Low Back and Lower Body Myofascial Pain Syndromes

Paul L. Reller L.Ac. / Last Updated: August 03, 2017

Treating Low Back Myofascial Pain and Impingement Syndromes

Much of the important information on treating myofascial and neuromuscular pain syndromes will be found in the article on this website entitled Myofascial Pain Syndromes, and you are encouraged to review this article. Low back pathologies are often a combination of joint degeneration and neuropathies coupled with myofascial neuromuscular problems, and so this article will address how these areas interrelate. To repeat the basic concept of myofascial pathology, since each striated muscle in the body may be affected by strain, either overuse or traumatic, and may generate a pattern of referred pain and associated symptoms, the subject of diagnosis and treatment of myofascial pain syndromes can be overly complex. It is therefore necessary to focus on the most pathological muscles and fascia. These are generally deep muscles that attach to important bones and joints, which may easily impinge the circulation of blood or nerve conduction, and which are often key stabilizers in postural mechanics. Since the chronic myofascial syndrome is essentially a neuromuscular pathology, treatment of the most pathological muscles has the potential to improve the function of the nervous system and may resolve broad neurological functions, even autonomic disorder. Attention to the stabilizing and impinging muscles will also significantly resolve chronic problems of joint instability and nerve conduction that contribute to all of the myofascial trigger points. In addition, myofascial syndromes contribute greatly to the common problems of degenerative joint and disc disease, and both contribute to and mimic common pathologies of the sciatic nerve pathway and other nerve pathologies, such as Meralgia Paresthetica and Chronic Pelvic Syndrome.

Incidence of lumbar degeneration in the United States population is very high. A study in 1998 by the NIH in Framingham followed case studies of over 600 patients who had lumbar radiographs at the average ages of 54 years and again at 79 years of age, with completed assessment of low back symptoms and functional assessments, and found that 12% of men and 25% of women at this age had significant degenerative slippage of vertebrae exceeding 3mm (PMID: 9762744). Forward displacement occurred predominantly in women and affected about one in six patients, and posterior displacement affected about one in twelve. On average, this slippage was between 11 and 25% of the diameter of the vertebra, which is quite alarming. Since displacement, or subluxation, of the vertebrae may easily impinge upon the nerve roots, and obviously cause painful pressure on joint tissues, this outcome of lumbar degeneration is quite alarming. What is equally as amazing as the high incidence of severe lumbar degenerative outcomes is the findings that only 32% of the subjects with severe lumbar slippage reported pain on most days, while 19% of subjects with no slippage reported daily significant pain and stiffness. Despite the severe bony displacement and obvious pressure on joint and nerve root tissues, as well as the spinal cord, the patients adapted to these severe joint deformities. These outcomes illuminate the fact that the lumbar area can adapt to even severe degenerative conditions and create healthy scar tissue and adaptive stabilization that allows good control of pain and prevents disability. Conservative care, in the form of a package of direct soft tissue mobilization, myofascial release, acupuncture, herbal and nutrient medicine, and instruction in therapeutic routines and neuromuscular reeducation, can achieve significant success with lumbar degenerative pathologies without surgical correction.

Clinically, our goal should be to prevent the type of severe degeneration of lumbar soft tissues mentioned above. These figures represent an unacceptable degree of severe lumbar deformity in the general aging population, and medical maintenance of the lumbar should be a priority for us all. Current medical strategies generally have favored pain alleviation with medication and rest during episodes of more severe pain, and eventually lumbar surgeries. In recent years the effectiveness of surgical therapy has been challenged by a number of large studies. A study at Harvard Medical School in 2005 assessed long-term outcomes of patients diagnosed with lumbar stenosis and treated either with surgery or without surgery (PMID: 15834339). The results, like a number of similar studies, showed no significant difference in 8-10 year follow-up between patients receiving surgery and those that opted to forgo surgery. In addition, 23% of surgical patients had needed at least one additional surgery by 10 years, a condition now frequently called "failed back syndrome". 39% of the patients that had foregone surgery initially had eventually opted for surgery, but these patients that opted for a surgical treatment had worse outcomes than the patients that continued to reject surgery. Typically, insurance coverage dictated the type of nonsurgical care, and this care was limited to pain medication and very short courses of physical therapy. In the United States, there has been virtually no standard treatment of lumbar degeneration utilizing an effective course of conservative care such as the treatment that is described in this article.

The problems of lumbar degeneration, referring to spinal stenosis with disc degeneration, disc bulging and impingement on the nerve roots, and facet joint tissue degeneration, with chronic hypertrophy and inflammatory irritation, are intricately tied to myofascial syndromes and neuromuscular disease. Stress imbalances from chronic muscle strain, contracture and weakness of stabilization, are the key components of lumbosacral degenerative pathologies. When these chronic myofascial pathologies are corrected, the joint tissues are allowed to heal, and if they are not corrected, even surgery will not prevent continuing degenerative changes. In addition, myofascial syndrome is proven to slowly expand and affect the entire neuron to the spine root, and eventually may affect the associated neurons innervating the motor and sensory aspects of other key muscles. As demonstrated with much study of the physiology of myofascial pain syndromes, chronic muscle strain frequently expands to a pathology that affects the central nervous system and autonomic nervous system as well, and puts increased stress on the immune system inflammatory regulation. From a holistic perspective, myofascial release and correction of key myofascial pathologies should be an integral part of all therapy of lumbar and pelvic pain pathology.

