Cohen, Steven P. MD
The sacroiliac (SI) joint is the largest axial joint in the body, with an average surface area of 17.5 cm2 (1). There is wide variability in the adult SI joint, encompassing size, shape, and surface contour. Large disparities may even exist within the same individual (2,3). The SI joint is most often characterized as a large, auricular-shaped, diarthrodial synovial joint. In reality, only the anterior third of the interface between the sacrum and ilium is a true synovial joint; the rest of the junction is comprised of an intricate set of ligamentous connections. Because of an absent or rudimentary posterior capsule, the SI ligamentous structure is more extensive dorsally, functioning as a connecting band between the sacrum and ilia (4). The main function of this ligamentous system is to limit motion in all planes of movement. In women the ligaments are weaker, allowing the mobility necessary for parturition (Figs. 1 and 2).
The SI joint is also supported by a network of muscles that help to deliver regional muscular forces to the pelvic bones. Some of these muscles, such as the gluteus maximus, piriformis and biceps femoris, are functionally connected to SI joint ligaments, so their actions can affect joint mobility. The potential for vertical shearing is present in approximately 30% of SI joints, owing to the more acute angulation of the short, horizontal articular component (5).
Age-related changes in the SI joint begin in puberty and continue throughout life. During adolescence, the iliac surface becomes rougher, duller, and coated in some areas with fibrous plaques. These senescent changes accelerate during the third and fourth decades of life and are manifested by surface irregularities, crevice formation, fibrillation and the clumping of chondrocytes. Degenerative changes on the sacral side generally lag 10–20 yr behind those affecting the iliac surface. In the sixth decade, motion at the joint may become markedly restricted as the capsule becomes increasingly collagenous and fibrous ankylosis occurs. By the eighth decade of life, erosions and plaque formation are inevitable and ubiquitous (4).
The innervation of the SI joint remains a subject of much debate. The lateral branches of the L4-S3 dorsal rami are cited by some experts as composing the major innervation to the posterior SI joint (1). Other investigators claim that L3 and S4 contribute to the posterior nerve supply (6,7). The innervation of the anterior joint is similarly ambiguous. Early 20th century German literature asserts the anterior SI joint is supplied by the obturator nerve, superior gluteal nerve and the lumbosacral trunk (8). More recent literature suggests the anterior joint is innervated by L2-S2 (1), L4-S2 (9), and the L5-S2 ventral rami (10). Some authors have even suggested that the anterior SI joint is devoid of nervous tissue (7,11). In a study testing the ability of L5 dorsal ramus and S1-4 lateral branch blocks to protect the SI joint from an experimental stimulus, 6 of 10 subjects retained the ability to perceive ligamentous probing (12).
A neurophysiologic study conducted in cats identified 29 mechanosensitive afferent units, 26 of which were found in the joint capsule and 3 in adjacent muscles (13). Twenty-eight of these units were classified as nociceptive and 1 as proprioceptive. Among these 29 receptive fields, 16 were located in the proximal third of the posterior SI joint and 11 in the middle third. The average mechanical threshold of an SI joint nociceptive unit was 70 g, as compared to the 6 g mean mechanical threshold for lumbar facet joint nociceptive units and the 241 g threshold for units residing in the anterior lumbar disk (14–16). This indicates that the pain sensitivity of the SI joints may be lower than that of the lumbar facet joints but higher than the anterior portions of lumbar discs. As all animals underwent posterior midline incisions, somatosensory units in the anterior SI joint were not stimulated.
Function and Biomechanics
The SI joints are designed primarily for stability. Their functions include the transmission and dissipation of truncal loads to the lower extremities, limiting x-axis rotation, and facilitating parturition. Compared to the lumbar spine, the SI joints can withstand a medially directed force 6 times greater but only half the torsion and 1/20th of the axial compression load (17). These last 2 motions may preferentially strain and injure the weaker anterior joint capsule (18).
There have been numerous attempts to discern the biomechanics of the SI joint. These motion studies can be summarized as follows: the SI joint rotates about all 3 axes, although the movements are very small and difficult to measure (19,20). Miller et al. (21) studied the load-displacement behavior of single and paired SI joints in 8 elderly cadavers. Various static test loads were applied in the superior, lateral, anterior and posterior directions, and rotations about all 3 axes were measured. These tests were conducted with one and both ilia fixed. The authors found that with 1 leg immobile, movements in all planes ranged from between 2 to 7.8 times more than that measured with both legs fixed. In a series of cadaveric studies, Vleeming et al. (22,23) found that the total range of motion during flexion and extension at the SI joint rarely exceeded 2 degrees, with 4 degrees being the upper limit during sagittal rotation. In another cadaver study, Brunner et al. (24) found that the main motion in male specimens tended to be translation, whereas in female specimens it was rotational. The maximum range of motion in this study was 1.2 degrees in men and 2.8 degrees in women. In a study by Egund et al. (25) examining SI joint movements in 4 volunteers using radiographic stereophotogrammetry, the authors found the maximal rotations and translations to be 2.0 degrees and 2.0 mm, respectively. A larger study (n = 24) by Jacob and Kissling (26) conducted in healthy young and middle-aged men and women found similarly small limits on rotation (1.7 degrees) and translation (0.7 mm). However, one individual with a history of SI joint pain exhibited more than 6 degrees of rotation about the y-axis. Finally, Sturesson et al. (27) measured multiple SI joint movements in 25 patients diagnosed with SI joint pain. Movements in all planes were found to be small, with translations never exceeding 1.6 mm, and rotations being limited to 3 degrees. No differences were found between symptomatic and asymptomatic joints, leading the authors to conclude that 3-dimensional motion analysis was not useful for identifying painful SI joints in most patients. Possible exceptions to the finding that hypermobility is not a typical cause of SI joint pain include traumatic instability, multiparity, muscular atrophy, and lower motor neuron disease (28).
