Are You Misdiagnosing Sacroiliac Joint Dysfunction?
The Value of Medical History and Physical Examination in Diagnosing Sacroiliac Joint Pain
Neural Therapy By Hunere
Epidemiology of pelvic pain and low back pain in pregnant women
An Integrated Model Of "Joint" Function And Its Clinical Application
Analysis of Hip Strength in Females
Pelvis and Sacral Dysfunction in Sports and Exercise
Role of Manual Therapy in the Evaluation and Treatment of a Surgically Stabilized Pelvis
The Sacroiliac Joint: An Underappreciated Pain Generator
Core Stability Measures as Risk Factors for Lower Extremity Injury in Athletes
Evaluation and treatment of the most common patterns of sacroiliac joint dysfunction
Functional and radiographic outcome of sacroiliac arthrodesis for the disorders of the sacroiliac joint
Hip Abductor Weakness in Distance Runners with Iliotibial Band Syndrome
Lumbar back and posterior pelvic pain in pregnancy
Management of Patellofemoral Pain Targeting Hip, Pelvis, and Trunk Muscle
Percutaneous Fixation of the Sacroiliac Joint
Renewed Treatment for Low Back Pain
Quadrupedalism, bipedalism, and human pregnancy
Reliability and Validity of the Active Straight Leg Raise Test in Posterior Pelvic Pain Since Pregnancy
Sacroiliac (S-I) Joint Dysfunction and Low Back Pain
Sacroiliac Joint Dysfunction in Athletes

* Please Note: The following article is provided by Body Mechanics & Gainesville PT for the sole purpose of educating and informing our current and future patients.

Sacroiliac Joint Dysfunction in Athletes

P. Gunnar Brolinson, DO, FAOASM, FAAFP*, Albert I. Kozar, DO, and Greg Cibor, DO
*Edward Via Virginia College of Osteopathic Medicine, Virginia Polytechnic Institute, 112 Merryman Center, Blacksburg, VA 24061, USA
Current Sports Medicine Reports 2003, 2:47-56 Current Science Inc. ISSN I 537-890x
Copyright 2003 by Current Science Inc.

The sacroiliac (SI) joint is a common source of low back pain in the general population. Because it is the link between the lower extremities and the spine, it sustains even higher loads during athletic activity, predisposing athletes to a greater probability of joint dysfunction and pain. The diagnosis and treatment of SI joint dysfunction remains controversial, due to complex anatomy and biomechanics, and a lack of universally accepted nomenclature and terminology, consistently reliable clinical tests and imaging studies, and consistently effective treatments. This article clarifies these issues by presenting a model of SI joint anatomy and function, a systematic approach to the diagnosis of dysfunction, and a comprehensive treatment plan.

General history
The concept of the sacroiliac (SI) joint as a pain generator is now well established. However, the evaluation and treatment of sacroiliac joint dysfunction (SIJD) is controversial. One issue is the broad categorization and terminology utilized for the anatomic etiologies of the pain by various health care practitioners. Controversy also exists because of the complex anatomy and biomechanics of the SI joint. There is no specific or salient historic issue, nor single clinical examination technique, that is both sensitive and specific for the diagnosis of SI dysfunction. To date, imaging studies do not distinguish the asymptomatic from symptomatic patient population, nor is there a gold standard for treatment [1]. This article reviews a number of studies and describes several different models put forth regarding this difficult clinical entity Further, it focuses on the functional significance and similarities between models, and illustrates how a functional and principle-centered approach to the diagnosis and management of this entity is essential in the athletic population. Although individual physical examination testing procedures appear to be unreliable, SI joint function and dysfunction are best evaluated by applying a consistent palpatory and functional examination technique, and adopting criteria and nomenclature to develop a systematic approach to this diagnostic dilemma. Accurate diagnosis is always based on a combination of historic clues, along with findings from static palpatory examination, segmental and regional motion testing overall functional biomechanical examination, and appropriate diagnostic testing.

