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8 Articles in Volume 5, Issue #2
Considerations in Treating Intractable Pain
Hospice Care Evolution
Myofascial Elements of Low Back Pain
Radiofrequency Neuroablation in Chronic Low Back Pain
State Pain Laws: A Case for Intractable Pain Centers Part III
Temporomandibular Joint Referred Pain
The ABC’s of Pain
Therapies for Chronic Pain and Fibromyalgia

Myofascial Elements of Low Back Pain

When treating myofascial trigger points (TrPs), contributing musculoskeletal, posture, and motion factors must be addressed in order to optimize outcomes.

Low back pain is one of the most significant health care issues in western society. Each year billions of dollars are expended, and millions of various office visits required for treating various aspects of low back pain. Despite such a significant impact on society and the focus by modern health care, the evaluation and treatment approaches remain far from uniform. In fact, a recent review of physicians in a tertiary academic medical center reported that “…the results found little agreement regarding low back pain judgments, and that the individual physicians held consistently to their opinions.” The conclusion was that “Management of low back pain may be idiosyncratic, potentially compromising patient care.”1

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Despite the specialization and sub-specialization of various medical disciplines to address pain specifically, the contemporary approaches continue to often bear little agreement between different pain management sub-specialties. In fact, differences between sub-specialists within a discipline may bear limited similarities. Many agencies are coming to the conclusion that the most effective approach to chronic pain treatment requires a multidisciplinary approach, where areas of expertise for each discipline may be incorporated for a more robust outcome.

Responses to various interventional ‘pain blocks’ often show more efficacy when combined with concurrent therapies that addresses contributing musculoskeletal and postural factors. For example, after leg-length discrepancy is corrected, trigger point injections may have a much more prolonged effect. Such a combined approach may be ‘curative’ rather than solely ‘pain treatment.’

It behooves the pain specialist to evaluate the multiple kinetic issues that may lead to recurrent stress or injury to the low back region. The purpose of this article is not to review the numerous postural, gait, and movement contributors to low back pain pathology, nor serve as a primer for treating low back pain. Instead, the focus is to raise the curiosity of the pain specialist to explore the multiple contributing factors — often classically within the realms of other allied specialists — before planning interventions. By learning and incorporating a few of the ‘pearls’ of multiple disciplines, a more complete evaluation and treatment plan will result.

Etiologies of Chronic Low Back Pain

The etiologies of chronic low back pain are many, and sometimes diverse. While herniated disc, spinal stenosis, spondylosis, and facet arthropathy are often considered along with myofascial origins, myofascial trigger points (TrPs) have been shown as coexisting with the other commonly accepted causes. Injection of active and painful myofascial trigger points from any origin may produce variable decreases in pain and improvements in mobility. Therefore, myofascial trigger point injections (TrPIs) are considered a significant treatment adjunct to low back pain.2

Often trigger point injections are carried out in a ‘follow the pain’ pattern, addressing primary and secondary trigger points and muscle spasms. Unfortunately, limited regard may be given to considering if the trigger point is in a shortened spastic muscle, or one that is weakened and overstretched from the opposing spastic muscles. Chronic postures may promote muscle force imbalances between the antagonistic muscle groups that lead to repetitive stretch trauma of the weaker muscle groups. As an example, shortened hamstring muscles may force secondary overstretching of lumbar extensor muscles during low back flexion. Therapies that address only those regional trigger points by promoting generalized lumbar extensor mobility, may actually promote excessive stretching of the already weakened over-stretched muscles, as well as contribute to more TrP formation. Moreover, if there is asymmetry of muscle strength and length between sides such approaches may also lead to areas of disproportionate relative mobility between individual spinal segments that may impact on less elastic non-muscular components. In situations of advanced muscle force imbalances, aggressive lumbar flexion exercises and TrPIs may also further weaken or overpower the posterior supporting ligamentous structures to allow segmental spinal movements which can lead to spondylosis and more pain generating processes.