This introduction to treatment of myofascial pain syndromes of the low back and pelvic region will focus on key muscles. The basic list will include quadratus lumborum, psoas, tensor fascial latae, gluteal muscles, and the piriformis. After this, key muscles of the limbs will be addressed. Superficial muscles, such as the paraspinals and serratus, may need to be addressed routinely in therapy as contributors, but are not key to the serious symptoms in most cases. Joint mobilization is extremely important in these low back myofascial pain syndromes, not only to address problems that directly affect the key muscles, such as impingement of the nerve supply to these muscles, but also to address therapy of the small multifidi muscles and to effectively resolve enthesopathy, or pathology of the myotendon attachment to the lumbar. The problems of myofascial syndromes of the low back are intricately tied together with lumbar joint pathology in a number of ways. To illustrate, the major hip flexor, the psoas, attaches not only to the transverse processes of the middle lumbar vertebrae, but also to the disc and facet tissues themselves at the same lumbar nerve root level that innervates the psoas muscle. This creates a feedback pathology, where chronic contracture and firing of the psoas muscle adds to impingement of the nerve that innervates this motor firing, leading to increased motor weakness potential and weak contracture with poor stability of the low back.

The Important and Most Pathological Muscles in Myofascial Pain Syndromes of the low back and pelvic region

It is important to understand that most myofascial syndromes involve more than one muscle, since problems with one muscle causes added strain on others, and overstrain is the etiology of the myofascial syndrome. The reason that fascia is included in the name of these syndromes is to stress that muscle tissues are interconnected and not isolated. Fascial tissues connect not only to adjacent muscle tissues but also to the joint tissues, resulting in both subluxation and capsular tissue pathologies. Over time, as calcification of tissues progress, ischemia prevents clearing of tissues, and other metabolites such as protein fragments accumulate in the tissues. Chronic inflammatory degeneration progresses. Neuropathies may be caused by both mechanical impingement of the nerve or nerve root, and by chronic inflammatory irritation of the nerves. If the pathology is an acute simple traumatic overstrain, an isolated muscle may be seen. If the pathology is chronic, usually the myofascial syndrome involves more and more muscles, as the body adapts to favored use and weakness of the pathological muscles, causing a broader pathology of increased strain on surrounding muscles and sometimes, eventually, opposite sides of the body and contralateral deep muscles. Exam and treatment usually includes the related muscles as well as the primary pathology. It is important to become familiar with the patterns of pathology as well as the location of trigger points with each important muscle.

A full explanation of myofascial pathology is available in the associated article on this website, and you should read this material if you haven't already read it, in order to understand the pathophysiology of the myofascial syndrome and neuromuscular disease mechanisms more thoroughly. The lumbar and pelvis are stabilized and moved primarily with a few deep muscles. Unfortunately, these muscles are not easy to treat. The Quadratus Lumborum, as the name implies, is a muscle that applies motor strength on four sides, which makes it much more complex to stretch and release than a typical muscle with connections to joint tissues at two ends. This muscle is joined intricately with the iliopsoas, which connects across the entire anterior pelvis, as well as the lumbar vertebrae, the twelfth rib, and the medial hip at the femur. The gluteal muscles and tensor fascial latae are also anatomically complex, with portions that wrap around the hip and exert motor and stabilizing forces at various angles, and join with a complex of ligaments and tendons that control the pelvis, sacrum and iliosacral joint. A number of large nerves besides the sciatic go between and through these muscle tissues, and chronic myofascial contracture and/or weakness may entrap or otherwise affect these major nerves, some of which also control motor function of these same muscles. Innervation of these key muscles is also complex, with multiple innervations evolved to both control the complex functions, as well as to provide back-up innervation if a nerve is traumatically damaged. This creates multiple trigger points. In general, all of these key muscles should always be addressed in therapy in order to insure successful outcome of low back and pelvic syndromes, even if only one of the muscles appears to be affected by acute strain.

