Lumbar Zygapophyseal Joint Back Pain

PATHOPHYSIOLOGY

LZ joint pain primarily results from repetitive load-bearing strain accumulated over a lifetime; rarely, LZ joint arthropathy is traced to one inciting event. During midlife, cartilaginous changes accelerate, and subchondral sclerosis and osteophytes growth are commonly observed phenomena. Intervertebral disk disease is the initial site of spinal degeneration; facet joint deterioration subsequently develops secondary to biomechanical effects. Mechanical consequences of disk degeneration include reduced disk height and segmental microinstability leading to increased facet load. This provokes joint subluxation and cartilage alteration with subsequent facet joint degeneration.

Rheumatoid arthritis, ankylosing spondylitis, synovial impingement, chondromalacia facetae, pseudogout, meniscoid entrapment, and capsular/synovial inflammation also predispose to chronic facet joint strain.

Lumbar facet joints are richly innervated with encapsulated, unencapsulated, and free nerve endings, and contain substance P, calcitonin gene–related peptide (CGRP), as well as neuropeptide Y. Nerve fibers occur within subchondral bone and intra-articular inclusions of lumbar zygapophyseal joints, thus signifying that facet-mediated pain may originate beyond the joint capsule. In models of degenerative lumbar spinal disorders, inflammatory mediators, such as prostaglandins and the inflammatory cytokines (interleukin [IL]-1beta, IL-6, and tumor necrosis factor-alpha [TNF]-alpha), occur within facet joint cartilage and synovial tissue.

PAIN-REFERRAL PATTERNS

Lumbar facet joints produce pain referred into the groin. Pain emanating from upper facet joints tends to extend into the flank, hip, and upper lateral thigh, whereas pain from the lower facet joints penetrates deeper into the posterolateral thigh.

CLINICAL PICTURE

Clinically, LZ joint–mediated back pain overlaps considerably with multiple other LBP etiologies. Although LZ joint pain is not associated with anatomically specific neurologic deficits, patients experiencing this referred somatic pain may demonstrate a pain-inhibited nonmyotomal weakness. Similarly, these individuals also report a nondermatomal referred extremity sensoryloss–type complaints reaching as far distal as the foot.

There are no specific radiographic computed tomography (CT) facet joint abnormalities identified to provide firm diagnosis of facet-mediated LZ pain. Single photon emission–computed tomography (SPECT) bone scintigraphy may sometimes help identify active inflammation with some facet-mediated sources in low back pain individuals.

LZ joint–mediated pain is a diagnosis made primarily by exclusion of other possible etiologies (see Plate 8-13). This is difficult to confirm, however; positive results with controlled analgesic injections may be supportive of this diagnosis. These nerve blocks are accomplished in two ways. The more reliable method targets the small nerve fibers branching from the dorsal spinal root known to innervate the facet joints, with the so-named medial branch block. Intra-articular anesthetic injection is also performed after an appropriate arthrogram. However, these injections have never been tested for validity.

MANAGEMENT

Controlled prospective studies comparing varied LZ joint pain treatments are limited despite increasing number of interventional therapies targeted at these joints. Conservative treatments, including medications, physical therapy, or manual therapy, lack specific analgesic efficacy for the joint pain per se. Nevertheless these modalities provide standard first-line treatment for acute-onset LBP.

Intra-articular steroid injection for treatment of LZ joint pain is a somewhat controversial subject. However, in general, it is concluded that intra-articular steroid injections may provide intermediate-term relief to LZ joint pain patients who appear to have active inflammation.

Lumbar medial branch neurotomy (LMBN) has the most evidence-based support. The thermal coagulation probe used for a medial branch neurotomy denaturates nerve proteins; therefore this provides a more superior clinical effect than medial branch anesthetic block. Several clinical trials have demonstrated LMBN efficiency in the treatment of LZ joint pain.

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