Cervical Facet Syndrome

Background

Neck pain is common in the general population and even more common in a chronic pain management practice. Very few reliable epidemiologic studies regarding the prevalence of neck pain exist; however, a Finnish study[1] and a Norwegian study[2] estimated the prevalence of neck pain in the general population to be approximately 34%. Furthermore, the prevalence of chronic neck pain, defined as lasting 6 months or longer, is estimated at approximately 14%.[1, 2]

In 1933, Ghormley coined the term facet syndrome to describe a constellation of symptoms associated with degenerative changes of the lumbar spine.[3] Relatively recently, the term cervical facet syndrome has appeared in the literature and implies axial pain presumably secondary to involvement of the posterior elements of the cervical spine.

Cervical facet syndrome.

Many pain generators are located in the cervical spine, including the intervertebral discs, facet joints, ligaments, muscles, and nerve roots. The facet joints have been found to be a possible source of neck pain, and the diagnosis of cervical facet syndrome is often one of exclusion or not considered at all.

Clinical features that are often, but not always, associated with cervical facet pain include tenderness to palpation over the facet joints or paraspinal muscles, pain with cervical extension or rotation, and absent neurologic abnormalities.[4] Imaging studies usually are not helpful, with the exception of ruling out other sources of pain, such as fractures or tumors. Signs of cervical spondylosis, narrowing of the intervertebral foramina, osteophytes, and other degenerative changes are equally prevalent in people with and without neck pain.[5]

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

NextEpidemiologyFrequencyUnited States

Aprill and Bogduk estimated the prevalence of cervical facet joint pain by reviewing the records of patients who had presented with neck pain for at least 6 months secondary to some type of injury.[6] These patients underwent discography, facet joint nerve blocks, or both at the request of the referring physicians.

A total of 318 patients were investigated, and 26% of the patients had at least one symptomatic facet joint. However, only 126 patients of the original study group had their facet joints investigated, and 65% of these patients had painful facet joints.[6] Furthermore, 62% of the patients who underwent both discography and facet joint nerve blocks had painful facet joints. This study indicated that the prevalence of cervical facet joint pain may be as low as 26% or as high as 65%, depending on how aggressively it is sought.[6]

A large study by Manchikanti et al involved 500 patients with chronic, nonspecific spine pain. The prevalence of facet joint pain was determined using controlled comparative local anesthetic blocks with 1% lidocaine followed by 0.25% bupivacaine.[7] This study indicated that the prevalence of cervical facet joint pain was 55%.

It seems apparent that the cervical facet joints may be a common source of neck pain; however, there are other pain generators in the cervical spine, such as the intervertebral discs, that may be involved as well. To evaluate the contribution of the disc to neck pain, a sample of 56 patients were selected from the previous study population. This group consisted of patients who had undergone both discography and facet joint nerve blocks at the same segment of the cervical spine as part of the diagnostic process.[8]

The results demonstrated that 41% of this group had a painful disc and facet joint at the same segment, and an additional 23% had a painful facet joint but not a painful disc at the same segment.[8] Therefore, most of the sample had a painful facet joint, but there was often a painful disc at the same level. This finding is not surprising when one considers how the facet joints and discs are intimately involved in motion of the cervical spine.

Cervical facet joint pain is a common sequela of whiplash injury. Barnsley and Lord et al studied the prevalence of chronic cervical facet joint pain after whiplash injury using double-blind, controlled, diagnostic blocks of the facet joints.[9] The joints were blocked randomly with either a short-acting or long-acting anesthetic, and, if complete pain relief was obtained, the joint was blocked with the other agent 2 weeks later. Of the 38 patients who completed the trial, 27 obtained complete relief from both anesthetics and longer relief from the longer acting agent.[9] Therefore, the prevalence of this sample is 54%, making cervical facet joint pain the most common cause of chronic neck pain after whiplash injury in this population.

Lord and Barnsley et al subsequently studied the prevalence of chronic cervical facet joint pain after whiplash injury using a double-blind, placebo-controlled protocol.[10] The sample consisted of 68 consecutive patients referred for neck pain secondary to a motor vehicle accident and longer than 3 months in duration. Those individuals with a predominant headache underwent a third occipital nerve block and were removed from the study if they received pain relief.[10] The third occipital nerve has a cutaneous branch and a branch to the C2-C3 facet joint; therefore, patients with pain from this segment could not participate in the placebo study because they would feel the effects of the local anesthetic. The remaining 41 patients underwent diagnostic blocks with either a short-acting or a long-acting local anesthetic, followed by a second block with either normal saline or the other anesthetic, followed by a third block with the remaining agent.

The investigators reported the positive responders experienced complete relief with each anesthetic and no relief with the normal saline. The prevalence of cervical facet joint pain after whiplash injury was found to be 60%, and the most common levels were C2-C3 and C5-C6.

PreviousNextFunctional Anatomy

The cervical spine is made up of the first 7 vertebrae and functions to provide mobility and stability to the head, while connecting it to the relative immobile thoracic spine (see the image below). The first 2 vertebral bodies are quite different from the rest of the cervical spine. The atlas, or C1, articulates superiorly with the occiput and inferiorly with the axis, or C2.

Cervical vertebra.

The atlas is ring-shaped and does not have a body, unlike the rest of the vertebrae. The body has become part of C2, and it is called the odontoid process, or dens. The atlas is made up of an anterior arch, a posterior arch, 2 lateral masses, and 2 transverse processes. The transverse foramen, through which the vertebral artery passes, is enclosed by the transverse process. On each lateral mass is a superior and inferior facet (zygapophyseal) joint. The superior articular facets are kidney-shaped, concave, and face upward and inward. These superior facets articulate with the occipital condyles, which face downward and outward. The relatively flat inferior articular facets face downward and inward to articulate with the superior facets of the axis.

The axis has a large vertebral body, which contains the fused remnant of the C1 body, the dens. The dens articulates with the anterior arch of the atlas via its anterior articular facet and is held in place by the transverse ligament. The axis is composed of a vertebral body, heavy pedicles, laminae, and transverse processes, which serve as attachment points for muscles. The axis articulates with the atlas by its superior articular facets, which are convex and face upward and outward.

