Cervical Radiculopathy

Background

Cervical radiculopathy is a dysfunction of a nerve root of the cervical spine. The seventh (C7; 60%) and sixth (C6; 25%) cervical nerve roots are the most commonly affected.[1, 2, 3, 4, 5, 6, 7]

Sagittal magnetic resonance image of the cervical spine. This image reveals a C6-C7 herniated nucleus pulposus. Axial magnetic resonance image of the cervical spine. This image reveals a C6-C7 herniated nucleus pulposus.

In the younger population, cervical radiculopathy is a result of a disc herniation or an acute injury causing foraminal impingement of an exiting nerve.[8] Disc herniation accounts for 20-25% of the cases of cervical radiculopathy. In the older patient, cervical radiculopathy is often a result of foraminal narrowing from osteophyte formation, decreased disc height, degenerative changes of the uncovertebral joints anteriorly and of the facet joints posteriorly.

Factors associated with increased risk include heavy manual labor requiring the lifting of more than 25 pounds, smoking, and driving or operating vibrating equipment. Other, less frequent causes include tumors of the spine, an expanding cervical synovial cyst, synovial chondromatosis in the cervical facet joint, giant cell arteritis of the cervical radicular vessels, and spinal infections.[9, 10] The purpose of this article is to provide information on the presentation, evaluation, differential diagnosis, and treatment of cervical radiculopathy.

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

NextEpidemiologyFrequencyUnited States

Cervical radiculopathy occurs at a much lower frequency than radiculopathy of the lumbar spine. The annual incidence is approximately 85 cases per 100,000 population.

PreviousNextFunctional Anatomy

Seven cervical vertebrae and 8 cervical nerve roots exist. The C1-2 (atlantoaxial) joint forms the upper cervical segment.[1, 3, 11, 12] This joint allows for 50% of all cervical rotation. The occipitoatlantal joint is responsible for 50% of flexion and extension. Below the C2-C3 level, lateral bending of the cervical spine is coupled with rotation in the same direction. This is due to the 45° inclination of the cervical facet joints.

The vertebral bodies of C3-C7 are similar in appearance and function. They articulate via the zygapophyseal or facet joints posteriorly. On the lateral aspect of the vertebral bodies are sharply defined margins, which articulate with the facet above. These articulations are called uncovertebral joints, or the joints of Luschka. These joints can develop osteophytic spurs, which can narrow the intervertebral foramina.

Intervertebral discs are located between the vertebral bodies of C2-C7. The discs are composed of an outer annular fibrosis and an inner nucleus pulposus and serve as force dissipators, transmitting compressive loads throughout a range of motion (ROM). The intervertebral discs are thicker anteriorly and therefore contribute to normal cervical lordosis.

The foramina are largest at C2-C3 and progressively decrease in size to the C6-C7 level. The nerve root occupies 25-33% of the foraminal space. The neural foramen is bordered anteromedially by the uncovertebral joints, posterolaterally by facet joints, superiorly by the pedicle of the vertebra above, and inferiorly by the pedicle of the lower vertebra. Medially, the foramina are formed by the edge of the end plates and the intervertebral discs. The nerve roots exit above their correspondingly numbered vertebral body from C2-C7. C1 exits between the occiput and atlas, and C8 exits below the C7 vertebral body. Degenerative changes of the structures that form the foramina can cause nerve root compression. This compression can occur from osteophyte formation, disc herniation, or a combination of the 2.

PreviousNextSport-Specific Biomechanics

Cervical radiculopathy in athletes can occur from several mechanisms. These injuries can occur from an extension, lateral bending, or rotation mechanism, which closes the neural foramen and results in ipsilateral nerve root injury. Conversely, a traction injury can occur with a sudden flexion or extension, coupled with lateral bending away from the affected nerve root.

Additionally, cervical disc herniations can occur with a sudden load with the neck in either flexion or extension. In elderly persons with osteophyte formation, repetitive neck extension and rotation in certain sports, such as swimming or tennis, may result in a more insidious injury.

PreviousProceed to Clinical Presentation , Cervical Radiculopathy

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Lumbosacral Facet Syndrome

Background

The facet joints are a pair of joints in the posterior aspect of the spine. Although these joints are most commonly called the facet joints, they are more properly termed the zygapophyseal joints (abbreviated as Z-joints; also commonly spelled as "zygapophysial joints"), a term derived from the Greek roots zygos, meaning yoke or bridge, and physis, meaning outgrowth. This “bridging of outgrowths” is most easily seen from a lateral view, where the Z-joint bridges adjoin the vertebrae. The term facet joint is a misnomer because the joint occurs between adjoining zygapophyseal processes, rather than facets, which are the articular cartilage lining small joints in the body (eg, phalanges, costotransverse and costovertebral joints). This joint is also sometimes referred to as the apophyseal joint or the posterior intervertebral joint.

