The Journal of Bone & Joint Surgery

The Journal of Bone & Joint Surgery, Volume 88, Issue suppl 2

Workshop Articles | April 01, 2006

Pain Generation in Lumbar and Cervical Facet Joints

John M. Cavanaugh, MD; Ying Lu, MS; Chaoyang Chen, MD; Srinivasu Kallakuri, MS

Note: The authors are grateful for the technical assistance of Amrita Vempati, Anita Singh, and Sowmya Surapaneni.

In support of their research for or preparation of this manuscript, one or more of the authors received grants or outside funding from the United States Centers for Disease Control and Prevention (CDC Grants # R49-CCR519751 and # R49-CE000455). None of the authors received payments or other benefits or a commitment or agreement to provide such benefits from a commercial entity. A commercial entity paid or directed, or agreed to pay or direct, benefits to a research fund, foundation, educational institution, or other charitable or nonprofit organization with which the authors are affiliated or associated (a Ford Biomedical Engineering Graduate Fellowship was provided by the Ford Motor Company).

The Journal of Bone and Joint Surgery, Incorporated

J Bone Joint Surg Am, 2006 Apr 01;88(suppl 2):63-67. doi: 10.2106/JBJS.E.01411

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Abstract

Facet joints are implicated as a major source of neck and low-back pain. Both cervical and lumbar facet syndromes have been described in the medical literature. Biomechanical studies have shown that lumbar and cervical facet-joint capsules can undergo high strains during spine-loading. Neuroanatomic studies have demonstrated free and encapsulated nerve endings in facet joints as well as nerves containing substance P and calcitonin gene-related peptide. Neurophysiologic studies have shown that facet-joint capsules contain low-threshold mechanoreceptors, mechanically sensitive nociceptors, and silent nociceptors. Inflammation leads to decreased thresholds of nerve endings in facet capsules as well as elevated baseline discharge rates. Recent biomechanical studies suggest that rear-end motor-vehicle impacts give rise to excessive deformation of the capsules of lower cervical facet joints. Still unresolved is whether this stretch is sufficient to activate nociceptors in the joint capsule.

To answer this question, recent studies indicate that low stretch levels activate proprioceptors in the facet-joint capsule. Excessive capsule stretch activates nociceptors, leads to prolonged neural afterdischarges, and can cause damage to the capsule and to axons in the capsule. In instances in which a whiplash event is severe enough to injure the joint capsule, facet capsule overstretch is a possible cause of persistent neck pain.

Figures in this Article

Lumbar Facet Pain

In a review of the lumbar facet syndrome, Mooney and Robertson¹ noted that the etiology of persistent pain arising from this joint remained elusive and pointed out that there appeared to be no conclusion as to why degenerative joints can be asymptomatic while normal-appearing joints can be painful. Schwarzer et al.² injected the lumbar facet joints of 176 patients who had nonspecific low-back pain and no definitive radiologic findings. Of these patients, 15% had pain relief with a shorter-acting anesthetic (lignocaine) and =50% improvement in pain with a longer-acting anesthetic (bupivacaine).

Biomechanical studies have confirmed or shown the contribution of the facets to load transmission in the spine and have indicated the possibility of facet overload. Yang and King³ showed that the lumbar facet superior articular process bottoms out on the lamina below when forces replicating the spinal extensor muscles are used to resist flexion loads. This loading also caused high strains to the facet-joint capsule⁴.