The remaining cervical vertebrae, C3-C7, are similar to each other, but they are very different from C1 and C2. They each have a vertebral body, which is concave on its superior surface and convex on its inferior surface. On the superior surfaces of the bodies are raised processes or hooks called uncinate processes, which articulate with depressed areas on the inferior aspect of the superior vertebral bodies called the echancrure or anvil. These uncovertebral joints are most noticeable near the pedicles and are usually referred to as the joints of Luschka.[11] These joints are believed to be the result of degenerative changes in the annulus, which leads to fissuring in the annulus and the creation of the joint.[12] The spinous processes of C3-C5 are usually bifid, in comparison to the spinous processes of C6 and C7, which are usually tapered.

The facet joints in the cervical spine are diarthrodial synovial joints with fibrous capsules. The joint capsules in the lower cervical spine are more lax compared with other areas of the spine to allow for gliding movements of the facets. The joints are inclined at 45° from the horizontal plane and angled 85° from the sagittal plane. This alignment helps to prevent excessive anterior translation and is important in weight bearing.[13]

The fibrous capsules are innervated by mechanoreceptors (types I, II, and III), and free nerve endings have been found in the subsynovial loose areolar and dense capsular tissues.[14] In fact, there are more mechanoreceptors in the cervical spine than in the lumbar spine.[15] This neural input from the facets may be important for proprioception and pain sensation and may modulate protective muscular reflexes that are important in preventing joint instability and degeneration.

The facet joints in the cervical spine are innervated by both the anterior and dorsal rami. The occipitoatlantal (OA) joint and atlantoaxial (AA) joint are innervated by the ventral rami of the first and second cervical spinal nerves. Two branches of the dorsal ramus of the third cervical spinal nerve innervate the C2-C3 facet joint, a communicating branch and a medial branch known as the third occipital nerve.

The remaining cervical facets, C3-C4 to C7-T1, are supplied by the dorsal rami medial branches that arise one level cephalad and caudad to the joint.[16, 17] Therefore, each joint from C3-C4 to C7-T1 is innervated by the medial branches above and below. These medial branches send off articular branches to the facet joints as they wrap around the waists of the articular pillars.

Intervertebral discs are located between each vertebral body caudad to the axis. The discs are composed of 4 parts, including the nucleus pulposus in the middle, the annulus fibrosis surrounding the nucleus, and 2 end plates that are attached to the adjacent vertebral bodies. The discs are involved in cervical spine motion, stability, and weight bearing. The annular fibers are composed of collagenous sheets called lamellae, which are oriented 65-70° from the vertical and alternate in direction with each successive sheet. Therefore, the annular fibers are prone to injury with rotation forces because only one half of the lamellae are oriented to withstand the force in this direction.[15] The middle and outer one third of the annulus is innervated by nociceptors, and phospholipase A2 has been found in the disc and may be an inflammatory mediator.[18, 19, 20]

Several ligaments of the cervical spine, which provide stability and proprioceptive feedback, are worth mentioning.[21, 22] The transverse ligament, the major portion of the cruciate ligament, arises from tubercles on the atlas and stretches across its anterior ring while holding the dens against the anterior arch. A synovial cavity is located between the dens and the transverse process. This ligament allows for rotation of the atlas on the dens and is responsible for stabilizing the cervical spine during flexion, extension, and lateral bending. The transverse ligament is the most important ligament in preventing abnormal anterior translation.[23]

The alar ligaments run from the lateral aspects of the dens to the ipsilateral medial occipital condyles and to the ipsilateral atlas. The alar ligaments limit axial rotation and side bending. If the alar ligaments are damaged, as in a whiplash injury, the joint complex becomes hypermobile, which can lead to kinking of the vertebral arteries and stimulation of the nociceptors and mechanoreceptors. This may be associated with the typical complaints of patients with whiplash injuries such as headache, neck pain, and dizziness. The alar ligaments prevent excessive lateral and rotational motions, while allowing flexion and extension.

The anterior longitudinal ligament (ALL) and the posterior longitudinal ligament (PLL) are the major stabilizers of the intervertebral joints. Both ligaments are found throughout the entire length of the spine; however, the anterior longitudinal ligament is closely adhered to the discs in comparison to the posterior longitudinal ligament, and it is not well developed in the cervical spine. The anterior longitudinal ligament becomes the anterior atlantooccipital membrane at the level of the atlas, whereas the posterior longitudinal ligament merges with the tectorial membrane. Both ligaments continue onto the occiput. The posterior longitudinal ligament prevents excessive flexion and distraction.[24]

The supraspinous ligament, interspinous ligament, and ligamentum flavum maintain stability between the vertebral arches. The supraspinous ligament runs along the tips of the spinous processes, the interspinous ligament runs between the spinous processes, and the ligamentum flavum runs from the anterior surface of the cephalad vertebra to the posterior surface of the caudad vertebra. The interspinous ligament and especially the ligamentum flavum control for excessive flexion and anterior translation.[24, 25, 26] The ligamentum flavum also connects to and reinforces the facet joint capsules on the ventral aspect. The ligamentum nuchae is the cephalad continuation of the supraspinous ligament and has a prominent role in stabilizing the cervical spine.

PreviousNextSport Specific Biomechanics

The patterns of motion of C2–C7 are determined by the orientation of the facet joints, the intervertebral discs, and the uncovertebral joints. The orientation of the facet joints lead to coupling of rotation and lateral flexion. For example, as the vertebral bodies laterally flex to the left, they also rotate to the left (the spinous processes move to the right). The degree of rotation that is coupled with lateral flexion decreases in the more caudal motion segments, possibly due to the difference in facet orientation in the caudal segments, which may contribute to unilateral facet joint dislocations in the lower cervical spine.[27]

The height of the articular process increases with caudal progression, which determines the quality of flexion and extension and allows more gliding motion in the cephalad segments.[28] Horizontal translation of a vertebral body more than 3.5 mm as measured on a lateral radiograph during flexion and extension is considered to be the upper limit of normal motion.[29]

The orientation of the facet joints alone does not determine the pattern of motion. In the lumbar spine, the pattern of motion does not change after the facets are removed, which implies that the discs and ligaments determine the pattern of motion.[30] Also, because of the orientation of the annular fibers in the disc, there is very little rotation in the lumbar spine.[31] However, it is known that there is a great deal of rotation in the cervical spine. Therefore, the discs do not seem to be the primary determinant of motion in the cervical spine.