Because of the unique nature of sport and the tremendous demands that most sporting activities place on the spine and pelvis, SIJD is well recognized by athletes and athletic medical practitioners. In fact, some authors describe SI dysfunction as a common problem in elite athletes, but a clinical entity that has been largely unstudied in the medical literature [2]. One study evaluating members of the United States Senior National Rowing Team indicated a prevalence of SI dysfunction in 54.1% of team members, and more common in sweep rowers (66%) than scullers (34%) [2]. SIJD may account for as much as 20% of low back pain complaints in the general population [3,4].

Rowers are a group of athletes at risk for SI dysfunction secondary to the biomechanical demands of rowing. The pelvis is relatively fixed while primarily transverse plane loads are applied through the lumbosacral region. These muscle action imbalances may disrupt the normal equilibrium of muscle function around the pelvis and SI region. Similarly, lumbosacral dysfunction has been described in cross country skiers, due to the increased use of the asymmetrical V-skating technique of high-performance skiers [5].

In addition to these specific examples, SIJD and the resultant symptomatology can develop in any sport that places significant biomechanical stress through the lumbar spine and pelvis. This region serves as a force transfer link between the lower extremities and torso, and as such is an at-risk region for athletic injury.

Muscles, ligaments, and neural structures of the low back
The anatomy of the SI joint must be viewed conceptually as the entire I umbosacral region and pelvis. From an anatomic perspective, this region is best viewed as a continuous, ligamentous stocking based on the interconnections of the various regional ligaments and fascial structures outlined in the literature [6]. This ligamentous stocking is the primary support of the osseous elements throughout the lumbosacral pelvic region, and is anchored through the thoracolumbar fascia of the back, and the hamstringsacrotuberous ligament complex of the pelvis (Fig. 1). Throughout this ligamentous sling is a large sheet of fascia that is the attachment site for multiple major muscle groups of the spine, abdomen, and upper and lower extremities. This fascia contains both a small-caliber, unmyelinated C-fiber system, typical of nociceptors and sympathetic axons, and a large-caliber fiber system with encapsulated endings, typical of mechanoreception and proprioreception. Force transfers through this region may be under the proprioceptive control of neural elements within this tissue. There are at least three separate sources of these small-caliber primary afferent fibers throughout the region 17o. Aside from their role in the maintenance of normal tissue tension and the propagation of possible prolonged inflammatory responses, the interactive role of these neural elements is essential to the normal trophic activity of this tissue. The stability and instability of this region is dependent upon these muscular and ligamentous relationships, and it is their breakdown and degeneration that can lead to chronic pain syndromes. The continuous nature of this ligamentous stocking gives the entire lumbosacral pelvic region a unitary function.

During the 10th week of gestation, a cavity begins to form in the area of the SI joint. This joint cavity fully develops into the SI joint by the 8th month of gestation [8]. During childhood, changes develop in the SI joint as the child starts to walk, and intra-articular ridges and depressions are developed secondary to an adaptation to gravitational stress through the SI joint Ultimately, the joint assumes an L-shape in the adult, the intended purpose to provide increased stability.

The adult SI joint demonstrates both a diarthrodial and a synovial joint [9]. it becomes a well-defined L-shaped articulation with an upper, long vertical pole and a short, lower horizontal pole. Some have described this as an S- or a C-shaped articulation [10]. There is significant variability of this joint between individuals [8]; it can vary widely with respect to size, shape, and surface contour, even within the same individual. The horizontal pole articular compartment of the SI joint always includes the second sacral segment, and rarely includes L4, L5, or 54 segments [11]. In approximately 30% of SI joints there is the potential for a vertical shearing effect based on the angle of articulation112,13].

Age-related changes
Moderate adaptive changes begin to occur on the iliac side of the joint as early as the third decade, especially in men [14]. There also appears to be an increase in size and number of elevations and depressions within the joint, which most likely represent adaptations to increased gravitational stress [8]. During the sixth and seventh decades there is progressive advancement of these adaptive changes, and thickening of the capsule; sometimes deep erosions exposing the subchondral bone, resulting in degenerative joint disease, is often noted. With increasing age, the capsule becomes less cellular and relatively more collagenous, and through the fifth and sixth decades becomes more thickened and fibrous.