Figure 1 A. Pelvic tilting forward increases the sacral angle to accentuate lumbar lordosis (G), while posterior tilt reduces lordosis by reducing sacral angle (E). Normal sacral angle and lumbar curve (F). From Nordin M and Frankel VH.4 Reprinted with permission. Figure 1 B. Ideal Lumbo-pelvic posture.5 Reprinted with permission. Figure 2. Faulty pelvic alignment as a result of (A): weak lengthen abdominal muscles, or (B) short stiff hip flexors; both of which exaggerate lumbar lordosis.5 Reprinted with permission.

Most spinal dysfunction is the product of cumulative microtrauma in multiple regional tissues from problems in trunk stabilization, alignment, and movement patterns. Core and spinal stabilization depends on balanced isometric support and movement control primarily provided by trunk musculature.3-5 When low back pain arises, one goal should include evaluation of directions for trunk and spinal alignment, stress, and movements that produce or increase pain.

A common denominator for most spinal related pain is an excessive relative flexibility at specific segments, rather than reduced flexibility from such factors as spasm.5,6 Those segments with reduced flexibility promote compensatory motion at the most flexible regions. While vertebral column pathology (disc herniations and bulges, spondylosis, facet arthropathy, and nerve compression) can promote pain independently, addressing trunk musculature issues first, and then those secondary abnormal spinal stresses, may reduce or alleviate the pain completely.5 The trunk muscles must hold the vertebral column and pelvis in optimal alignment, as well as prevent potentially injurious segmental movement. Therefore, observing body mechanics during various positions and movement may shed light on relative flexibility of various regions, and the impact on spinal stresses which produce pain. In some less chronic back pain syndromes, addressing posture, such as how one wears a backpack, may be the only intervention required to produce a cure.7

Figure 3. Oblique view of Iliopsoas Muscle complex with force vectors, as indicated by arrows. Pubic bone structure, and adjacent attached muscles (pectineus, tensor fascia latae, etc.) have been removed to allow view of distal attachments. Figure 4. Upper anterior thigh muscular attachments.8 Reprinted with permission.

Spinal Mechanics

An initial observation of spinal mechanics should include lumbar curvature. Decreased lumbar curvature may result in a ‘flat back’, while increased curvature may result in excessive lordosis “sway back.” Judging the lumbar curve may be difficult, due to issues with obesity, or paravertebral muscle hypertrophy (see Figure 1). The lumbar curvature may be affected by pelvic tilt. An anterior tilt of the pelvis increases lordosis, while a posterior tilt reduces the lordosis4 (see Figure 2). Weakened or lengthened abdominal muscles may not adequately support the anterior pelvis, allowing increased tilt, and exaggerated lordosis (see Figure 3). Additionally, shortened hip flexors, such as the iliacus, psoas muscles (originate in the posterior pelvis and lumbar vertebrae; see Figure 4), rectus femoris, sartorius, tensor fascia latae, and pectineus (originate from anterior pelvis) can enhance forward pelvic rotation to exaggerate lumbar lordosis by essentially pulling the structures forward (see Figure 5). Shortened hamstrings, with weakened hip flexors may promote a posterior pelvic tilt, and flattening of the lumbar lordosis. Length or strength differences in groups between sides may promote asymmetry as one side of the pelvis rotates more, leading to additional rotational forces on the spine.6 These rotational forces are even more exaggerated through trunk or lower extremity movement.

A simple test for hip flexor length and mobility involves a supine psoas stretch maneuver (see Figure 6). The patient is asked to lie supine, with flexed hips and knees, leaving the feet on the testing table surface. The examiner will palpate the lumbar lordosis as the patient slides the foot out, extending the hip and knee. A dramatic forward rotation of the pelvis, and exaggeration of the lumbar lordosis, along with an onset of pain, suggests that hip flexor shortening is a major contributor to the posture promoting the pain. If the examiner holds the lower leg with extension of the knee as the hip is extended, the contribution of the rectus femoris, sartorius, and tensor fascia latae is negated. Continued pain with this maneuver suggests that the iliacus and psoas are the major contributors to the back pain, since the pectineus is such a small muscle.