The joints of Luschka are suggested to be involved primarily in rotation and may aid in the coupling of rotation and lateral flexion.[32] Another purpose of the joints of Luschka may be to protect the disc from injury as it ages and loses its water content. This may explain why these joints are not present at birth but develop later in childhood.[33]

The orientation of the OA joints allow for substantial flexion and extension (13°), less lateral flexion (8°) and rotation (10°), and minimal translation (1 mm).[34, 35] The AA joints allow for axial rotation of 65°, which is 40-50% of the total cervical spine rotation, negligible lateral flexion, 10° of flexion and extension, and lateral translation of 4 mm.[34, 36] This degree of axial rotation can cause kinking of the vertebral arteries that run in the transverse foramina of C6 to the atlas. The contralateral artery begins to kink at 30° and the ipsilateral artery at 45°.[37] Consequences include nausea, vomiting, visual problems, vertigo, and stroke.[38]

With axial rotation of the atlas on the axis, there is a coupled movement of vertical translation of the atlas, so that it is at its lowest position at the extremes of right and left rotation and at its highest position at neutral. This coupling of translation with rotation is secondary to the orientation of the facets.[4] The instantaneous axis of rotation (IAR) is a term used to describe the motion of one vertebral body in relation to the vertebral body below.

The IAR has been estimated at the OA joint,[36] the AA joint,[34] and in the cervical spine from C2-C3 to C6-C7.[39] In the middle and lower cervical spine, the IAR has been measured for each segment from C2-C3 to C6-C7 in asymptomatic people.[40] In a subsequent study, the IARs were measured in persons with neck pain, who had not received a diagnosis after examination and imaging of the cervical spine.[39] Abnormal IARs were found in 46% of the patients, and an additional 26% had marginal findings. However, the location of the abnormal motion segments did not correlate with the findings on discography or facet joint blocks.

PreviousProceed to Clinical Presentation , Cervical Facet Syndrome

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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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Little League Elbow Syndrome

Background

Little league elbow (LLE) syndrome is a valgus overload or overstress injury to the medial elbow that occurs as a result of repetitive throwing motions. Over the past several decades, the number of organized sports for children has grown significantly, with millions of children participating in organized athletics each year. This increase in participation has been paralleled by an increase in sports-related injuries in the pediatric population.[1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11]

Increased single-sport participation with year-round training, higher intensities at young ages, and longer competitive seasons are contributing factors to the increased injury rates seen in pediatric athletes. Conditioning and training errors also contribute significantly to the risk and frequency of injury. Although briefly discussed below, injuries to the lateral, posterior, and anterior elbow are separate entities and should not be confused with the medial injuries referred to as little league elbow syndrome.

During the throwing motion, valgus stress is placed on the elbow. This valgus stress results in tension on the medial structures (ie, medial epicondyle, medial epicondylar apophysis, medial collateral ligament complex) and compression of the lateral structures (ie, radial head, capitellum). Repeated stress results in overuse injury when tissue breakdown exceeds tissue repair. Recurrent microtrauma of the elbow joint can lead to little league elbow, a syndrome that encompasses (1) delayed or accelerated growth of the medial epicondyle (medial epicondylar apophysitis), (2) traction apophysitis (medial epicondylar fragmentation), and (3) medial epicondylitis.[1, 8, 12, 13, 14, 15]

Medial epicondylar apophysitis and stress fractures through the medial epicondylar epiphyses caused by repetitive valgus stress generally manifest with progressive medial pain, decreased throwing effectiveness, and decreased throwing distance.

Other causes of medial elbow pain include avulsion fractures of the medial epicondyle and ulnar collateral ligament (UCL) sprains or tears. Although a fracture is usually an acute traumatic event, a preceding history of medial elbow pain is common and is thought to be a risk factor for progression to acute fracture. Therefore, any thrower who is experiencing medial elbow pain should refrain from pitching until he or she has had a thorough evaluation.[1, 3, 5, 8, 16]

A medial epicondyle fracture manifests as point tenderness and swelling over the medial epicondyle, often with an elbow flexion contracture greater than 15°. Repetitive medial stress can also cause attenuation and microstretching of the UCL complex, causing mild instability over time.[1]

UCL injuries can manifest as acute ligament tears following a single valgus stress or as overuse sprains following repetitive valgus overloads. The clinical presentation is similar to little league elbow; however, the typical age range of the athlete is the older teenager who is skeletally mature. Suspected UCL injuries should be referred for further evaluation by a sports medicine specialist. Athletes with UCL injuries should not be allowed to pitch until they have been evaluated.

Although uncommon in children, neurologic injuries such as C8-T1 radiculopathy and ulnar neuritis can manifest as medial elbow pain and should be included in the differential diagnosis (see Differentials and Other Problems to Be Considered).

Lateral compression of the elbow most frequently results in injuries to the capitellum and radial head. Osteochondrosis of the capitellum (known as Panner disease) generally occurs in children aged 7-12 years and manifests as dull, achy, activity-related lateral elbow pain. Swelling, clicking, and decreased range of motion are uncommon associated symptoms. Panner disease tends to be a benign self-limited condition that does well over time and is treated with complete rest from inciting activities such as throwing and weight bearing on the elbow. Osteochondral injuries can also be observed in the radial head.