Quadratus lumborum and Iliopsoas

The Quadratus Lumborum is the main stabilizing muscle of the low back, as well as being the prime mover of the lumbar in lateral flexion and raising of the hip. Acting bilaterally, the QL extends the lumbar spine and also assists forced exhalation, as in coughing. The right and left QL act antogonistically, as well as synergistically, to move and stabilize, and so therapy must always be directed to both muscle sets. Anatomical attachments are to the 12th rib, transverse processes of all 5 lumbar vertebrae, the crest of the ilium, and the iliolumbar ligament. The muscle fibers are overlayed in 3 distinct groups, from superficial to deep, the iliocostal, the iliolumbar, and the lumbocostal. The trigger points involve 2 deep and 2 superficial areas primarily, but due to the numerous sections of the muscle, actual trigger points are probably more numerous. The problem with access to these trigger points is that the muscle is deep and not very thick. QL pathology involves contracture most of the time that also diminishes the anatomical access to the various muscle bellies and trigger points, with little space between the ribs and the iliac crest. Manual trigger point release is accomplished by stretching the muscle primarily in two ways, with the leg and pelvis in extension and external rotation, and then with the hip flexed and the pelvis in internal rotation. The physician must move the thumb to find the triggering lesion or knotted tissue, or must alter the needle direction to best trigger the various trigger points. In actuality, these trigger points are very close together. In normal acupuncture therapy, two of the trigger points would correspond to UB23 and UB25, while a third would be addressed by UB52 or GB24. Deep needling must be done with care, although if the needle is directed away from, or parallel to the thoracic cage, the organ tissues are easily avoided, and the low back is almost entirely muscle fiber.

Pain referred from the Quadratus Lumborum typically is felt across the iliac crest and the sacroiliac joint, as well as the deep upper buttock. Pain may also be referred to the lower buttock and around the greater trochanter. Pain is aggravated by turning in sleep, standing upright and walking, and painful spasm inhibiting an upright posture is typical of acute strain or exacerbation. Coughing or sneezing is often very painful in this case, as is turning in bed. Often the acute exacerbation occurs with minimal movement of the lumbar in the morning, after the strained muscle is held in a shortened position through the night. The patient will often report that onset of the painful spasm occurred as they got out of the shower and reached for the towel, or when twisting, bending and reaching for something in the kitchen. Often, the patient reports that they were unable to stand at all due to pain and had to crawl back to bed. Less acute onset, or gradual worsening of this pain pattern usually occurs with patients that sit for prolonged periods at work without getting up and moving around. Postural strain from sleeping position may also be an important aggravating factor.

Typically, most low back pain felt across the iliac crest and sacroiliac involves the QL, and most pain felt as a pattern up and down alongside the spine involves the psoas. Since these muscles are overlapping anatomically, often the patient with chronic problems has problems in both sets of muscles. Differentiation in diagnosis allows the physician to focus on the more problematic muscles. With the QL syndrome, the patient will often complain that they cannot lie on a particular side due to soreness at the greater trochanter of the hip. A wide variety of pain complaints have been recorded in relation to the QL, though, including episodes of sharp shooting pain from the ASIS to the patella on the lateral anterior thigh. Differential diagnosis of common low back pain involves proper assessment of both the various similar myofascial pain patterns, and the neuropathic pain from radiculopathy or inflammatory nerve irritation around the facet joint. Myofascial patterns that mimic QL pain include the paraspinal longisimmus thoracis and multifidi (small muscles that stabilize the vertebrae), the iliopsoas, and the lower rectus abdominus, which typically refers a pain pattern moving across the PSIS and SI joints. In addition, the complex of gluteal muscles and quadratus lumborum may create a trigger point pattern resembling sciatic pathology. This myofascial syndrome is nearly identical to sciatic nerve pathology, and is sometimes referred to as "pseudo-disc syndrome". Differential diagnosis clarifies these patterns when the trigger points of the QL and gluteus minimus stimulate the sciatic pattern, when myofascial release or trigger point needling of the Gluteus minimus inactivates the sciatica component, or when inactivation of the QL trigger points eliminates both the low back and sciatic patterns. Differential diagnosis of the radiculopathy or facet syndrome should be achieved with MRI and EMG studies, although a number of nonspecific orthopedic tests are helpful in diagnosis. Osteoarthritic changes, predominantly bone spurs or disc space narrowing, may also be a significant source of low back pain, but a high percentage of patients with moderate degenerative changes have no pain. Often, the patients with osteoarthritic degenerative changes find that their low back pain is relieved when QL myofascial trigger points are effectively treated.

Chronic dysfunction and weakness may contribute to QL pathology, and innervation may involve tissue lesions affecting the nerve roots from T12 to L4. In this sense, lumbar degenerative pathology, neuropathy, and inflammatory dysfunction may contribute to poor motor firing and weak stabilization by the QL, also creating a feedback pathology. In other words, typical lumbar spine pathology, bulging discs, and facet joint hypertrophy from chronic inflammation, may effect the nerve conduction and response to the Quadratus lumborum and Iliopsoas, which in turn would cause poor muscle stabilization and mechanical stress from chronic contracture affecting the joint tissues and nerves. In these cases, improvement in the QL myofascial pathology combined with effective lumbar mobilization may lead to greater lumbar stabilization and improvement in the lumbar degeneration, neuropathy, and inflammatory problems.