As is true of any synovial joint, the Z-joint is a potential source of pain. In fact, the Z-joint is one of the most common sources of low back pain (LBP). The first discussion of the Z-joint as a source of LBP was by Goldwaith in 1911.[1] In 1927, Putti illustrated osteoarthritic changes of Z-joints in 75 cadavers of persons older than 40 years.[2] In 1933, Ghormley coined the term facet syndrome, suggesting that hypertrophic changes secondary to osteoarthritis of the zygapophyseal processes led to lumbar nerve root entrapment, which caused LBP.[3] In the 1950s, Harris and Mcnab[4] and McRae[5] determined that the etiology of Z-joint degeneration was secondary to intervertebral disc degeneration.

Hirsch et al were later able to reproduce LBP with injections of hypertonic saline solution into the Z-joints, thus affirming the role of the Z-joints as a source of LBP.[6] Mooney and Robertson also performed provocative hypertonic saline Z-joint injections and recorded pain referral maps with radiation mainly to the buttocks and posterior thigh.[7]

Thus, the history and presence of Z-joint pain has been well published. However, despite all of these studies, the diagnosis of Z-joint–mediated pain remains a challenge because no history findings or examination maneuver has been found to be unique or specific to this entity.[8, 9] Schwarzer et al and other authors have reported up to a 45% false-positive diagnostic rate when the physical examination findings are correlated to diagnostic medial branch blocks of the posterior rami.[10, 11, 12, 13, 14]

Authors have concluded that in most cases, Z-joints are not the single or primary cause of LBP. In many cases, Z-joint pain is mistaken for discogenic pain. Thus, many clinicians agree that correlating historical or physical examination findings with pain emanating from the Z-joint is a challenge. This review may help broaden the clinician's knowledge of this entity and may assist in making the diagnosis of lumbosacral facet joint syndrome.

For excellent patient education resources, see eMedicineHealth's patient education articles Low Back Pain, Sprains and Strains, and Slipped Disk.

Related Medscape Reference topics include the following:

Mechanical Back PainDegenerative Disk DiseaseDegenerative Lumbar Disc Disease in the Mature AthleteLumbar Degenerative Disk DiseaseLumbar Disk Problems in the AthleteLow Back Pain and SciaticaNextEpidemiologyFrequencyUnited States

LBP is the most common musculoskeletal disorder of industrialized society and the most common cause of disability in persons younger than 45 years. Given that 90% of adults experience LBP sometime in their lives, the fact that it is the second leading cause for visits to primary care physicians and the most frequent reason for visits to orthopedic surgeons or neurosurgeons is not surprising. As the primary cause of work-related injuries, LBP is the most costly of all medical diagnoses when time off from work, long-term disability, and medical and legal expenses are taken into account.

The lumbosacral Z-joint is reported to be the source of pain in 15-40% of patients with chronic LBP. Ray believed that Z-joint–mediated pain is the etiology for most cases of mechanical LBP,[15] whereas other authors have argued that it may contribute to nearly 80% of cases. Thus, the diagnosis and treatment of this entity may help alleviate LBP in a significant number of patients.

International

International data on lumbosacral facet syndrome have not been clearly established.

PreviousNextFunctional Anatomy

The spine is composed of a series of functional units. Each unit consists of an anterior segment, which is made up of 2 adjacent vertebral bodies and the intervertebral disc between them, and the posterior segment, which consists of the laminae and their processes. One joint is formed between the 2 vertebral bodies, wherea the other 2 joints, known as the Z-joints, are formed by the articulation of the superior articular processes of one vertebra with the inferior articular processes of the vertebra above. Thus, the Z-joints are part of an interdependent functional spinal unit consisting of the disc-vertebral body joint and the 2 Z-joints, with the Z-joints paired along the entire posterolateral vertebral column.

In the lumbar spine, the superior articular processes face anterolaterally, whereas the inferior articular processes face posteromedially. The superior articular process has a concave orientation in order to accommodate the more convex orientation of the inferior articular process. The upper lumbar Z-joints are oriented in a sagittal plane, whereas the lower lumbar Z-joints approach a more frontal orientation. Thus, as the lumbosacral Z-joints maintain a progressive coronal orientation, greatest at the S1 level, they are functionally able to resist rotation in the upper lumbar region as well as resist forward displacement in the lower lumbosacral region.

The Z-joint is considered a motion-restricting joint, able to resist stress and withstand both axial and shearing forces. In back extension, the Z-joints, along with the intervertebral discs, absorb a compressive load. In addition, the transmission of the Z-joint load occurs through contact of the tip of the inferior articular process with the pars of the vertebra below. The overloaded Z-joint then causes posterior rotation of the inferior articular process, resulting in stretching of the joint capsule.

If one considers the disc and each of the adjacent Z-joints as an interdependent functional spinal unit, degenerative changes within this 3-joint complex can influence each of the segments. Thus, degeneration of the discs can lead to loss of disc height, resulting in a relative increase in Z-joint load that is found in compression and extension maneuvers. One theory is that these excessive Z-joint loads cause the inferior articular process to pivot about the pars and stretch the joint capsule, in addition to causing rostrocaudal subluxation (ie, Z-joint malalignment). Thus, some authors postulate that Z-joints undergo osteoarthritic changes in response to disc degeneration secondary to changes in loading.

