordotic curve is flattened. The cervical spine is then less able to dissipate the exerted forces in this situation, leading to fracture(s) and possible spinal cord injury. This proposed mechanism is supported by biomechanical studies that replicate it. In individuals with straight cervical spines, less energy is needed to fail under an axial load than in those with a normal lordotic curve; this finding underlines the importance of the cervical musculature in maintaining proper lordosis.

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