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Techniques in Regional Anesthesia and Pain Management (2011) 15, 40-50

Sacroiliac joint dysfunction: From a simple pain in thebutt to integrated care for complex low back pain

Alfred L. Clavel Jr, MD

From the Fairview Pain Management Centre, Fairview-University of Minnesota Medical Center, Minneapolis, Minnesota,

and Minnesota Head and Neck Pain Clinic, St. Paul, Minnesota.

In the last 40 years, significant advances have been made in the understanding of the neurophysiologicprocesses involved in the experience of trauma and pain. This knowledge, together with the rapidgrowth and understanding in the behavioral health sciences, has expanded to include a much betterappreciation of how these fields are converging and contribute to a process called neuroplasticity. Thesebasic mechanisms common to all patients have important implications for clinical outcome and forimproving clinical practice. This article is written for clinicians who manage patients with sacroiliacjoint dysfunction, a specific type of nonspecific low back pain.© 2011 Elsevier Inc. All rights reserved.

KEYWORDS:SI joint dysfunction;Low back pain;Neuroplasticity;Integrated care

The approach to sacroiliac joint dysfunction (SIJD) andpain begins with establishing its place in the management oflow back pain (LBP). These 2 conditions are so interrelatedit is an oversimplification to separate them completely. Inthe United States, LBP is the second most common neuro-logic complaint after headache.1 It is the fifth most commoneason for all physician visits2 and is the reason for 50% ofll outpatient physical therapy visits.3 Men and women

appear equally susceptible with up to 80% of the populationexperiencing back pain during their lifetime.4 The preva-lence of LBP increases with age, peaking in the elderlypopulation between ages 70 and 79.5 The economic andsocial impact of LBP is well recognized with high rates ofdisability, lost productivity, and medical expenditures.

Any approach to low back pain must start with therealization that many conditions can contribute to or causeLBP. Many are rare and easily identified. Others are ex-tremely common even in asymptomatic individuals. Fortu-

The author has no conflicts of interest to disclose.Address reprint requests and correspondence: Alfred L. Clavel Jr, MD,

Fairview Pain Management Centre, Fairview-University of Minnesota Medi-cal Center, Suite 600, 606 24th Avenue S., Minneapolis, MN 55454

E-mail address: dclavel@comcast.net.

1084-208X/$ -see front matter © 2011 Elsevier Inc. All rights reserved.doi:10.1053/j.trap.2011.06.002

nately, most causes of acute and chronic LBP are benign.However, their impact is not. Traditional approaches dividepatients into acute and chronic categories. Patients withacute pain are divided into 3 categories, those with “redflags” for serious conditions, such as spinal compressionfracture; those with progressive neurologic signs and symp-toms, such as radiculopathy; and those with benign or non-specific low back pain. Sacroiliac (SI) joint dysfunction andpain fits into the latter category. You might say it is aspecific type of nonspecific low back pain. The literaturesuggests that nonspecific LBP accounts for 85% of acuteLBP syndrome.6 Recently, an additional classification hasemerged to include “yellow flags” or risk factors for delayedrecovery or progression from acute to chronic LBP. Manyfactors have been identified to predict the onset and delayedrecovery from acute LBP. Table 1 is 1 such classificationfrom Koes et al.7

Table 1 lists only a few of the accepted risk factors fordelayed recovery. Figure 1 (Fricton JR, unpublished data)shows how pain, risk factors, and chronicity can be inter-related. This diagram is hypothetical, but does illustrate afew very important themes, such as the progression from

peripheral to more central factors and the increasing level of

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41Clavel Sacroiliac Joint Dysfunction

complexity over time. However, the scale across the bottomof the graph can be quite variable. In some patients, thescale could be changed to either weeks or days with rapidaccumulation of risk factors for recovery. In some patients,they present with many premorbid risk factors making treat-ment complex from the beginning.

This article reviews our current evolving understandingof how these factors can be expressed through the nervousand musculoskeletal system and how these factors can com-plicate management and contribute to SI joint dysfunctionand “nonspecific” LBP.

Understanding SI joint dysfunction: Structuraljoint pathology vs joint dysfunction?