The Z-joint is a common pain generator in the lower back. The 2 common mechanisms for this generation of pain are either (1) direct, from an arthritic process within the joint itself, or (2) indirect, in which overgrowth of the joint (eg, Z-joint hypertrophy or a synovial cyst) impinges on nearby structures.

The Z-joints are diarthrodial joints with a synovial lining, the surfaces of which are covered with hyaline cartilage, which is susceptible to arthritic changes and arthropathies. Repetitive stress and osteoarthritic changes to the Z-joint can lead to zygapophyseal hypertrophy. Like any synovial joint, degeneration, inflammation, and injury can lead to pain with joint motion, causing restriction of motion secondary to pain and, thus, deconditioning. In addition, Z-joint arthrosis, particularly trophic changes of the superior articular process, can progress to narrowing of the neural foramen. In addition, as is the case for any synovial joint, the synovial membrane can form an outpouching and, thus, a cyst. Z-joint cysts are most commonly seen at the L4-L5 level (65%), but they are also seen at the L5-S1 (31%) and L3-L4 (4%) levels. These synovial cysts can be clinically significant, particularly if they impingeonnearbystructures(eg,theexistingnerve root).

The neural foramen is bordered by the superior articular process, pars interarticularis, and posterior portion of the vertebral body. Z-joint hypertrophy or a synovial cyst can contribute to lateral and central lumbar stenosis, which can lead to impingement on the exiting nerve root. Thus, Z-joint pain can occasionally produce a pain referral pattern that is indistinguishable from disc herniation.

To understand the pattern of pain generation from the Z-joint, knowledge of the innervation pattern is essential. This pattern is frequently misunderstood even by experienced practitioners. Each Z-joint is innervated by branches of the dorsal ramus, termed the medial branch. The medial branch is 1 of 3 branches of the dorsal ramus, with the other 2 being the lateral branch (which does not exist for the L5 dorsal ramus) and the intermediate branch. The lateral branch innervates the iliocostalis muscle, and the intermediate branch innervates the longissimus muscle. The medial branch innervates many structures, including the Z-joint, but it also innervates the multifidus, interspinales, and intertransversarii mediales muscles, the interspinous ligament, and, possibly, the ligamentum flavum (see image below).

Dorsal ramus innervation (medial and lateral branches). MAL23 = mamillo-accessory ligament bridging the mamillary and accessory processes of L2 and L3; Z-joint = zygapophyseal joint.

After the medial branch splits off from the dorsal ramus, it courses caudally around the base of the superior articular process of the level below toward that level’s Z-joint (eg, the L2 medial branch wraps around the L3 superior articular process to approach the L2-L3 Z-joint). The medial branch then continues in a groove between the superior articular process and transverse process (or, in the case of the L5 medial branch, between the superior articular process of S1 and the sacral ala of S1, which is the homologous structure to the transverse processes of the lumbar vertebrae). As it makes this course, the medial branch is held in place by a ligament joining the superior articular process and the transverse process, termed the mamillo-accessory ligament (MAL) (see image below).

Dorsal ramus innervation (medial and lateral branches). MAL23 = mamillo-accessory ligament bridging the mamillary and accessory processes of L2 and L3; Z-joint = zygapophyseal joint.

The MAL is so named because it adjoins the mamillary process of the superior articular process to the accessory process of the transverse process (see image below). The MAL is clinically important because it allows precise location of the medial branch of the dorsal ramus using only bony landmarks, which is essential for fluoroscopically guided procedures.

Mamillary process anatomy.

After passing underneath the MAL, the medial branch of the dorsal ramus gives off 2 branches to the nearby Z-joints. One branch innervates the Z-joint of that level, and the second branch descends caudally to the level below. Therefore, each medial branch of the dorsal ramus innervates 2 joints—that level and the level below (eg, the L3 medial branch innervates the L3-L4 and L4-L5 Z-joints). Similarly, each Z-joint is innervated by the 2 most cephalad medial branches (eg, the L3-L4 Z-joint is innervated by the L2 and L3 medial branches). Some authors have also suggested that the L5-S1 Z-joint has a unique triple innervation; in addition to the expected innervation by the L3 and L4 medial branches, the S1 medial branch emerging from the S1 posterior sacral foramen ascends cranially to also innervate the L5-S1 Z-joint. This has not, however, been consistently reported.

Understanding of this anatomy is crucial for procedures that attempt to obliterate Z-joint–mediated pain by blunting the innervation, whether through anesthesia (eg, a medial branch block) or denervation (eg, medial branch radiofrequency ablation [RFA]).[16] Practitioners commonly make the mistake of thinking that each Z-joint is innervated by the 2 adjoining medial branches (eg, that the L4-L5 Z-joint is innervated by the L4 and L5 medial branches of the dorsal rami, when it is actually innervated by the L3 and L4 medial branches). Two common reasons are cited for why practitioners make this mistake.