Osteochondritis dissecans (OCD) of the capitellum occurs in adolescents aged 13-17 years. This is a localized injury to subchondral bone that results from repetitive lateral compression of the elbow during overhead motions. These patients report a general dull elbow pain that worsens with activity, often have a flexion contracture of 15° or greater, and may have mechanical symptoms of clicking or popping. Loose body formation, residual capitellum deformity, and elbow degenerative joint disease are potential sequelae. Different treatment options are used based on the age and skeletal maturity of the patient and the type of lesion present.

Osteochondritis dissecans lesions can be separated into type I, which has no displacement and no articular cartilage fracture; type II, which has evidence of articular cartilage fracture or partial displacement; and type III, which is completely displaced with loose bodies in the joint.

Posterior elbow injuries also occur as a result of throwing. During the follow-through stage of throwing, extension overload and valgus stress can result in injury of the olecranon. These athletes present with posterior elbow pain, clicking, and possible loss of elbow extension. Loose bodies and olecranon nonunion can occur in younger athletes. Older athletes may experience olecranon fractures or secondary osteophyte formation. These injuries are sometimes treated surgically.[1, 3, 4, 5, 6, 7, 9, 10, 11, 17]

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

NextEpidemiologyFrequencyUnited States

Annually, an estimated 4.8 million children aged 5-14 years participate in baseball and softball. The incidence of all baseball-related overuse injuries is 2-8% per year. The incidence of overuse injuries in the 9- to 12-year-old range for baseball is 20-40%, and in the adolescent age group is 30-50%. The true incidence of sports-related injuries is unknown because a large number of athletes never seek medical care. Early recognition of little league elbow syndrome is important, because it leads to better outcomes and decreases the risk of persistent functional disabilities in the athletes.

International

No data are available for the annual incidence of little league elbow syndrome in the international community.

PreviousNextFunctional Anatomy

Evaluation of the young adolescent elbow presents some anatomic challenges to the healthcare provider in that the elbow consists of numerous ossification centers and cartilaginous physes. Becoming familiar with the chronologic order of appearance and ossification of these growth centers is important. Consider the mnemonic CRITOE (ie, capitellum, radius, internal epicondyle, trochlea, olecranon, external epicondyle).

Each of the ossification centers appears at a relatively predictable time starting around age 1-2 years, with 2-year intervals between the next center's appearance. Closure of each of the apophyses occurs from age 14 to 16 years, with the medial epicondyle specifically closing at approximately age 15 years. The elbow likely reaches full skeletal maturity by the late teen years, at which time injuries to the UCL are far more common. Until then, the young thrower is at risk for little league elbow syndrome.[1, 4, 12, 16, 18]

The static stabilizers around the elbow include the bony articulations, the joint capsule, and the various ligament bundles. The medial (ulnar) collateral ligamentous complex consists of the anterior oblique bundle, posterior oblique bundle, and transverse ligament. These structures are the primary medial support of the elbow during valgus stress. The lateral (radial) ligamentous complex, composed of the lateral collateral, lateral ulnar collateral, and accessory lateral collateral ligaments, provides support during varus stress.

The dynamic stabilizers primarily include the muscles that cross the elbow joint, such as the triceps, biceps, and brachioradialis. The flexor-pronator group stabilizes against valgus stress, and the extensor-supinator group stabilizes against varus stress.

Elbow biomechanics include flexion/extension range of motion and pronation/supination. Slight hyperextension 5-15° through flexion of approximately 150° is within normal limits. Baseball pitchers with years of throwing experience often have relative 5-10° flexion contractures on their dominant side; however, in the young thrower, a flexion contracture can be a sign of injury. Pronation of 75° and supination of 85° is normal. Varus-valgus laxity of 3-4° is normal.

PreviousNextSport-Specific Biomechanics

One should be familiar with the stages of throwing to understand the complexities of the biomechanical forces that contribute to the young thrower's risk of injury, such as in little league elbow syndrome. The pitching or throwing motion can be divided into 6 stages. Medial elbow injuries are the most common type seen in throwers and occur most commonly in the cocking and acceleration phases of throwing, owing to the presence of maximum valgus extension or distraction forces.[1, 12, 13, 14, 15]

Windup begins with the pitcher balancing his weight over his rear leg, with the elbow flexed and the forward leg flexed at least 90°. Stride starts with the lead leg beginning to descend toward the plate, and the 2 arms separate. The elbow moves from extension into flexion of 80-100°. Cocking occurs when the humerus is in extreme abduction and external rotation and the elbow is flexed. The lead foots contacts the ground, the pelvis and trunk rotate, and elbow torque transfers valgus force across the elbow joint. During this phase, medial tension and lateral compression forces are applied to the elbow. Acceleration is the shortest pitching phase, lasting from maximal external shoulder rotation to ball release. In this phase, the trunk rotates as the elbow extends. Maximum elbow angular velocity is comparable during fastballs, sliders, and curveballs, but it less during the change-up pitch. Velocity comes from rotation of the trunk, shoulder, and hips. Varus torque forces during this phase act to resist the valgus extension "overload" phenomenon and can contribute to posterior elbow (olecranon) impingement. Deceleration is initiated at ball release and ends when the shoulder has reached full internal rotation. The body must decelerate the arm and dissipate forces in the elbow and shoulder. Follow-through is the final phase of the baseball pitch and ends with the pitcher reaching a balanced fielding position with full-trunk rotation and the body weight fully transferred from the rear leg to the forward leg. During follow-through, the elbow flexes into a relaxed position and crosses the body. PreviousProceed to Clinical Presentation , Little League Elbow Syndrome

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Iliotibial Band Syndrome

Background

Iliotibial band (ITB) syndrome (ITBS) is the most common cause of lateral knee pain among athletes.[1, 2, 3, 4, 5, 6] ITBS develops as a result of inflammation of the bursa surrounding the ITB and usually affects athletes who are involved in sports that require continuous running or repetitive knee flexion and extension.[1, 2, 3, 7, 8, 9, 10] This condition is, therefore, most common in long-distance runners and cyclists. ITBS may also be observed in athletes who participate in volleyball, tennis, soccer, skiing, weight lifting, and aerobics.[11]

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

See also the following on Medscape Reference:

Iliotibial Band Friction Syndrome [in the Orthopedic Surgery section]

Physical Medicine and Rehabilitation for Iliotibial Band Syndrome

See also the following Medscape resource:

CME Medical Interventions Effectively Treat Overuse Injuries in Adult Endurance Athletes

NextEpidemiologyFrequencyUnited States

ITBS is the most common cause of lateral knee pain in runners. Although few studies are available regarding the incidence of ITBS in athletes, some studies cite this condition with an incidence as high as 12% of all running-related injuries.[12] Several studies of US Marine Corps recruits undergoing basic training determined the incidence of ITBS among this group to vary from 5.3 to 22.2%.