Of neste; there do appear to be accessory articulations, with an incidence of anywhere from 8% to 35%, that seem most likely to develop in the posterior portion of the articulationnear 52. These are possibly acquired as a result of weight-bearing stress [8].

History of the motion argument
There have been conflicting studies regarding the mobility of the SI joints. For some time it was generally accepted that there was motion early in life, but progressively less motion as the degenerative changes of the joint took place, and many investigators felt that the joints eventually fused. Clinicians now feel that motion occurs throughout life [1]. Hypocrites. first described pregnancy-related motions of the SI joint in the fifth century BC. In 1589, Dimerbroch 1864, Von Luschka was the first to categorize the SI joint as a diarthrosis, suggesting the idea of motion. In 1905, Goldthwaith and Osgood described ST joint overuse and hyper-mobility leading to lumbar plexus irritation and ischialgia. In 1909, Albee described it as synovial and mobile. Many of these early studies were conducted on cadavers, and led to conflicting reports in the literature. In 1920, Halladay was the first to study unembalmed corpses, and found asymmetrical SI joint movements. He found that these movements also led to movements in the pubic symphysis, and that back hyperextension leads to displacement of the sacrum with respect to L5. Much of his work was the basis for spinal mechanics, further developed by the osteopathic profession. In 1921, Smith-Peterson described an SI joint arthrodesis that was effective for ischialgia, and in 1934 Cyriax stated that the SI joint subluxation can be measured by comparing leg lengths.

In the modern area, Bowen and Cassidy [8] were the first to demonstrate that the SI joint is patent throughout life, and in 1991 Ostgaard et al. [15] reported that SI joint pain was one of the most common etiologies of low back pain during pregnancy. In a number of studies throughout the 1990s, Vleeming et al. [16,17] showed that the intraarticular ridges and depressions that are found as we progress through life are actually adaptations to the forces on the SI joint. These adaptations increase the stability of the joint, and imply its underlying mobility.

Actual validation of SI motion has been dearly established in the modem era via dinical evidence and biomechanical studies. These studies note motion in both prolonged and abrupt load patterns. Vleeming et al. [18,19] showed that in vitro, loading tests showed SI joint mobility into old age, and that prolonged loading caused creep of ligaments. Buyruk et al. [20] used color Doppler imaging to assess joint stiffness and motion in live subjects in 1995, and the actual innervation of the joint was confirmed by Fortin et al. [21-23].

Biomechanical models of function have developed from the first description of load transfer from the spine to the lower extremities crossing through the SI joint, to the description of an integrated model of joint function [24oo].

Axis of motion
The osteopathic profession espouses that there are at least seven described axes of motion [25.]; however, these axes should not be thought of as absolutes, but as functional axes that occur pending the direction of forces applied through the joint. These include a left and right oblique axis, a vertical and anteroposterior (AP) axis, a vertical and sagittal axis, and three horizontal axes. It should be noted that none of these axes is rigid. The actual axis used depends on the motion and the summation of forces that move through the joint with a particular action.

In the normal gait cycle, there are combined activities that occur conversely in the right and left innominates, and function in connection with the sacrum and spine (Fig. 2) [26]. As one steps forward with the right foot, at heel strike the right innominate rotates posterior and the left innominate rotates anterior. During this motion, the anterior surface of the sacrum is rotated to the left and the superior surface is level, while the spine is straight but rotated to the left. Toward midstance, the right leg is straight and the innominate is rotated anterior. The sacrum is rotated right and side-bent left, while the lumbar spine is side-bent right and rotated left. At left heel strike, the opposite sequence will occur and the cycle is repeated.