The hallmarks of physical exam usually reveal some inhibition of lumbar flexion with pain, as well as restriction of lateral movement of the lumbosacral joint. The patient typically shows some muscle guarding restricting lumbar and SI movement with walking, lying down, turning over, getting up from the table, or when rising from a chair. The postural exam will reveal the lateral pelvis higher on the side with the contracted QL. A functional scoliosis, or lateral curve, may also be observed, which disappears when the lumbar is flexed fully. A flattened lumbar, or loss of lumbar lordotic curve, is often typical due to the vertebral rotation. Flexion is usually more restricted than extension or rotation. In lumbar joint capsular patterns, on the other hand, extension and rotation are most restricted. Side bending is restricted toward the pain-free side in QL pathology, but is best assessed with the patient sitting to eliminate other side bending restrictors. Deep palpation of the QL and trigger points reveals pathology, but the tight space between the tenth rib and the crest of the ilium with QL contraction, and the fact that the QL is under the sometimes thick paraspinals presents problems for the physician with less experience positioning and palpating the QL. For this reason, a contracted quadratus lumborum also presents problems with locating the trigger points for trigger point needling.

Traumatic injury or aggravation of QL pathology is also common. Lifting and twisting, awkward strain of a near fall while twisting, and motor vehicle accidents all typically injure the QL. Studies show that the QL develops trigger points in about 80% of rear-end, frontal, and drivers' side auto collisions. Often, the muscle was chronically strained with latent trigger point pathology before the trauma. The QL is the most commonly overlooked muscular source of low back pain, which affects up to 60% of the adult population, according to Travell and Simons. These authors state that in any one year, an estimated 10-15% of adults have some work disability caused by back pain, and in studies of musculoskeletal pain complaints of U.S. Army personell, the QL was the most commonly involved muscle. Since most low back pain is chronic, perpetuating factors are very important to identify in chronic QL pathology. Poor body mechanics, or ergonomics, with prolonged sitting is commonly involved, especially if the patient is frequently twisting the torso to read material to the side, answering the phone, etc. or driving. Onset of pain often is reported as the patient rises from the chair or car seat, twisting the torso. Mechanical factors are also frequently involved, such as a lower limb-length inequality, a small hemipelvis, or weak support from deconditioned abdominal or gluteal muscles. A lower limb-length inequality of only 1/8 to 1/4 inch (3-6 mm) may perpetuate QL trigger points. Carrying a wallet in the back pocket and sitting on this wedge may elevate the pelvis to one side and also perpetuate QL trigger points.

The abnormalities of assymetrical growth in the pelvis and bones of the leg are common in the population, and may be easily assessed and addressed in treatment if a few simple facts are kept in mind. A lower leg length inequality of as little as 1/8 inch has been found to perpetuate QL TrPs. Studies presented by Travell and Simons over time showed that between 15-30% of subjects with low back pain had a structural lower leg length inequality of 3/8 inch (10 mm). Frquently, a lower leg length inequality was correlated with a small hemipelvis. Treatment strategies involve orthotic shoe lifts or use of a pad under a small hemipelvis when seated. Adaptive strategy involves increased stretch and toning of the key muscles affected, especially the quadratus lumborum, iliopsoas, gluteals and TFL, as well as myofascial release. The diagnosis of lower leg length inequality is often diagnosed without proper assessment, and this practice should be stopped. Diagnosis of lower leg length inequality by assessing pelvic rise on one side or by eyeballing the heels when lying does not give a proper assessment. Correct diagnosis involves proper radiological assessment, and methods of tape measurement hip-to-ankle, or navel to medial malleollus have been proven notoriously faulty. Unfortunately, medical doctors are reluctant to perform these radiologic assessments, and insurers are reluctant to approve payment. Some more reliable assessment methods clinically involve pelvic rise on one side sitting (small hemipelvis), knee height with the patient supine and the heels against the buttocks (unequal femurs), and height of the heels with the patient prone and the the knees flexed 90 degrees (unequal tibias). Use of othotic shoe lifts or small pads under the small hemipelvis will serve to remove strain and aid therapy when structural abnormalities are confirmed with radiologic assessment, but if these structural abnormalities are not present, these measures may serve to perpetuate strain.

Pelvic tilt and scoliosis may also be involved in QL pathology. Once again, assessment may not be as simple as one would like. There are two types of scoliosis, functional and structural. Structural scoliosis occurs when the bones are developing, and almost all patient adapt muscularly. By far, the most prevalent type of scoliosis presented with low back pain involves functional scoliosis, sometimes called compensatory. This may occur due to lower leg length inequality, small hemipelvis, or pelvic angulation. Radiologic assessment should be performed ideally to rule out these problems or treat with mechanical lifts. Various studies over time cited by Travell and Simons showed that as many as 58% of patients with both lower back pain and lumbar scoliosis showed a lower leg length inequality of 3/8 inch (10 mm). Most often, functional scoliosis develops with chronic imbalance between the contractures of deep stabilizing muscles, whether a lower leg length inequality exists or not. A contracted QL on one side, perhaps compounded by a weak QL on the opposite side, may eventually cause a C-curve functional scoliosis. An S-curve scoliosis is usually seen with more chronic cases when deep stabilizing upper back muscles are eventually strained. Functional scoliosis can usually be assessed by having the patient stand and flex forward slowly to touch the toes. With structural scoliosis the curvature will remain, but with functional scoliosis the spine will straighten. If the scoliosis is primarily associated with lower leg length inequality, placing a small riser under one foot, such as a small book, will correct or worsen the curvature. If the QL contracture is strong, though, this may not straighten the spine.