There is no other cause of back pain like SI joint dysfunc-tion and pain that challenges every clinician. This aspect ofcare is a source of passing disinterest to some, fascinationand keen focus for others, and frustration and confusion tomany clinicians who treat patients with low back pain. SIjoint pathology is not the same as SI joint dysfunction.Many pathologic conditions affect the sacroiliac joint. In-fection, traumatic disruption, metabolic bone diseases, andthe spondylarthropathies are a few well-described and ac-

Table 1 Risk factors for occurrence and chronicity of LBP

Risk factor Occurrence

Individual Age; physical fitness; weakness of back and ab

Psychological Stress; anxiety; negative mood or emotions; popain behavior

Occupational Manual material lifting; bending, and twisting;job dissatisfaction; monotonous tasks; poor wosocial support

Adapted by permission from BMJ Publishing Group Limited.7

Figure 1 Contributing factors. Reproduced by permission of J.

bFricton.

cepted pathologic states identified by imaging studies thatinvolve the SI joint. These inflammatory or pathologicstates typically do not cause any diagnostic confusion. Bycontrast, sacroiliac dysfunction and pain is a syndromecaused by a combination of pelvic rotation, joint locking,hypo/hypermobility, and/or muscular imbalance. There isno demonstrable radiographic joint pathology and the diag-nosis is made by physical examination. The examination isbased on pelvic alignment and mobility tests and provoca-tive maneuvers that stress the SI joint attempting to repro-duce the patient’s pain complaints. At the turn of the 19thcentury, as first reported by Goldwaith and Osgood,8 jointsprains were felt to be the primary cause of sciatica. Thisconcept lasted until 1930, when Barr and Mixter discovereda herniated disk and nerve root compression at surgery in apatient with refractory LBP treated for “SI joint sprain.” Theera of the disk either herniated or degenerative officiallystarted and has dominated most approaches to LBP.9 Un-ortunately, this conceptualization is not helpful in the vastajority of people with nonspecific LBP. Often, the disk

bnormalities appear to represent normal spinal matura-ion or are of insignificant magnitude to explain theatient’s complaints. So, where does SI joint dysfunctiont into the diagnosis or management? Many different

umbar stabilization patterns exist, as outline by Kendallt al10 in the book, Muscles Testing and Function withosture and Pain. SIJD represents an additional twisted

umbar stabilization pattern relying heavily on asymmet-ic activation of hip girdle structures. The forces createdy this pattern produce excessive tension or repetitivehear and torsional forces across the joint. Specific to thiswisted stabilization pattern are 3 possibilities: SI jointathology without SI joint dysfunction, SI joint pathol-gy with SI joint dysfunction, and SI joint dysfunctionlone. This article focuses on the latter, although it coulde applied to SIJD with pathology as long as the jointathology is addressed concurrently.

What is SIJD?

As described by Lewit,11 the SI joint is 1 of 3 joints in the

Chronicity

al muscles; smoking Obesity; low educational level; highlevels of pain and disability

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42 Techniques in Regional Anesthesia and Pain Management, Vol 15, No 2, April 2011

ment of the joint. However, the joint can be placed understrain indirectly and held in a rotated position by a group ofmuscles acting through the pelvic ring. In essence, thepatient is using their hip girdle to help stabilize the lumbro-sacral spine. Porterfield12 and Schamberger13 reviewed therelationships between different SI joint malalignment pat-terns and muscular dysfunction. Many different patterns andmuscular combinations exist. Sorting these out requirescareful physical examination and each pattern requires adifferent individualized treatment plan. For this article, themost common pattern is discussed: right anterior and leftposterior innominant rotation with sacral torsion. Figure 2shows how this pattern appears and leads to compensatorylumbar scoliosis and sacral torsion.

Figure 3 shows how activation of the right anterior hipgirdle muscles by a pattern of habitual activation and short-ening, acute guarding response from trauma, or both main-tains the rotation. Weakness or deconditioning of the corestabilizers allows this pattern to become dominant. Addi-tionally, the right piriformis muscle, if shortened or inspasm, will pull the sacrum against the ileum on the right,essentially locking the joint. Typically, in this state, manualtherapy or muscle energy techniques, in addition to relaxedstretching of the piriformis, is necessary to release the joint.While patients are aware of the “crooked” pelvis, theytypically do not know how to correct it. As muscles, ten-dons, or joints become sensitized from pain or trauma, thisbecomes the habitual guarding response. Over time, thispattern is subject to operant learning patterns, conditionedfear responses, and a stress response leading to increased

Figure 2 Right anterior-left posterior innominate rotation. ThisImplications for Medicine and Sport. By permission of Copyright

complexity. B

How prevalent is the condition?

