Showing posts with label Lumbosacral. Show all posts
Showing posts with label Lumbosacral. Show all posts

Tuesday, February 4, 2014

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 brancDorsal 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 brancDorsal 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. 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

Monday, February 3, 2014

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

Sunday, February 2, 2014

Lumbosacral Spondylolisthesis

Background

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

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

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

Spondylolisthesis can be classified into the following 6 distinct categories.

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

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

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

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

Isthmic spondylolisthesis is further divided into the following 3 subtypes:

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

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

NextEpidemiologyFrequencyUnited States

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

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

PreviousNextFunctional Anatomy

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

PreviousNextSport-Specific Biomechanics

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

PreviousProceed to Clinical Presentation , Lumbosacral Spondylolisthesis

Saturday, January 18, 2014

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 brancDorsal 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 brancDorsal 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. 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

Lumbosacral Spine Acute Bony Injuries

Background

Injuries to the lumbar spine have received only a small amount of attention compared with other athletic injuries. This can be explained by a number of reasons. Spinal fractures are relatively uncommon in sports participation compared with other types of injuries; most injuries to the lumbar spine are relatively minor and fit into the category of soft-tissue injuries. These soft-tissue injuries are usually self-limited and resolve without coming to the attention of healthcare professionals.

The mechanisms and severity of sports-related lumbar spinal injuries reflect a competitive and risk-taking culture.[1, 2, 3, 4, 5, 6] Lumbar spine bony injuries are often limited to specific sports, most frequently seen in sports such as automobile or motorcycle racing,[7, 8, 9] skydiving[10] (see the image below), power weight lifting,[11, 12] wrestling,[13] gymnastics,[14, 15, 16] football,[17, 18, 19, 20, 21, 22] hockey,[23] rowing,[24] horseback riding,[25, 26] and high-speed snow sports.[27, 28, 29, 30, 31] This article reviews the diagnosis and management of acute lumbar vertebral fractures.

Sagittal computed tomography scan reconstruction oSagittal computed tomography scan reconstruction of a young female who had a skydiving accident. The parachute deployed, but the patient landed on concrete and sustained a lower-extremity fracture and a fracture of L1. She was neurologically intact but required an open reduction with a fusion and instrumental fixation of the fracture.

For excellent patient education resources, see eMedicineHealth's patient education articles Vertebral Compression Fracture and Low Back Pain.

Related Medscape Reference topics:

Lumbar Disk Problems in the Athlete

Lumbar Spine Fractures and Dislocations

Lumbar Spine Trauma Imaging

Lumbosacral Disc Injuries

Lumbosacral Discogenic Pain Syndrome

Related Medscape resources:

Resource Center Exercise and Sports Medicine

Resource Center Joint Disorders

Resource Center Spinal Disorders

CME/CE Back Pain in a 39-Year-Old Man from Guatemala

CME Early Surgery for Severe Sciatica Relieves Pain Faster Than Conservative Treatment

CME/CE Low Back Pain: Evaluating Presenting Symptoms in Elderly Patients

NextEpidemiologyFrequencyUnited States

The epidemiology of thoracic and lumbar spine injuries in athletes is very difficult to document. Most epidemiologic studies on lumbar spine injuries in athletes lack prospective data. The thoracolumbar junction and lumbar spine are common sites for fractures due to the high mobility of the lumbar spine compared with the more rigid thoracic spine. Injury to the cord or cauda equina occurs in approximately 10-38% of adult thoracolumbar fractures and in as many as 50-60% of fracture dislocations. The rate of bony injury without neurologic consequence is undoubtedly higher.

In the United States, Keene reported an overall rate of 7% for sport-related lumbar injuries in the athlete population.[30] Most of these injuries occurred during practice or preseason conditioning, and only 6% occurred during actual competition. Lumbar spine injuries were significantly more common in football[17, 18, 19, 20] and gymnastics.[14, 15, 16]

Statistics from the US Air Force Academy indicated that 9% of all athletic injuries affect the spinal column. In an analysis of injuries in a professional football team, Ryan et al reported a 6% rate of spinal injuries.[9] Snook reviewed all musculoskeletal injuries sustained by college wrestlers and female gymnasts and found a rate of thoracolumbar spine injuries of 2% for the wrestlers[13] and 13% for the female gymnasts.[32]

Related Medscape Reference topics:

Cauda Equina and Conus Medullaris Syndromes

Lumbosacral Facet Syndrome

Lumbosacral Radiculopathy

Lumbosacral Spondylolisthesis

Lumbosacral Spondylolysis

Related Medscape resources:

Resource Center Exercise and Sports Medicine

Resource Center Osteoporosis

Specialty Site Orthopaedics

International

Information on the incidence of sports-related spinal injuries in other countries is also limited and difficult to determine due to differences in data collection and reporting among countries. In England, Williams estimated that spinal injuries accounted for 15% of all injuries sustained in sports.[10] Furthermore, injuries to the thoracic and lumbar spine seemed to be more frequent in automobile racing, horseback riding, parachuting, mountain climbing, and weightlifting.

PreviousNextFunctional Anatomy

The lumbar spine consists of a mobile segment of 5 vertebrae, located between the relatively immobile segments of the thoracic and sacral segments at either end. The thoracic spine is stabilized by the attached rib cage and intercostal musculature, whereas the sacral segments are fused, providing a stable articulation with the ilium. The lumbar vertebrae are particularly large and heavy compared with the cervical and thoracic vertebrae. The bodies are wider, the pedicles are shorter and heavier, and the transverse processes project somewhat more laterally and ventrally when compared with other spinal segments. The laminae are shorter vertically than the bodies and are bridged by strong ligaments. Finally, the spinal processes are broader and stronger than those in the thoracic and cervical spine.[33]

The lumbar spine must transmit compressive, bending, and twisting forces that are generated between the upper and lower body. Consequently, as one moves more caudally into the lumbar spine, the muscle groups and ligaments become larger and stronger.

The intervertebral discs consist of 2 components, the annulus fibrosus and the nucleus pulposus. The annulus is a dense fibrous ring located at the periphery of the disc, which has strong attachments to the vertebrae and serves to confine the nucleus pulposus. The lumbar spine is surrounded by powerful musculature and ligaments, which dynamically stabilize the spine.

Related Medscape Reference topic:

Topographic and Functional Anatomy of the Spinal Cord

PreviousNextSport-Specific Biomechanics

The lumbar spine is a complex, 3-dimensional (3-D) structure that is capable of flexion, extension, lateral bending, and rotation. In the spine, the total range of motion is the result of a summation of the limited movements that occur between the individual vertebrae. Strong muscles and ligaments are crucial for supporting the bony structures and for initiating and controlling movement.

The most common movement of the lumbar spine is flexion. During flexion, anterior compression of the intervertebral disc and widening of the spinal canal occurs along with some sliding movement of the articular process in the zygapophyseal joint. This movement is limited by the posterior ligamentous complex and the dorsal muscles. Extension of the lumbar spine is more limited, producing posterior compression on the disc, narrowing of the spinal canal, and a sliding motion of the zygapophyseal joint. The anterior longitudinal ligament, ventral muscles, lamina, and spinous processes limit the extension of the lumbar spine.

Lateral bending involves lateral compression of the intervertebral disc, along with sliding separation of the zygapophyseal joint on the convex side. An overriding of the zygapophyseal joint occurs on the concave side. The intertransverse ligaments limit the lateral bending of the spine. Rotation of the lumbar spine involves compression of the annulus fibrosus fibers. It is limited by the geometry of the facet joints and the iliolumbar ligaments. The motion of the lumbar spine cannot be considered without evaluating the synchronous movements of the cervical and thoracic spine. The entire spinal column moves as one unit in all planes of motion. Each region of the spine has its own characteristic curvature. These curves allow an upright posture while maintaining the center of gravity over the pelvis and lower limbs. Although most rotation is accomplished at the cervical spine, flexion and lateral bending are primarily cervical and lumbar functions.

Spinous process fractures may occur as a result of direct trauma to the posterior spine or as a result of forcible flexion and rotation. These injuries are usually not associated with neurologic deficits. Violent muscular contraction or direct trauma can cause fractures of the transverse processes. For example, a football helmet blow to the back can cause fractures of either the spinous or transverse processes. Burst fractures (see the images below) are usually associated with axial loading and compression of the spine. Acute traumatic spondylolisthesis is usually associated with major trauma and extreme hyperextension of the spine.

