Lumbar Facet Arthropathy

Bones of the spine articulate anteriorly by intervertebral disks and posteriorly by paired joints. The latter, formally known as zygapophyseal joints (but commonly termed facet joints), are true synovial joints, with a joint space, hyaline cartilage surfaces, a synovial membrane, and a fibrous capsule. Two medial branches of the dorsal rami innervate the facet joints. Medial branches of the lumbar dorsal rami issue from their respective intervertebral foramina, cross the superior border of the transverse process, and then run medially around the base of the facet joint before innervating the joints.[19]

In studies, autonomic nerves and nociceptive, substance P–immunoreactive nerve fibers have been identified in the lumbar facet joint capsule and synovial folds. Douglas and colleagues identified substance P–immunoreactive nerve fibers in erosion channels that extended through the subchondral bone and calcified cartilage into the articular cartilage. Giles and Harvey identified them in the inferior recess capsule and synovial folds, whereas Ashton and coauthors found them running freely in the facet capsule stroma.[20, 21] Grönblad and colleagues demonstrated sparsely distributed substance P–immunoreactive nerve fibers in facet joint plical tissue.[22]

The presence of nociceptive nerve fibers in the various tissue structures of facet joints, as well as the existence of autonomic nerves there, suggests that these structures may cause pain under increased or abnormal loads. Substance P is a well-known inflammatory mediator that may sensitize nociceptors to them and other mediators, resulting in chronic pain.

Like other joints, the facet joints consist of bone, cartilage, synovial tissue, and menisci that are rudimentary invaginations of the joint capsule. In the synovial fluid of patients with rheumatoid arthritis, osteoarthritis, or traumatic joint disease, increased levels of prostaglandins have been measured and are implicated as an important cause of pain. Prostaglandin, a known inflammatory mediator, also is released from facet joints.

A study by Netzer et al indicated that in patients with facet joint osteoarthritis associated with lumbar spinal stenosis, the subchondral bone in the osteoarthritic facet joints is characterized by the infiltration of macrophage-rich tissues into the marrow and by enhanced de novo bone formation.[23]

Biomechanically, facet joints assume a prominent role in resisting stress, and their importance is well established. A cadaveric study by Adams and Hutton demonstrated that the facet joints resist most of the intervertebral shear force and share in resisting the intervertebral compressive force, albeit only in lordotic postures.[24] In the rotation of the spine, the facet capsular ligaments are the spinal ligaments that undergo by far the most strain. They protect the intervertebral disks by preventing excessive movement.[25]

A study by Pan et al indicated that persons with LBP tend to have greater subchondral bone mineral density in their lumbar facet joints than do asymptomatic individuals, possibly as a result of “increased load bearing by the facets secondary to disc degeneration,” as well as “misdistribution of loading within the joint.”[26]

Frequency

United States

The prevalence of facet joint pain in the general population or in persons with acute back pain has not been investigated. The reported rate of facet joint pain for patients with chronic low back pain (LBP) ranges from 4-75%. The reported prevalence seems to be a function of the size of the sample studied and the conviction of the authors.

Three studies report the prevalence of lumbar facet joint pain among chronic LBP patients based on 100% relief of pain using less than 2 mL of intra-articular diagnostic injection. In 1988, Jackson and colleagues reported that 7.7% of 454 patients with chronic LBP had 100% relief with diagnostic injection.[27] In 1991, Carette and coauthors reported that 11 (5.8%) of 190 patients experienced complete relief of symptoms with a single lidocaine injection.[28] In 1994, Schwarzer and colleagues reported that 7 (4%) of 176 patients reported 100% relief.[29, 30] This last study was the most stringent of the 3 because the authors performed a second confirmatory block with bupivacaine, documenting longer relief of pain commensurate with the longer half-life of the local anesthetic.