Throughout this cycle there is a rotatory motion at the pubic symphysis, which is essential to allow normal motion through the SI joint. According to Greenman [26,27], pubic symphysis dysfunction in walking is one of the essential or leading causes of the development of SIJD. In static stance, when one bends forward and the lumbar spine regionally extends, the sacrum regionally flexes, with the base moving forward and the apex moving posterior. During this motion, both innominates go into a motion of external rotation and out-flaring. This combination of motion during forward bending is called natation of the pelvis. The opposite occurs in extension, which is called counternutation. As the sacrum goes into extension with the base moving posterior and the apex anterior, the innominate components internally rotate and in-flare. This motion is dearly demonstrated and illustrated by Kapandji [28].

Motion and respiration
The relationship of motion and respiration is very easy to demonstrate, by placing one's hand on the sacrum of a prone patient. As the patient inhales the sacrum extends (the base comes posterior and the apex moves anterior). This actually involves a whole countemutation of the pelvis (sacral extension and innominate out-flare/external rotation). The axis of motion in the SI joint is horizontal, and most likely roughly through the second sacral segment [29].

Motion Dysfunction
As previously noted, throughout later decades of life, the SI joint becomes less mobile due to adaptive changes in both the joint articulation and connective tissues. Some believe that these changes are actually the result of hypermobility in the joint and the body's own response to this motion [11]. Hypomobility in general appears to be common in clinical practice, in both acute low back and SI joint pain syndromes.

In the osteopathic profession, SIJD is broken down into iliosac_ral and SI dysfunctions [25o,27]. This is primarily a differentiation in terminology for identifying which part of the anatomy plays the major role in motion restriction. Fur. ther, the dysfunctions are named for their bony position of ease. Somatic dysfunction implies impaired or altered function of the related components of the somatic (body framework) system: skeletal, arthroidal, and myofascial structures and related vascular, lymphatic, and neural elements. There are three types of primary iliosacral dysfunction: 1) innominate shears, superior and inferior; 2) innominate rotations, anterior and posterior; and 3) innominate in-flare and out-flare. There are two main types of dysfunction: 1) sacral torsions, flexion and extension; and 2) unilateral sacral lesions, flexion and extension.

Torsions have both a right and left anterior and right and left posterior types. These are diagnosed when rotation is the primary component, although there is an additional side-bending component as well. Unilateral lesions tend to have a primary flexion or extension plus side-bending component, as opposed to a rotatory component. A bilat-, erally flexed or extended sacrum is also possible, which is often found in certain decompensated postures and during pregnancy [25o,27,29].

Gross SI joint instability is rare, but microinstability is a relatively common component seen in patients with recurrent SIJD. This microinstability often leads to chronic pain syndromes and must be Treated as part of these complex pain presentations. Instability often occurs as a result of the loss of the functional integrity of any of the systems of the lumbosacral and pelvic region that provide stability. The myofascial or the osteoarticular and ligamentous components may be affected, as with chronic spondylolisthesis. Understanding this concept is critical, because it implies that a thorough evaluation of the lumbosacropelvic function must be carried out in the evaluation for SIJD, regardless of the origin of pain.

Subluxation indicates gross instability of the SI joint and is quite rare in the general athletic population. It is primarily described in injuries resulting in significant energy input, such as car and motorcyde accidents. Some evidence for this phenomenon has been described in the orthopedic and radiographic literature vis a vis joint arthrography with use of contrast, indicating some form of traumatic disruption of the SI joint [30].

Role of Sacroiliac Joint Coupling Between the Spine, Pelvis, Legs, and Arms
Biomechanics between the spine and pelvis
In 2001, Vleeming et al. [24oo] described their integrated model of joint dysfunction. This functional description comes from extensive study of the SI joint over the past 10 to 15 years, and is the most studied and supported model for SIJD. It integrates structure (form and anatomy), function (forces and motor control), and the mind (emotions and awareness) on human performance. Integral to the biomechanics of SI joint stability is the concept of a self-locking mechanism. The SI joint is the only joint in the body that has a flat joint surface that lies almost parallel to the plane of maximal load. It's ability to self-lock occurs through two types of dosure, form and force. Form closure describes how specifically shaped, closely fit contacts provide inherent stability independent of external load. Force closure describes how external compression forces add additional stability. It had long been thought that only the ligaments in this region provided that additional support. It is the fascia and muscles within the region that provide significant self-bracing or self-locking to the SI joint and its ligaments through their cross-like anatomic configuration. Ventrally, this is formed by the external abdominal obliques, linea alba, internal abdominal obliques, and transverse abdominals, whereas dorsally the latissimus dorsi, thoracolumbar fascia, gluteus maximus, and iliotibial tract contribute significantly. Additionally, there appears to be an arthrokinetic reflex mechanism by which the nervous system actively controls this added support system. These supports are critical in asymmetric loading, when the SI joint is most prone to subluxation. The important concept to gain from this understanding of integrated function with regard to treatment and prevention of low back pain is that SIJD is a "neuromyofascialmusculoligamentous" injury.