Sagittal T1-weighted magnetic resonance imaging stSagittal T1-weighted magnetic resonance imaging study of a professional driver who was in a rollover motor vehicle accident while racing his car. This figure shows a T-10 unstable burst fracture producing severe kyphotic deformity of the spine. The abnormal signal on the vertebral body and the extradural defect represents a subacute hematoma producing spinal cord compression. The patient had severe paraparesis and underwent an emergency operation. The procedure involved an anterolateral retroperitoneal approach with a corpectomy and vertebral reconstruction. Postoperative plain x-ray film of a professional dPostoperative plain x-ray film of a professional driver who experienced a burst fracture in a rollover motor vehicle accident while racing his car. This image shows a vertebral reconstruction with the use of a titanium cage filled with bone and the arthrodesis with a Z plate. Sagittal computed tomography scan reconstruction oSagittal computed tomography scan reconstruction of an athlete who had a burst fracture.

The intervertebral discs are thick and strong. The annulus fibrosus receives most of the forces that are transmitted from one vertebral body to another, and it is designed to resist tension and shearing forces. The nucleus pulposus is designed to resist compression forces; it receives primarily vertical forces from the vertebral bodies and redistributes them in a radial fashion to the horizontal plane. This structure allows the intervertebral discs to dissipate the axial loading.

Related Medscape Reference topics:

Disk Herniation Imaging

Herniated Nucleus Pulposus

Lumbar Compression Fracture

Lumbosacral Spine Sprain/Strain Injuries

Lumbosacral Spondylolisthesis

Lumbosacral Spondylolysis

Related Medscape resources:

Resource Center Spinal Disorders

Specialty Site Neurology & Neurosurgery

Specialty Site Orthopaedics

PreviousProceed to Clinical Presentation , Lumbosacral Spine Acute Bony Injuries

Saturday, December 21, 2013

Lumbosacral Spondylolysis

Background

Lumbosacral spondylolysis (lumbar spondylolysis) is a unilateral or bilateral defect of the pars interarticularis that affects one or more of the lumbar vertebrae. See the images below.

Radiograph of L4 defect in the pars interarticularRadiograph of L4 defect in the pars interarticularis. Computed tomography scan demonstrating defects in Computed tomography scan demonstrating defects in the left and right pars interarticularis.

The term spondylolysis is derived from the Greek words spondylos, meaning vertebra, and lysis, meaning break or defect. Numerous hypotheses have been proposed on the etiology of lumbosacral spondylolysis (lumbar spondylolysis), as follows:

Separate ossification centersFracture during postnatal lifeStress fracture[1, 2] Increased lumbar lordosisImpingement of the articular process on the pars articularisWeakness of supporting structures[3] Growth[2, 4] Pathologic changes in the pars articularisDysplasia of the pars interarticularis

However, mechanical factors are widely believed to be the cause or at least the trigger of the development of lumbosacral spondylolysis (lumbar spondylolysis), especially when congenital abnormalities are present.[5] Moreover, lumbosacral spondylolysis (lumbar spondylolysis) is argued to be related to the human erect posture and lumbar curve.[1]

Ambulation may have a role in the genesis of lumbosacral spondylolysis (lumbar spondylolysis) because no known cases exist in nonambulatory patients.[6] As an acquired condition, no reports exist of its occurrence in stillborn fetuses or in the newborn.[7] Heredity is also implicated.[8]

When the defect in the pars interarticularis is not associated with a forward displacement, the term spondylolysis applies.[9] The term spondylolisthesis is derived from spondylos and listhesis, meaning movement or slipping, and refers to the slipping forward of one vertebra on the next caudal vertebra (see the image below).

Lateral radiograph of the lumbar spine shows spondLateral radiograph of the lumbar spine shows spondylolysis at L5 with spondylolisthesis at L5 through S1. On this single view, it is not possible to determine if these pars defects are unilateral or bilateral. Oblique views may help resolve this issue.

Lumbosacral spondylolysis (lumbar spondylolysis) is most common at L5, accounting for 85% of all cases,[10] and may be observed as high as L2.[11] Therefore, a slip is most common at the level of L5 slipping forward on S1. Lumbosacral spondylolysis (lumbar spondylolysis) is the cause of the most common type of spondylolisthesis.[4] Moreover, Ariyoshi et al reported a case of lumbosacral spondylolysis (lumbar spondylolysis) that occurred at 3 sites in L5 that involved the bilateral pars interarticularis and the center of the right lamina.[12]

For excellent patient education resources, see eMedicineHealth's patient education article Low Back Pain.