Since radiologic exams expose the patient to harmful radiation, and may be difficult to get approved or recommended, the general rule is to first treat the patient with myofascial release and neuromuscular reeducation, and if these measures fail to relieve symptoms, to try to schedule the radiologic assessment. Correction of the Quadratus lumborum trigger points and myofascial syndrome are the most important focus in this approach, and assessment and treatment of the iliopsoas, piriformis, gluteals and tensor fascial latae may also be important. If the S-curve functional scoliosis is observed, treatment of the key upper back stabilizers, the lattissimus dorsi, subscapularis, splenii, levator scapuli and scalenes may also be necessary, as well as the paraspinals and multifidi. A thorough approach to myofascial syndromes is always recommended. If this thorough conservative approach with myofascial release and acupuncture is not completely successful in correcting functional scoliosis, a competent radiologic assessment of lower leg length inequality and small hemipelvis, and consideration of orthotic lifts and pelvic risers is recommended. If all of these measures are unsuccessful, more extensive radiologic assessment with X-ray and MRI may be needed to find the structural cause of pelvic tilt.

Treatment of the Quadratus Lumborum trigger points

Palpating and treating quadratus lumborum trigger points (QL TrPs), as noted, is problematic because the space between the lower rib cage and the pelvis is usually tight when the QL is contracted. Sustained pressure on any of the QL TrPs may reproduce symptom patterns, but penetration of the TrPs with the needle is a more reliable way of eliciting the myofascial pain pattern. These TrPs are palpated between the edges of the overlying latissiumus dorsi and external oblique at the level of about the L3-4, with the patient side-lying, a pad under the low back to facilitate QL stretch, the arm and rib cage extended, and the hip and leg extended. Deeper palpation reveals the thickest part of the muscle between the crest of the ilium and the paraspinals. When the muscle is felt, the finger may slowly search for the TrP. After identifying the TrP and attempting release, the needle may be inserted and slanted toward the lower lumbar and away from the thoracic cage, liver and kidney edges. A second TrP region exists along the inner crest of the ilium where the muscle fibers attach. A second approach to the TrPs may be achieved by stretching the deeper QL fibers by flexing the hip while you palpate. Manual pressure release alone is recommended in this position as needling is awkward.

Since the QL is complex in anatomy and function, attention to common secondary TrPs is essential in therapy. These TrPs, or order of importance, are the contralateral QL, the ipsilateral iliopsoas, the intercostalis between T11 and L3, and occasionally the long latissiumus dorsi and obliques. Satellite TrPs to the gluteals and piriformis are also important in therapy, especially if the referred pain zone includes the deep buttock area or legs. Usually, these contributing TrPs should be treated prior to release of the QL TrP to have the most complete effect.

The iliopsoas is the second most pathological muscle in low back pathology, and is also complex in anatomy and difficult to treat directly, due to its anatomical depth and dlfficulty reaching TrPs. The most problematic part of the muscle is perhaps the psoas minor, which is usually originating at the vertebral bodies of the T12 and L1, including this vertebral disc and foraminal tissues, and attaching to the iliacus, pubic bone and inguinal ligament. The TrP and body of the muscle lies anterior to the psoas major, and may be indirectly released with manual pressure throught the abdomen midway from the prominence of the ASIS to the navel, just medial to McBurney's point. Successful needling involves a combination of distal meridian points and local acupuncture points with shallow needling depth affecting the muscle. The Dai Mai extraordinary meridian is of most value, although the opposite ST36 and same side ST28 may also be useful. Variations of anatomy in the population are significant, though, with abscence of the psoas minor in up to 50% of the population, and anatomical variations at the sites of origin and attachment commonly seen. Patients without the psoas minor muscle per se are treated effectively by addressing TrPs in the psoas major, which may be located at various points at the location described above or inferior. Manual palpation and release of the psoas TrPs requires slow and careful pressure coordinated with the patient breathing. Guarding in the abdomen is a problem in most patients and must be relieved by using the opposite hand to apply broad pressure to the abdomen and by slowly achieving depth of pressure at the TrP. The actual pressure on the psoas is achieved by pressing on the abdominal wall, and the patient must be relatively comfortable and the abdominal wall relaxed with deep breathing.