Although it is widely acknowledged that dysfunctional SI joints may cause low back pain (LBP), the prevalence of this condition has not been well studied. Prevalence studies are further compromised by the fact that most have used either physical examination findings and/or radiological imaging techniques to make the diagnosis of SI joint pain. The largest of these is a retrospective study by Bernard and Kirkaldy-Willis (29), who found a 22.5% prevalence rate in 1293 adult patients presenting with LBP. Diagnoses in this series were based predominantly on physical examination.
Schwarzer et al. (30) conducted a prevalence study involving 43 consecutive patients with chronic LBP principally below L5-S1 using fluoroscopically guided SI joint injections. Fifty-seven other patients with LBP were excluded on the basis of more rostral symptoms. Three criteria were used to diagnose SI joint pain: analgesic response to local anesthetic (LA), abnormalities on post-arthrography computed tomography (CT) scanning, and concordant pain provocation during joint distension. Using significant pain relief after LA injection as the sole criterion for diagnosis, the prevalence of SI joint pain in the 43 subjects was determined to be 30% (95% confidence interval [CI], 16%–44%), with 4 patients obtaining complete pain relief. Using analgesic response combined with a ventral capsular tear (the most common radiologic finding) as the criteria, the prevalence decreased to 21% (95% CI, 9%–33%). Only 7 patients satisfied all 3 diagnostic criteria, for a lower limit prevalence rate of 16% (95% CI, 5%–27%). The presence of groin pain was the only referral pattern found to distinguish patients with SI joint pain from those with LBP of non-SI joint origin.
Maigne et al. (31) conducted a prevalence study in 54 patients with unilateral LBP using a series of blocks done with different LA based on International Spinal Injection Society guidelines (32). Nineteen patients had a positive response (≥75% pain relief) to the lidocaine screening block. Among these patients, 10 (18.5%) responded with >2 h pain relief after the confirmatory block with bupivacaine and were considered to have true SI joint pain (95% CI, 9%–29%). Based on these studies, the prevalence of SI joint pain in carefully screened LBP patients appears to be in the 15%–25% range.
Mechanism of Injury
The mechanism of SI joint injury has previously been described as a combination of axial loading and abrupt rotation (18). On an anatomic level, pathologic changes affecting many different SI joint structures can lead to nociception. These include capsular or synovial disruption, capsular and ligamentous tension, hypomobility or hypermobility, extraneous compression or shearing forces, abnormal joint mechanics, microfractures or macrofractures, chondromalacia, soft tissue injury, and inflammation. Mechanistically, there are numerous reported etiologies for SI joint pain. To simplify matters, these causes can be divided into intraarticular and extra-articular sources. Arthritis and infection are two examples of intraarticular causes of SI joint pain. Extra-articular sources are the more common of the two and include enthesopathy, fractures, ligamentous injury, and myofascial pain. Clinical studies have demonstrated significant pain relief after both intraarticular and periarticular SI joint injections (33–36).
In addition to etiologic sources, there are numerous factors that can predispose a person to gradually develop SI joint pain. Risk factors that operate by increasing the stress borne by the SI joints include true and apparent leg length discrepancy (37), gait abnormalities (38), prolonged vigorous exercise (39), scoliosis (40), and spinal fusion to the sacrum (41). Whereas increased SI joint uptake using scintigraphy has been demonstrated after lumbar spine fusion (42), at least one study examining the long-term effects of spinal fusion on SI joint function concluded that neither biomechanical nor anatomical changes were more common in fusion patients than in those who underwent decompression procedures (43). Lumbar spine surgery has also been purported to trigger SI joint pain for reasons unrelated to increased force transmission. These factors include SI ligament weakening and/or surgical violation of the joint cavity during iliac graft bone harvest (44) and postsurgical hypermobility (45).
Pregnancy predisposes women to SI joint pain via the combination of increased weight gain, exaggerated lordotic posture, the mechanical trauma of parturition, and hormone-induced ligamental laxity (46,47). The laxity associated with pregnancy is attributable to increased levels of estrogen and relaxin, and it predisposes parturients to sprains of the SI joint ligaments. SI subluxation has also been reported to cause back pain in pregnancy (48).
Inflammation of one or both SI joints is considered to be an early and prominent symptom in all seronegative and HLA-B27-associated spondylarthropathies (49). Although the precise etiology of spondylarthropathy remains unknown in most patients, the strong association with HLA-B27 supports the view that these conditions are attributable to a genetically determined immune response to environmental factors in susceptible individuals. In a subset of patients with Reiter's syndrome/reactive arthritis, the disease is clearly induced by infection (50) (Table 1).
The specific etiologies that can result in SI joint pain are widespread and protean. Potential causes range from rare events such as pyogenic infection (51) and malignancy (52), to more mundane occurrences such as bracing one's legs in a motor vehicle accident (53), falls (53), athletic injuries (54), prolonged lifting and bending (55), and torsional strain (55). In a retrospective study by Chou et al. (56) assessing the inciting events in 54 patients with injection-confirmed SI joint pain, the authors found trauma was the cause in 44% of patients, 35% were idiopathic, and 21% were attributed to the cumulative effects of repeated stress. In the 24 patients who cited trauma as the source of their pain, the most common events were motor vehicle accidents (n = 13), falls onto the buttock (n = 6), and childbirth (n = 3).
Diagnosis and Presentation
History and Physical Examination
One of the most challenging aspects of treating SI joint pain is the complexity of diagnosis. Literally dozens of physical examination tests have been advocated as diagnostic aids in patients with presumed SI joint pain (57). Many involve distraction of the SI joints, with 2 of the most common ones being Patrick's test and Gaenslen's test. Despite the plethora of diagnostic tests, clinical studies have for the most part demonstrated that neither medical history nor physical examination findings are consistently capable of identifying dysfunctional SI joints as pain generators (30, 58, 59) (Table 2). In addition, Dreyfuss et al. (60) found 20% of asymptomatic adults had positive findings on 3 commonly performed SI joint provocation tests.