International

Data are not available regarding the international incidence of ITBS.

PreviousNextFunctional Anatomy

The ITB is the condensation of fascia formed by the tensor fascia lata and the gluteus medius and minimus muscles. The ITB is a wide, flat structure that originates at the iliac crest and inserts at the Gerdy tubercle on the lateral aspect of the proximal tibia. This band serves as a ligament between the lateral femoral condyle and the lateral tibia to stabilize the knee. The ITB assists in the following 4 movements of the lower extremity:

Abducts the hipContributes to internal rotation of the hip when the hip is flexed to 30°Assists with knee extension when the knee is in less than 30° of flexionAssists with knee flexion when the knee is in greater than 30° of flexion

The ITB is not attached to bone as it courses between the Gerdy tubercle and the lateral femoral epicondyle. This lack of attachment allows it to move anteriorly and posteriorly with knee flexion and extension. Some authors hypothesize that this movement may cause the ITB to rub against the lateral femoral condyle, causing inflammation. Other investigators hypothesize that injury of the ITB results from compression of the band against a layer of innervated fat between the ITB and epicondyle. Furthermore, a potential deep space is located under the ITB as it crosses the lateral femoral epicondyle and travels to the Gerdy tubercle. This bursa may become inflamed and cause a clicking sensation as the knee flexes and extends. The inflamed bursa may add another component to ITB tendinitis.

See also the following on Medscape Reference:

Bursitis in Emergency Medicine

Bursitis [in the Orthopedic Surgery section]

Tendonitis

PreviousNextSport-Specific Biomechanics

In runners, the posterior edge of the ITB impinges against the lateral epicondyle of the femur just after foot strike in the gait cycle.[7, 8] This friction occurs at or slightly below 30 º of knee flexion.[2, 3, 7] Downhill running and running at slower speeds may exacerbate ITBS as the knee tends to be less flexed at foot strike.[13, 14]

In cyclists, the ITB is pulled anteriorly on the pedaling downstroke and posteriorly on the upstroke. The ITB is predisposed to friction, irritation, and microtrauma during this repetitive movement because its posterior fibers adhere closely to the lateral femoral epicondyle.

PreviousProceed to Clinical Presentation , Iliotibial Band Syndrome

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Cervical Discogenic Pain Syndrome

Background

Cervical intervertebral disc disease accounts for 36% of all spinal intervertebral disc disease, second only to lumbar disc disease, which accounts for 62% of all spinal intervertebral disc disease. Cervical problems tend to be less debilitating than lumbar problems, and they do not cause individuals to miss work as often as lumbar spine problems do.[1, 2]

One of 5 visits to an orthopedic practice is for cervical discogenic pain (CDP), with C5-6 and C6-7 accounting for approximately 75% of visits. C7 is the most common nerve root involved.[3] Cervical discogenic pain syndrome (CDPS) presents with proximal symptoms first, and, later, it can progress to brachialgia.

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 intervertebral disc disease accounts for 36% of all spinal intervertebral disc disease. This condition is somewhat more common in women. Although acute attacks may start at a very young age with episodes of acute torticollis or "wry neck," the incidence peaks when persons are aged 45-50 years (see image below).

Appearance of torticollis as a result of sternomastoid fibrosis in a young child.

Of all sports-related injuries, 2-3% are spinal injuries and the majority of these happened during unsupervised activities such as football, soccer, wrestling, diving, surfing, skiing and sand lot games.[4] The majority of the available literature, however, is found for football and this group is the most likely to sustain cervical trauma.

Statistical estimates of the incidence of cervical injury for football players varies ranging from 1 quadriplegic injury per 7,000 to 1 injury per 58,000.[5] Another review reported that since 1977, there has been an annual incidence of fewer than 10 cases of permanent injury to the cervical spinal cord among football players.[6] In 1976, the National Collegiate Athletic Association football rules committee disallowed the technique of spear tackling or the technique of using the helmet to butt or ram an opponent. This resulted in a remarkable decrease in the incidence of catastrophic neck injuries over the next 9 years.[7]

PreviousNextFunctional Anatomy

The cervical spine permits a wide range of motion (ROM) of the head in relation to the trunk. A degree of stability and flexibility is required to control the motion and dissipate the forces applied to the spine. Great differences in anatomy and function exist between the occiput-C1, the C1-2 (upper complex), and C3-C7 (lower complex) levels. Eight motion segments occur between the occiput and T1. No disc exists between C1 and C2; therefore, the first intervertebral disc is between C2 and C3.

The intervertebral disc consists of an outer annulus fibrosus and an inner nucleus pulposus. The intervertebral disc is thicker anteriorly, contributing to the normal cervical lordosis. The C6-7 disc is the thickest disc of the cervical spine. The nucleus pulposus and the inner one half of the annulus fibrosus are avascular and receive nutrition through diffusion, compression, dehydration, and imbibition of fluids.[8]

The annulus fibrosus, particularly the outer one third, has been found to be innervated by the sinuvertebral nerve and the vertebral nerve. The sinuvertebral nerve arises from the ventral ramus (somatic root), whereas the vertebral nerve (autonomic root) is derived primarily from the sympathetic nervous system. However, the vertebral nerve has connections with the cervical ventral rami, which suggests the possibility of the vertebral nerve also conveying somatic afferents from the disc.[9, 10, 11]

The nociceptors and mechanoreceptors in the annulus fibrosus mediate pain transmission from structural disruption of the intervertebral disc itself or from the chemically mediated inflammatory effect of phospholipase A2.[10, 12] Pacinian corpuscles and Golgi tendon organs present in the posterolateral region of the outer one third of the annulus transmit proprioceptive information from the intervertebral disc.[8, 12, 13, 14, 15]

The adult cervical disc has a crescentic shape anteriorly, with the apex of the crescent at the uncovertebral joints on each side. The posterior annulus has multiple vertical fissures allowing for a very degenerative appearance during discography and on gross examination. In addition, the nucleus of the cervical disc tends to be poorly centralized when compared with the lumbar disc. In the lumbar disc, the nucleus tends to be well localized in the center of the disc, and the posterior annulus tends to remain relatively intact when compared with the cervical disc. Annular fissures in the lumbar disc tend to be circumferential and/or radial in nature.