NextEpidemiologyFrequencyUnited States

Lumbosacral spondylolysis (lumbar spondylolysis) is more commonly observed in males,[10] but this difference may not be significant.[13, 14]

In the United States, a reported difference exists between the sexes and races, with an incidence of lumbosacral spondylolysis (lumbar spondylolysis) of 6.4% in white men, 2.8% in black men, 2.3% in white women, and 1.1% in black women. A pars defect is twice as common in boys than in girls, although high-grade slippage is 4 times more common in girls than in boys. Alaskan Eskimos (26%) have the highest incidence, with the highest rate in Eskimos from north of the Yukon River.[4]

PreviousNextFunctional Anatomy

Repetitive axial loading, especially in an extended lumbar spine is thought to be the most important contributing mechanism causing lumbosacral spondylolysis (lumbar spondylolysis), leading to fatigue fracture of the pars interarticularis. Shear stresses on the isthmic pars are greater when the lumbar spine is extended. When repetitive extension stresses occur, the pars interarticularis becomes impinged from the inferior facet of the cephalad vertebrae, which results in microfractures and attempts at repair.[15] See the images below.

Long TR (T2-weighted) fat suppressed sagittal magnLong TR (T2-weighted) fat suppressed sagittal magnetic resonance image shows increased signal in the pars interarticularis on the left at L5 (same patient in Images 3-4). This is an acute stress reaction. Sagittal short TR (T1-weighted) magnetic resonanceSagittal short TR (T1-weighted) magnetic resonance image shows decreased signal in the pars interarticularis on the left at L5 (same patient in Images 3-4). PreviousNextSport-Specific Biomechanics

Lumbosacral spondylolysis (lumbar spondylolysis) occurs in 3-7% of the general population[14] The athletic population is believed to be more prone to the development of this condition,[15] because the incidence of lumbosacral spondylolysis (lumbar spondylolysis) in competitive athletes is higher than the percentage reported for the nonsports population.[16]

The overall percentage of lumbosacral spondylolysis (lumbar spondylolysis) among athletes in a study by Soler et al was about 8%, a figure not significantly higher than that among the general population.[14] However, certain sporting events were found to contribute higher percentages when each sport was considered separately, with the highest percentages of lumbosacral spondylolysis (lumbar spondylolysis) occurring in throwing sports (26.67%), artistic gymnastics (16.96%), and rowing (16.88%).[14] In an earlier series, a high percentage of lumbosacral spondylolysis (lumbar spondylolysis) was been observed in diving (43.13%), wrestling (29.82%), and weight lifting (22.68%).[16]

Other sports with high incidence rates of lumbosacral spondylolysis (lumbar spondylolysis) are ballet, dancing, football, volleyball, and fast bowlers in cricket. In ballet, the higher incidence rate is due in part to an inability to reach or maintain proper turn-out and thus overcompensation with lordosis.

In general, the presence of the repetitive actions of flexion, extension, rotation, and torsion, either alone or in combination, that are often associated with resistance are the biomechanical movements that show the highest prevalence of lumbosacral spondylolysis (lumbar spondylolysis).[14]

PreviousProceed to Clinical Presentation , Lumbosacral Spondylolysis

Friday, December 20, 2013

Lumbosacral Spine Sprain/Strain Injuries

Background

Low back pain (LBP) is a well-known health concern in the United States. Although the incidence of low back injuries is much less in athletes than in a corresponding population of industrial workers, such injuries are still seen in many athletes. The most common causes of LBP in athletes are musculoligamentous sprains and strains, which occur mainly at the lumbosacral region. This is true of both high-performance, world-class athletes and of "weekend athletes." With over 30 million Americans now involved in organized sports, these back injuries present health concerns on the national level.

(See also the Medscape Reference articles Mechanical Low Back Pain [in the Physical Medicine and Rehabilitation section], Lumbar Disk Problems in the Athlete [in the Sports Medicine section], and Low Back Pain and Sciatica [in the Neurology section], as well as Pain Measurement in Patients With Low Back Pain, Guidelines Issued for Management of Low Back Pain, and Epidemiology of Adolescent Spinal Pain: A Systematic Overview of the Research Literature on Medscape.)