When less stringent criteria are used, higher prevalences of lumbar facet joint pain are reported. In 1988, Moran and colleagues reported relief in 9 (16.7%) of 45 patients using 1.5 mL of bupivacaine.[31] Pain provocation followed by pain relief with local anesthetic was used as the diagnostic criterion. In 1992, Schwarzer and co-investigators reported relief in 9 (9.8%) of 92 patients, using a 50% reduction of pain as the criterion and employing double-block screening with lidocaine and confirmatory bupivacaine block.[32] In a separate investigation, Schwarzer and colleagues reported a prevalence of 26 (15%) of 176 patients, using the same diagnostic criterion.[29, 30]

In another study, Schwarzer and coauthors reported that 23 (40.3%) of 57 patients obtained pain relief of 50% or more pain with bupivacaine but experienced no relief with saline control injection.[33] A 2004 study by Manchikanti and colleagues reported a 27% prevalence rate of lumbar facet pain, using controlled, comparative local anesthetic blocks of the dorsal medial nerves.[34]

Higher prevalence rates are reported when control blocks are not used. In 1984, Raymond and Dumas—using a strict intracapsular technique but no control block—reported a 16% prevalence rate.[35] In 1992, Revel and coauthors reported that 22 (55%) of 40 subjects had pain relief of 75% or more and that 17 (42.5%) of 40 patients had greater than 90% relief of their pain with a single intra-articular lidocaine injection.[36]

As seen from these data, reports of prevalence are a function of the investigators' choice of selection criteria. Studies requiring the most stringent criteria (100% relief of symptoms after a diagnostic block) report a 4-7.7% prevalence rate of facet joint pain among chronic LBP patients. Investigations using double blocks and requiring 50% relief report prevalence rates of about 10-15%. Numerous other studies using a single diagnostic block report prevalence rates of 16-75%.

International

In a sample of 472 South Korean adults, aged 20-84 years, Ko et al found the prevalence of lumbar facet osteoarthritis, as derived through multidetector computed tomography (MDCT) scanning, to be 17.58%. The prevalence increased with age.[37]

See also Frequency/United States.

Mortality/Morbidity

No studies specifically address the mortality and morbidity of chronic back pain from facet joint – mediated pain. The mortality and morbidity of chronic low back pain, however, have been extensively addressed.

Race

No studies have specifically addressed the correlation between the prevalence of facet-mediated chronic low back pain and race.

Sex

No studies have specifically addressed the male-to-female prevalence ratio of chronic, facet-mediated low back pain.

Age

A higher prevalence among the older population would be expected if the etiology of facet joint–mediated back pain arose from degenerative changes of the joint, similar to the way it does in other osteoarthritic joint damage. One small study by Revel and colleagues and a larger investigation by Jackson and coauthors noted that older patients responded more commonly to diagnostic injections.[27, 36] The 1995 study by Schwarzer and colleagues involving 57 patients reported higher positive response rates in older patients (40%), even with the use of saline control injections.[33] They noted that the average age of patients was 59 years, which was higher than the average age in studies reporting much lower prevalence rates.

A 2008 report by Manchikanti et al looked at the rate of facet joint–related chronic low back pain in 424 patients, separated into 6 age groups.[38] According to their retrospective analysis, the prevalence ranged from 18% (in individuals aged 31-40 years) to 44% (in persons aged 51-60 years).

Little controversy surrounds the facet joint as a possible source of chronic low back pain (LBP). Innervation and possible inflammatory mediators of the joint have been elucidated. Pain upon provocation of the joint, relief upon anesthetization of the same joint in healthy volunteers, and chronic LBP in patients have been documented. Although initially described as a syndrome, investigators now prefer to term it facet joint pain. By definition, a syndrome is a group of signs and symptoms that occur together and characterize a particular abnormality; however, no signs or symptoms have been identified as unique to facet-mediated pain.[39]

A major source of frustration for clinicians has been the fact that no reliable means exist to document a clinical diagnosis of lumbar facet joint pain without the use of invasive techniques. If the true prevalence of facet joint pain was 40-75%, as initially reported, a clinical profile might not be crucial, because all chronic LBP patients would warrant investigation for this disorder. However, a prevalence of 10-15% would indicate that a clinical profile would be important in preventing the indiscriminate use of diagnostic and/or therapeutic blocks.

Biomechanical studies of the facet joint during extension and of facet capsular ligaments strained during rotation initially provided the belief that facet joint pain is worse with extension and rotation. Early studies by Helbig and Lee provided initial credence to this belief, but later studies by Revel and coauthors and by Schwarzer and colleagues did not support it.

Revel's investigation found that an increase in pain during hyperextension and extension-rotation was, in fact, less frequent in the group that responded to the facet joint injection than in the group that did not.[36]

The characteristics of lumbar facet joint pain include the following:

• Location of pain.

  • Lumbar facet joint pains are lateralized and can radiate below the knee. They rarely, if ever, cause axial or central back pain.