Other significant TrPs in the iliopsoas involve the broad iliacus palpated inside of the iliac crest, and the tendon attachment at the lesser trochanter of the hip, where both the muscle fibers of the iliacus and the tendon attachment of the psoas major may harbor TrPs. If the ilacus is tight, some flexion of the hip and support with a small pillow under the hip may be needed to comfortably release the TrPs. The TrPs at the less trochanter may be released both with manual pressure with the muscle stretched by slightly extending the hip with the leg off of the side of the table, and also with active release technique, palpating across the tendon as the patient breathes deeply and flexes the hip actively. Iliopsoas pathology is most often associated with TrPs in other muscles, though, and complete therapy may involve TrP release in the QL, opposite iliopsoas, TFL, paraspinals and gluteals. A general rule would involve a holistic approach to treatment and attention to all of these key muscles in the treatment of low back pain. This requires a time intensive treatment, but without this approach, complete relief of the myofascial pathology and sustained release of TrPs may not be achieved.

The iliopsoas is the prime hip flexor and serves to assist lumbar extension and flexion. The psoas may be continuously active while sitting or standing, and typically produces myofascial pain more acutely when rising from the seat after prolonged sitting, or when ascending stairs. The pattern of pain is typically up and down along the spine, worse when standing, with a diffuse nagging low back ache when recumbent. Pain may worsen when lying supine without flexing the hips, and especially when lying prone for a prolonged period. Reports of first pain often involve rising from bed in the morning. Due to the deep abdominal location, psoas pain may be aggravated by dry constipation and by the cramping or spasm accompanying menstrual flow. Uterine fibroids may aggravate the iliopsoas. Complaints of anterior thigh and groin pain are also common, and there may be involvement in meralgia paresthetica syndromes, often related to the inguinal ligament and nerve impingement or entrapment. When both psoas muscles are involved, pain may be felt across the low back, mimicing the QL pattern. Travell and Simons refer to the iliopsoas as the Hidden Prankster because of its potential involvement in a variety of musculoskeletal problems. Chronic iliopsoas contracture and pain may cause distortion in postural mechanics affecting and overloading a number of stabilizing muscles from the neck to the knees. Chronic contracture and swelling of the iliopsoas may contribute to compression of the iliac vein and artery, and compression syndromes causing episodic lower extremity swelling, cellulitis, or dystrophy. These vessels are typically compressed between the psoas major and fifth lumbar vertebral body.

Sacroiliac pathology may also aggravate the iliopsoas. A locked sacroiliac (SI) joint is a common aspect of chronic low back and lumbosacral pain syndromes. While the SI joint is not a highly mobile joint, the motion of the joint is complex, with simultaneous rotations and movements in three dimensions that primarily transmit and dissipate the complex mechanical forces at the lumbosacral. Each time a person engages the low back and pelvis in torsion with flexion and leg movement, the SI joint must adjust mechanical forces, lock and unlock. When a combination of myofascial and joint pathologies occurs, the SI joint may maintain a locked position, creating added strain for a variety of stabilizing tissues, including the iliacus. While the SI is one of three joints in the body for which movement can neither by caused by, nor opposed by, muscular activity, muscle contracture can cause the joint to be held in a locked or displaced position. Asymmetric muscle tension on the pelvis from myofascial problems of the gluteus minimus muscles are often a key contributor. A combination of joint mobilization, myofascial release, and active release technique is necessary to fully correct this problem. Techniques described by Warren Hammer utilizing active release technique (ART) as well as soft tissue mobilization, or Tui Na, including a maneuver named after Dr. Janet Travell's father and described in her book, are helpful as parts of a comprehensive therapeutic regimen when SI joint locking is diagnosed. These maneuvers involve muscle and soft tissue stretch and mobilization. Most experts today agree that research has shown that both diagnosis and treatment of the SI pathology is difficult and must involve improvement of stability of the surrounding soft tissues and reduction of mechanical stresses and strains from poor postural mechanics. Once again, a holistic, or comprehensive, therapeutic routine, utilizing acupuncture, Tui Na, myofascial release and neuromuscular reeducation is best suited to correct the SI pathology. If this is a prime contributor to chronic iliacus strain, the low back syndrome that includes iliopsoas myofascial neuromuscular pathology must include this therapeutic protocol to achieve complete success.

The other key muscles commonly causing or contributing to low back pain

Travell and Simons state that low back pain is frequently referred from the gluteal muscles and lower rectus abdominus, as well as the paraspinals and small muscles of the lumbar, such as the rotares. While the QL and psoas are the prime suspects, these muscles must also be addressed in therapy. Mobilization and acupuncture with therapeutic stretch are usually sufficient to release TrP pathology of the paraspinals and rotares, as well as the rectus abdominus. A group of synergistic pelvic stabilizers with focus on the gluteals are important in the pathology of the low back pain, and should be treated as a group. The gluteals, TFL (tensor fascia latae) and piriformis are thus the prime muscles of pathological concern with myofascial release. Manual and trigger point needling are both relatively easy to perform for these muscles. As usual, the TrP release is best performed with the muscle in a stretched position.

