INTRODUCTION

Low back pain is ubiquitous to mankind by virtue of our upright posture. Traditionally, it has been believed that most episodes of spinal pain are short lived and that at least 90% of patients with low back pain recover in about 6 weeks with or without treatment.^1–3

Contrary to this prior assumption of only 10–20% patients experiencing recurrent or chronic symptoms after an initial episode of low back pain, recent literature puts that number as high as 35–79%.^4–7

The challenge lies, in this subgroup of subjects, to identify the specific pain generator so that appropriate interventional therapy may be initiated as and when indicated. The study by Kuslich et al.⁸ identified along with intervertebral disc, dura, ligaments, fascia, and muscles, zygapophyseal or facet joints as capable of transmitting pain in the low back region. Even prior to this anatomical study, Goldthwait⁹ in 1911 first recognized lumbar zygapophyseal joints as potential source of low back pain. He believed that joint asymmetry could result in pain secondary from nerve root pressure. Subsequently, in 1933, Ghormley¹⁰ first coined the term ‘facet syndrome’ as lumbosacral pain with or without sciatic pain, occurring after a twisting or rotary strain of the lumbosacral region. Badgley¹¹ in 1941 suggested that facet joints by themselves could be a primary source of low back pain separate from the nerve compression component. However, it was not until 1963 when Hirsch et al.¹² demonstrated that the low back pain distributed along the sacroiliac and gluteal areas with referral to the greater trochanter could be induced by injecting hypertonic saline in the region of the lumbar facet joints. In 1976, Mooney and Robertson,¹³ and three years later McCall et al.¹⁴ used fluoroscopy to confirm the location of intra-articular lumbar facet joint injections in asymptomatic individuals, demonstrating reproduction of back and leg pain after injection of hypertonic saline. Eventually, Marks¹⁵ in 1989, followed by Fukui et al.¹⁶ in 1997, described the distribution of pain patterns after stimulating the lumbar facet joints.

Recent literature¹⁷ indicates that the prevalence of chronic lumbar zygapophyseal joint-mediated pain has a wide range that varies from 15% in the relatively younger patients, with confidence limits of 10–20%. This prevalence can be as high as 40% among the elderly population with confidence limits of 27–53%.¹⁸

ANATOMY

The lumbar facet or zygapophyseal joints are paired, true synovial, diarthrodial joints that form the posterior aspect of the respective intervertebral foramina. The joint consists of hyaline cartilage, a synovial membrane, a fibrous capsule, and nociceptive fibers transmitted via the medial branches of the dorsal rami.^19,20 These facet joints are innervated by the medial branches of the dorsal rami (posterior primary rami) that exit the intervertebral foramina. The posterior primary rami travel posteriorly over the base of the transverse process. The dorsal ramus divides into a medial, an intermediate, and a lateral branch. The lateral branch ascends from the dorsal ramus just before it reaches the transverse process. The medial branch passes under the mammilloaccessory ligament and sends branches to the adjacent facet joint, the facet joint below, and the more medial erector spinae muscles. Thus, the joint is typically innervated from a branch at the same level and a branch originating from the foramen above. In contrast, the dorsal ramus at the fifth lumbar vertebral level (L5) travels between the ala of the sacrum and its superior articular process, which divides into the medial and lateral branches at the caudal edge of the process, the medial branch continuing medially, where it innervates the lumbosacral joint.^21–23

Neuroanatomical studies^12,24–26 indicate that the facet joint capsule is richly innervated, containing both free and encapsulated endings, and can undergo extensive stretch under physiological loading.²⁷ It has been reported that protein gene product (PGP) 9.5, substance P (SP), calcitonin gene-related peptide (CGRP), dopamine β-hydroxylase (DBH), vasoactive intestinal polypeptide (VIP), neural peptide Y (NPY), and choline acetyl transferase (chAT) immunoreactive (IR) fibers are present within the human facet joint capsule.^{21,26,28–30} Ashton et al.³¹ confirmed immunoreactivity for SP, CGRP, and VIP in surgically removed human facet joint capsule. A subsequent anatomical study confirmed higher concentration of inflammatory cytokines in facet joint tissue from patients with lumbar spinal stenosis than in lumbar disc herniations, suggesting that these cytokines may have some contribution to the etiology of symptoms in degenerative spinal stenosis.³²