  • In their study of 26 patients selected by way of differential diagnostic blocks, Schwarzer and colleagues observed that no patients with central pain responded to diagnostic blocks of the facet joints.[29, 30] This study also refuted the commonly held notion that pain below the knee is unlikely to be referred from the facet joint.

• Clinical features of facet joint pain.

  • In their large 1988 study, Jackson and coauthors could not identify clinically specific facet syndromes or predict with any degree of accuracy which patients were more likely to respond to facet diagnostic blocks.[27] They concluded that facet syndrome is not a reliable clinical diagnosis.

  • Studies addressing the pattern of referred pain have been unable to distinguish pain from different levels. However, a generally held belief is that facet joint pain is more prevalent among the older population, is more lateralized, and is a more likely diagnosis when radiographic findings show severe facet arthritis.

See History.

The cause of most lumbar facet pain is unknown. On occasion, the lumbar facet joints are affected by systemic inflammatory arthritides, such as rheumatoid arthritis and ankylosing spondylitis. The following is a more specific look at sources of low back pain (LBP).[40]

Microtrauma

Microtrauma of the facet joints can produce pain. Small fractures, capsular tears, splits in the articular cartilage, and hemorrhage have been documented on postmortem studies of trauma victims who had normal radiographic findings. Whether these abnormalities were painful was not recorded.

Osteoarthritis

Osteoarthritis is another cause of lumbar facet joint pain. However, not all cases of facet arthritis are painful; the radiographic changes of osteoarthritis are as common in patients with LBP as in those without it. Some studies report that severely degenerated joints are more likely to cause symptoms. In a 2008 report, multidetector computed tomography (CT) scanning in 188 individuals revealed lumbar facet osteoarthritis in 59.6% of males and 66.7% of females.[41] In this study population, however, the report found no association between osteoarthritis at any level of the lumbar spine and the development of LBP.

Reports indicate that the orientation of the facet joints is associated with the development of spinal osteoarthritis. In a study of 150 patients, Linov et al found that a particularly sagittal orientation of the L4 and L5 facet joints appeared to be linked to the disease.[42]

A study by Yoshiiwa et al indicated that ligamentum flavum hypertrophy is related to severe facet joint osteoarthritis, as well as to lumbar segmental instability and severe disk degeneration and a sagittalized facet joint orientation.[43]

Synovial capsule distention and inflammation

Dory attributed LBP from facet syndrome to distention and inflammation of the synovial capsule, with resultant stimulation of the nociceptive nerve endings.[44] Expanded synovial recesses may also compress nerve roots in the spinal canal and neural foramina, which may explain the presence of radicular pain in patients with facet syndrome. Lippitt attributed pain in facet syndrome to a combination of synovitis, segmental instability, and degenerative arthritis.[45]

Rheumatoid arthritis

Using magnetic resonance imaging (MRI) scans, a study by Yamada et al of 201 patients with rheumatoid arthritis found erosion of the lumbar facets and endplates in 76.6% and 70.6% of patients, respectively, with the erosion occurring at 38.7% and 33.8% of intervertebral levels, respectively. Facet and endplate erosion both occurred most commonly at the midlumbar and lower-lumbar areas. A correlation was seen between facet erosion and the presence of spondylolisthesis.[46]

Other

Other theories regarding the causes of LBP include meniscoid entrapment, synovial impingement, joint subluxation, chondromalacia facette, capsular and synovial inflammation, mechanical injury to the joint capsule, and the restriction of normal articular motion from soft or articular causes.

A study by Hawellek et al found a positive correlation between the amount of cartilage calcification in the lumbar facet joints and degeneration of the facet joints and intervertebral disks. The study did not find cartilage calcification in the lumbar facet joints to be associated with patient age, although a correlation was found between age and cartilage calcification in the lumbar intervertebral disks.[47]

No specific laboratory studies are necessary when a diagnosis of lumbar facet arthropathy is being considered.

Abnormalities on plain radiographs, computed tomography (CT) scans, and magnetic resonance imaging (MRI) scans[14] are not specific for patients with back pain; degenerative changes are often found in asymptomatic persons. Although some clinicians may use plain radiography and CT scanning to investigate or even diagnose facet joint pain, no radiographic findings identify lumbar facet joints as the source of low back pain and referred lower extremity pain.[48]

A limited number of studies have attempted to establish correlation between osteoarthritic changes and response to blocking of the joints. While some earlier studies demonstrated such a relationship, others have failed to do so. Furthermore, findings from MRI scans, CT scans, dynamic bending radiographs, and radionuclide bone scans cannot be used to reliably help predict lumbar facet joint pain.