"Sciatica is a symptom, not a diagnosis; its cause should be identified"

The piriformis is the primary hip lateral rotator and stabilizer in medial rotation. Contracture of the muscle frequently causes problems, both adding strain to other low back and pelvic stabilizers, and also potentially irritating the sciatic nerve (piriformis syndrome), as well as creating nerve impingement on a variety of other key nerves. The sciatic nerve may take any combination of three routes through or around the piriformis, depending on the anatomical variations of the individual. The greater sciatic foramen of the pelvis lies under the inferior part of the piriformis attachment under the edge of the sacrum. There are a number of anatomical variations in the path of the sciatic nerve as it destributes from the cauda eqina to the leg. In studies, 85% of subjects showed the sciatic nerve trunk anterior to the piriformis between the muscle and rim of the foramen. In 10% of subjects, the sciatic branched at the foramen and the peroneal portion passed through the muscle, while the tibialis portion passed anterior to the muscle. In 2-3% of subjects, the peroneal portion passed posterior, or over the piriformis, and the tibialis portion passed anterior. In 1% of subjects, both portions of the nerve passed through the muscle. Of course, these 11% of patients with the sciatic nerve passing through the belly of the piriformis present with problems of intense sciatic nerve impingement, entrapment, and irritation when the piriformis is not healthy.

The piriformis may develop problems both via strain (myofascial TrP syndrome and neuromuscular disease), and/or with lumbosacral pathlogy affecting the innervation of the muscle at the S1-2 root. These pathologies may cause chronic contracture, weakness, or both. Both the contracted piriformis and the weak slackened piriformis may irritate the sciatic nerve. The weak muscle may cause more periodic sudden trauma to the nerve with activity, while the contracted muscle may cause continuous impingement and increased symptoms with use. Both types of impingement may cause episodic sciatic symptoms and mimic the sciatic radiculopathy. In these cases, standard tests for sciatic pathology may be negative, such as the straight leg raise with medial rotation. Entrapment symptoms may occur in the approximately 11% of the population in which a portion of the sciatic nerve passes through the belly of the muscle, after 45 minutes of gentle continuous pressure with postural mechanics in a sustained posture, or after 2 hours of localized blood flow stagnation. Prolonged sitting on a fat wallet may be a contributing factor. Entrapment of a portion of the sciatic nerve may result in a 50% reduction in nerve conduction, effecting motor responses of the lower extremity. Loss of motor nerve conduction from a sacral radiculopathy could have significant consequences, also, as the piriformis is a key stabilizer and mover both with weight bearing and with rising from the seat. It is also thought to be a key stabilizer of the hip joint, holding the top of the femur into the acetabulum. With walking or running, the piriformis is needed to restrain medial rotation of the thigh, and in a seated position, the piriformis is a prime mover of hip abduction as we turn and rise from the seat. Sacroiliac function is also stabilized by the piriformis, and a slow and weak muscle could lead to significant sacroiliac dysfunction. A chronic contracted or slack piriformis could contribute to femoral acetabular impingement or degenerative arthritis of the fibrocartilaginous labrum of the hip socket.

Treatment and identification of TrPs in the piriformis is more difficult than many muscles because the piriformis lies under the large gluteus maximus. The size and shape of the piriformis may also vary considerably between patients. It is usually a thick bulky muscle, but may be thin, and in rare cases, absent. It attaches to the underside of the edge of the sacrum, which may harbor satellite trigger points, and originates on the superior edge of the greater trochanter of the femur, but also may adhere to the hip joint. The tendon is thought to be a prime stabilizer of the femur into the hip, and a weak or slack piriformis could contribute to a hypermobile hip and arthritic degeneration. To palpate the piriformis one should draw a mental line between the superior edge of the great trochanter and the lower sacral border at about the sciatic notch. The inferior edges of the overlying gluteus medius and minimus should be palpated and this reveals the piriformis just inferior to their edge. The muscle should be stretched with the patient side-lying and the hip medially rotated to be most effective. Releasing the overlying gluteal maximus manually first, as well as the gluteus medius/mimimus, is often necessary to properly palpate and treat the piriformis TrP. Two distinct TrPs should be addressed, the point corresponding to the acupuncture point GB30, of course, and the TrP near and deep to the sacral border. The most effective stretch of the muscle has been found to be with the hip fully flexed and laterally rotated. Normally, the piriformis is a lateral rotator, but with full hip flexion, it is a medial rotator, because the attachment is to the rotated superior head of the femur.