PreviousNextSport-Specific Biomechanics

Biomechanics is the study of the changes in the anatomic structures occurring during body movements. The movements of the cervical spine include flexion and extension in the sagittal plane, lateral flexion in the coronal plane, and rotation in the horizontal plane. Lateral flexion and rotation occur as coupled movements. Other movements of the cervical spine include protrusion (ie, the head is moved as far forward as possible with the neck outstretched and maintaining forward-facing position) and retraction (ie, the head is moved as far backward as possible and maintaining a forward-facing position).

Fifty percent of rotation of the cervical spine occurs in the upper cervical complex with the atlas rotating ipsilaterally around the odontoid. Protrusion causes upper cervical spine extension and lower cervical spine flexion, whereas retraction causes upper cervical spine flexion and lower cervical spine extension. At the occiput-C1 and C1-2 levels, ROM is greater with the protruded and retracted position than with full-length flexion and full-length extension positions.[16] See the image below.

Three-dimensional computed tomography scan of C1.

The annular fibers are made up of collagenous lamellae with alternating directions of inclination oriented 35° from the horizontal. The annulus is more susceptible to injury with rotation and translation movements due to resistance offered only by the lamella oriented in the direction of movement. In the cervical spine, as in the lumbar spine, the intervertebral disc dissipates the transmission of compressive loads throughout the ROM by slowing the rate at which these forces are transmitted through the spine. By diverting the load via temporarily stretching the annular fibers, the disc protects the vertebra from taking the entire load at once.

In asymmetric loading, the nucleus pulposus migrates toward the area with less load. Thus, in flexion movements of the cervical spine, anterior offset loading of the intervertebral disc occurs, in which the nucleus pulposus moves posteriorly and the posterior annular wall is stretched. In addition, the cervical lordosis reduces, the vertebral canal lengthens, and the intervertebral foramina open.[2]

In extension movements of the cervical spine, posterior offset loading of the intervertebral disc occurs, in which the nucleus moves anteriorly and the anterior annular wall is stretched. Shortening of the vertebral canal and closing of the intervertebral foramen also occur.[2] In lateral flexion and rotation (coupling movement) of the cervical spine, there is offset loading of the intervertebral disc on the side of flexion and rotation, with nuclear material moving to the opposite side (site of the convexity), and the posterolateral annular wall is stretched.[2]

The intervertebral foramina house the exiting cervical nerves. The largest cervical spine foramen is at the C2-3 level, and the smallest foramen is at the C6-7 level.[17] The cervical foramina become very dynamic during cervical spine ROM. The intervertebral foramina enlarge with flexion and decrease with extension. In rotation, the ipsilateral side becomes smaller, and the contralateral side enlarges. The extreme changes of the foramina occur with coupled movements (ie, flexion-rotation and extension-rotation-lateral flexion).[18]

In addition to the above biomechanical concerns, cervical spinal stenosis has been evaluated with regard to catastrophic cervical sports injuries. The Torg/Pavlov ratio (measured by dividing the sagittal diameter of the spinal canal by the sagittal diameter of the vertebral body) when less than 0.8 was thought to subject the football player to high risk of cervical cord injury due to suspected cervical stenosis (see image below). However, subsequent studies found that this ratio may be erroneously low in players that have wide vertebral bodies. A study by Cantu suggested that functional stenosis as documented by myelogram or magnetic resonance imaging (MRI) may be a more appropriate measure of stenosis.[6]

Lateral cervical spine plain radiograph illustrating the Torg/Pavlov ratio. Classification of athletic cervical spine injuries

A review by Bailes and Maroon classified athletes with cervical injuries into 3 types[4] :

Type I injuries were those that caused permanent spinal cord damage, including conditions such as anterior cord syndrome, Brown-Sequard syndrome, central cord syndrome, and mixed incomplete syndrome.Type II injuries were classified as those that occur transiently after athletic trauma with normal neurologic examination and normal radiologic evaluation. Type II injuries included spinal concussion neurapraxia, and "burning hands" syndrome. The burning hands syndrome was described as suspected injury to the spinothalamic and corticospinal tracts, resulting in arm and hand weakness with burning dysesthesias.[19] This is distinct from the burner or stinger injury that is a common cervical injury in football players and is thought to be due to traction on the upper trunk of the brachial plexus. In this condition, athletes typically have a burning, dysesthetic pain that begins in the shoulder region and radiates unilaterally into the arm and hand, with C5-C6 distribution numbness or weakness. Type III injuries were classified in athletes with only radiologic abnormalities but without neurologic deficit. These included congenital spinal stenosis, acquired spinal stenosis, herniated cervical disc, an unstable fracture, fracture/dislocation, ligamentous injury, and spear-tackler’s spine. Spear tackler’s spine was described by Torg et al described athletes that were at high risk for quadriplegic injury. These athletes had developmental cervical canal stenosis, reversal of the cervical lordosis, preexisting posttraumatic cervical radiographic abnormalities, and documentation of using spear-tackling techniques. PreviousProceed to Clinical Presentation , Cervical Discogenic Pain Syndrome

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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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Thoracic Outlet Syndrome

Background

Thoracic outlet syndrome is not the name of a single entity, but rather a collective title for a variety of conditions attributed to compression of these neurovascular structures as they traverse the thoracic outlet.[1, 2, 3, 4, 5] The thoracic outlet is bordered by the scalene muscles, first rib, and clavicle. Neurovascular structures pass from the neck and thorax into the axilla through this space. Thoracic outlet syndrome remains one of the most controversial clinical entities in medicine.[6, 7, 8] See the image below.