Schwarzer and colleagues concluded that CT scanning has no place in the diagnosis of lumbar facet joint pain.[49] They used the stringent criteria of 80% pain relief for the duration of bupivacaine anesthesia and negative relief with saline control injection. The investigators did not observe any correlation between CT-scan findings and response to diagnostic injections.

 

The use of diagnostic blocks is fundamental to a diagnosis of lumbar facet joint pain. Regardless of the symptoms, one characteristic that all patients with such pain share is the relief of pain once a local anesthetic has been injected. Fluoroscopically guided blocks of the joints constitute the only available standard to correlate with any clinical or radiographic test for facet joint pain.[13]

Single diagnostic blocks are a poor standard. Those employed without the provision of controls led to a false-positive rate of 38% in a lumbar study[29] and a 27% false-positive rate in a cervical study, with a 32% placebo rate in still another investigation. If an investigator relied on a single, uncontrolled block, 1 of every 3 apparently positive blocks would be a false positive. A reliable diagnosis must be accompanied by observation in relation to control subjects.

Control observation can be achieved either with saline injection around the joint while shielding the patient from view of the injections or through use of a confirmatory block. In a confirmatory block, relief achieved with the first local anesthetic is accompanied by relief provided by a second injection for a duration commensurate with the half-life of the second local anesthetic. A patient with genuine facet joint pain should experience relief with the first injection and feel no relief if injected with saline or, if injected with the confirmatory block, experience the same relief that he/she did with the first injection, but for a longer period of time.

The use of double blocks to confirm facet pain is not without limitations. When an appropriate duration of relief with a confirmatory block was required, Lord and colleagues found in cervical studies that specificity was high (88%) but that sensitivity was low (54%) in comparison with double-blinded, randomized, placebo-controlled triple blocks.[50] When diagnostic criteria for the double blocks were expanded to include all patients with reproducible relief, regardless of duration, sensitivity increased to 100% but specificity was lowered to 65%. The authors concluded that a clinician's choice of controls depends on the implications of the results. If innocuous therapy is prescribed, relief of pain, regardless of duration, with a double block may suffice. When diagnostic certainty is critical, such as in a medicolegal context or when surgical intervention is contemplated, placebo-controlled blocks are recommended.

The use of saline around the joint for control observation also has limitations. Of the various possible combinations of responses to 2 injections, pain relief in the same patient with local anesthetic and with saline poses a dilemma. The clinician could conclude that the patient does not have facet joint pain, having falsely responded to the local anesthetic and to the saline. However, a response to the saline injection does not necessarily negate the validity of the first injection with local anesthetic; it may instead indicate that the patient responded to a placebo. The individual may have true facet pain in addition to being a placebo responder. Because of this, some clinicians often proceed with RF neurotomy in patients who obtain 80% relief with lidocaine and with saline, depending on the clinical presentation. Studies are being conducted to report outcomes based on such an approach.

Facet diagnostic blocks can be performed intra-articularly and at the dorsal medial branches that supply the joint. The latter site is used if the joint is not accessible or as a means of avoiding the theoretical risk of needle damage to the joint. Barnsley and Bogduk found that local anesthetic blocks of the cervical medial branches are a specific test for the diagnosis of cervical facet joint pain. In their study, local anesthetic always reached the target nerve and did not affect any other diagnostically important structures.[51] Dreyfuss and colleagues determined that, with the use of appropriate technique, lumbar medial branch blocks are target specific.[52] The use of 0.5 mL of lidocaine adequately bathed the site of the target nerve and trivialized the spread to the dorsal root or the epidural spread to other potential pain generators.

With well-controlled studies reporting 7-14% prevalence rates for facet joint pain, clinicians must adopt stringent criteria for diagnosing facet joint pain. In this way, they can avoid unnecessarily subjecting a large portion of patients with chronic low back pain to various treatments aimed at facet joint pain.

Physical Therapy

No studies have compared the efficacy of one type of physical therapy over another in the treatment of lumbar facet arthropathy. Once the diagnosis of facet joint pain has been confirmed and pain has been brought under control with appropriate treatment, experienced clinicians generally recommend physical therapy for reconditioning, as well as lumbar stabilization exercises.

Currently, no surgical intervention is advocated for lumbar facet joint pain.