Developmental studies by Pearson14,15 examining chil-dren found some degree of pelvic obliquity in 93% ofradiographs between ages 8 and 13. Longitudinal studies ofchildren and teenagers by Kline16 showed a gradual increas-ng prevalence of pelvic obliquity in boys from elementary75%) to junior (86%) to senior high school (92%). Most ofhese children were asymptomatic, clearly suggesting thatelvic malalignment is probably related to posture, musclembalance, and stabilization patterns. Thus, pelvis malalign-ent can exist with minimal clinical consequence. The

revalence of SIJD is unknown, but is estimated to rangerom 15% to 25% of patients with low back pain.17 In 1

large series of 1293 patients with LBP, SIJD was felt to bethe primary diagnosis in 22.5%.18 As noted in the compre-hensive review by Cohen,19 there are no standard long-termreatments. Additionally, recent studies have questioned theiagnostic validity of previously accepted physical exami-ation findings, provocative tests, and radiographic imag-ng. Even the once-accepted practice of diagnostic blocks toid in the assessment has been questioned with recent ad-ances in the neurobiology of pain and associated centrallasticity changes that occur in all patients in response to theain experience.17 Adding to this diagnostic confusion is theimultaneous occurrence of SIJD and other spinous pro-esses that cause LBP. In the review sited above18 of 1293atients with LBP 33% with SIJD were found to haveoexisting spinal sources of pain. The most common in-luded SIJD and posterior facet syndrome, lateral recessyndrome, and herniated nucleus pulposis, respectively.

was published in Schamberger W. The Malalignment Syndromeier.

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ernard and Kirkaldy-Willis18 found SI joint dysfunction in

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43Clavel Sacroiliac Joint Dysfunction

30% of patients with L5-S1 isthmic spondylolisthesis. Heconcluded the x-ray finding was incidental in these patients.In an additional study, Bernard and Cassidy19 found 43.6%f 250 patients had associated conditions contributing toBP. These included posterior facet syndrome (38), lateral

ecess spinal stenosis (31), herniated nucleus pulposus (15),umbar discogenic syndrome (20), and arachnoiditis (5).

Figure 3 Actions anterior hip flexors and piriformis in lockingSyndrome Implications for Medicine and Sport. By permission of

orty-two percent had a history of lumbar surgery. As noted s

y Shaw,20 the SI joint absorbs much of the rotational forcesf the typical reciprocal gait. In SI joint dysfunction, theseorces are transmitted to the longitudinal axis of the lumbarpine. This increased rotational strain would be maximal at4-5 and secondarily at L5-S1. Any coexistent structuralbnormality would be aggravated and may become symp-omatic. The compensatory scoliosis would cause additional

his picture was published in Schamberger W. The Malalignmentright Elsevier.

SIJ. T

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44 Techniques in Regional Anesthesia and Pain Management, Vol 15, No 2, April 2011

eral myofascial patterns21 refer to the SI joint area. Theseinclude, but are not limited to, the piriformis, the gluteusmaximus and medius, and the quadratus lumborum. Thesemuscular pain syndromes can coexist with both spinal con-ditions and SI joint dysfunction or occur separately addingto diagnostic confusion. Therefore, any attempt to diagnosisand manage LBP with SI joint dysfunction must be madewith care and must include an understanding of how thiscondition can interact and sabotage treatments aimed atother sources of pain. Simply lumping these conditionstogether as nonspecific is an oversimplification of a com-plex condition.

Diagnosing SIJD

The precise diagnosis of SIJD is often difficult to makesince it can be associated with spinal pathology. Themost consistent pain pattern is unilateral pain localizedpredominantly below the L5 spinous process.22-26 Pa-tients often point directly to the SI joint (Fortins’ fingertest). Pain in the buttock over the SI joint, lower lumbar,lower extremity, groin, and upper lumbar are the mostfrequent described locations in decreasing order of oc-currence. Referral patterns can extend below the kneeand into the foot, sometimes confounding the diagnosiswhen there is coexisting spinal pathology. There are nodefinitive diagnostic tests for SIJD. Numerous physicalexamination maneuvers have been described to aid in thediagnosis of SI joint pain, but all suffer from poor intert-ester and intrarater reliability.27,28 False-positive resultson 3 tests were found in 20% of asymptomatic individ-uals.28 In clinical practice, physical examination tests are

ivided into provocative SI joint maneuvers or align-ent/mobility tests. Generally, reproducibility is greater

or provocative than for mobility/alignment tests18 andultiple positive tests may improve the diagnostic reli-

bility.29 Additional information can be integrated intohe assessment, by including a rectal examination search-ng for either referred pain from the prostate, rectum, orterus. Pelvic floor muscle spasm or myofascial tender-ess is often associated with SIJD. Myofascial examina-ion often discloses the appropriate muscle imbalancesnd posture asymmetries, guarding responses, and theatient’s preferred lumbosacral stabilization pattern. Thettuned observer may even notice ideomotor responsesssociated with various arousal states during the historynd physical examination. Lumbosacral stabilization rep-esents a learned movement pattern, is stored in proce-ural memory, and thus changes depending on the phys-ological state of the individual. The sitting-lying test orhe supine long sit test is often helpful as an initialcreening test for pelvic rotation. In this test, the apparenteg length paradoxically switches as the patient movesrom lying to sitting long leg position.