Coupled motion of contralateral latissimus dorsi and gluteus maximus
Vleeming et al. [31] defined the posterior layer of the thoracolumbar fascia as a mechanism of load transfer from the ipsilateral latissimus dorsi and the contralateral gluteus maximus (Fig. 3). This load transfer is critical during rotation of the trunk, helping to stabilize the lower lumbar spine and pelvis. This was demonstrated through cadaveric and electromyelographic (EMG) studies [32]. The stretched tissue of the posterior thoracolumbar fascia assists the muscles by generating an extensor influence, and by storing elastic energy during lifting to improve muscular efficiency.

Lumbopelvic rhythm and the hamstrings
Recent studies show there is both a functional and anatomic connection between the biceps femoris muscle and the sacrotuberous ligament [33-35]. This relationship allows the hamstring to play an integral role in the intrinsic stability Of the SI joint. It appears that the biceps femoris, often found to be short on the pathologic side in low back pain, may actually be a compensatory mechanism via the previously described arthrokinetic reflexes to help stabilize the SI joint. In healthy individuals, a normal lumbopelvic rhythm exists, during which the first 65 of forward bending is via the lumbar spine, followed by the next 30 via the hip joints. Increased hamstring tension prevents the pelvis from tilting forward, which diminishes the forward-bent position of the spine, which results in reducing the spinal load [36]. Normalization of the lumbopelvic rhythm is an essential component to treatment of low back papa and SIJD.

Gravitational strain
The model of suboptimal posture, though incomplete, has shown to be effective when used as a model to guide treatment [37-39]. Posture can be defined as the size, shape, and attitude of the musculoskeletal system with respect to gravitational force [40]. Subtle departure from ideal posture has been implicated as an important biomechanical factor in athletes with regard to injury because it results in increased mechanical stress throughout the body. Posture must always be evaluated as part of the biomechanical evaluation. The size, shape, and attitude of three cardinal bases of support should always be included: standing surface, the feet, and the base of the sacrum.

Tensegrity approach to the pelvis
Although still in development, a new biomechanical model of body design is tensegrity [41], which refers to a self-stabilizing system in which tension is continuously transmitted across all elements. Therefore, the stability of a tensegrity structure lies not in the strength of individual members but in the ability of all the members to distribute and balance mechanical forces. Current biomechanical models of spinal mechanics view the spine as a column or pillar. The sacrum as the base locks into the pelvis as a wedge or other gravity-dependent dosure. For human postures, this model may not explain the functionality present. According to Levin [42o], "the hallmark of a pillar is stability, but the hallmark of a spine is flexibility and movement." In the tensegrity model, triangulated structures (a truss) form the basis for inherently stable structures. When viewed three-dimensionally, they become the tetrahedron, octahedron, and icosahedron. Further, the sacrum, as opposed to being viewed as a wedge or base, is suspended as a compression element within-the ligamentous tension system of muscles, ligaments, and fascia. To date, cellular structure and mechanotransduction are established by this system [43-45].