First, in the cervical region, the Z-joints are innervated by the 2 medial branches of the same name (eg, the C3-C4 Z-joint is innervated by the C3 and C4 medial branches), with the transition occurring at the T1-T2 Z-joint, which is innervated by the C8 and T1 medial branches. The second reason practitioners commonly confuse the innervation pattern is because they fail to recognize that the medial branch descends one level to reach the Z-joint. For example, the L2 medial branch courses around the L3 superior articular process, crosses underneath the L3 MAL, and then sends branches to the L2-L3 and L3-L4 Z-joints. Therefore, in a medial branch block, the medial branches closest to the Z-joint are targeted; they simply descended from a higher level.

Moreover, it is important to note that the medial branch of the posterior rami also innervates other posterior back structures. This has several important clinical implications. First, pain relief from anesthetizing the medial branch does not necessarily implicate the Z-joints as the primary pain generator, because one of the other structures innervated by the medial branch may have been the pain generator. Second, denervation of the medial branch by RFA may affect the nerve supply to the multifidus muscle. This is important because lumbosacral radiculopathy is often another consideration in the differential diagnosis of LBP.

One test to confirm the diagnosis of a lumbosacral radiculopathy is electromyography (EMG) of the multifidus muscle. Normally, denervation potentials in the multifidus muscle of a patient with LBP might be interpreted as evidence of a lumbosacral radiculopathy. However, in the context of a patient who has had RFA of the medial branch of the dorsal rami for the treatment of Z-joint pain, an alternative explanation for the denervation potentials in the multifidus would be denervation from the RFA, not from a lumbosacral radiculopathy.

The Z-joints contain nociceptive nerve fibers from nerves of the sympathetic and parasympathetic ganglia, which can be activated by local pressure and capsular stretch. Nociceptive type IV receptors have been identified in the fibrous capsule and represent a plexus of unmyelinated nerve fibers and type I and II corpuscular mechanoreceptors. In addition, encapsulated type I and II nerve endings have been found to be primarily mechanosensitive and likely provide proprioceptive and protective information to the central nervous system.

In addition, the Z-joints have been found to undergo sensitization of neurons by naturally occurring inflammatory mediators such as substance P and phospholipase A2. Peripheral nerve endings release chemical mediators such as bradykinin, serotonin, histamine, and prostaglandins, which are noxious and can cause pain. Substance P has been implicated because of its ability to act directly on nerve endings or indirectly through vasodilation, plasma extravasation, and histamine release. Phospholipase A2 hydrolyzes phospholipids to produce arachidonic acid, causing an inflammatory reaction, edema, and prolonged nociceptive excitation.

In all, many sources of pain can be found at the Z-joint, ranging from degenerative changes to irritated nerve endings (chemical and mechanical) to concomitant nerve root entrapment.

Related Medscape Reference topics include the following:

Herniated Nucleus PulposusLumbosacral Disc InjuriesLumbosacral Spine Acute Bony InjuriesLumbosacral Spine Sprain/Strain InjuriesLumbosacral SpondylolisthesisLumbosacral SpondylolysisSpinal StenosisPreviousNextSport-Specific Biomechanics

Athletes involved in nearly any type of sport are susceptible to Z-joint injury. From linemen on a football team, who may sustain repetitive and compressive forces to an extended spine, to baseball players or golfers, who perform repeated spinal rotational maneuvers, lumbosacral facet syndrome can impact athletes in most sports.

Related Medscape Reference topics include the following:

Degenerative Lumbar Disc Disease in the Mature AthleteLumbar Disk Problems in the AthletePreviousProceed to Clinical Presentation , Lumbosacral Facet Syndrome

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Lumbosacral Discogenic Pain Syndrome

Background

Spinal abnormalities are more common in athletes than in nonathletes in the general population. Any spinal injury pattern can be observed in athletes who are subjected to trauma. Athletes are susceptible to degenerative disc changes at an early age because of the repetitive loading activities involved in sports.

Back pain is second only to the common cold as a cause of lost time from work and results in more lost productivity than any other medical condition. It has been estimated to result in 175.8 million days of restricted activity annually in the United States, and at any given time, 2.4 million Americans are disabled secondary to low back pain. Of these 2.4 million Americans, one half are chronically disabled. Data from the National Ambulatory Medical Care Survey from 1989-1990 revealed that there were almost 15 million office visits for low back pain, ranking this as the fifth reason for all physician visits.

In most industrialized nations, the lifetime prevalence of back pain exceeds 70%, and in the United States, a 15-20% 1-year prevalence rate has been estimated.[1] In 1990, 400,000 industrial low back injuries resulting in disability occurred in the United States. In 1985, a prospective Swedish study of adults aged 20-65 years conducted over an 18-month period reported over 7,500 work absences related to acute low back pain. Of these episodes, 57% of workers recovered within 1 week, 90% in 6 weeks, and 95% after 12 weeks. In 1987, Deyo reported a slower recovery rate in the United States, with only 33.2% of patients recovering in less than 1 month, 33% recovering in 1-5 months, and 32.7% taking longer than 6 months to recover. Finally, recurrence rates from 60-85% have been reported during the first 2 years following an acute back injury.