Radiographic studies are helpful in diagnosing SI joint

athology but both plain films and computed tomography

cans demonstrate abnormal degenerative changes in upo 24% of asymptomatic individuals over the age of 50.27

Many of the above studies used “diagnostic” SI jointinjections as the gold standard for diagnosis. Interpretationsof diagnostic injections attempting to block the “pain gen-erator” become problematic once central sensitization andneuroplastic changes have developed. In a recent meta-analysis focusing on the diagnostic validity of the Interna-tional Association for the Study of Pain criteria for SI jointpain by Szadek et al,30 the thigh thrust test, the compressionest, and 3 or more positive screening tests had discrimina-ive power for diagnosing SI joint pain. Because no goldtandard exists, combining a careful history with a physicalxamination, judicious use of diagnostic tests, and “diag-ostic” injections is always warranted.

CNS response to injury, trauma, and adaption

It is impossible to develop treatment plans for LBP andignore the trauma response and its implication for long-termoutcomes. Similarly, it is impossible to discuss SIJD with-out addressing how the central nervous system (CNS) re-sponds to trauma. It is well established that repetitive noci-ceptive stimuli can lead to lasting changes in synapticplasticity in the dorsal horn of the spinal cord in a processcalled central sensitization.31,32 A similar, but physiologi-cally distinct process, leads to peripheral sensitization.33

Reorganization of nociceptive and nonnociceptive afferentsoccurs throughout the brain in cortical and subcortical re-gions, the brain stem, and spinal cord.34 Thus, the CNSchanges in response to the pain experience. The pain re-sponse is not “hardwired” and unchangeable, but is plasticand malleable. This process includes the contributions ofmicroglia,35,36 thus implicating the immune system as partf the normal processing of experience. In this way, thendividual is capable of learning, changing, and adapting toast experiences. This psychophysiologic response includeshanges in neuronal, immunologic, and hormonal systemsacilitating communication from the body to the mind andise versa. The ability to increase sensitivity followingxposure to an injurious sensation allows future responseso occur readily and with a reduced threshold.37 This height-

ened sensitivity leads to both misinterpretation of innocuousstimuli as a potential threat and exaggerated response toboth painful and nonpainful sensations. These responses canbe confusing to both patients and providers without aware-ness of central sensitization. These patients may becomedesperate looking for a “fix” to their pain and becomeincreasingly vulnerable following failed treatment. Somewill agree to almost anything that could possibly help.Furthermore, as pointed out by Waddell et al,38,39 patientswith these exaggerated responses are poor surgical candi-dates. This would make sense, since the physiologicalchanges in the CNS would not likely respond to a peripheralanatomic treatment and may only increase after furthertrauma from surgery. Thus surgery by itself would be ex-

pected to have poor outcomes when behavioral responses

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45Clavel Sacroiliac Joint Dysfunction

and examination findings suggest associated CNS changes.Examples of his phenomena of heightened sensation arepresent in many published articles on LBP. For example,Carragee et al40 found a false-positive lumbar discographyrate of about 25% in asymptomatic individuals. These find-ings correlated with annular disruption, abnormal psycho-metric findings, and chronic pain states, suggesting degen-erative changes, emotional states, increased arousal withchronic pain, or some combination of all 3 or other factorsthat can contribute to this response. In a related articledemonstrating altered sensory processing, Carragee et al41

found asymptomatic patients with prior iliac bone harvest-ing for nonlumbar surgery could not separate spinal (dis-cography) from nonspinal sources of pain, again suggestingthis misinterpretation of stimuli. This misinterpretation ofstimuli raises questions about the practice of blocking the“pain generator” as an appropriate isolated treatment forpatients with both peripheral and central sensitization.

As outlined by Perry et al,42 the neurobiology of traumand adaptation involves multiple systems within the brainnd spinal cord well beyond the facilitation or sensitizationf the nociceptive stimulus. These response patterns canead to hyperarousal or dissociation, but typically, someombination of the 2. The fight or flight response is asso-iated with changes in norepinephrine and epinephrine andigrostriatal dopamine, while the dissociative response isssociated with changes in endorphins, mesolimbic andesocortical dopamine, and �-aminobutyric acid. Clini-

ally, some patients remain guarded and braced with ele-ents of conditioned fear response; others disconnect from

heir bodies (pain) and repress affect and somatic percep-ion, while others have elements of both.