The reliability of provocative SI joint maneuvers and alignment/mobility tests has also been questioned, with most studies conducted by chiropractors and physical therapists. Whereas some of these studies have found moderate to high inter-examiner reliability (61–63), most have not (64–68). Generally, reproducibility has been found to be greater for provocative tests than for mobility and alignment assessments. In the Dreyfuss et al. study (59) conducted in 85 patients with injection-confirmed SI joint pain, there was moderate agreement (kappa = 0.6) between chiropractors and medical doctors with regard to provocative maneuvers of painful joints. Even when agreement was perfect, the maneuvers were still found to lack diagnostic utility.
Results of studies examining radiologic findings in patients with SI joint pain have been similarly disappointing. In studies by Maigne et al. (69) and Slipman et al. (70), the investigators found sensitivities of 46% and 13%, respectively, for the use of radionuclide bone scanning in the identification of SI joint pain. Despite the high specificites in these studies (89.5% for Maigne et al. and 100% for Slipman et al.), the low sensitivies indicate bone scanning is a poor screening test for SI joint pain. Poor correlation with diagnostic injections and symptoms have also been found for CT and radiographic stereophotogrammetry (71,27). In a retrospective analysis by Elgafy et al. (71), CT imaging was found to be 57.5% sensitive and 69% specific in diagnosing SI joint pain.
Pain Referral Patterns
There have been several attempts to identify pain referral patterns from SI joints. In one of the earliest studies conducted in 10 asymptomatic volunteers, Fortin et al. (72) performed provocative SI joint injections using contrast and lidocaine. Sensory changes were localized to the ipsilateral medial buttock inferior to the posterior superior iliac spine in 6 of the 10 subjects. In 2 subjects, the area of hyperesthesia extended to the superior aspect of the greater trochanter. The last 2 subjects experienced sensory changes radiating into the upper thigh. In a follow-up study, independent examiners selected 16 individuals among 54 with chronic LBP whose pain diagrams most closely resembled the pain referral patterns obtained in the first study (73). These 16 patients proceeded to undergo provocative SI joint injections with contrast and LA. All 16 experienced concordant pain during the injection, with 14 obtaining pain relief after deposition of LA. Ten patients reported ≥50% pain reduction. Six of the 16 patients had ventral capsular tears revealed during arthrography. After the SI joint injections, provocative discography and lumbar facet joint injections were performed in 9 patients each. In none of the patients was either test positive.
Slipman et al. (74) conducted a retrospective study to determine the pain referral patterns in 50 patients with injection-confirmed SI joint pain. In contrast to the findings by Fortin et al. (72) and Schwarzer et al. (30), the authors found the most common referral patterns for SI joint pain to be radiation into the buttock (94%), lower lumbar region (72%), lower extremity (50%), groin area (14%), upper lumbar region (6%), and abdomen (2%). Twenty-eight percent of patients experienced pain radiating below their knee, with 12% reporting foot pain. Based on the existing data, the most consistent factor for identifying patients with SI joint pain is unilateral pain (unless both joints are affected) localized predominantly below the L5 spinous process (30,59,72–74).
It is often assumed that an analgesic response to a properly performed diagnostic block is the most reliable method to diagnose SI joint pain. Although this may seem to be self-evident, the validity of intraarticular SI joint blocks remains unproven. There are many factors that can impact on the sensitivity and specificity of diagnostic blocks. These include the placebo effect, convergence and referred pain, neuroplasticity and central sensitization, expectation bias, unintentional sympathetic blockade, systemic absorption of LA, and psychosocial issues (75). In addition, SI joint block can be one of the most challenging spinal injection procedures. Extravasation of LA to surrounding pain-generating structures such as muscles, ligaments, and lumbosacral nerve roots can lead to false-positive blocks. Conversely, failure to obtain adequate LA spread to the anterior and cephalad portions of the SI joint can result in false-negative blocks. In a classic study by North et al. (76) examining the specificity and sensitivity of a battery of lumbosacral LA blocks in 33 patients with a chief complaint of sciatica, the authors found the specificity of all blocks to be exceedingly low. SI joint blocks were not performed in this study.
In a pilot study by Fortin et al. (72) mapping SI joint referral patterns in asymptomatic volunteers, extravasation of contrast (mean 1.6 mL injected) occurred in 9 of 10 subjects during SI joint injection, with half having at least moderate spread outside the joint. After the injection of LA, 40% of subjects noted lower extremity numbness, indicating inadvertent anesthetization of the lumbosacral nerve roots. In the Maigne et al. (31) study, 3 of the initial 67 patients were excluded because of “sciatic palsy” after the screening block and another 7 were excluded because penetration of the SI joint was impossible. Other investigators have reported much less frequent (<5%) failure rates with fluoroscopically guided SI joint injections (30,59,77). Technical difficulties may be more frequently encountered in elderly patients and those with spondylarthropathies, in whom degenerative changes are more pronounced. If persistent difficulties entering the SI joint are encountered using fluoroscopy, the 3-dimensional imaging capabilities of CT may facilitate entry into the joint (34, 78) (Fig. 3).
Regardless of the imaging modality used to confirm intraarticular injection, SI joint injections should never be performed blindly. Rosenberg et al. (79) performed a double-blind study in 37 patients (39 joints) to determine the accuracy of clinically guided SI joint injections using CT imaging as the standard. The authors found that intraarticular injection was accomplished in only 22% of patients, whereas sacral foraminal spread occurred 44% of the time. In 3 patients, no contrast was seen on CT scanning, indicating probable vascular uptake. In 24% of injections, contrast extended into the epidural space.
