Myofascial pain is a common source of discomfort in the lower back. It is a painful condition that results in localized trigger points in the affected muscle. Myofascial pain syndrome was first clearly defined by Simons et al ¹ in the 1980s. It is characterized by trigger points in a specific muscle that may or may not respond to snapping palpation with a local twitch response and secondary decreased range of motion caused by the pain.¹ A trigger point is a localized taut band of muscle that is tender to palpation and produces pain that radiates when palpated. Tactile pressure to trigger points result in known, reproducible but nondermatomal referral patterns, also known as zones of reference.^1,² There is significant variability among practitioners in the identification of trigger points for the diagnosis of myofascial pain syndrome, although there is some evidence that the interrater reliability can be significantly improved with training.³ There is currently no gold standard test for trigger point identification, leaving a fair amount of subjectivity in the diagnosis. The twitch response is the most specific clinical test of a trigger point.¹ Trigger points are either active or latent.¹ Both active and latent trigger points have tender taut bands within the muscle, but latent trigger points are not associated with spontaneous pain. Latent trigger points may be the result of prior injury that then becomes painful with reinjury. Trigger points may be further subdivided into primary, secondary, and satellite trigger points.^1,² Primary trigger points become active as a result of trauma, overload or overuse injury, or after leaving a muscle in a prolonged contracted or shortened position.¹ Primary trigger points are in a discrete and separate location, with adjacent secondary trigger points that are often the result of spasm. Satellite trigger points are felt in the area of the referred pain remote from the primary trigger point location. The more irritable the trigger point, the more painful and extensive the referred pain; muscle size does not affect the amount or extent of the referred pain. Producing referred pain requires less pressure applied to an active than to a latent trigger point.¹ Latent trigger points, by definition, are inactivated when key trigger points are inactivated. ^1,² Although in the past their mere existence was questioned, we now know that trigger points can be documented by electromyography (EMG). Hubbard and Berkoff⁴ in their 1993 article were the first to report spontaneous needle EMG activity at the trigger point site now described as spontaneous electrical activity (SEA).⁴ Endplate noise that has been recorded from specific myofascial trigger points are thought to be attributable to excessive acetylcholine release in the neuromuscular junction.¹ Sympathetic activity appears to play a role in the activity of trigger points, with increased EMG amplitude seen under conditions of psychological stress and reduced firmness after a stellate ganglion block.^5,⁶

Myofascial pain is not the same as the pain endured by those with fibromyalgia, which is a more diffuse, centralized musculoskeletal condition with many associated symptoms (e.g., irritable bowel). Predisposing factors are anything that increases or changes the demands on the muscle. These may include repetitive use, deconditioning, poor posture, and occupational or recreational injury related to muscle imbalances.⁶ If treated early, the prognosis for myofascial pain is good. Treatment includes physical therapy, including stretching and strengthening or conditioning; trigger point injections; acupuncture; biofeedback; transcutaneous electrical nerve stimulation (TENS); and some medications. It is not entirely clear why trigger points are painful because there is no direct evidence of inflammation or enhanced nociceptors within the trigger point sites. However, after the pain is initiated, sensitization at the level of the dorsal horn may occur, which then progresses to the development of central sensitization and the subsequent development of chronic myofascial pain.⁶

Although local anesthetic is the substance most often used by pain physicians in trigger point injections, there is not much evidence for its superiority over normal saline or dry needling. It does appear that the best response to trigger point injections occurs if a local twitch response is elicited.⁷ Part of the problem is that placebo-controlled studies of local anesthetic injections are extremely difficult to accomplish. Many of the studies do not have consistent criteria for trigger points, and some do not distinguish between the tender points of fibromyalgia and the trigger points of myofascial pain. The relief from the local anesthetic consistently outlasts the half-life of the local anesthetic, giving some credence to central sensitization in myofascial pain syndrome. All local anesthetics are somewhat myotoxic, with bupivacaine being the most myotoxic by far, but the muscle quickly regenerates with little long-term ill effect.⁸ The mechanism of bupivacaine’s effect appears to be on the calcium release related to the channel-ryanodine receptor of skeletal muscle.⁸^–¹⁰ Injected steroid can also be myotoxic and should be used in low doses. Dry needling has been used with varied success but has the disadvantage of postneedling soreness, depending on the sensitivity of the patient before and during the procedure and whether or not acupuncture needles, associated with less soreness, were used.⁶ Although not all acupuncture points (e.g., in the ear) are the same as trigger points, there is a striking similarity between acupuncture points and those used for dry needling and for trigger point injections.