An athlete who presents with pain in the area of the SI joints requires a thorough history and physical examination. Elements of the history should include the following factors:

1. The age of the patient, because many conditions occur within certain age ranges (ankylosing spondylitis versus osteoarthritis).
2. The type of sport in which the patient is involved.
3. The acuteness or chronicity of the pain. Was there an acute traumatic injury or a chronic repetitive injury?
4. The mechanism of injury.
5. For active pregnant women, remembering that pregnancy causes laxity of the SI joint and predisposes women to pain or injury.
6. Identification of provocative and palliative measures.The duration and frequency of the pain.
7. The quality and intensity of the pain as well as any radiation or referred pain (usually unilateral, dull, and deep, with radiation to buttock, posterior thigh, or groin).
8. Notation of previous low back injuries, with the treatments and outcomes.
9. The presence of red flags signaling more serious pathology including , but not limited to, weight loss, night pain and night sweats (cancer); fevers and chills (infection); dysuria and hematuria (nephrolithiasis); epigastric pain with nausea, vomiting and/or heartburn (peptic ulcer disease or pancreatitis); left-sided abdominal pain with melena, hematochezia, diarrhea and/or constipation (diverticular disease); pulsating abdominal pain with radiation to groin (abdominal aortic aneurysm [AAA]); and numbness, tingling, weakness and/or incontinence (radiculopathy or cauda equine syndrome).

Physical examination
The physical examination begins with observation of the athlete both statically and dynamically. One should evaluate the patient in standing, supine, and prone positions, and assess symmetry of the heights of the iliac crests, anterior superior iliac spines, posterior superior iliac spines, ischial tuberosities, gluteal folds, and greater trochanters, as well as symmetry of the sacral sulci, inferior lateral angles and pubic tubercles. Next, determine if there is any leg length discrepancy. One should realize that true leg length discrepancies will generally cause asymmetry and pain, whereas a functional leg length discrepancy is usually the result of SI joint and/or pelvic dysfunction. Assess posture for increased lumbar lordosis, which can result from sacral torsions.

Dynamic observation assesses for any asymmetry during both gait and specific motions characteristic of the patient's sport (eg, rowing). SI joint pain, pathology, and restriction may cause a decrease in stride length, leading to a limp of cause reflex inhibition of the gluteus medius, leading to a Trendelenburg gait.

Next, the examiner should look for decreases in both passive and active range of motion of the entire spine, hips, and knees. If pain with motion testing occurs, the patient should specifically identify the area of pain. One should always perform a thorough examination of the lumbar spine, hips, and knees because pathology in these areas can refer pain to the SI joint. A neurologic examination for radiculopathy should also be conducted, in addition to evaluating abdominal strength and overall flexibility.

There have been numerous functional (motion) and provocative (pain-producing) tests reported in the literature; however, none have consistently been shown to reliably diagnose SI joint dysfunction [3,46-48]. We feel that there are two major flaws in how these studies and others like them have been carried out. Dreyfuss et al, [3] assumed that pain production is an essential prerequisite to dysfunction. We feel that SIJD can be diagnosed based on motion restriction and tissue texture changes, especially in chronic pain syndromes when pain location can very greatly due to muscle imbalance and other factors. They all focus on assessing each test individually; however, SI screening tests must always be followed up with segmental motion testing and tissue palpation. When these tests are used together with a thorough history to create a clinical picture, they become significantly more reliable [49], much like physical exam tests for meniscal tears. Research is currently underway using SI joint injections under fluoroscopy to compare different provocative tests for reliability and accuracy. A detailed discussion of the numerous tests described for SIJD is beyond the scope of this review, but the reader is referred to several excellent sources [25o,27,.50]. Common tests include standing forward flexion, sitting forward flexion, stork (Gillet), Gaenslen, supine-to-sit, Patrick (Faber), side-lying approximation, and supine gapping. In osteopathic medicine, SI joint somatic dysfunction is diagnosed primarily by the standing and seated flexion tests, stork test, and asymmetry of pelvic and sacral bony landmarks [27].

Differential diagnosis
The differential diagnosis of SIJD is broad, and includes infection, inflammation (arthritic, metabolic and spondyloarthropothies), tumor (primary or metastatic), fractures (stress or traumatic), pregnancy, osteitis condensans illi, radiculopathies, spinal stenosis, facet syndrome, disco-genic pain, hip disease, and vascular (AAA), gastrointestinal, and genitourinary etiologies [1].