As for facet blocks, some experts have advocated using a series of SI joint blocks to reduce the incidence of false-positives. In a prospective study involving 67 patients with unilateral LBP, SI joint-compatible referral patterns and joint tenderness, Maigne et al. (31) sought to determine the prevalence of SI joint pain using a series of blocks with 2 different LA. In the 54 patients who completed the study, 19 obtained ≥75% pain relief with the lidocaine screening block. After the bupivacaine confirmatory block, only 10 of the 19 patients achieved ≥75% pain relief lasting 2 or more hours, for a prevalence rate of 18.5%. The false-positive rate of 17% in this study is less than that previously reported for lumbar facet blocks (80). Yet without a diagnostic “gold standard,” there is no way of determining how many true positives were false positives and how many false positives were actually true positives. In clinical practice confirmatory SI joint blocks are almost never performed because a) the block itself is considered to be definitive treatment; b) double-blocks are not cost-effective (81); and c) the negative consequences of obtaining a false false-positive block (misdiagnosing true SI joint pain) outweigh the ramifications of overdiagnosing the condition. In summary, there is no infallible, universally accepted method for diagnosing pain originating in the SI joint(s).
The treatment of SI joint pain is widely acknowledged to be one of the most challenging problems confronting pain physicians. Evidence supporting this statement can be seen by the plethora of different therapies that have been advocated for this disorder. Generally, these treatments can be divided into 2 categories: those directed at correcting the underlining pathology and those aimed at alleviating symptoms. For both of these categories, the evidence supporting any one therapy is limited by the lack of controlled outcome studies.
Recent studies have provided incontrovertible evidence that psychopathology and other psychosocial factors can influence both the development of chronic pain conditions and the response to treatment. In a study by Polatin et al. (82) conducted in 200 chronic LBP patients, the authors found that 77% met lifetime criteria and 59% demonstrated current symptoms for at least one psychiatric diagnosis, with the most common being depression, substance abuse, and anxiety disorders. Notably, more than 50% of those with depression and more than 90% of patients with substance abuse or an anxiety disorder experienced symptoms before the onset of LBP. Most, but not all, studies have shown untreated psychopathology to negatively affect LBP treatment outcomes (83).
In addition to psychiatric illness, social factors have been demonstrated to impact the prognosis of LBP. These include return-to-work issues, secondary gain, catastrophizing, poor role models, codependency behavior, inadequate coping mechanisms, and attitudes, beliefs, and expectations (84). To optimize outcomes, the identification and treatment of concomitant psychosocial issues is of paramount importance. This is best accomplished via a multidisciplinary approach.
The non-interventional management of SI joint pain should ideally address the underlining pathology. In patients with true or apparent leg length discrepancy, this might include the use of shoe inserts to more equitably distribute the load borne by the SI joints. Because leg length discrepancies are frequently found in asymptomatic individuals (37) and many patients already compensate for their lower extremity length difference by altering their gait or posture, most experts recommend starting out cautiously with inserts that correct only half the incongruity. For SI joint pain resulting from altered gait mechanics and spine malalignment, physical therapy and osteopathic or chiropractic manipulation have been reported to reduce pain and improve mobility (85,86). However, there are no prospective, controlled studies supporting these modalities.
Nonsurgical stabilization programs have been advocated for SI joint pain. These range from the application of pelvic belts that reduce the sagittal rotation of incompetent SI joints in pregnant women (87,88) to exercise-induced pelvic stabilization programs (89). In a study by Mooney et al. (89), the authors found that 5 women with injection-confirmed SI joint pain had electromyographic-documented hyperactivity of the ipsilateral gluteus muscles and contralateral latissimus muscle compared with 15 asymptomatic control patients. After a 2-1/2 month exercise program, all 5 patients achieved a significant reduction in pain and a return of myoelectric activity to normal patterns.
Ankylosing spondylitis (AS), the most well known and studied spondylarthropathy, is an inflammatory rheumatic disease characterized by spine and SI joint involvement that manifests as spondylitis and sacroiliitis. There are numerous studies assessing the efficacy of various pharmacologic treatment modalities in AS and other spondylarthropathies, but the conclusions that can be drawn from these studies are limited by several factors. These include the protean nature of rheumatic involvement, the systemic manifestations accompanying the disorders, and the fact that although the outcome measures generally include changes in pain complaints and mobility, most do not specifically address SI joint pain. Table 3 lists the evidence supporting various pharmacotherapies for AS and other spondylarthropathies.
Intraarticular injections with steroid and LA often serve the dual function of being therapeutic and aiding in diagnosis. To summarize these studies, most but not all investigators have found radiologically guided SI joint injections to provide good to excellent pain relief lasting from 6 mo to 1 yr (Table 4). Along with a multitude of studies demonstrating prolonged pain relief after intraarticular SI joint steroid injections, double-blind studies have shown a beneficial effect for periarticular corticosteroid treatment as well (35,36).
Radiofrequency Denervation Procedures
Several investigators have performed radiofrequency (RF) denervation procedures in an attempt to provide prolonged pain relief to patients suffering SI joint pain. The techniques used have ranged from denervating the nerves supplying the SI joint (90–92) to cre-ating lesions in the joint itself (93), with one study using a combination of the two (94). The success rates of studies targeting the nerve supply are higher than those focusing on the joint itself, with approximately two thirds of patients reporting significant pain relief. The major drawback to percutaneous RF denervation procedures is that they should not be expected to alleviate pain emanating from the ventral SI joint. In the study by Schwarzer et al. (30), ventral capsular pathology was shown to account for 69% of all CT pathology in the 13 patients with a positive response to diagnostic SI joint blocks. Complicating matters further are that the nerves lesioned during RF procedures innervate other pain-generating structures besides the SI joint, and the SI joint is likely innervated by other nerves inaccessible for denervation (Table 5).
Surgical and Other Invasive Interventions
In 1999, Srejic et al. (95) reported 12–16 mo of significant pain relief in 4 patients with SI joint pain who received a series of 3 intraarticular injections with hyaluronic acid. Three of these patients had postsurgical SI joint pain and one suffered from severe osteoarthritis of the spine. The rationale for this treatment stems from studies demonstrating long-term pain relief with hyaluronic acid injections in degenerative joint disease of the knee (96). However, one meta-analysis found only scant evidence for the use of viscosupplementation in knee osteoarthritis, especially when lower molecular weight hyaluronate formulations are used (97). In addition to questionable efficacy, another factor that mitigates against intraarticular hyaluronic acid injections for SI pain is that degenerative joint disease accounts for only a small percentage of cases.