Lumbar Flexion

Lumbar flexion from a standing position is a common daily activity. During the forward bending motion, the initial motion is a posterior sway of the pelvis as the hips flex, which allows the center of gravity to remain within the base of support. As the hips begin flexion, the lumbar spine starts to reverse its lordosis (forward curve). After complete reversal of the lordosis, the remaining motion is through hip flexion. The lumbar spine should not complete more than 50% of its motion into flexion before hip flexion begins. At complete flexion, there should be a straightening or flattening of the lumbar region9 (see Figure 6). The lumbar range of motion value is based on a normal starting position of approximately 20 to 30 degrees of extension while standing erect, and bending forward to a maximal flexion curvature of 20 degrees. For a patient with a flattened lordosis, at which standing alignment approaches zero degrees of extension; 50 degrees of flexion will not be attainable without considerable lumbar stress motions. Any flexion greater than 25 to 30 degrees is considered excessive.10

Moreover, flexion impairment is considered if it reaches greater than 50% of its range before hip flexion begins or if more motion occurs in the lumbar spine than the hips during the 30 to 60 degree phase of bending forward.9 Each segment should contribute to the motion, and a failure of one or more segments will force other segments to move beyond their optimal range as compensation to allow regional motion. Because of the compensatory excessive movement, care must be taken to ensure against promoting hypermobility in some segments while others remain hypomobile.5 Vigorous stretches, and trigger point injections into hypermobile regions may potentially promote instability of the region.

Returning to erect posture from forward flexion should be initiated by hip extension, followed by concurrent lumbar and hip extension motions until an upright position is reached. If lumbar extension initiates, or predominates the initial phase, excessive compressive force on the spine may result.4,11 Moreover, this type of motion pattern typically relies less on the hip mobility and forces exaggerated lumbar movement requirements for daily activities. This promotes ‘wear and tear’ on muscular and less elastic spinal elements.

Figure 5. The Psoas stretch technique as a screen for iliopsoas muscle dysfunction as a contributor to low back pain. In the supine position, with a flexed hip posture, the patient may be without back discomfort, and a normal lumbar lordosis is palpated. With a ‘heal-slide’ maneuver, the hip and knee joint are slowly extended, while the lumbar lordosis and anterior superior iliac spine are palpated. A positive test is considered when the pelvis rotates forward, with an enhancement of the lumbar lordosis, as the patient notes onset of discomfort (pain or increased stiffness) in the lumbar region. Figure 6. Variations in lumbar motion during forward bending and quadruped rocking.5 Reprinted with permission.

Lumbar Extension

Lumbar extension involves an increase in the anterior curve, and may be highly variable in range.5 More problems arise from excessive extension forces on one or two individual spinal segments, than from restricted overall lumbar mobility. Lumbar extensor muscles, which restrain back flexion, are located on the dorsal spine regions.12 However, lumbar extension is typically restrained by the abdominal muscles and hip flexors (located anteriorly); as well spinous processes, disks, and apophyseal joints (located posteriorly).11 Hyperextension and hyperflexion damages interspinous ligaments and can cause sudden disc prolapse and long-term structural disk damage. The anterior longitudinal ligament contributes marginally to large extension forces, as disks degenerate, it is not pulled as taut and thus allows extension motions through progressive hypertrophy this condition may contribute to stenosis of the bony canal.

Rotational Motion

Rotational motion of the L-Spine is estimated at approximately 13 degrees, with each segment between T10 and L5 as contributing about 2 degrees. The rotation between L5 and S1 is normally 5 degrees. Facet joint orientation plays a significant role in rotational restriction in this region.12 The thoracic spine mobility plays a greater role than L-spine for trunk rotation. Asymmetry in abdominal muscle group strengths and lengths, especially the oblique muscle groups, limit rotation mobility and produce a postural rotation of the spine. Asymmetry of the paraspinal muscles may be attributed to this rotation and produce a virtual muscle mass difference, as the shortened anterior groups rotate the weakened antagonistic paravertebral muscles outward, thereby appearing as a larger muscle mass.5 Lateral flexion to the side opposite the greater bulk is restricted due to increased muscle stiffness; but if the asymmetry is due to postural rotation, lateral flexion toward the same side with perceived increased mass is more restricted.12