The diagnosis of lumbar facet arthropathy (LFA) can be made by a practitioner who is proficient in diagnostic spinal injections and who has specialty training in musculoskeletal spine medicine. Interventional physiatrists are uniquely qualified to evaluate LFA because they possess the technical skills required to administer spinal injections and have an appreciation of musculoskeletal medicine.

Facet joint pain is usually not considered until conservative measures for treating low back pain (LBP) have been tried without success. No current studies advocate or assess the efficacy of specific physical therapy or manipulations aimed at treating facet joint pain.

Treatments for facet joint pain include (1) intra-articular steroid/local anesthetic injection under fluoroscopic guidance (see images below) and (2) radiofrequency ablation to block the joint from all sensory input. Some authorities have also advocated the use of pulsed radiofrequency[15] at a lower temperature. Prior to radiofrequency ablation, medial branch blocks or intra-articular facet injections are typically done. Medial branch blocks appear to have better prognostic outcomes than intra-articular facet injections.[16]  A retrospective study by Han et al found that in patients with chronic lower lumbar facet joint pain, medial branch blocks did not differ significantly in analgesic effect or resulting functional improvement whether administered using ultrasonographic or fluoroscopic guidance. However, the time needed to perform ultrasonographically guided medial branch blocks was significantly shorter than that for the fluoroscopically guided blocks.[53]

A retrospective study by Nedelka et al indicated that shock-wave therapy produces better long-term results in alleviating lumbar facet joint pain than do corticosteroid injections and suggested that the treatment is almost as effective as RF neurotomy. The report, on 62 patients with unilateral chronic lumbar facet pain, also found that shock-wave treatment and RF neurotomy provided long-term improvement in the performance of daily activities.[54]

Another treatment option is surgical fusion of the joint, but no published reports describe such treatment for lumbar facet arthropathy.

Details about treatment with injection or ablation are as follows.

Intra-articular facet joint injection

Numerous early studies of this procedure are not worth mentioning because of their serious flaws with diagnostic criteria, the location of injections, and the injection volumes used. A study by Lynch and Taylor was able to demonstrate that intra-articular injection was superior to extra-articular injection, but, after 6 months of follow-up, the statistical significance had disappeared.[55]

In 1989, Lilius and colleagues prospectively studied 109 patients with chronic LBP. They were distributed randomly into 1 of 3 groups that received injections of intra-articular cortisone/anesthetic, intra-articular saline, or pericapsular cortisone/anesthetic. Although pain relief was substantial, with 36% of patients reporting benefits that persisted for up to 3 months, no significant differences were noted between groups. These results led the authors to conclude that facet joint injection is a nonspecific method of treatment and that good results reflect the tendency of LBP to undergo spontaneous remission. Two critical flaws are noted in this study. First, the authors did not preselect subjects with diagnostic facet joint injections. Second, the intra-articular facet joint injection volumes of up to 8 mL were excessive.

In 1991, a controlled study by Carette and coauthors randomized patients into 2 groups; one group received an intra-articular methyl prednisolone/local anesthetic mixture and the other received intra-articular saline.[28] Patients were preselected with local anesthetic into the facet joints at L4-5 and L5-S1 and reported pain relief of greater than 50%. When the patients were tracked for 6 months, no difference in pain relief was noted between the 2 groups, with the data suggesting that intra-articular facet joint injections with corticosteroids were not effective in treating chronic LBP. This study was flawed in that only a single lidocaine injection, which is subject to false-positive readings and placebo responses, was used to determine the presence of facet joint pain. Furthermore, the assumption that saline is a true inert placebo may be flawed.

Other studies have shown that saline provides pain relief to a greater degree than would be expected from placebo. At 6-month follow-up, 46% of the steroid group and 15% of the saline group had good pain relief; however, the authors invalidated this finding because only a portion of both groups that reported pain relief at 1 month had actual pain relief at 6 months.

A study by Huang indicated that fluoroscopically guided lumbar facet joint injections employing an interlaminar approach and loss-of-resistance technique can provide a successful alternative means of injecting osteoarthritic facet joints, particularly when osteophytes and/or extreme joint curvature in the transverse plane interfere with direct posterior access to severely arthritic joints.[56]

RF neurotomy

Five controlled studies of RF neurotomy of the dosal medial nerve branch have reported on the effectiveness of this procedure, and 1 study has reported on the effectiveness of repeated RF neurotomy for lumbar facet pain.