Proliferative therapy (a.k.a. “prolotherapy”) has been advocated as a treatment for nonspecific LBP and SI joint pain (98). The rationale behind the use of “prolotherapy” is that the ligaments and other soft tissue structures are of primary importance in the development of LBP. Thus, the injection of a drug promoting fibroblast hyperplasia should theoretically increase the strength and reduce sensitization of these structures. In a double-blind study, Ongley et al. (99) found that LBP patients who received 6 wk of proliferant therapy had lower pain scores and disability indices at their 6-mo follow-up than “control” patients who received saline injections. Despite these findings, the lack of specific diagnoses, the numerous other treatment differences between groups, and the targeting of pain generators outside the SI joints limit the relevance of this study.
In patients with SI joint pain unresponsive to more conservative measures, several investigators have advocated surgical stabilization. Unfortunately, all published reports on SI joint fusion have been small case series or retrospective studies. Whereas the primary indications for SI joint fixation are either joint instability or fractures (100,101), successful arthrodesis has also been reported for degenerative joint disease (102). In some patients, successful stabilization can be done percutaneously using CT guidance (103). Regardless of the underlying etiology, based on the existing studies the long-term success rate for SI joint fusion appears to be in the range of 70% (100–102). Neuroaugmentation of the third sacral nerve root has also been reported to provide adequate pain relief in 2 patients with severe SI joint pain unresponsive to conventional therapy (104).
The SI joint is a real yet underappreciated pain generator in an estimated 15% to 25% of patients with axial LBP. Whereas historical and physical examination findings have been previously advocated as useful tools in identifying patients with SI joint pain, more recent studies have demonstrated they have limited diagnostic value. Presently, small-volume diagnostic blocks remain the most commonly used method for diagnosing this disorder, although their validity remains unproven. Owing to the complexity of the joint, the mechanisms of SI pain are numerous and ill-defined. When a pathological condition such as leg length discrepancy or altered gait mechanics is present, correcting the underlying defect is the safest and most reliable treatment option. Intraarticular and periarticular corticosteroid injections have been shown in most, but not all, studies to provide good to excellent pain relief lasting up to 10 mo in patients with and without spondylarthropathy. One promising area in the treatment of SI joint pain is RF denervation, although the conclusions that can be drawn are limited by the heterogeneous methods used and the lack of controlled studies.
1. Bernard TN, Cassidy JD. The sacroiliac syndrome. Pathophysiology, diagnosis and management. In: Frymoyer JW, ed. The adult spine: principles and practice. New York: Raven, 1991;2107–30.
2. Dijkstra PF, Vleeming A, Stoeckart R. Complex motion tomography of the sacroiliac joint: an anatomical and roentgenological study [in German]. Rofo 1989;150:635–42.
3. Ruch WJ. Atlas of common subluxations of the human spine and pelvis. Boca Raton, FL: CRC Press, 1997.
4. Bowen V, Cassidy JD. Macroscopic and microscopic anatomy of the sacroiliac joint from embryonic life until the eighth decade. Spine 1981;6:620–8.
5. Mitchell FL Jr. The muscle energy manual, Vol. 1. East Lansing, MI: MET Press, 1995.
6. Murata Y, Takahashi K, Yamagata M, et al. Sensory innervation of the sacroiliac joint in rats. Spine 2000;16:2015–9.
7. Grob KR, Neuhuber WL, Kissling RO. Innervation of the sacroiliac joint in humans [in German]. Z Rheumatol 1995;54:117–22.
8. Pitkin HC, Pheasant HC. Sacrarthrogenic telalgia I: a study of referred pain. J Bone Joint Surg 1936;18:111–33.
9. Solonen KA. The sacroiliac joint in the light of anatomical, roentgenological and clinical studies. Acta Orthop Scand 1957;27(suppl):1–27.
10. Ikeda R. Innervation of the sacroiliac joint: macroscopic and histological studies. J Nippon Med Sch 1991;58:587–96.
11. Fortin JD, Kissling RO, O'Connor BL, Vilensky JA. Sacroiliac joint innervation and pain. Am J Orthop 1999;28:68–90.
12. Dreyfuss P, Park K, Bogduk N. Do L5 dorsal ramus and S1–4 lateral branch blocks protect the sacroiliac joint from an experimental pain stimulus? A randomized, double-blinded controlled trial. Presented at the International Spinal Injection Society 8th Annual Scientific Meeting, San Francisco, CA, September 8–10, 2000.
13. Sakamoto N, Yamashita T, Takebayashi T, et al. An electrophysiologic study of mechanoreceptors in the sacroiliac joint and adjacent tissues. Spine 2001;26:E468–71.
14. Yamashita T, Cavanaugh JM, El-Bohy AA, et al. Mechanosensitive afferent units in the lumbar facet joint. J Bone Joint Surg (Am) 1990;72:865–70.
15. Yamashita T, Minaki Y, Oota, et al. Mechanosensitive afferent units in the lumbar intervertebral disc and adjacent muscle. Spine 1993;18:2252–6.
16. Minaki Y, Yamashita T, Ishii S. An electrophysiological study on the mechanoreceptors in the lumbar spine and adjacent tissues. Neurol Orthop 1996;20:23–35.
17. Dreyfuss P, Dreyer SJ, Cole A, Mayo K. Sacroiliac joint pain. J Am Acad Orthop Surg 2004;12:255–65.
18. Dreyfuss P, Cole AJ, Pauza K. Sacroiliac joint injection techniques. Phys Med Rehabil Clin North Am 1995;6:785–813.
19. Walker JM. The sacroiliac joint: a critical review. Phys Ther 1992;72:903–16.
20. White AA, Panjabi MM. Clinical biomechanics of the spine. 2nd ed. Philadelphia: JB Lippincott, 1990.
21. Miller JA, Schultz AB, Andersson GB. Load-displacement behavior of the sacroiliac joints. J Orthop Res 1987;5:92–101.