Lateral Flexion

The greatest lateral flexion mobility occurs in the lower thoracic segments (8-9 degrees per segment), because they are not restricted by ribs. The lumbar and other thoracic segments average 6 degrees of side-bending, while the lumbosacral segment L5S1 has only 3 degrees of lateral flexion. Lateral flexion produces lumbar rotation toward the curve convexity. Rightward lateral flexion produces lumbar rotation to the left. With 6 degrees of motion for each lumbar segment, the lumbar contribution may reach 27 degrees. Although limited by ribs, thoracic lateral flexion may reach 75 degrees.

Because lateral flexion and segmental rotation motions are coupled, impairments of motion or alignment of either movement impacts the other. A malaligned spine rotated to one side will have lateral flexion to that side limited. A spine that is posturally rotated to the right will have limited rightward side-bending, because the spine segments will be unable to rotate to the left. Leftward side-bending will be unimpeded, because the segmental rotation to the right has already taken place.5,12

Figure 7. The classic location for Iliopsoas TrPs (Xs), and the pain referral distributions, as indicated by the red demarcation. Note that there are no active TrP that can be activated or palpated by a posterior approach to the lumbar musculature.2 Reprinted with permission. Figure 8. Classic Iliopsoas muscle and trigger point injection technique. With the patient in a supine position, and an extended slightly externally rotated hip, the distal TrPs of the iliopsoas complex may be palpated and activated. As suggested in the right-side diagram, injectate spread to the more proximal muscle mass would be expected to be minimal, especially to the majority of the psoas muscle mass.2 Reprinted with permission.


The preceding brief review should emphasize the importance of evaluating multiple muscle groups when planning a treatment program. Often overlooked, are the relations of weakened and lengthened abdominal muscles, and shortened spastic hip flexors to the movement processes that promote TrPs, as well as segmental spinal instability, arthropathy, and even radiculopathy as a process continuum.

Exercise programs that focus on back strengthening, without including lengthening of the opposing hip flexors, or strengthening of the abdominal muscle groups, when indicated, may not lead to improved pain control, or a functional recovery. Classical sit-ups or abdominal crunches may actually incorporate more force generation and further shortening of the hip flexors, rather than abdominal muscle groups. Such activity may actually promote the pathology. Isometric abdominal strengthening with gentle supine ‘heal slides ‘maneuvers to allow stretching of the hip flexors may address more of the specific muscular imbalances that produce back pain.

Trigger Point injections are best focused on the shortened and spastic muscles. If side-bending to the right is restricted by TrPs in the quadratus lumborum muscles on the left, the left sided TrP should be a primary focus for therapy. If low back extension appears inhibited by opposing hip flexors, TrPs in the Iliopsoas muscle may be considered as primary foci. (see Figure 8) Injection of these muscles is described in multiple texts, with the primary site located near the femoral neck2 (see Figure 9). Other approaches to the components have been described, especially as how these muscles are injected with other agents such as botulinum toxins.5 Whatever injection technique is chosen, the proper physical therapy should be coordinated to allow maximal benefit of the treatment. If only transient benefit is produced by the coordinated TrPI and PT program, consideration of a longer acting muscle relaxation injection may be in order. Prolonged relaxation of hip flexor groups through the use of botulinum neurotoxins (ex. Botox, and Myobloc ) as adjuncts to physical therapy have been described as beneficial.13


Whichever injection protocol or drug regimen is to be utilized, it is hoped that careful consideration of the various muscle and postural forces will be included in the diagnostic and treatment planning. Evaluation of movement, gait, and posture when incorporated with the knowledge of drug effects, and injection techniques should promote a more specific and hopefully more effective treatment program for patients with chronic low back pain, as well as multiple other pain syndromes. The textbook by Dr. Sahrmann5 is a very valuable resource for evaluation of multiple pain syndromes. n

Last updated on: December 13, 2011
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