In the first study, from 1994, Gallagher and colleagues reported successful outcomes at up to 6 months of follow-up in patients who were treated with RF, compared with those who underwent sham treatments.[57] Single intra- or extra-articular diagnostic injections were used, with an inclusion criterion of good or equivocal response. Shortcomings of the study were the small number of subjects, short duration of follow-up, and poor diagnostic criteria. Differential blocks were not used.

In the second study, from 1999, van Kleef and coauthors reported that a 1-year follow-up, significant pain reduction was found in 7 of 15 patients who were treated with RF, compared with 2 of 15 patients who had undergone sham treatment.[58] The diagnostic criterion was a single diagnostic joint injection with subsequent pain relief of 50% or more. Shortcomings of the study were the number of subjects and the fact that differential blocks were not used.

In the third study, from 2000, Dreyfuss and co-investigators reported a rate of successful outcome of 87% at 1-year follow-up in 15 patients; the individuals were treated with RF after successful differential diagnostic injections.[59] Weaknesses of this study were the number of subjects and the lack of a control group. However, strict diagnostic criteria were used, including 80% pain relief and differential blocks with lidocaine and bupivacaine.

In the fourth study, from 2001, Leclaire and colleagues reported on 70 patients who were randomized to RF treatment versus sham treatment after single diagnostic facet injections yielded good pain relief.[60] No differences in outcome between the groups were noted at 12 weeks of follow-up. A large patient population was used, but the diagnostic criterion was poor. Single diagnostic injections with good relief are not valid to differentiate a facet joint pain population.

In the fifth study, from 2005, van Wijk and coauthors reported on 81 patients randomized to RF treatment versus sham treatment after a single diagnostic facet joint injection yielded 50% pain relief.[61] No differences in outcome were noted between the groups. This study was again flawed by the limitation of single diagnostic injections. Careful reading of the study shows that although the authors reported on 462 patients, after accounting for excluded patients and dropouts, 37 had negative responses to the diagnostic injection and 81 had positive responses to the diagnostic injection, yielding an unusually high prevalence of facet joint pain.

In 2004, Schofferman and Kine retroactively reported on the effectiveness of repeated RF neurotomy for lumbar facet pain.[62] In 20 patients who had undergone a repeat RF treatment, an 85% success rate at a mean duration of 11.6 months was achieved.

Conclusions

Of the first 5 studies reviewed above, 3 showed favorable outcomes, and 2 did not. Although the 2 studies that demonstrated no significant favorable outcomes utilized a larger population of patients, their use of a single diagnostic injection and their employment of a rather loose inclusion criterion of 50% pain relief or good pain relief were inadequate for differentiating a facet joint population. The study that used a strict 80% pain relief with differential block criterion did demonstrate a rather high success rate with RF treatment. However, this study lacked a control group.

RF ablation appears to be safe, with most studies reporting no associated complications. The complications that have been previously reported related to electrical faults and included cases of small superficial burns. A 2004 report by Kornick and colleagues on 616 treated lesions showed a 1% complication rate for neuritis.[63] The investigators reported no other complications.

In 2013, the American Society of Interventional Pain Physicians (ASIPP) released an update of their guidelines for interventional techniques in patients with chronic spinal pain. The guidelines state that evidence for the therapeutic efficacy of lumbar facet joint nerve blocks is fair to good but that there is only limited evidence for the efficacy of intra-articular lumbar injections.[17, 18]

The ASIPP guidelines also state that there is good evidence for the therapeutic efficacy of RF ablation in lumbar facet joint interventions but that evidence for the efficacy of pulsed RF is limited.[17, 18, 64]

A literature review by Manchikanti et al found level II evidence for long-term lumbar spine improvement with RF neurotomy and level III evidence for long-term improvement with lumbosacral intra-articular injections.[1]

American Society of Pain and Neuroscience

Best practice guidelines from the American Society of Pain and Neuroscience on RF neurotomy included the following for the lumbar spine[65] :

• Lumbar RF neurotomy (LRFN) is primarily employed for symptoms of low back pain with no radicular symptoms
• MRI or CT scanning should be used prior to LRFN, to rule out other possible etiologies; imaging, however, is not effective in diagnosing facet-mediated pain, and the use of LRFN is not necessarily excluded by the presence of discogenic changes
• In terms of success with LRFN, intra-articular facet injections are generally considered to be less predictive than medial branch blocks
• In instances of recurrent pain, repeat LRFN’s efficacy has been found to be highly reproducible
• Although additional evidence is needed, electrodes are optimally positioned parallel to the target nerves
• Prior to LRFN, in order to make sure that the electrode tip has been appropriately placed and to avoid unintentional lesioning of the ventral ramus or other structures, motor and sensory testing is recommended
• The supporting evidence is strongest for the use of conventional thermal RF (60-80°C) for 60-90 seconds