Thoracic outlet syndrome in a 16-year-old volleyball player with a stenotic right subclavian vein (arrow) secondary to fibrosis.

For excellent patient education resources, see eMedicineHealth's patient education articles Shoulder and Neck Pain and Electromyography (EMG).

NextEpidemiologyFrequencyUnited States

The wide variability of symptoms and signs in patients with thoracic outlet syndrome and the lack of an objective confirmatory test for the diagnosis makes correctly identifying patients with thoracic outlet syndrome difficult.[9] Therefore, determining its exact incidence remains elusive; estimates range from 3-80 cases per 1000 population.[10] Thoracic outlet syndrome is more common in women, particularly those with poor muscular development, poor posture, or both.[11]

PreviousNextFunctional Anatomy

The neurovascular bundle courses through 3 spaces, or triangles, as it exits the neck to reach the axilla and proximal arm. All 3 spaces can be the source of compression of the various components of the neurovascular bundle, including the brachial plexus and the subclavian vessels.[12] These spaces are small at rest and become even smaller with certain arm maneuvers, such as abduction and external rotation.[13, 14] This can aid in the diagnosis of thoracic outlet syndrome and forms the basis for provocative testing, which is discussed later (see Clinical, Physical).

The first space is the interscalene triangle. It is bordered by the anterior scalene muscle, the middle scalene muscle, and the upper border of the first rib. This space contains the trunks of the brachial plexus and subclavian artery. The interscalene triangle is the most common site for neural compression, vascular compression, or both.[10]

The second space is the costoclavicular triangle, which is bordered by the clavicle, first rib, and scapula and contains the subclavian artery and vein and the brachial nerves.

The third and final space is beneath the coracoid process just deep to the pectoralis minor tendon; it is referred to as the subcoracoid space.

PreviousNextSport-Specific Biomechanics

Thoracic outlet syndrome is most often seen in patients who engage in repetitive motions that place the shoulder at the extreme of abduction and external rotation. An example of such activity is swimming, especially with the freestyle stroke, butterfly stroke, and backstroke. When a swimmer reports tightness and pain around the shoulder, neck, and clavicle as his or her hand enters the water, thoracic outlet syndrome should be suspected.

In addition to swimmers, other athletes affected by thoracic outlet syndrome include water polo, baseball, and tennis players and athletes in any other activity that places repetitive stress on the shoulder at the extremes of abduction and external rotation. These individuals may present with neurologic and arterial or venous symptoms. Venous thoracic outlet syndrome most commonly develops in young male athletes in whom the upper extremity musculature is overdeveloped as a result of work or physical conditioning. Baseball players, whose sport requires repetitive throwing motions, are at increased risk for arterial thoracic outlet syndrome in their dominant arm.

PreviousProceed to Clinical Presentation , Thoracic Outlet Syndrome

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Little League Elbow Syndrome

Background

Little league elbow (LLE) syndrome is a valgus overload or overstress injury to the medial elbow that occurs as a result of repetitive throwing motions. Over the past several decades, the number of organized sports for children has grown significantly, with millions of children participating in organized athletics each year. This increase in participation has been paralleled by an increase in sports-related injuries in the pediatric population.[1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11]

Increased single-sport participation with year-round training, higher intensities at young ages, and longer competitive seasons are contributing factors to the increased injury rates seen in pediatric athletes. Conditioning and training errors also contribute significantly to the risk and frequency of injury. Although briefly discussed below, injuries to the lateral, posterior, and anterior elbow are separate entities and should not be confused with the medial injuries referred to as little league elbow syndrome.

During the throwing motion, valgus stress is placed on the elbow. This valgus stress results in tension on the medial structures (ie, medial epicondyle, medial epicondylar apophysis, medial collateral ligament complex) and compression of the lateral structures (ie, radial head, capitellum). Repeated stress results in overuse injury when tissue breakdown exceeds tissue repair. Recurrent microtrauma of the elbow joint can lead to little league elbow, a syndrome that encompasses (1) delayed or accelerated growth of the medial epicondyle (medial epicondylar apophysitis), (2) traction apophysitis (medial epicondylar fragmentation), and (3) medial epicondylitis.[1, 8, 12, 13, 14, 15]

Medial epicondylar apophysitis and stress fractures through the medial epicondylar epiphyses caused by repetitive valgus stress generally manifest with progressive medial pain, decreased throwing effectiveness, and decreased throwing distance.

Other causes of medial elbow pain include avulsion fractures of the medial epicondyle and ulnar collateral ligament (UCL) sprains or tears. Although a fracture is usually an acute traumatic event, a preceding history of medial elbow pain is common and is thought to be a risk factor for progression to acute fracture. Therefore, any thrower who is experiencing medial elbow pain should refrain from pitching until he or she has had a thorough evaluation.[1, 3, 5, 8, 16]

A medial epicondyle fracture manifests as point tenderness and swelling over the medial epicondyle, often with an elbow flexion contracture greater than 15°. Repetitive medial stress can also cause attenuation and microstretching of the UCL complex, causing mild instability over time.[1]

UCL injuries can manifest as acute ligament tears following a single valgus stress or as overuse sprains following repetitive valgus overloads. The clinical presentation is similar to little league elbow; however, the typical age range of the athlete is the older teenager who is skeletally mature. Suspected UCL injuries should be referred for further evaluation by a sports medicine specialist. Athletes with UCL injuries should not be allowed to pitch until they have been evaluated.

Although uncommon in children, neurologic injuries such as C8-T1 radiculopathy and ulnar neuritis can manifest as medial elbow pain and should be included in the differential diagnosis (see Differentials and Other Problems to Be Considered).