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

NextEpidemiologyFrequencyUnited States

Studies document that 7-13% of all sports injuries in intercollegiate athletes are low back injuries. The most common back injuries are muscle strains (60%), followed by disc injuries (7%). Athletes are more likely to sustain injuries in practice (80%) than during competition (6%).[1] American football (17%) and gymnastics (11%) are reported to have the highest rates of low back injury.[1]

International

Exact numbers regarding the international frequency of low back injuries are not known, however, a recent French study reported over 50% of French individuals aged 30-64 years had experienced at least 1 day of LBP over the previous 12 months, and 17% had suffered LBP for more than 30 days in the same 12-month period.[2] The authors noted that the prevalence of LBP varied between men and women, that there was an increased incidence with increasing age for LBP that lasted more than 30 days, and that these data were similar to those of other countries.

In an African study, the mean LBP point prevalence among adults was 32%, with an average 1-year prevalence of 50% and an average life-time prevalence of 62%.[3]

PreviousNextFunctional Anatomy

Sprains are ligamentous injuries that are caused by a sudden violent contraction, sudden torsion, severe direct blows, or a forceful straightening from a crouched position. All major ligaments (ie, anterior longitudinal, posterior longitudinal, yellow, intertransversal, capsular, interspinosus, supraspinosus) can sustain sprains; however, the posterior ligaments are more prone to injury. The posterior longitudinal ligament, for example, is the biggest of this group of ligaments and is less developed than its anterior counterpart.

Strains are defined as tears, either partial or complete, of the muscle-tendon unit. Muscle strains and tears most frequently result from a violent muscular contraction during an excessively forceful muscular stretch. Any posterior spinal muscle and its associated tendon can be involved, although the most susceptible muscles are those that span several joints.

Combined with injured tendons and ligaments, all embedded structures may be temporarily or permanently damaged. Of major interest are proprioceptors that play a crucial role in the motor control of the spine. An inhibited motor control weakens spinal stability and may lead to chronic back problems or reinjury.

PreviousNextSport-Specific Biomechanics

The lumbar spine bears tremendous loads: the large, superimposed body weight interacts with additional forces that are generated by lifting as well as other activities that involve powerful forces.[4, 5, 6, 7, 8] The lumbar spine and the hips are responsible for the mobility of the trunk. The L4-5 and L5-S1 areas bear the highest loads and tend to undergo the most motion. Consequently, these areas are found to sustain the most spinal strain or sprain injuries. In addition, load-bearing strain and sprain injuries most frequently occur during the strongest coupling patterns (ie, lateral bending with flexion-extension, axial rotation with lateral bending).

The bony architecture and the ligamentous elements constitute the structural components of the spine.[9] The muscles and tendons constitute the dynamic elements. With all elements intact, the biomechanical function of the spine is normal. The intrinsic translatory and rotatory stability of the spine is provided by the ligaments. The contribution of a given ligament depends not only upon its particular strength, but also upon its location. Moreover, a ligament may contribute relatively more to either the translatory or rotatory stability, depending upon the loading circumstances. Assuming that all ligaments are made of the same material, the strength of a ligament is proportional to its cross-sectional area. A ligament with a larger cross-sectional area provides greater stability and less displacement when the functional spinal unit (FSU) is subject to physiologic loads.

Another factor that contributes to spinal stability is the distance of a ligament from the center of rotation.[10] A ligament that is located close to the center of rotation provides much less stability against bending than a ligament that is further away from the rotation center. The interspinous ligaments in the adult lumbar spine are frequently absent, ruptured, or degenerated and do not contribute to stability of the spine. However, supraspinous ligaments do play a role in stabilizing the spine. Muscles provide stability to the spine during all dynamic movements and actions. Injured trunk muscles can decrease spinal stability if the intact muscles are not able to compensate for the dysfunction of the injured unit.

Spinal instability can occur as a result of trauma, disease, surgery, or some combination of the 3 causes. Clinical instability is defined as a loss of the ability of the spine to maintain relationships between vertebrae under physiologic loads in such a way that (1) there is neither initial nor subsequent damage to the spinal cord or nerve roots, and (2) there is no development of incapacitating deformity or severe pain. Instability leads to abnormal kinetics (stiffness) and/or kinematics (coupling patterns).

When the tissues surrounding the spine are damaged, structures embedded within those tissues may also become temporarily or permanently harmed. Proprioceptors, including muscle spindles, Golgi tendon organs, and joint receptors, are of great importance for postural control. Damaged proprioceptors weaken the stability of the spine and may lead to reinjuries or chronic problems. Although some studies document changes in the normal quality and quantity of motion, there has been no compelling correlation of either with pain behavior.