22. Vleeming A, van Wingerden JP, Dijkstra PF, et al. Mobility in the sacroiliac joints in the elderly: a kinematic and radiological study. Clin Biomech 1992;7:170–6.
23. Vleeming A, van Wingerden JP, Snijders CJ, et al. Load application to the sacrotuberous ligament: influence on sacroiliac joint mechanics. Clin Biomech 1989;4:204–9.
24. Brunner C, Kissling R, Jacob HA. The effects of morphology and histopathologic findings on the mobility of the sacroiliac joint. Spine 1991;16:1111–7.
25. Egund N, Olsson TH, Schmid H, Selvik G. Movements in the sacroiliac joints demonstrated with roentgen stereophotogrammetric analysis. Acta Radiol Diagn 1978;19:833–45.
26. Jacob H, Kissling R. The mobility of the sacroiliac joints in healthy volunteers between 20 and 50 years of age. Clin Biomech 1995;10:352–61.
27. Sturesson B, Selvik G, Uden A. Movements of the sacroiliac joints: a roentgen stereophotogrammetric analysis. Spine 1989;14:162–5.
28. Harrison DE, Harrison DD, Troyanovich SJ. The sacroiliac joint: a review of anatomy and biomechanics with clinical implications. J Manipulative Physiol Ther 1997;20:607–17.
29. Bernard TN, Kirkaldy-Willis WH. Recognizing specific characteristics of nonspecific low back pain. Clin Orthop 1987;217:266–80.
30. Schwarzer AC, Aprill CN, Bogduk N. The sacroiliac joint in chronic low back pain. Spine 1995;20:31–7.
31. Maigne JY, Aivaliklis A, Pfefer F. Results of sacroiliac joint double block and value of sacroiliac pain provocation tests in 54 patients with low back pain. Spine 1996;21:1889–92.
32. Bogduk N. International Spinal Injection Society guidelines for the performance of spinal injection procedures. Part I: zygapophysial joint blocks. Clin J Pain 1997;13:285–302.
33. Maugars Y, Mathis C, Berthelot JM, Charlier C, Prost A. Assessment of the efficacy of sacroiliac corticosteroid injections in spondyloarthropathies: a double-blind study. Br J Rheumatol 1996;35:767–70.
34. Braun J, Bollow M, Seyrekbasan F, et al. Computed tomography guided corticosteroid injection of the sacroiliac joint in patients with spondyloarthropathy with sacroiliitis: clinical outcome and follow-up by dynamic magnetic resonance imaging. J Rheumatol 1996;23:659–64.
35. Luukkainen R, Nissila M, Asikainen E, et al. Periarticular corticosteroid treatment of the sacroiliac joint in patients with seronegative spondyloarthropathy. Clin Exp Rheumatol 1999;17:88–90.
36. Luukkainen R, Wennerstrand PV, Kautiainen HH, et al. Efficacy of periarticular corticosteroid treatment of the sacroiliac joint in non-spondyloarthropathic patients with chronic low back pain in the region of the sacroiliac joint. Clin Exp Rheumatol 2002;20:52–4.
37. Schuit D, McPoil TG, Mulesa P. Incidence of sacroiliac joint malalignment in leg length discrepancies. J Am Podiatr Med Assoc 1989;79:380–3.
38. Herzog W, Conway PJ. Gait analysis of sacroiliac joint patients. J Manipulative Physiol Ther 1994;17:124–7.
39. Marymont JV, Lynch MA, Henning CE. Exercise-related stress reaction of the sacroiliac joint: an unusual cause of low back pain in athletes. Am J Sports Med 1986;14:320–3.
40. Schoenberger M, Hellmich K. Sacroiliac dislocation and scoliosis. Hippokrates 1964;35:476–9.
41. Katz V, Schofferman J, Reynolds J. The sacroiliac joint: a potential cause of pain after lumbar fusion to the sacrum. J Spinal Disord Tech 2003;16:96–9.
42. Onsel C, Collier BD, Meting K, et al. Increased sacroiliac joint uptake after lumbar fusion and/or laminectomy. Clin Nucl Med 1992;17:283–7.
43. Frymoyer JW, Howe J, Kuhlmann D. The long-term effects of spinal fusion on the sacroiliac joint and ilium. Clin Orthop 1978;134:196–201.
44. Ebraheim NA, Elgafy H, Semaan HB. Computed tomographic findings in patients with persistent sacroiliac pain after posterior iliac graft harvesting. Spine 2000;25:2047–51.
45. Frymoyer JW, Hanley E, Howe J, et al. Disc excision and spine fusion in the management of lumbar disc disease: a minimum ten-year follow-up. Spine 1978;3:1–6.
46. Albert H, Godskesen M, Westergaard J. Prognosis in four syndromes of pregnancy-related pelvic pain. Acta Obstet Gynecol Scand 2001;80:505–10.
47. Berg G, Hammar M, Moller-Nielsen J, et al. Low back pain during pregnancy. Obstet Gynecol 1988;71:71–5.
48. Daly JM, Frame PS, Rapoza PA. Sacroiliac subluxation: a common treatable cause of low-back pain in pregnancy. Fam Pract Res J 1991;11:149–59.
49. Bollow M, Braun J, Hamm B. Sacroiliitis: the key symptom of spondylarthropathies. 1. The clinical aspects [in German]. Rofo 1997;166:95–100.
50. Cush JJ, Lipsky PE. Reiter's syndrome and reactive arthritis. In: Koopman WJ, ed. Arthritis and allied conditions: a textbook of rheumatology, Vol. 1, 14th ed. Philadelphia: Lippincott Williams& Wilkins, 2001:1324–44.