In a neurophysiologic study with use of a rabbit model, thirty mechanosensitive units were identified at the lumbar facet joint and twenty-seven were identified in the muscles and tendons near their insertion into the facet⁵. The facet joint contained a much higher proportion of high-threshold, low-conduction velocity units than muscle did. It is these latter units—nociceptors—that are likely to transmit pain. In rabbit facet joints injected with Type-II carrageenan, the multiunit background discharge rate showed an increase that can be divided into two phases—a first phase from zero to thirty minutes, and a second phase from forty-five to 150 minutes⁶. Units that were previously silent appeared in the first fifteen minutes and persisted beyond seventy-five minutes. Thresholds of the characterized units ranged from 1.23 g to >30 g and decreased with time. Histologic examination revealed inflammatory changes in carrageenan-injected tissues, vasodilatation and edema in the capsule, and leukocyte infiltration in the perivascular space within surrounding muscle tissue. In another study, after the injection of substance P (10 µg) into rabbit lumbar facet-joint receptive fields, 54.2% of the units showed immediate onset and 29.2% of the units showed slow onset of the excitation⁷. One-third of the units showed decreased von Frey threshold responses after the application of substance P. These neurophysiologic studies reveal the following in support of lumbar facet pain of capsular origin: (1) a population of high-threshold, small-diameter sensory neurons in the capsule, (2) sensitization and increased discharge of facet-joint neurons in the presence of inflammation, and (3) demonstration of the effects of substance P on these neurons. In addition, Beaman et al.⁸ demonstrated substance P-containing nerves in subchondral bone in osteoarthritic facet joints, which suggests that facet pain of subchondral origin may also occur in cases of joint degeneration.

Cervical Facet Pain

Whiplash-associated disorders are among the most common injuries associated with motor-vehicle accidents. In the United States, more than 59% of insurance claimants for motor-vehicle injury reported neck injuries in 1997⁹. Studies of the natural history of whiplash-associated disorders have suggested that chronic pain with continued symptoms develops in 6% to 33% of acutely injured victims¹⁰. The societal cost of whiplash injury, including medical and legal expenses, is enormous, as high as $29 billion annually in the United States alone¹¹.

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Figs. 1-A and 1-B: Surgical preparation and positioning of capsule markers. Two holes are shown drilled in the rostral end of the freed C5 process to attach it to the actuator via two stainless-steel hooks. (Reproduced, with modification, from: Lu Y, Chen C, Kallakuri S, Patwardhan A, Cavanaugh JM. Neurophysiological and biomechanical characterization of goat cervical facet joint capsules. J Orthop Res. 2005;23:779-87. Reprinted with permission.) Loading paradigm for quasistatic tests. Tests were run in 2-mm increments with a four-minute rest period between tests. Each load pattern consisted of a 0.5 mm/sec loading ramp, a ten-second hold, and a 0.5 mm/sec unloading ramp. FJC = facet-joint capsule.

Many research studies have focused on determining the mechanisms of whiplash injury and appropriate countermeasures. Several regions of the cervical spine are postulated to be a source of whiplash injury and pain generation, including facet joints, intervertebral discs, ligaments and muscles, and spinal nerve roots. Dwyer et al.¹² injected the C2-C3 to C6-C7 facet joints and Dreyfuss et al.¹³ injected the lateral atlantoaxial and atlanto-occipital joints with contrast medium under fluoroscopic control to determine if they are potential pain generators. Injection into each joint produced pain patterns replicating clinical neck-pain patterns.

The incidence of cervical facet pain appears to be greater than that of lumbar facet pain. In a study reported by Aprill and Bogduk¹⁴, 128 patients with chronic neck pain underwent diagnostic blocks to the cervical facets; eighty-two obtained complete relief of pain. To account for false positives, a second study was performed on fifty consecutive patients¹⁵ with use of lignocaine and bupivacaine. Of thirty-eight patients who completed the study, twenty-seven had pain relief from both injections and longer-duration relief with bupivacaine. The prevalence of cervical facet pain was concluded to be at least 54% (twenty-seven of fifty). A similar study indicated that 55% of patients with chronic, nonspecific cervical spinal pain had pain of facet origin¹⁶.

A chronic pain condition (late whiplash syndrome) without detectable lesions was reported to occur in subjects with a whiplash injury of the neck^17,18. The facet joint is a potential source of pain in these cases. Percutaneous radiofrequency neurotomy of the dorsal rami branches was shown to offer pain relief by denaturing the nerves that innervate the facet joint at the level of pain¹⁹. Long-term relief can be maintained by multiple treatments to overcome axon regeneration. Kallakuri et al.²⁰ demonstrated nerve profiles that were immunoreactive to substance P and calcitonin gene-related peptide in human cervical facet-joint capsules, strongly suggesting that the capsule does contain nerves that can signal pain.