These physiological processes become learned in a stateependent fashion.43 In either case, patients tend to be

unaware of their responses and appear frozen and guarded,hoping someone can fix them, usually focused on a periph-eral treatment. A person’s acute stress (fight, flight, orfreeze) response to injury and trauma varies in length de-pending on the injury and tissue damage and innate factorssuch as an individual’s resilience, supports, and underlyingvulnerability. The introduction to this article included apartial list of some of these factors important to LBP. Anindividual’s response to repetitive trauma (repetitive backinjuries) will develop in a use-dependent fashion based onthe accumulation of experiences. Thus the acute stress re-sponse will gradually become increasingly sensitized overtime, leading to heightened and prolonged responses. Thispattern can generalize to surrounding tissues. This repetitivepattern leads to tonic hyperarousal and conditioned fear ofmovement. The old adage, “once bitten, twice shy” is thewell-recognized behavioral correlate to this physiologicalpattern. The memory of the experience is stored not only inour consciousness, but also in our body. This is the differ-ence between explicit (conscious) and implicit (subcon-scious) memory systems. The subconscious refers to thesubcortical brain areas, the brain stem, spinal cord, and

peripheral nervous system. In the child, the typical response

becomes the organizing template for future adaptation tostress and pain, explaining the risk factor of child maltreat-ment for chronic pain.44 In the adult, repetitive traumaticxperiences or persistent pain can be built upon the originalemplate in the process of central sensitization and implicitearning to reorganize the receptive fields throughout thepinal cord, brain stem, and brain. This helps explain howepeated injury or strains leads to prolonged reactionschronic pain), exaggerated responses, and generalization ofhe response. In this way, the nervous tissue is able toniquely store each experience and unfortunately each in-ury. These neuroplastic changes lead to central sensitiza-ion and more complex behavior responses such as muscleemory, guarding responses, and muscle tension.This heightened responsive state includes cutaneous,

eep muscular (myofascial) and joint tenderness, and eveneferred visceral responses. Central sensitization, a naturallyccurring neurobiological form of learning from experi-nce, can be modified by classical and operant conditioning,hus either increasing or decreasing its magnitude.45

Many of these central changes can be altered and reducedwith specific therapy and rehabilitation. Hyperarousal anddissociation can be addressed with specific forms of ther-apy, decreasing autonomic nervous system activation, andincreasing somatic awareness, while mental rehearsal, im-agery, and physical practice produce changes in the brainmotor systems and in cortical receptive fields.46 These

ovements must be very specific. An analogy would beomeone learning to play the piano. Practicing a specificong 1 to 2 hours a day, physically, mentally, or withmagery, leads to learning and gradual mastery. Randomlyitting keys in no sequence or pattern does not have theame effect. This means rehabilitation for SIJD must bepecific to the unique malalignment pattern and the uniquerauma/adaptive response of the individual. Failure to ad-ress either the peripheral or the central pattern leads toncomplete recovery and chronic pain.

Treatment of complex pain and trauma requires address-ng the unique adaptive response of the individual. A num-er of factors tend to trap patients in the “cycle of immo-ility.” Re-experiencing pain, fear, or rage is common withttempted reactivation and movement, economic hardshipnd daily financial worry,47 feeling trapped in the workersompensation systems, and being told you have degenera-ive spine disease and nothing can be done. Most individualsecome frozen in worry, fear, and eventually hopelessness.reatment requires reversing these ideas with carefully de-igned programs that simultaneously address all factors.

Treatment planning

Over the past three decades, several emerging areas ofinvestigation have provided evidence on the important im-pact that stress, mood, and psychophysiologic states canhave on the development, course, and outcome of medical

illness.48

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46 Techniques in Regional Anesthesia and Pain Management, Vol 15, No 2, April 2011

Recent breakthroughs in our understanding of painmechanisms including central sensitization, wind-up, neu-rogenic inflammation, neuroplasticity, cortical reorganiza-tion, and our understanding of psychoneuroimmunologycontinue to shape our understanding and resultant treat-ments for those who suffer from chronic painful conditions.These advances are transforming our understanding of ill-ness and disease from a clinicopathologic view of structure,function, and pathology to a deeper appreciation of under-lying dynamic physiological and molecular processes thatmodulate the pain experience and healing process. At thesame time, our knowledge and understanding in the behav-ioral health sciences has expanded to include a much betterappreciation of underlying molecular and physiological pro-cesses. It is only natural to notice how these 2 systems notonly overlap but also are intimately connected and related.The line between peripheral and central processes has gonefrom separate to blurred to overlapping in the last decade asit is now accepted that both factors influence each other ona cellular and molecular basis. These new developments arechallenging our traditional approaches to the treatment andmanagement of both acute and chronic conditions. Initially,from an empiric observation, and now, from a molecularand physiological perspective, we are rapidly discoveringthe neurobiological mechanisms that provide the connectiv-ity and interaction between the mind and body. Treatment ofSIJD requires a working appreciation of these factors be-cause ignoring either peripheral or central factors can com-promise treatment outcomes.