51. Dunn EJ, Bryan DM, Nugent JT, Robinson RA. Pyogenic infections of the sacro-iliac joint. Clin Orthop 1976;118:113–7.
52. Humphrey SM, Inman RD. Metastatic adenocarcinoma mimicking unilateral sacroiliitis. J Rheumatol 1995;22:970–2.
53. Fortin JD. Sacroiliac joint dysfunction: a new perspective. J Back Musculoskeletal Rehabil 1993;3:31–43.
54. Baquie P, Brukner P. Injuries presenting to an Australian sports medicine center: a 12-month study. Clin J Sport Med 1997;7:28–31.
55. LeBlanc KE. Sacroiliac sprain: an overlooked cause of back pain. Am Fam Physician 1992;46:1459–63.
56. Chou LH, Slipman CW, Bhagia SM, et al. Inciting events initiating injection-proven sacroiliac joint syndrome. Pain Med 2004;5:26–32.
57. Cohen SP, Rowlingson J, Abdi S. Low back pain. In: Warfield CA, Bajwa ZA, eds. Principles and practice of pain medicine. 2nd ed. New York: McGraw-Hill, 2004: 273–84.
58. Slipman CW, Sterenfeld EB, Chou LH, et al. The predictive value of provocative sacroiliac joint stress maneuvers in the diagnosis of sacroiliac joint syndrome. Arch Phys Med Rehabil 1998;79:288–92.
59. Dreyfuss P, Michaelsen M, Pauza K, et al. The value of medical history and physical examination in diagnosing sacroiliac joint pain. Spine 1996;21:2594–2602.
60. Dreyfuss P, Dreyer S, Griffin J, et al. Positive sacroiliac screening tests in asymptomatic adults. Spine 1994;19:1138–43.
61. Laslett M, Williams M. The reliability of selected pain provocation tests for sacroiliac joint pathology. Spine 1994;19:1243–9.
62. McCombe PF, Fairbank JC, Cockersole BC, Pynsent PB. Reproducibility of physical signs in low-back pain. Spine 1989;14:908–18.
63. Kokmeyer DJ, Van der Wurff P, Aufdemkampe G, Fickenscher TC. The reliability of multitest regimens with sacroiliac pain provocation tests. J Manipulative Physiol Ther 2002;25:42–8.
64. Riddle DL, Freburger JK. Evaluation of the presence of sacroiliac joint region dysfunction using a combination of tests: a multicenter intertester reliability study. Phys Ther 2002;82:772–81.
65. Potter NA, Rothstein JM. Intertester reliability for selected clinical tests of the sacroiliac joint. Phys Ther 1985;65:1671–5.
66. Freburger JK, Riddle DL. Measurement of sacroiliac joint dysfunction: a multicenter intertester reliability study. Phy Ther 1999;79:1134–41.
67. Carmichael JP. Inter- and intra-tester reliability of palpation for sacroiliac joint dysfunction. J Manipulative Physiol Ther 1987;10:164–71.
68. Meijne W, van Neerbos K, Aufdemkampe G, Van der Wurff P. Intraexaminer and interexaminer reliability of the Gillet test. J Manipulative Physiol Ther 1999;22:4–9.
69. Maigne JY, Boulahdour H, Chatellier G. Value of quantitative radionuclide bone scanning in the diagnosis of sacroiliac joint syndrome in 32 patients with low back pain. Eur Spine J 1998;7:328–31.
70. Slipman CW, Sterenfeld EB, Chou LH, et al. The value of radionuclide imaging in the diagnosis of sacroiliac joint syndrome. Spine 1996;21:2251–4.
71. Elgafy H, Semaan HB, Ebraheim NA, Coombs RJ. Computed tomography findings in patients with sacroiliac pain. Clin Orthop 2001;382:112–8.
72. Fortin JD, Dwyer AP, West S, Pier J. Sacroiliac joint: pain referral maps upon applying a new injection/arthrography technique. Part I: asymptomatic volunteers. Spine 1994;19:1475–82.
73. Fortin JD, Aprill CN, Ponthieux B, Pier J. Sacroiliac joint: pain referral maps upon applying a new injection/arthrography technique. Part II: clinical evaluation. Spine 1994;19:1483–9.
74. Slipman CW, Jackson HB, Lipetz JS, et al. Sacroiliac joint pain referral zones. Arch Phys Med Rehabil 2000;81:334–8.
75. Hogan QH, Abram SE. Neural blockade for diagnosis and prognosis: a review. Anesthesiology 1997;86:216–41.
76. North RB, Kidd DH, Zahurak M, Piantadosi S. Specificity of diagnostic nerve blocks: a prospective, randomized study of sciatica due to lumbosacral disease. Pain 1996;65:77–85.
77. Dussault RG, Kaplan PA, Anderson MW. Fluoroscopy-guided sacroiliac joint injections. Radiology 2000;214:273–7.
78. Bollow M, Braun J, Taupitz M, et al. CT-guided intraarticular corticosteroid injection into the sacroiliac joints in patients with spondyloarthropathy: indication and follow-up with contrast-enhanced MRI. J Comput Assist Tomogr 1996;20:512–21.
79. Rosenberg JM, Quint DJ, de Rosayro AM. Computerized tomographic localization of clinically-guided sacroiliac joint injections. Clin J Pain 2000;16:18–21.
80. Schwarzer AC, Aprill CN, Derby R, et al. The false-positive rate of uncontrolled diagnostic blocks of the lumbar zygapophysial joints. Pain 1994;58:195–200.
81. Bogduk N, Holmes S. Controlled zygapophysial joint blocks: the travesty of cost-effectiveness. Pain Med 2000;1:24–34.
82. Polatin PB, Kinney RK, Gatchel RJ, et al. Psychiatric illness and chronic low-back pain. The mind and spine: which goes first? Spine 1993;18:66–71.
83. Fayad F, Lefevre-Colau MM, Poiraudeau S, et al. Chronicity, recurrence, and return to work in low back pain: common prognostic factors [in French]. Ann Readapt Med Phys 2004;47:179–89.