Several facet-joint injury mechanisms have been proposed, including facet-joint impingement, synovial fold pinching, and facet-joint capsule strain injury. Krafft et al.²¹ studied crash recorder-equipped cars and noted no neck injury in impacts with peak accelerations of 6 g or less, temporary neck symptoms at 10 g or less, and long-term disability at 13 g and 15 g. The magnitude of facet-joint capsule deformation in these higher "g" whiplash events may possibly result in capsular injury and persistent pain.

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Fig. 2: Neural response of a group-IV unit to 18-mm stretch. (Top) A: Single unit histogram. Only the discharges that template-matched the waveform of the unit were counted. The afterdischarge was evident for more than four minutes. Only 125 seconds of the time course is shown here (twenty-five seconds per division). (Middle) B: Capsule load. (Bottom) C: Actuator displacement scheme. (Reprinted, from: Lu Y, Chen C, Kallakuri S, Patwardhan A, Cavanaugh JM. Neural response of cervical facet joint capsule to stretch: a study of whiplash pain mechanism; with permission of the Stapp Association. Stapp Car Crash J. 2005;49:49-56.)

Recent Studies Addressing Cervical Facet Pain

To study the possible link between facet capsule stretch and pain generation, our group has developed an in vivo goat model for neurophysiologic and mechanical characterization of facet-joint capsules in the cervical spine^22-25. These studies are summarized below.

Materials and Methods

Adult LaMancha or Alpine anesthetized female goats (33 to 55 kg) were used. A C4-C7 laminectomy was performed to expose the C6 dorsal rootlets. The spinal cord and roots were immersed in mineral oil at 37°C. The left C5-C6 facet joint was isolated and the C5 inferior articular process was then freed from the pedicle. Two stainless-steel hooks were inserted into holes in this process and connected to an actuator system. A spine fixator, a stereoimaging system, and a computer-controlled actuator coupled with a miniature 50-lb load cell were used to stretch the C5-C6 capsule and measure load and strain²³. An array of tantalum spheres or acrylic paint targets was applied on the capsule surface (Fig. 1-A) for later strain characterization.

Neural activity of the left C6 dorsal rootlets was recorded with a custom-designed miniature bipolar electrode as described by Chen et al.²² (Fig. 1-A). Electrical stimuli (0.1 or 0.3 msec duration, 8 or 15 V) were then applied to the capsule at nine locations with a bipolar stimulating electrode. The facet-joint capsule then underwent a series of stretch tests at a loading and unloading rate of 0.5 mm/sec. The first test included 2-mm actuator displacement, followed by increases, in 2-mm increments, for subsequent tests until the capsule sustained rupture (Fig. 1-B).

Waveforms of single sensory units were identified by the action potentials evoked by electrical stimulation. Each waveform was then used as a template by matching the waveform to the individual unit in the multiunit discharge²³. Image-tracking software was used to track the capsule targets, and linear quadrilateral membrane elements were developed with use of the target positions as nodes. Digitized marker-displacement history was imposed on the nodes to reconstruct capsule deformation, and finite element strain analysis was performed. The finite elements at the targets were used to describe strain distribution at the nine electrically stimulated areas in which sensory units were identified. Thus, the strain history of a corresponding element was approximated for each unit. An illustration of the data collected from a group-IV unit in an 18-mm stretch test is shown in Figure 2²⁵.