Reality

The reality of clinical practice is that practitioners treatpeople, not neurons, disks, joints, or muscles. Many treat-ment approaches work with some patients some of the time,which explains why some clinicians are adamant about 1therapy or another. The art of medicine involves knowingwhat therapy to use on a particular problem or patient at aparticular time. This includes identifying what constitutesmeaningful spinal pathology. Thus, individualizing care re-quires matching specific treatment options to the needs ofthe patient vs asking the patient to conform to 1 approach.Additionally, patients present with beliefs about the treat-ment they desire, with various degrees of readiness fordifferent treatments, and with limitations in insurance cov-erage and financial concerns. Understanding and adjustingtreatment to the patient’s complexity often leads to moreengaging response from the patient. Comprehensive conser-vative care requires balancing all of these factors in thetreatment planning process and decision-making. Informedconsent is all about providing information and educationabout both peripheral and central factors so the patient canunderstand relevant clinical options and recommendations.This is especially true before surgery, as surgery in essencerepresents a peripheral treatment and additional trauma tothe region potentially worsening central sensitization, a cen-

tral process, and thus creating chronic pain. Dr. Macrae q

discusses the growing recognition of chronic postsurgicalpain as a significant risk and public health concern.49 It alsosuggests that preparing people for surgery by addressingcentral factors and modifying their trauma response beforeexperiencing the trauma of surgery could lead to improvedsurgical outcomes. Are LBP and SIJD a peripheral disorder,a central disorder, or both? How you conceptualize LBP andSIJD will have profound implications in treatment.

From the discussion above, pelvic malalignment is acommon finding in asymptomatic people. This is similar toother physical examination findings in the general popula-tion such as poor posture, limited lumbar stability, loss offlexibility, and deconditioning. Similarly, the same can besaid for magnetic resonance imaging findings of the lumbarspine. When is it important to treat SIJD as part of themanagement of LBP? The following discussion describesthe continuum of care for patients with SIJD. Standardmedical treatments with nonsteroidal anti-inflammatorydrugs, muscles relaxants, adjuvants, and pain medicationshave been omitted for clarity, but in clinical practice areused to help facilitate treatment and rehabilitation.

Distinguishing simple from complex SIJD

SIJD can range from simple postural syndromes tohighly complex mind-body syndromes involving multiplecontributing factors. The difficulty in treatment involves theintegration of peripheral factors of SIJD and associatedspinal conditions with central factors of stress, trauma, andadaptation with the needs and skills of the individual. Fail-ure to assess for and address the entire problem may lead tovariable effectiveness of treatments. Not understanding themeaning of the pain in the person’s life could represent anoversimplification of the problem. For example, teachingrelaxation exercises as the only treatment to someone witha fractured arm is obviously ineffective. Similarly, casting afractured arm in someone whose injury occurred in a motorvehicle accident involving the death of a loved one missesthe complex nature of traumatic injuries and central re-sponses that contribute to illness and/or healing. Thus, it isvery important to match treatments to the complexity of theproblem to maximize success.50 Simple SIJD presents asingle, rather than multiple, pain diagnoses of recent onsetnd with defined behavioral factors. Patients are motivatedor self-care, can achieve muscular relaxation, and are ableo identify multiple triggers for increased pain. There isood marital and family support and work record. Centralensitization is minimal. Complex SIJD patients presentith multiple diagnoses evolving over time, mixture ofsychosocial and behavioral factors, have trouble relaxing,nd have poor motivation for self-care. Additionally, mar-tal and family dysfunction, poor social supports, litigation,ultiple medications and treatment failures complicateanagement over time. Regional or generalized central

ensitization patterns exist. Last, premorbid psychologicalnd adjustment difficulties or significant tissue injury re-

uiring prolonged recovery suggests the need to expand

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47Clavel Sacroiliac Joint Dysfunction

treatment to an integrated multidisciplinary team of provid-ers from the onset.