Frymoyer reported that 40% of patients experience leg pain in association with back pain; a much lower percentage reported numbness and weakness; and only 1% of adult respondents in the United States reported symptoms indicative of true sciatica. Herniated discs occur primarily in the second through the fifth decades of life and have a slight male preponderance. The L4-5 disc has been shown to be the most commonly herniated disc, resulting an L5 radiculopathy. The L5-S1 disc is a close second in frequency of herniation. Translating the frequency of back pain into economic terms emphasizes the magnitude of the problem. Lower back injuries account for approximately 22% of compensable workplace injuries, but they account for 31% of compensation payments. In the United States, the direct costs of spinal disorders were estimated to be in excess of $23 billion during 1990. This represented an increase of nearly 47% over the estimated costs in1984.

NextEpidemiologyFrequencyUnited States

Thoracolumbar spinal abnormalities are more common in athletes than in nonathletes in the general population. Studies investigating spinal injuries in athletes are largely limited to those injuries that are severe enough to limit participation. Many athletes do not report injuries that allow continued competition, and they participate with chronic low back pain.

Nearly 50% of college football linemen experience low back pain during a typical season, while 10-27% of all college football players experience lumbar spinal symptoms.

The rate of lumbar spinal injury in gymnasts has been directly related to the level of competition. Evidence from magnetic resonance imaging (MRI) scans that support this relationship is found in 9% of pre-elite, 43% of elite, and 63% of Olympic level gymnasts.[2, 3]

Noncontact sports, such as golf and cycling, are also associated with increased low back pain, largely related to repetitive forces or long-term postures.

PreviousNextFunctional Anatomy

The lumbar spine has an average of 5 vertebrae (normal range 4-6), with an intervertebral disc interposed between adjacent vertebral bodies. A cartilaginous endplate exists between the disc and the adjacent vertebral bodies and is considered part of the disc.

The disc itself is comprised of a central nucleus pulposus surrounded peripherally by the annulus fibrosis. In healthy young adults, the nucleus is a semifluid mass of mucoid material. The nucleus is comprised of approximately 70-90% water in a young healthy disc, but this percentage generally decreases with age. The primary nuclear constituents include glycosaminoglycans, proteoglycans, and collagen. Type II collagen predominates in the nucleus. Proteoglycans are the largest molecules in the body and possess an enormous capacity to attract water through oncotic forces. These forces increase their weight by 250% and result in a gellike composition. Biomechanically, the nucleus can display properties of either a solid or a liquid substance, depending on the transmitted loads and its posture.

The annulus fibrosis consists of 10-20 type I concentric collagen fiber layers that surround the nucleus. The layers are arranged in an alternating orientation of parallel fibers lying approximately 65 º from the vertical.

The vertebral endplate is a thin layer of cartilage located between the vertebral body and the intervertebral disc. While normally composed of both hyaline and fibrocartilage in youth, older endplates are virtually entirely fibrocartilage. Because the intervertebral disc is the largest avascular structure in the body, it is dependent on diffusion across the endplate for nutrition and waste removal. The endplate is considered part of the disc because the endplate almost always remains with the disc when the disc is traumatically displaced from the vertebral body.

The principal functions of the disc are to allow movement between vertebral bodies and to transmit loads from one vertebral body to the next. When axial loads are transmitted to the spine, the annulus and nucleus display a complex intertwined role allowing for pressure dispersal. The nucleus has the capacity to sustain and transmit pressure; this function is principally invoked during weight-bearing. In this circumstance, it transmits loads and braces the annulus. The annular lamella is capable of sustaining an axial load on the basis of its bulk. When an axial load is applied to the nucleus, it tends to shorten. The nucleus attempts to radially expand, thereby exerting pressure on the annulus. Annular resistance efficiently opposes this outward pressure, creating a hoop tension effect. The intervertebral disc is so effective at resisting these axial loads that a 40-kg load to a disc causes only 1 mm of vertical compression and only 0.5 mm of radial expansion.

During movement, the annulus acts like a ligament to restrain movements and partially stabilize the interbody joint. The oblique orientation of the annular fibers provides resistance to vertical, horizontal, and sliding movements. The alternation in the direction of the annular fibers in consecutive lamellae causes the annulus to resist twist poorly. When the segment twists one way, the fibers oriented in that direction are placed on stretch while those fibers oriented the opposite direction are placed on slack; therefore, the annulus resists the twisting motion with less than its full complement of fibers.