Results

The following findings are presented in greater detail by Lu et al.^24,25. Strains of 30% to 41% at the 12-mm stretch test and below did not produce apparent tissue damage. Between the 12-mm stretch and the 22-mm stretch, progressive capsular injury occurred. At the 22-mm stretch, the capsule strains ranged from 41% to 73%, beyond which the capsules typically ruptured. Fifty units were analyzed for their neural properties in relation to strain. These units were categorized by their conduction velocity into thirty-two group-III (thinly myelinated fibers) and eighteen group-IV (unmyelinated C fibers) units. Forty-two units responded to stretch with low-strain thresholds (10.2% ± 4.6%), while eight units responded only to high strains (47.2% ± 9.6%). No significant difference was observed in threshold between groups III and IV. Thirty-five of the forty-two low-strain threshold units displayed discharge saturation at the strains of 44.2% ± 16.7%. No significant difference was seen in saturation threshold between groups.

Twelve low-threshold units and two high-threshold units exhibited afterdischarge. Afterdischarge lasting longer than thirty seconds but less than four minutes occurred after peak strains of 38.5% ± 12.4%; afterdischarge lasting longer than four minutes appeared after 45.0% ± 15.1% strains.

Discussion

Lu et al.²⁵ demonstrated a quantitative relationship between capsule sensory discharges and applied capsule stretch from cervical facet joints. Their study indicated that capsular strains of 47.2% ± 9.6% are most likely noxious and trigger nociceptive discharges from the capsules, which are transmitted to the central nervous system for pain sensation. Strains that correspond to the onset of nociceptive discharge and to afterdischarge may indicate strain ranges that are injurious or painful in whiplash²⁶. In contrast, most of the capsular neural receptors responded in the physiologic range of capsule stretch and fired at strains of 10.2% ± 4.6%.

A majority (83%) of low-threshold units showed saturated responses at high strains of 44.2% ± 16.7%. These responses may play a role in warning the body of potential injury. Similar observations were made in studies in other tissues in which saturation occurred in response to higher-magnitude mechanical stimuli of different modes, including tension, compression, and joint rotation.

This study demonstrated high strain thresholds at 47.2% ± 9.6% for nociception and saturation strains at 44.2% ± 16.7%. These are comparable with the strains that lower cervical facet-joint capsules experienced during whiplash loading, and also fall within the range of partial failure strains in human cadaver facet-joint capsule studies^27,28. Thus, this study supports a capsule-strain-injury mechanism of whiplash and further provides a neurophysiologic basis for it.

Persistent afterdischarge was observed in this study after capsular strains of 45.0% ± 15.1% and may be related to nerve injury or capsular injury with the release of inflammatory mediators into the surrounding tissue. This peripheral sensitization may lead to central sensitization of pain pathways in the spinal cord. Spinal cord sensitivity can be seen within minutes of tissue injury²⁹. More vigorous and longer-lasting afterdischarge may lead to more extensive central sensitization, which may eventually evolve to chronic whiplash pain. Several studies have observed central hypersensitivity to neck stimulation in whiplash patients^30-33.

Our preliminary data demonstrated that axonal swelling and retraction balls (indicators of axonal injury) occurred after capsule strains of 62% to 82%. These axonal changes may lead to hyperexcitability, spontaneous firing, and neuropathic pain³⁴.

Conclusions

Clinical studies indicate that the facet joint is the origin of a good percentage of lumbar and cervical spinal pain. Studies using diagnostic blocks suggest that the incidence of cervical facet pain is higher than that of lumbar facet pain. Many of these patients have no obvious radiographic abnormalities, and pain may be of capsular origin. Biomechanical studies support overstretch of cervical facet-joint capsules as a possible source of whiplash injury. The neurophysiologic studies reported here support injured facet-joint capsules as a source of the facet syndrome. These latter studies demonstrate high-threshold nociceptors, saturation of mechanoreceptors, and afterdischarges at high strains. Inflammation of the facet joints leads to elevated baseline discharge and decreased thresholds of capsule receptors. High capsular strain may also lead to damaged axons in the capsular tissue, which may then lead to persistent pain. ?

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Topics

pain ; whiplash injuries ; zygapophyseal joint

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John M. Cavanaugh, Ying Lu, Chaoyang Chen, Srinivasu Kallakuri; Pain Generation in Lumbar and Cervical Facet Joints. The Journal of Bone & Joint Surgery. 2006 Apr;88(suppl_2):63-67.

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