Diagnostic testing
There is no specific gold standard imaging test to diagnose SIJD, due largely to the location of the joint and overlying structures that make visualization difficult. However, standard radiographs taken at a 25 to 30 from the AP axis, and lateral views may show degenerative changes, ankylosis, demineralization or fracture [1]. Degenerative changes are usually first noted on the iliac side of the joint. If sclerosis involves the lower two thirds of the joint on both sides, sacroiliitis is common [51]. It should be noted that in adolescents, the SI joints can show widening and irregularity, and consequently can make diagnosis difficult.

Bone scans identify osteoblastic activity, and may signal infection, tumor, fracture, or a metabolic process. Computerized tomography will identify fractures, osteoid osteomas, and degenerative changes. Ultrasound Doppler imaging can capture SI motion in pregnant women with SI pain [ 52]. Finally, magnetic resonance imaging (MRI) helps to identify fractures, tumor, soft tissue pathology, and lumbar disc disease. MRI is most sensitive for identifying inflammatory sacroiliitis [1].

Traditional treatments of SIJD include analgesics, anti-inflammatory agents, ice, heat, and physical rehabilitation. We believe that a principle-centered, functional approach to evaluation and rehabilitation must be undertaken [53oo]. Physical therapy must focus rehabilitation on the entire abdomino-lumbo-sacro-pelvic-hip complex addressing articular, muscular, neural, and fascial restrictions, inhibitions, and deficiencies. The transverses abdominis has been shown to be the key muscle to functional retraining the core, due to its observed patterns of firing before and independent of the other abdominal musdes [54]. Exercise techniques that promote independent contraction of the transverses abdominis have been shown to lower recurrence rates after an acute low back pain episode [55], and lower pain and disability in chronic low back pain [56o]. Most recently, a study by Richardson eta!. [57o] appears to show that these clinical benefits focusing on the transverses abdominis occur due to significantly reduced laxity in the SI joint. Correction of leg length discrepancies, somatic dysfunction, inflexibility, and poor posture is fundamental. SI belts may be helpful in pregnant patients with hypermobile joints. Prolotherapy of the lumbo-sacral-iliac region has been shown to be effective in those athletes with chronic lumbar and SI joint pain due to instability [58o,59-62].

Sacroiliac joint injection with or without fluoroscopy has not been consistently shown to be effective [1,63-65], although, theoretically it should help to diagnose the SI joint as the source of pain. Similarly, periarticular injections also show inconsistent results [66,67]. In osteopathic medicine, manipulation is frequently used to treat SIJD. These dysfunctions are termed restrictions, that is, pelvic and sacral hypomobility. Osteopathic manipulation has been shown to be as efficacious as standard medical care in the treatment of patients with acute and subacute low back pain [68o]. In addition, patients treated with osteopathic manipulation typically required less medication and physical therapy. Several osteopathic techniques are utilized in the treatment of SIJD, including soft tissue technique, muscle energy, rnyofascial release, functional technique, straincounterstrain, cranial-sacral technique, and high velocity-low amplitude. Explanations of these techniques and their specific applications to the SI joint can be found in several excellent sources [25o,27,29].

Sacroiliac joint instability
Chronic stress can cause connective tissue structures to degenerate arid lose their ability to compensate. Eventually ligamentous laxity and hypermobility can occur. With a joint already prone to subluxation based on its anatomy, to which, chronic additional stresses are applied, resultant SI joint instability is not all that uncommon. Indirect instability can also occur through the additional forces applied once levels above the SI joint become hypermobile. This is commonly seen with spondylolisthesis and at times in spondylolysis. Failure to identify the enthesopathy or tendonopathy that develops in the iliolumbar, SI, and sacrotuberous ligaments, and the attachments of the gluteals, and erector spinae, can lead to incomplete resolution of sympt,,mc nr fnillirp of treatment. These hypermobile areas with commonly seen with spondylolisthesis and at times in spondylolysis. Failure to identify the enthesopathy or tendonopathy that develops in the iliolumbar, SI, and sacrotuberous ligaments, and the attachments of the gluteals, and erector spinae, can lead to incomplete resolution of symptoms or failure of treatment. These hypermobile areas with chronic micromotion can be treated with prolotherapy when gross instability and neurologic injury are absent.