The muscles involved in myofascial pain of the lower back can be divided into the posterior (superficial to the transverse process) and anterior (deep to the transverse process) muscles. The posterior muscles include the multifidus (located closest to the spinous process) and the adjacent erector spinae muscles. The latissimus dorsi are attached to the spine by the thoracolumbar fascia, which envelops the multifidus and erector spinae muscles posterior to the quadratus lumborum. The thoracolumbar fascia extends distally and is in contact with the contralateral gluteus maximus and is thus thought an important factor in the transfer of load from the spine to the lower extremities. The quadratus lumborum is replaced distally by the iliolumbar ligament, one of the strongest ligaments in the body and the one responsible for much of the stability of the lumbosacral segment. More anteriorly and inferiorly to the quadratus are the iliopsoas muscles. These descend into the pelvic brim and attach to the lesser trochanter of the femur.¹¹

Pain involving the quadratus lumborum and iliopsoas muscles can be either primary myofascial or secondary in nature, reflecting pathology in the spine or other nearby organs. The quadratus lumborum, psoas major, and iliacus (which comes together to form the iliopsoas) muscles make up the major muscles of the posterior abdominal wall (Fig. 22-1).

Fig. 22-1 Lumbar region of back: cross section.

Quadratus Lumborum Injections

Establishing a Diagnosis

The diagnosis of myofascial pain is a clinical one, largely dependent on the findings of the history and physical examination. The quadratus lumborum muscle allows lateral movement and extension of the mid and lower back. This muscle is a common source of myofascial pain because of its frequent use in normal daily activities such as walking and sitting; it is made worse by poor posture.² Pain is felt in the flank, lower back, hip, and sometimes the buttocks but is mostly above the iliac crest and exacerbated by movement of the spine. It may mimic radicular or even sacroiliac joint pain because of its attachment to the iliac crest. Acute myofascial pain of the quadratus lumborum may be precipitated by sudden movements (e.g., lifting in a way that twists the lower back), and even the most mundane of movements such as coughing or deep breathing become painful. Even sleep can be problematic because patients are unable to find a comfortable position in which to sleep because of pain with any lateral movement of the spine. Patients describe pain with arising from the supine position. Because of its proximity to the abdominal organs, disease of these organs, particularly kidney disease, may present as low back pain and must be excluded. Pronounced asymmetry of the dominant quadratus lumborum in elite cricket players (fast bowlers) and resultant pars fractures involving the nondominant side have been reported in the literature in several case reports.¹² Pain from the quadratus lumborum may be confused with pain that comes from injury to the iliolumbar ligament.¹³ The iliolumbar ligament connects the transverse process of L5 to the iliac crest. This very strong, thick ligament stabilizes the L5 body to the ilium and prevents axial rotation and translational movement on the sacrum. Pain from the quadratus lumborum may be distinguished from pain caused by iliolumbar ligament injury because of the absence of pain around the area of the flank with iliolumbar pain. The quadratus lumborum lies deep to the erector spinae muscles and the thoracolumbar fascia, so it may be difficult to distinguish these muscles from the erector spinae just on the basis of palpation.¹⁴

Physical examination involves observation and palpation for trigger points. When the patient is standing, the practitioner should look from behind for obvious signs of spasm causing a functional scoliosis or tilt and should look for elevation of the posterior superior iliac spine. The practitioner should observe for an antalgic gait and palpate for tender trigger points just below the twelfth rib and around the area of the iliac crest; this may be increased with back rotation. Part of the physical examination includes looking for a functional leg length discrepancy caused by spasm of the quadratus lumborum. The shortened leg is associated with the side of quadratus spasm and subsequent contraction resulting in upward motion of the pelvis.¹⁵ Provocative maneuvers include palpation of trigger points while twisting the back.

Anatomy

The quadratus lumborum is shaped like a quadrangle and has as its origin the aponeurosis of the iliolumbar ligament and part of the iliac crest. It is posterior to the psoas muscle and lateral to the thoracolumbar fascia. It inserts at the twelfth rib and the transverse processes of L1 to L4. It serves as an anchor between the twelfth rib and the pelvis, and the majority of the fibers attach to the twelfth rib.¹⁶ This creates a stable base for the diaphragm, allowing for its function as a basic muscle of respiration.¹³ The quadratus lumborum pulls down on the diaphragm and laterally flexes the lumbar spine (unilateral) and aids in back extension (bilateral). Its innervation is from the ventral rami of T12 to L4.

Phillips et al ¹³ in their cadaver study of the anatomy of the quadratus lumborum showed that although there is considerable variation in the presence and location of the muscle fascicles, the muscle exists in three broad layers, and about half of the quadratus lumborum fascicles acts on the twelfth rib and the rest exert their actions on the lumbar vertebra. The compressive forces exerted by the quadratus lumborum is insignificant compared with that exerted by the erector spinae and multifidus, and thus there is little evidence for a major stabilizing role of the quadratus lumborum on the lumbar spine.¹³

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