PreviousNextSport Specific Biomechanics

Any factor that creates excessive demand can lead to injury. Excessive mechanical loading may occur by repetitive fatigue overload, supramaximal overload, or unexpected overload.[4] Improper technique in activities such as in blocking or tackling, poor body mechanics, or improper training can lead to overload. Unexpected overloads result from falls, collisions, or improper technique. Good coaching, proper technique, and safety measures help to minimize fatigue overload and limit dangerous sport situations.

PreviousProceed to Clinical Presentation , Lumbosacral Discogenic Pain Syndrome

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Lumbosacral Spondylolisthesis

Background

Spondylolisthesis is defined as forward translation of a vertebral body with respect to the vertebra below.[1, 2, 3, 4, 5, 6] The term is derived from the Greek roots spondylo, meaning spine, and listhesis, meaning to slide down a slippery path.

Spondylolisthesis can occur at any level of the spinal column, although it is most common in the lower lumbar spine. Most cases are thought to result from minor overuse trauma, particularly repetitive hyperextension of the lumbar spine. Spondylolysis, a break in the vertebra typically in the region of the pars interarticularis, may or may not be associated with a spondylolisthesis. If the pars defect is bilateral, it may allow slippage of the vertebra, typically L5 on S1, resulting in spondylolisthesis.

Both spondylolysis and spondylolisthesis are often asymptomatic, and the degree of spondylolisthesis does not necessarily correlate with the incidence or severity of symptoms, even when a patient is experiencing back pain. However, these 2 entities have been reported to be the most common underlying causes of persistent low back pain among children and adolescents, despite the fact that most cases are asymptomatic.[3, 5, 7, 8, 9]

Spondylolisthesis can be classified into the following 6 distinct categories.

Type I Congenital (dysplastic)Caused by agenesis of the superior articular facetType II Isthmic (spondylolytic)Caused by pars interarticularis defectsType III DegenerativeSecondary to articular degenerationType IV TraumaticCaused by fracture or dislocation of the lumbar spine, not involving the parsType V PathologicCaused by malignancy, infection, or other types of abnormal boneType VI Postsurgical (iatrogenic)

A new computer-assisted classification has been recommended by the Spinal Deformity Study Group based on slip grade, pelvic incidence, and sacro-pelvic and spinal balance. Software enabled observers to identify all 6 types of spondylolisthesis and to identify 7 anatomical landmarks on each radiograph.[10]

A variety of methods are also used to measure the degree of spondylolisthesis. The primary focus of this article is isthmic spondylolisthesis only, because it is the most common variety and because it is relevant to sports medicine.

Isthmic (spondylolytic) spondylolisthesis usually occurs in children older than 5 years, most commonly in those aged 7-8 years, and it rarely occurs before walking begins. Slip progression is minimal after skeletal maturity.

Isthmic spondylolisthesis is further divided into the following 3 subtypes:

Type IIA, or lytic spondylolisthesis, involves a defect in the pars area and is thought to result from recurrent microfractures from the impact of the articular processes against the pars while in extension. This defect usually occurs by age 6 years and is occasionally associated with developmental anomalies such as lumbarization, sacralization, and spina bifida occulta. Type IIB involves an intact but elongated pars, probably resulting from repetitive microfractures that heal in an elongated position, much like pulled toffee. Type IIC spondylolisthesis, a rare form, results from an acute fracture of the pars interarticularis during significant trauma.

For excellent patient education resources, see eMedicineHealth's patient education articles Low Back Pain, Slipped Disk, and Lumbar Laminectomy.

NextEpidemiologyFrequencyUnited States

The prevalence rate of isthmic spondylolisthesis is approximately 5% at age 5-7 years, with an increase to 6-7% by age 18 years. This condition is twice as common in males as in females, and the prevalence is lower in blacks (2.8%, black men; 1.1%, black women) than in whites (6.4%, white men; 2.3%, white women). Despite the higher prevalence in males, progression, although still rare, has been reported to be more common in females.

Additional risk factors include having a first-degree relative with a slip, occult spina bifida at S1, and the presence of scoliosis.

PreviousNextFunctional Anatomy

Mechanical stresses play an important role in this process. Erect posture produces a constant downward and forward thrust on the lumbar vertebrae. Stresses on the pars interarticularis are accentuated during repetitive hyperextension, which results in increased contact of the caudal edge of the L4 inferior articular facet with the L5 pars interarticularis. This collective trauma may eventually result in a stress fracture of the pars interarticularis. Spondylolisthesis may occur when bilateral pars defects are present, which allows forward slippage of the vertebra (typically L5 on S1). Spondylolisthesis has never been reported in quadrupeds or people who are chronically bedridden.