When choosing hypermobile segments for prolotherapy, one must try to differentiate between functional and structural hypermobility, because treatment can be quite different [69]. Structural hypermobility implies a fixed defect, whereas functional hypermobility implies a compensatory change that is able to be altered through manual procedures and or exercise. Not all hypermobile regions are structural.

Hypomobile somatic dysfunction can produce functional or compensatory hypermobility in the early stages. If the somatic dysfunction is left untreated, over time the dysfunctional segments will have structural hypermobility. Clues to structural hypermobility are the bony exostoses at attachments of postural muscles and ligaments on radiography, which develop as a joint attempts to stabilize itself. Comprehensive neuromuscular rehabilitation to supplement the function of weakened ligaments should be accomplished. Prolotherapy can then be used as an adjunctive treatment to eliminate the remaining residual structural hypen-nobility.

Gravitational strain
Recurrent somatic dysfunction and altered postural alignment should clue the physician in to the diagnosis of gravitational strain or postural imbalance. Gravitational strain is a systemic neuromuscular response of postural alignment and muscle firing patterns to chronic gravitational stress. Other findings may include chronic or recurrent sprains/strains, pseudoparesis, recurrent articular dysfunction, recurrent myofascial trigger points, muscle imbalance, and ligamentous laxity. Gravitational stress, an obligatory consequence of bipedal posture, is a constant and a greatly underestimated systemic stressor [70]. It is most important that one understand that postural imbalance is a systemic neuromuscular dysfunction. Initial treatment in these chronic pain states must focus on the reeducation of the neuromuscular system. This is accomplished by seeking optimization of posture. This can be achieved through the use of one or more of the following modes of physical manipulation [40]: 1) contoured orthotics worn in the shoes to optimize foot and lower extremity biomechanics; 2) a flat orthotic of sufficient thickness to level the sacral base; 3) manipulation and/or mobilization directed to restore resilience to soft tissues and motion of restricted joint segment; 4) daily practice of a therapeutic posture for 20 minutes to counter the bias of soft tissues reflective of the initial posture; and 5) use of pelvic belts (sacral belts) or a levitor device for sacropelvic support during the postural retraining process.

During the implementation of the above, a principle-centered, functional rehabilitation program [53o0] that focuses first on the stretching of tight, hypertonic postural muscles, strengthening of weak phasic muscles, and proprioceptive pelvic belts (sacral belts) or a levitor device for sacropelvic support during the postural retraining process.

During the implementation of the above, a principle-centered, functional rehabilitation program [53oo] that focuses first on the stretching of tight, hypertonic postural muscles, strengthening of weak phasic muscles, and proprioceptive retraining must be carried out [71,72o,73,74]. It is critical to remember that muscle imbalances must be eliminated, and coordinated movement patterns returned to normal before strengthening of the core can begin effectively.

Sacroiliac joint dysfunction is a well known clinical entity in the athletic population. Despite this, its diagnosis, evaluation, and treatment remains problematic. Given the number of sports that can potentially stress and injure this region, we must continue to refine our biomechanical models and treatment paradigms to better serve athletes with SlID and pain. We believe that a comprehensive functional approach based on historic clues and appropriate diagnostic testing will lead to an accurate diagnosis. The appropriate therapeutic approach can then be selected. Our experience is that a multimodal approach works best, and often includes SI joint mobilization or manipulation. Identification and correction of functional or anatomic leg-length discrepancy is an important but often overlooked clinical entity. The influence of proximal or distal structures is poorly appreciated, but must be considered, especially with regard to postural retraining. Finally, the biomechanical demands of the athlete's sport must be carefully evaluated in the design of the rehabilitative environment, ultimately resulting in the successful return of the athlete to his or her sport.