PreviousProceed to Clinical Presentation , Lumbosacral Spine Sprain/Strain Injuries

Lumbosacral Radiculopathy

Background

Some of the major causes of acute and chronic low back pain (LBP) are associated with radiculopathy. However, radiculopathy is not a cause of back pain; rather, nerve root impingement, disc herniation (see the image below), facet arthropathy, and other conditions are causes of back pain.[1, 2, 3]

Sagittal magnetic resonance image showing loss of Sagittal magnetic resonance image showing loss of intervertebral disc height at L5/S1. Herniations of the nucleus pulposus are noted at L4/5 and L5/S1. Courtesy of Barton Branstetter, MD.

Lumbosacral radiculopathy, like other forms of radiculopathy, results from nerve root impingement and/or inflammation that has progressed enough to cause neurologic symptoms in the areas that are supplied by the affected nerve root(s).

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NextEpidemiologyFrequencyUnited States

Lumbosacral radiculopathy occurs in approximately 3-5% of the population, and men and women are affected equally, although men are most commonly affected in their 40s, whereas women are most commonly affected between ages 50-60.[4] Of those who have this condition, 10-25% develop symptoms that persist for more than 6 weeks.

PreviousNextFunctional Anatomy

The anatomy of the lumbar epidural space is the key to understanding the mechanism of lumbosacral radiculopathic pain. The sinuvertebral nerves innervate structures in the lumbar epidural space; these nerves originate distal to the dorsal root ganglion, then run back through the intervertebral foramen to supply the arteries, venous plexi, and lymphatics. At the inner aspect of the intervertebral foramen, the sinuvertebral nerves divide into ascending and descending branches that freely communicate with corresponding branches from the segment above, from the segment below, and from the opposite side.

The sinuvertebral nerve supplies the posterior longitudinal ligament, superficial annulus fibrosus, epidural blood vessels, anterior dura mater, dural sleeve, and posterior vertebral periosteum. The 2 structures capable of transmitting neuronal impulses that result in the experience of pain are the sinuvertebral nerve and the nerve root. The posterior rami of the spinal nerves supply the apophyseal joints above and below the nerve as well as the paraspinous muscles at multiple levels.

Herniation of the intervertebral disc can cause impingement of the above neuronal structures, thus causing pain. The presence of disc material in the epidural space is thought to initially result in direct toxic injury to the nerve root by chemical mediation and then exacerbation of the ensuing intraneural and extraneural swelling, which results in venous congestion and conduction block. Notably, the size of the disc herniation has not been found to be related to the severity of the patient's pain.

Pain is also believed to be mediated by inflammatory mechanisms that involve substances such as phospholipase A2, nitric oxide, and prostaglandin E. These mediators are all found in the nucleus pulposus itself. Phospholipase A2 has been found in high concentrations in herniated lumbar discs; this substance acts on cell membranes to release arachidonic acid, a precursor to other prostaglandins and leukotrienes that further advance the inflammatory cascade. Additionally, leukotriene B4 and the substance thromboxane B2 have been found to have direct nociceptive stimulatory roles.

From a biomechanical standpoint, the lumbar intervertebral discs are highly susceptible to herniation because they are exposed to tremendous forces, principally by the magnification of the forces that result from the lever effect of the human arm in lifting; the forces generated by the upper trunk mechanics with rotation, flexion/extension, and side-bending on the discs below; and by the vertical forces associated with the upright position. Because each intervertebral disc is a fluid system, hydraulic pressure is generated whenever a load is placed on the axial skeleton. The hydraulic pressure mechanisms then multiply the force on the annulus fibrosus of the intervertebral disc to make it 3-5 times that which is exerted on the axial skeleton.

PreviousNextSport-Specific Biomechanics

Dancers are prone to both acute and chronic back problems, including lumbosacral radiculopathy, which develop secondary to the combination of 2 factors that are required in most dance routines: extreme physical flexibility and exposure of the spine to the extremes of its range of motion.[1] Additionally, female dancers are predisposed to disc herniation secondary to the positioning that is required in certain movements, such as the pas de deux (in which excess lumbar lordosis is present), as well as the large jumps that these dancers often perform.

Golfers are also very susceptible to disc disease and lumbosacral radiculopathy because of the repetitive torsional motion that is used in the sport.[5] The golf swing can produce up to an estimated 7500 N of compressive force across L3-L4. Competitive weight lifters and football linemen have been noted to experience even larger compressive loads.

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