PreviousNextSport-Specific Biomechanics

Sports that involve repetitive hyperextension and axial loading of the lumbar spine may result in repetitive microtrauma to the pars interarticularis, resulting in spondylolysis and sometimes spondylolisthesis. Examples of such activities include gymnastics, football (lineman), wrestling, weight lifting (particularly standing overhead presses), rowing, pole vaulting, diving, hurdling, swimming (especially the butterfly stroke), baseball (especially pitching), tennis (especially serving), sailing (particularly the hiking maneuver), and volleyball. Gymnastics and football are generally considered the highest risk sports.[4, 5, 6, 11]

PreviousProceed to Clinical Presentation , Lumbosacral Spondylolisthesis

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Sacroiliac Joint Injury

Background

Lower back pain is one of the most prevalent sports maladies, affecting athletes in nearly every sport. Diagnosing the cause of a back injury is quite difficult and challenging because multiple structures in the lower back region can cause pain. However, an accurate diagnosis is paramount to providing successful treatment of the spine injury.

Although still somewhat controversial, the sacroiliac joint (SIJ) is generally accepted as an anatomic structure within the lumbar complex that if injured can be a cause of lower back pain. Mechanical dysfunction, inflammation, infection, trauma, and degeneration all have been attributed to the SIJ. Once the diagnosis of SIJ injury is established, specifically directed treatment can lead to satisfying results. This article discusses the diagnosis, management, and rehabilitation of sacroiliac injuries and pain.

For excellent patient education resources, visit eMedicineHealth's Osteoporosis Center. Also, see eMedicineHealth's patient education articles Low Back Pain and Lumbar Disc Disease.

NextEpidemiologyFrequencyUnited States

The incidence of lower back pain in humans parallels the incidence of the common cold, with a lifetime rate approaching 95%. Goldwaith and Osgood first discussed the possibility that SIJ injury could cause low back pain as early as 1905.[1] In the decades since then, several attempts have been made to establish the prevalence of SIJ syndrome in persons with back pain, and the results of these reports vary widely.

Schwarzer et al remarked that "the prevalence of sacroiliac pain would appear to be at least 13% and perhaps as high a 30%" in patients with low back and buttock pain.[2] Bernard and Kirkaldy-Willis reported the prevalence rate to be 22.5% in 1293 patients with back pain.[3]

PreviousNextFunctional Anatomy

The SIJ is a true diarthrodial joint that joins the sacrum to the pelvis.[4, 5, 6] In this joint, hyaline cartilage on the sacral side moves against fibrocartilage on the iliac side. The joint is generally C shaped with 2 lever arms that interlock at the second sacral level. The joint contains numerous ridges and depressions, indicating its function for stability more than motion. However, studies have documented that motion does occur at the joint; therefore, slightly subluxed and even locked positions can occur.[2, 7]

Stability is provided by the ridges present in the joint and by the presence of generously sized ligaments. The ligamentous structures offer resistance to shear and loading. The deep anterior, posterior, and interosseous ligaments resist the load of the sacrum relative to the ilium. More superficial ligaments (eg, sacrotuberous ligament) react to dynamic motions (eg, straight-leg raising during physical motion). The long dorsal sacroiliac ligament can become stretched in periods of reduced lumbar lordosis (eg, pregnancy).

Many large and small muscles have relationships with these ligaments and the SIJ, including the piriformis, biceps femoris, gluteus maximus and minimus, erector spinae, latissimus dorsi, thoracolumbar fascia, and iliacus. Any of these muscles can be involved with a painful SIJ. As a true joint, the SIJ is a pain-sensitive structure richly innervated by a combination of unmyelinated free nerve endings and the posterior primary rami of L2-S3. The wide possibility of innervation may explain why pain emanation from the joint can manifest in so many various ways, with different and unique referral patterns for individual patients.

PreviousNextSport-Specific Biomechanics

The function of the SIJ is to dissipate loads of the torso through the pelvis to the lower extremities and vice versa. The pelvis acts as a central base through which large forces are accepted and dissipated. Although the main role of the joint is to provide stability, the SIJ has limited motion that allows it to dissipate and transfer significant loads and stresses. Studies by Weisel indicate that most movement occurs when rising from the sitting to the standing position. However, the amount of motion is small, making assessment of sacroiliac motion during physical examination quite difficult. Selvik suggested that hyperextension produces the greatest degree of motion (2° on average, with only minimal translation of 0.5-1.6 mm).

If the motion in the pelvis is asymmetric, then dysfunction can occur. Some conditions that cause asymmetric motion include leg-length inequalities, a unilaterally weak lower limb (eg, polio), tight myofascial structures (eg, iliopsoas), and scoliosis. Hip osteoarthritis can lead to leg-length shortening and SIJ pain.

Women may be at increased risk for SIJ problems because their broader pelvises, greater femoral neck anteversion, and shorter limb lengths lead to different, possibly predisposing, biomechanics. In addition, pregnancy often leads to stretching of the pelvis, specifically targeting the sacroiliac ligaments and possibly leading to dysfunction, hypermobility syndromes, and chronic pain.

Innervation

The nerve supply of the SIJ originates from multiple lumbosacral root levels with partial innervation from L2 (anterior joint) to S3 (posterior joint). Because the root innervation can vary so widely, the pain referral patterns from primary sacroiliac pain can also vary. Fortin et al interviewed multiple patients documented to have sacroiliac pain by anesthetizing the joint with lidocaine injections under fluoroscopic guidance.[8, 9] He found referral patterns ranging from localized buttocks pain to frank radicular leg pain and many other descriptions in between.