Treatment

Simple SIJDHow do we apply this approach to SIJD? On 1 side of the

spectrum, SIJD represents a simple developmental or habit-ual stabilization pattern in which asymmetric activation ofhip girdle muscles have become increasingly involved inlumbar stabilization. Normally, hip girdle muscles are in-volved primarily with movement and secondarily with staticstabilization. However, with certain habitual postures orstances, certain muscles become shortened and strong whileother muscles become elongated and weak. As mentionedearlier, many different lumbar stabilization patterns exist asoutline by Kendall et al.10 SIJD represents a twisted lumbarstabilization pattern relying heavily on asymmetric activa-tion of hip girdle structures. Frequently, the individual isunaware or vaguely recognizes the postural asymmetry. Atthis stage, most people are either asymptomatic or avoidcertain activity that causes problems. While many patternsare possible, the most common pattern is seen in patientswith a right anterior and left posterior innominant rotation.Importantly, at this stage no significant central sensitizationhas developed; behavioral factors are easily defined, and notrauma response exists. Thus, most involved structures,right SI joint and right anterior hip girdle muscles, rightpiriformis, and left posterior hip girdle muscles, are mini-mally tender to touch or mildly sore with overuse or stretch-ing. Patients may recognize hip girdle stiffness and rotatedstance. Stress and muscle tension issues are manageable.Treatment is fairly simple, focusing on helping the patientfirst recognize the asymmetry with proprioceptive and kin-esthetic awareness exercises and self-monitoring, then self-mobilization exercises such as muscle energy techniques,self-myofascial release techniques such as ischemic com-pression or relaxed stretching, followed by therapeutic ex-ercises to correct the muscular imbalances and promoteproper lumbar stabilization. Notice the heavy reliance onself-management. This is a chronic pattern that will simplyreturn again and again unless a new pattern is createdfocusing on the transverse abdominis, multifidis, and thepelvic floor as the primary static stabilizers. The routinemust be repeated multiple times during the day for 15 to 30seconds to gradually create a new learned dominant patternof stabilization over 3 to 6 months. Many patients feel muchbetter with the simple program and it is often self-re-en-forcing over time with patients developing both a sense ofmastery and confidence.

Intermediate SIJD

Intermediate cases typically develop around a fewthemes. The first theme is people with preexisting rotations

where changes in stress or prolonged overuse cause exces-

sive tension or repetitive shear and torsional forces acrossthe joint. Pregnancy with related hormonal changes or in-juries to 1 lower extremity leading to altered gait dynamicswould fall in this group. People with preexisting rotationswill guard in the rotated pattern as their dominant form ofstabilization. Treatment must focus on managing the guard-ing response, addressing the stress response, correcting themalalignment with self-mobilization, and performing ther-apeutic exercises to restore muscle balance and stabiliza-tion. Pacing recovery is often needed. This is similar to thesimple group except additional care must address stress andbehavioral factors. Reactive anxiety or frustration is oftenpresent. The second theme is people with acute traumacausing the rotational pattern. Common initiating injuriesare falling on the buttock (ischial tuberosity), misstep off acurb or stair, or lifting a heavy object while in a twisted bentposition. These are accompanied by different degrees ofinjury, pain, muscular guarding, and central sensitization.The people with acute traumatic causes can be treated ef-fectively with manual techniques and SI joint injections ifdone before the guarding response becomes overlearned oroperant to environmental factors. In these cases, breakingthe pain response by blocking the peripheral pain generatorleads to rapid recovery. Fritz et al3 set a cutoff of 16 daysefining recent onset when traditional manual techniquesre most effect. They reviewed recent advances in the sub-rouping of patients with acute LBP to match therapy toatients instead of directing patients to respond to the pre-erred treatment of the provider. However, the longer theotation and guarding response persists, the greater centralssues such as central sensitization, learning, and stressecome contributing factors. Boudreau et al46 reviewed the

role of motor learning and neuroplasticity in designing re-habilitation plans for this more complicated group. He notesthat a simple walking, reconditioning, or strengthening pro-gram is insufficient or lacks the specificity to change corti-cal and other central changes. The movement patterns arestored in procedural memory and can only be changed byhard work on the part of the patient. Think of how muchwork would be required to change the way you walk on aregular daily basis. The movement pattern changes muststart while working directly with the physical therapist,but are later cued independently by the patient at home orwork under all levels of stress. Fortunately, no one needsto have perfect stabilization, but to develop awareness oftheir different patterns and regulate or manage them.Thus, intermediate cases can be differentiated from sim-ple cases by the additional complex central factors thatrequire time to modify and change before the new stabi-lization pattern becomes dominant. At this stage, treat-ment must include the management of both central andperipheral factors, recalling that peripheral factors affectcentral processes and central factors affect peripheralmechanisms in a reciprical fashion and must be managed

simultaneously.