Nonsteroidal anti-inflammatory drugs (NSAIDs) are recommended for medical therapy for lumbar facet arthropathy (LFA). Peripherally acting analgesics include NSAIDs and acetaminophen. NSAIDs are the DOC in the initial pharmacologic treatment of acute episodes of LFA or following acute exacerbation of chronic pain.

Class Summary

Have analgesic, anti-inflammatory, and antipyretic activities. Their mechanism of action is not known, but they may inhibit cyclo-oxygenase (COX) activity and prostaglandin synthesis. Other mechanisms may include inhibition of leukotriene synthesis, lysosomal enzyme release, lipoxygenase activity, neutrophil aggregation, and various cell membrane functions.

Aspirin (Anacin, Bayer Aspirin, Ascriptin)

Best-known NSAID. It is widely available and has cardioprotective, cerebroprotective, and anticoagulation properties. Aspirin treats mild to moderate pain. The drug inhibits prostaglandin synthesis, which prevents the formation of platelet-aggregating thromboxane A2.

Ibuprofen (Ibuprin, Motrin)

DOC for patients with mild to moderate pain. The drug inhibits inflammatory reactions and pain by decreasing prostaglandin synthesis.

Naproxen (Naprelan, Naprosyn, Aleve)

For the relief of mild to moderate pain. Naproxen inhibits inflammatory reactions and pain by decreasing the activity of COX, which results in decreased prostaglandin synthesis.

Nabumetone (Relafen)

Nonacidic NSAID that is rapidly metabolized after absorption, becoming a major active metabolite that inhibits the COX enzyme (thereby inhibiting pain and inflammation).

Ketorolac (Toradol)

Inhibits prostaglandin synthesis by decreasing the activity of COX, which results in the decreased formation of prostaglandin precursors.

Class Summary

Although increased cost can be a negative factor, the incidence of costly and potentially fatal GI bleeding is clearly less with COX-2 inhibitors than with traditional NSAIDs. Ongoing analysis of cost and avoidance of GI bleeding will further define populations that will most benefit from COX-2 inhibitors.

Celecoxib (Celebrex)

Primarily inhibits COX-2. COX-2 is considered an inducible isoenzyme; it is induced by pain and inflammatory stimuli. The inhibition of COX-1 may contribute to NSAID GI toxicity. At therapeutic concentrations, COX-1 isoenzyme is not inhibited; thus, the incidence of GI toxicity, such as endoscopic peptic ulcers, bleeding ulcers, perforations, and obstructions, may be decreased in comparison with nonselective NSAIDs. Seek the lowest dose for each patient.

COX-2 neutralizes circulating myelin antibodies through anti-idiotypic antibodies; down-regulates pro-inflammatory cytokines, including INF-gamma; blocks Fc receptors on macrophages; suppresses inducer T and B cells and augments suppressor T cells; blocks complement cascade; promotes remyelination; and may increase CSF IgG (10%).

COX-2 has a sulfonamide chain and is primarily dependent on cytochrome P450 enzymes (hepatic enzymes) for metabolism.

Class Summary

Analgesics ensure patient comfort, promote pulmonary toilet, and have sedating properties, which are beneficial for patients who experience pain.

Acetaminophen (Tylenol, Feverall)

Ensures patient comfort, promotes pulmonary toilet, and has sedating properties

See the list below:

• Various treatments are available in an outpatient setting for patients with facet joint arthropathy. Please refer to the Treatment section for a more complete discussion.

See the list below:

• Lumbar facet arthropathy does not require inpatient management; outpatient workups and treatments are adequate.

See the list below:

• Patients need to be educated in all aspects of their diagnosis and to be informed of all treatment options. As with any condition affecting the back, patients need to have a good understanding of proper body mechanics and back safety techniques; they also require daily activities to prevent worsening of symptoms. Participation in physical therapy may be helpful in improving spinal range of motion and strength. The patient should be instructed in a lumbar spine stabilization program when appropriate.

• For excellent patient education resources, see eMedicineHealth's patient education articles Low Back Pain, Chronic Pain, and Pain Medications.