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Thoracic Disc Injuries

Background

Thoracic disc injury, first described in 1838, is an uncommon site of injury owing to the stabilizing effect of the rib cage.[1] The similarity of symptoms to lumbar disc herniation makes the diagnosis of a thoracic disc injury difficult,[2, 3, 4, 5, 6] but the process tends to be self-limiting and rarely requires surgical intervention.[4]

(See also the articles Disk Herniation and Thoracic Spine, Trauma [in the Radiology section], Thoracic Discogenic Pain Syndrome [in the Sports Medicine section], Lumbar Disc Disease [in the Neurosurgery section], and Herniated Nucleus Pulposus [in the Orthopedic Surgery section], as well as Return to Contact Sports After Spinal Surgery and Thoracoscopic Spine Surgery for Decompression and Stabilization of the Anterolateral Thoracic and Lumbar Spine on Medscape.)

For patient education resources, see the Bone Health Center, Back, Ribs, Neck, and Head Center, Back, Neck, and Head Injury Center, and Muscle Disorders Center, as well as Back Pain and Chronic Pain.

NextEpidemiologyFrequencyUnited States

The incidence of thoracic disc injuries is 1 in 1 million persons per year, and these injuries account for 0.25-0.75% of all disc herniations.[7]

PreviousNextFunctional Anatomy

The thoracic discs are unusually stable compared with the cervical and lumbar discs. The stability of the thoracic discs is secondary to the surrounding rib cage, with the stabilizing effect of the rib articulations. However, the blood supply of the thoracic spine is more tenuous than the cervical and lumbar spine, especially at the T4-T9 watershed area, which is more prone to ischemic injury.

PreviousNextSport-Specific Biomechanics

The facet orientation in the thoracic spine is vertical, with a slight medial angulation. This orientation allows for easier lateral bending and rotation versus pure bending. Biomechanical studies have shown that intervertebral discs are at the highest risk of injury when combined with bending and torsional forces. Therefore, the thoracic spine discs are at a decreased risk of injury because of the decreased bending potential in this segment of the spine.

The spinal cord-to-canal ratio (the ratio of the cross-sectional area of the cord to the cross-sectional area of the spinal canal) is 40% in the thoracic spine versus 25% in the cervical spine. The thoracic spine is also naturally kyphotic. These 2 facts make the thoracic spine more sensitive to cord compression from disc herniation.

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Bicipital Tendonitis

Background

Bicipital tendinitis, or biceps tendinitis, is an inflammatory process of the long head of the biceps tendon and is a common cause of shoulder pain due to its position and function.[1, 2, 3, 4, 5] The tendon is exposed on the anterior shoulder as it passes through the humeral bicipital groove and inserts onto the superior aspect of the labrum of the glenohumeral joint. Disorders of the biceps tendon can result from impingement or as an isolated inflammatory injury. Other causes are secondary to compensation for rotator cuff disorders, labral tears, and intra-articular pathology.

For patient education resources, see the Arthritis Center and Sports Injury Center, as well as Tendinitis, Rotator Cuff Injury, and Repetitive Motion Injuries.

NextEpidemiologyFrequencyUnited States

Bicipital tendinitis is frequently diagnosed in association with rotator cuff disease as a component of the impingement syndrome or secondary to intra-articular pathology, such as labral tears.[6]

PreviousNextFunctional Anatomy

As its name implies, the biceps has 2 proximal heads with a common distal insertion onto the radius. The long head of the biceps merges with the short head of the biceps to form the body of the biceps brachii muscle. This muscle is a powerful supinator and flexor of the forearm.

The long head biceps tendon lies in the bicipital groove of the humerus between the greater and lesser tuberosities and angles 90° inward at the upper end of the groove, crossing the humeral head to insert at the upper edge of the glenoid labrum and supraglenoid tubercle. The long head of the biceps tendon helps to stabilize the humeral head, especially during abduction and external rotation.

See the image below.

Biceps muscle and tendons. PreviousNextSport-Specific Biomechanics

Bicipital tendinitis frequently occurs from overuse syndromes of the shoulder,[7] which are fairly common in overhead athletes such as baseball pitchers, swimmers, gymnasts, racquet sport enthusiasts (eg, tennis players), and rowing/kayak athletes.[8, 9, 10, 11] Trauma may occur because of direct injury to the biceps tendon when the arm is passed into excessive abduction and external rotation. This pattern of shoulder injury can also occur in the left shoulder of right-handed golfers. Many overuse injuries coexist with some degree of bicipital tendinitis and rotator cuff tendinitis.

The athletic shoulder differs qualitatively from the biomechanics of the shoulder in daily life because of the higher energies and repetitive motions that are involved in athletic activities. Sports activities that require repetitive overhead motion with inadequate reparative time may cause the biceps tendon to break down.

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