48 Techniques in Regional Anesthesia and Pain Management, Vol 15, No 2, April 2011

Complex SIJD

Complex cases start with elements of either simple orintermediate cases, but have preexisting or rapidly accu-mulate central factors in addition to peripheral factors.Now the complex interplay of pain, altered movementpatterns, learned responses, and memory is stored in bothperipheral and central sensitization and neuroplasticitychanges throughout the CNS. These changes are based onrepeated neuronal firing in a use-dependent process andcan only be changed in a similar but different repetitivepattern. Recall from earlier discussions that repeatedstates become traits. Early on in treatment, conditionedfear of movement, coexisting depression and anxiety, orlow motivation for self-care suggest complexity from theoutset. Problems created by personal injury and workerscompensation if present are additive. An especially com-plex situation can develop when certain adaptive re-sponses to trauma and pain become state dependent,43

meaning the combination of flight/fight/freeze responsesare associated with high levels of somatic disconnection.These people have trouble relaxing, have poor awarenessof muscle tension and guarding responses, and strugglewith regulating and integrating change into their life thatinjury and treatment require. Basically, as people cope byignoring, disconnecting, or pushing-away pain, all ini-tially adaptive in coping with acute pain, over time, thiscoping style can become problematic by reducing so-matic awareness needed for later recovery and changingmovement and stabilization patterns. Central sensitiza-tion can seem to spread to adjacent structures or gener-alize. These patients often appear stuck in the “acute painmodel” looking for the missed diagnosis or the quickresolution to their condition and poorly tolerate rehabil-itation and pain management strategies. This group re-quires comprehensive integrated treatment plans withexpectations of incremental change and improvementover time. Helping the patient safely reconnect to theirbody by strategies that incrementally improve somaticawareness while managing fear and autonomic arousal iscritical for success. Outcome is dependent on patient’swillingness to address all peripheral, behavioral, and psy-chosocial factors and health providers offering treatmentstrategies that match the patient complexity. Complexpatients need to be managed by an interdisciplinary teamof health professionals in a supportive environment toeffectively modify contributing factors and illness behav-iors while progressive rehabilitation, new motor learning,and neuroplastic change develop. Also, complex casescan be present from the outset, develop rapidly depend-ing on the severity of injury or the individual’s responseto trauma and injury, or gradually develop over time withaccumulation of contributing factors. While no controlledstudies exist using this treatment classification, recent

studies provide evidence indicating enhanced outcomes

in patients with LBP by addressing contributingfactors.51,52

Coexisting spinal pathology

The treatment of SIJD includes the management ofcoexisting spinal pathology that can create altered move-ment patterns, guarding responses, central sensitization,and neuroplasticity. These changes can become inter-twined with patterns created in SIJD. For example, thecompensatory scoliosis that accompanies pelvic obliquitycan aggravate lower lumbar degenerativespine or facetdisease. The complete discussion of managing the oftencoexisting conditions is beyond the scope of this article,but all patients must be fully assessed and an individu-alized treatment approach developed to address factorsfrom all 3 areas.

Conclusions

In summary, recent advances in the neurobiology of painhave provided incontrovertible evidence indicating al-tered CNS processing is critical to our understanding ofLBP. Understanding and developing a treatment strategyfor SIJD, a specific type of “nonspecific” LBP requiresintegrating this information with traditional “peripheraltreatments” for this challenging disorder. Additionally,addressing psychosocial and behavioral factors simulta-neously with strategies promoting new motor learningand neuroplastic changes with progressive rehabilitationprovides an opportunity to more effectively treat complexpatients and improve outcomes. The conceptualization ofboth peripheral and central factors and their integrationinto treatment simultaneously, by matching patient needsand complexity, allows for addressing all salient aspectsof care. This approach accepts central changes as a nor-mal response to injury and pain, while affording theopportunity to design treatment strategies that addressbehavioral factors, neuroplastic changes, and psychoso-cial elements with peripheral treatments in an integratedfashion. This approach places increased importance onself-care and self-reliance inviting the patient to be partof the process and solution. The development of compe-tence and mastery helps reduce fear, anxiety, and uncer-tainty, which is necessary to reduce central amplificationof pain. Last, this model illustrates how treatment mustmove beyond aerobic reconditioning and strengthening toinclude approaches designed to facilitate new motorlearning and neuroplasticity changes.

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