Lateral compression of the elbow most frequently results in injuries to the capitellum and radial head. Osteochondrosis of the capitellum (known as Panner disease) generally occurs in children aged 7-12 years and manifests as dull, achy, activity-related lateral elbow pain. Swelling, clicking, and decreased range of motion are uncommon associated symptoms. Panner disease tends to be a benign self-limited condition that does well over time and is treated with complete rest from inciting activities such as throwing and weight bearing on the elbow. Osteochondral injuries can also be observed in the radial head.

Osteochondritis dissecans (OCD) of the capitellum occurs in adolescents aged 13-17 years. This is a localized injury to subchondral bone that results from repetitive lateral compression of the elbow during overhead motions. These patients report a general dull elbow pain that worsens with activity, often have a flexion contracture of 15° or greater, and may have mechanical symptoms of clicking or popping. Loose body formation, residual capitellum deformity, and elbow degenerative joint disease are potential sequelae. Different treatment options are used based on the age and skeletal maturity of the patient and the type of lesion present.

Osteochondritis dissecans lesions can be separated into type I, which has no displacement and no articular cartilage fracture; type II, which has evidence of articular cartilage fracture or partial displacement; and type III, which is completely displaced with loose bodies in the joint.

Posterior elbow injuries also occur as a result of throwing. During the follow-through stage of throwing, extension overload and valgus stress can result in injury of the olecranon. These athletes present with posterior elbow pain, clicking, and possible loss of elbow extension. Loose bodies and olecranon nonunion can occur in younger athletes. Older athletes may experience olecranon fractures or secondary osteophyte formation. These injuries are sometimes treated surgically.[1, 3, 4, 5, 6, 7, 9, 10, 11, 17]

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

NextEpidemiologyFrequencyUnited States

Annually, an estimated 4.8 million children aged 5-14 years participate in baseball and softball. The incidence of all baseball-related overuse injuries is 2-8% per year. The incidence of overuse injuries in the 9- to 12-year-old range for baseball is 20-40%, and in the adolescent age group is 30-50%. The true incidence of sports-related injuries is unknown because a large number of athletes never seek medical care. Early recognition of little league elbow syndrome is important, because it leads to better outcomes and decreases the risk of persistent functional disabilities in the athletes.

International

No data are available for the annual incidence of little league elbow syndrome in the international community.

PreviousNextFunctional Anatomy

Evaluation of the young adolescent elbow presents some anatomic challenges to the healthcare provider in that the elbow consists of numerous ossification centers and cartilaginous physes. Becoming familiar with the chronologic order of appearance and ossification of these growth centers is important. Consider the mnemonic CRITOE (ie, capitellum, radius, internal epicondyle, trochlea, olecranon, external epicondyle).

Each of the ossification centers appears at a relatively predictable time starting around age 1-2 years, with 2-year intervals between the next center's appearance. Closure of each of the apophyses occurs from age 14 to 16 years, with the medial epicondyle specifically closing at approximately age 15 years. The elbow likely reaches full skeletal maturity by the late teen years, at which time injuries to the UCL are far more common. Until then, the young thrower is at risk for little league elbow syndrome.[1, 4, 12, 16, 18]

The static stabilizers around the elbow include the bony articulations, the joint capsule, and the various ligament bundles. The medial (ulnar) collateral ligamentous complex consists of the anterior oblique bundle, posterior oblique bundle, and transverse ligament. These structures are the primary medial support of the elbow during valgus stress. The lateral (radial) ligamentous complex, composed of the lateral collateral, lateral ulnar collateral, and accessory lateral collateral ligaments, provides support during varus stress.

The dynamic stabilizers primarily include the muscles that cross the elbow joint, such as the triceps, biceps, and brachioradialis. The flexor-pronator group stabilizes against valgus stress, and the extensor-supinator group stabilizes against varus stress.

Elbow biomechanics include flexion/extension range of motion and pronation/supination. Slight hyperextension 5-15° through flexion of approximately 150° is within normal limits. Baseball pitchers with years of throwing experience often have relative 5-10° flexion contractures on their dominant side; however, in the young thrower, a flexion contracture can be a sign of injury. Pronation of 75° and supination of 85° is normal. Varus-valgus laxity of 3-4° is normal.

PreviousNextSport-Specific Biomechanics

One should be familiar with the stages of throwing to understand the complexities of the biomechanical forces that contribute to the young thrower's risk of injury, such as in little league elbow syndrome. The pitching or throwing motion can be divided into 6 stages. Medial elbow injuries are the most common type seen in throwers and occur most commonly in the cocking and acceleration phases of throwing, owing to the presence of maximum valgus extension or distraction forces.[1, 12, 13, 14, 15]

Windup begins with the pitcher balancing his weight over his rear leg, with the elbow flexed and the forward leg flexed at least 90°. Stride starts with the lead leg beginning to descend toward the plate, and the 2 arms separate. The elbow moves from extension into flexion of 80-100°. Cocking occurs when the humerus is in extreme abduction and external rotation and the elbow is flexed. The lead foots contacts the ground, the pelvis and trunk rotate, and elbow torque transfers valgus force across the elbow joint. During this phase, medial tension and lateral compression forces are applied to the elbow. Acceleration is the shortest pitching phase, lasting from maximal external shoulder rotation to ball release. In this phase, the trunk rotates as the elbow extends. Maximum elbow angular velocity is comparable during fastballs, sliders, and curveballs, but it less during the change-up pitch. Velocity comes from rotation of the trunk, shoulder, and hips. Varus torque forces during this phase act to resist the valgus extension "overload" phenomenon and can contribute to posterior elbow (olecranon) impingement. Deceleration is initiated at ball release and ends when the shoulder has reached full internal rotation. The body must decelerate the arm and dissipate forces in the elbow and shoulder. Follow-through is the final phase of the baseball pitch and ends with the pitcher reaching a balanced fielding position with full-trunk rotation and the body weight fully transferred from the rear leg to the forward leg. During follow-through, the elbow flexes into a relaxed position and crosses the body. PreviousProceed to Clinical Presentation , Little League Elbow Syndrome

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