PATHOPHYSIOLOGY

With aging, the changes that occur in the zygapophyseal joints are the same as those seen in any diarthrodial joint. The earliest change is synovitis, which may persist with the formation of a synovial fold which projects into the joint space itself. Later, degenerative changes set in gradually, and eventually become more marked. Eventually, the capsular laxity allows for subluxation of the joint surfaces. Continued degeneration mainly due to repeated torsional strains results in the formation of subperiosteal osteophytes, and possibly subchondral synovial cysts. The end result is that of gross articular degeneration, with almost complete loss of articular cartilage, and formation of bulbous zygapophyseal joints and marked periarticular fibrosis. The pathogenesis of a degenerative cascade in the context of a three-joint complex involving the intervertebral disc and the adjacent zygapophyseal joint also leads to the assumption that the degenerative changes within the disc are also believed to lead to associated facet degeneration.^33–35

PAIN PATTERNS

The clinical presentation of lumbar zygapophyseal joint-mediated low back pain appears to overlap considerably with the presentation of low back pain due to various other etiologies. Lumbar facet joints have been shown to be capable of producing pain in the low back and referred pain in the lower extremity in normal volunteers.^13–16 McCall et al.¹⁴ concluded that pain referral patterns overlap between the upper and lower lumbar spine. Marks¹⁵ also studied patterns of pain induced from lumbar facet joints, from the posterior primary rami of L5, and from the medial articular branches of the posterior primary rami from T11 to L4. He observed no consistent segmental or somatic referral pattern. Marks also concluded that pain referred to the buttocks or trochanteric region occurred mostly from the L4 and L5 levels, while inguinal or groin pain was produced from L2 to L5. This latter finding led to the conclusion that the nerves innervating the joints gave rise to distal referral of pain more commonly than the facet joint itself. Fukui et al.¹⁶ concluded that the major site of referral pain from the L1–2 to L4–5 joints was the lumbar region itself. However, stimulation of the L5–S1 joint caused referred spinal pain as well as gluteal pain. Referred pain into the lower extremities was not observed by Fukui et al.¹⁶ as was reported by Mooney and Robertson.¹³ However, it must not be overlooked that in the study by Mooney and Robertson, the relatively large volume of the injectate (3 cc) used may very well have inadvertently anesthetized structures other than the facet joint intended. In essence, these studies indicate that there is no clear dermatomal or somatic pattern that is diagnostic of lumbar facet joint-mediated pain and an overlap with a varied pattern is the norm.

DIAGNOSIS

All this being said, there is no identified correlation between a clinical picture or any imaging study used, such as the magnetic resonance imaging (MRI), computed tomography (CT) scan, single photon emission computed tomography (SPECT), or radionuclide bone scan in diagnosing pain mediated via the lumbar zygapophyseal joint.^36–40 Simple static radiographs of the lumbar spine, and also dynamic images including standing flexion–extension films, may reveal evidence of arthritis involving the lumbar zygapophyseal joint as commonly in asymptomatic individuals as in patients with axial low back pain. What remains contentious is how lumbar zygapophyseal joint-mediated pain should be diagnosed.

Another point not to be overlooked is the fact that psychological factors can be involved in cases of chronic low back pain. Long before the monumental work of Freud, it was recognized that emotional states could be associated with physical symptoms in the absence of an organic pathology. Consequently, it behooves the primary spine care provider to learn how to identify these patients, how to diagnose their conditions, how to treat them, and how, when, and from whom to seek consultation. Unless chronic spinal pain is simultaneously understood and treated from a musculoskeletal and psychological perspective, treatment failure will be the norm. Treatment modalities directed only at a physical or mechanical problem will not be sufficient or helpful if there is an associated unrecognized or ignored psychological problem. Diagnosis is the cornerstone of a rational treatment approach to any kind of illness. Spine physicians confronted with a patient describing chronic or ongoing back pain are pressed to establish a diagnosis. Appropriately, any clues derived from the history and from the physical examination are pursued toward that end. Schemata describing the great classifications of disease illustrate the breadth and scope of physical pathologic conditions that can be associated with low back pain. Thus, the differential diagnosis in a patient presenting with chronic low back encompasses numerous entities. Clinical problems tend to become complex when there is difficulty in establishing a diagnosis or when then the treatment options are unclear or difficult to implement. In approximately a quarter of the patient population there is a coexisting lesion responsible for the patient’s symptoms. Up-to-date laboratory and imaging techniques notwithstanding, nothing supplants and nothing exceeds the diagnostic accuracy of a thorough history and a careful physical examination. Because the causes of back pain are legion and involve virtually every organ system as well as the psyche, a truncated history, focused only on the spine should be avoided. A tunnel vision, essentially blinding oneself, will only lead to diagnostic followed by therapeutic pitfalls.