84. Seres JL. Evaluating the complex chronic pain patient. Neurosurg Clin N Am 2003;14:339–52.
85. Cibulka MT, Delitto A. A comparison of two different methods to treat hip pain in runners. J Orthop Sports Phys Ther 1993;17:172–6.
86. Osterbauer PJ, De Boer KF, Widmaier R, et al. Treatment and biomechanical assessment of patients with chronic sacroiliac joint syndrome. J Manipulative Physiol Ther 1993;16:82–90.
87. Vleeming A, Buyruk HM, Stoeckart R, et al. An integrated therapy for peripartum pelvic instability: a study of the biomechanical effects of pelvic belts. Am J Obstet Gynecol 1992;166:1243–7.
88. Damen L, Spoor CW, Snijders CJ, Stam HJ. Does a pelvic belt influence sacroiliac joint laxity? Clin Biomech 2002;17:495–8.
89. Mooney V, Pozos R, Vleeming A, et al. Exercise treatment for sacroiliac pain. Orthopedics 2001;24:29–32.
90. Cohen SP, Abdi S. Lateral branch blocks as a treatment for sacroiliac joint pain: a pilot study. Reg Anesth Pain Med 2003;28:113–9.
91. Buijs EJ, Kamphuis ET, Groen GJ. Radiofrequency treatment of sacroiliac joint-related pain aimed at the first three sacral dorsal rami: a minimal approach. Pain Clinic 2004;16:139–46.
92. Yin W, Willard F, Carreiro J, Dreyfuss P. Sensory stimulation-guided sacroiliac joint radiofrequency neurotomy: technique based on neuroanatomy of the dorsal sacral plexus. Spine 2003;28:2419–25.
93. Ferrante FM, King LF, Roche EA, et al. Radiofrequency sacroiliac joint denervation for sacroiliac syndrome. Reg Anesth Pain Med 2001;26:137–42.
94. Gevargez A, Groenemeyer D, Schirp S, Braun M. CT-guided percutaneous radiofrequency denervation of the sacroiliac joint. Eur Radiol 2002;12:1360–5.
95. Srejic U, Calvillo O, Kabakibou K. Viscosupplementation: a new concept in the treatment of sacroiliac joint syndrome: a preliminary report of four cases. Reg Anesth Pain Med 1999;24:84–8.
96. Petrella RJ, DiSilvestro MD, Hildebrand C. Effects of hyaluronate sodium on pain and physical functioning in osteoarthritis of the knee: a randomized, double-blind, placebo-controlled trial. Arch Int Med 2002;162:292–8.
97. Lo GH, LaValley M, McAlindon T, Felson DT. Intra-articular hyaluronic acid in treatment of knee osteoarthritis: a meta-analysis. JAMA 2003;290:3115–21.
98. Hauser RA. Punishing the pain: treating chronic pain with prolotherapy. Rehab Manag 1999;12:26–30.
99. Ongley MJ, Klein RG, Dorman TA, et al. A new approach to the treatment of chronic low back pain. Lancet 1987;2:143–6.
100. Simpson LA, Waddell JP, Leighton RK, et al. Anterior approach and stabilization of the disrupted sacroiliac joint. J Trauma 1987;27:1332–9.
101. Dabezies EJ, Millet CW, Murphy CP, et al. Stabilization of sacroiliac joint disruption with threaded compression rods. Clin Orthop 1989;246:165–71.
102. Waisbrod H, Krainick JU, Gerbershagen HU. Sacroiliac joint arthrodesis for chronic lower back pain. Arch Orthop Trauma Surg 1987;106:238–40.
103. Arand M, Kinzl L, Gebhard F. Computer-guidance in percutaneous screw stabilization of the iliosacral joint. Clin Orthop 2004;422:201–7.
104. Calvillo O, Esses SI, Ponder C, et al. Neuroaugmentation in the management of sacroiliac joint pain: report of two cases. Spine 1998;23:1069–72.
105. Broadhurst NA, Bond MJ. Pain provocation tests for the assessment of sacroiliac joint dysfunction. J Spinal Disord 1998;11:341–5.
106. Young S, Aprill C, Laslett M. Correlation of clinical characteristics with three sources of chronic low back pain. Spine J 2003;3:460–5.
107. Maugars Y, Mathis C, Vilon P, Prost A. Corticosteroid injection of the sacroiliac joint in patients with seronegative spondylarthropathy. Arthritis Rheum 1992;35:564–8.
108. Gunaydin I, Pereira PL, Daikeler T, et al. Magnetic resonance imaging guided corticosteroid injection of the sacroiliac joints in patients with therapy resistant spondyloarthropathy: a pilot study. J Rheumatol 2000;27:424–8.
109. Hanly JG, Mitchell M, MacMillan L, et al. Efficacy of sacroiliac corticosteroid injections in patients with inflammatory spondyloarthropathy: results of a 6 month controlled study. J Rheumatol 2000;27:719–22.
110. Pereira PL, Gunaydin I, Duda SH, et al. Corticosteroid injections of the sacroiliac joint during magnetic resonance: preliminary results [in French]. J Radiol 2000;81:223–6.
111. Pereira PL, Gunaydin I, Trubenbach J, et al. Interventional MR imaging for injection of sacroiliac joints in patients with sacroiliitis. AJR Am J Roentgenol 2000;175:265–6.
112. Ojala R, Klemola R, Karppinen J, et al. Sacro-iliac joint arthrography in low back pain: feasibility of MRI guidance. Eur J Radiol 2001;40:236–9.
113. Karabacakoglu A, Karakose S, Ozerbil OM, Odev K. Fluoroscopy-guided intraarticular corticosteroid injection into the sacroiliac joints in patients with ankylosing spondylitis. Acta Radiol 2002;43:425–7.
114. Fischer T, Biedermann T, Hermann KG, et al. Sacroiliitis in children with spondyloarthropathy: therapeutic effect of CT-guided intra-articular corticosteroid injection [in German]. Rofo 2003;175:814–21.
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