Piriformis syndrome, or sciatic irriation, is reported to produce a wide variety of symptoms. Travell and Simons report that pain and paresthesia may be felt in the low back, groin, perineum, buttock, hip, posterior thigh and leg, foot and in the rectum during defecation. In studies of patients with sciatic neuropathy, the number of patients diagnosed with piriformis syndrome have been greater than those diagnosed with a nerve root pathology related to disc protrusion. Females acquired piriformis syndromes over males 6:1. A gynecologist reported that 8.3% females attending a clinic for chronic low back pain had contracted, swollen and tender piriformis that was considered responsible for their pain. While the piriformis TrP does not usually cause low back pain per se, piriformis pathology may be a cause or contributor in a significant number of low back pain syndromes, and piriformis syndrome has produced a variety of low back pain complaints. In 15% of studied subjects, the inferior gluteal nerve also passes through the piriformis, always accompanied by the peroneal branch of the sciatic nerve, and nerve entrapment could thus effect the gluteal muscles as well. The deep gluteus minimus is also referred to as the pseudo-sciatica muscle because the TrP pain patterns of this muscle so closely resemble the classic sciatic pain pattern along the posterior and lateral thigh and lower leg. Once again, it must be emphasized that low back and pelvic pain syndromes often involve the whole array of key muscles, and the physician is wise that treats all of these muscles in the treatment protocol.

A great percentage of patients that complain of low back pain actually point to the buttocks and sacrum when identifying the location of the pain. The gluteal muscles are frequently causing or contributing to this pain syndrome. The Gluteus maximus typically causes complaints of pain with prolonged sitting or walking uphill or up stairs. There is little referred pain from the 3 gluteus maximus TrPs, and most complaints occur deep along the sacrum or to the lower buttock. The gluteus maximus is the largest muscle in the body, and this is because it is integral to the evolution of the upright posture peculiar to humans. The muscle maintains pelvic tilt and extension of the hip, and works synergistically with a variety of key muscles, from the low back erector spinae to the hamstrings, including the piriformis, tensor fascia latae and iliopsoas. This large muscle is rarely strained acutely, as it only uses its full strength potential in strenuous situations, but is often gradually weakened when the pelvic stability is not well maintained by other muscles, or when the innervation is diminished by a variety of problems affecting either the lumbosacral nerve roots or the gluteal nerve. Chronic problems often involve muscle contracture and ischemia of blood and nerve flow. Few patients actually maintain the gluteal muscles and piriformis with targeted stretch and strength exercises. We take our buttocks for granted most of the time.

"Pseudo-Sciatica" is the term Travell and Simons apply to the typical pain distribution associated with the gluteus minimus myofascial pattern, and many studies show that a majority of patients with "Sciatica" actually have pain of muscular or ligamentous origin

The three gluteal muscles both overlap and overlay. The gluteus minimus is the deepest and most superior, attaching across the ilium all the way to the anterior superior iliac spine (ASIS), and is a counterpart to the iliopsoas in this regard, which lies just on the other side of the pelvic bone. This muscle works with the overlying gluteus medius to maintain pelvic stability during walking, and stress imbalances between the iliopsoas and the gluteal muscles may contribute to repetitive postural strain and low back pain, as well as the pseudo-sciatic pain syndrome associated with gluteus minimus TrPs. A common test for gluteus minimus and medius weakness is the Trendelenburg Sign, which tests the ability of these gluteal muscles to hold the pelvis stable when the patient stands on one leg. To observe this sign, crouch behind the standing patient with fingers on the iliac crests. Ask the patient to raise the leg of the unaffected side and stand completely on the leg of the painful side. These gluteal muscles on the side supporting the body weight should be strong enough to keep the opposite hip and pelvis from falling. Wait 30 seconds and see if the opposite hip and pelvis start to drop. Mild weakness could be due to chronic myofascial trigger point pathology, while dramatic weakness may be due to lumbosacral disc pathology and radiculopathy, gluteal nerve impingement or palsy, or even advanced degenerative arthritis of the hip.

Since the gluteus minimus and medius attachments wrap around the hip joint and attach across the superior aspect of the femur and joint capsule, hip degeneration and arthritis may also be linked to chronic problems with these muscles. Most of the osteoarthritic degeneration in the hip is seen in the superior and lateral aspects of the joint, where these gluteal muscle tendons overlay. Bursitis in this area, called trochanteric bursitis, is also one of the most common causes of hip pain, and may be caused by contracted gluteals and enthesopathy. Since the TFL (tensor fascia latae) lies over the end, or lateral side, of the gluteus miniumus, contracture of this muscle could also contribute to gluteus minimus pathology, and also may contribute to the trochanteric bursitis. The orthopedic test, Sign of the Buttock, indicates problems with hip pathology, such as trochanteric bursitis. This simple test is a variation of the sciatic stress test, the straight leg raise. In this test, the patient lies supine, the affected leg is passively raised with full knee extension, or straight leg, and the patient may complain of pain to the leg and hip at an elevation of about 70-90 degrees. When this occurs, the physician allows the knee to flex and observes if the leg can be more fully flexed at the hip until pain recurs. If the pain remains the same with the knee flexed, and is felt in the buttock, hip and leg, this is a positive sign that gluteal contracture or enthesopathy may be causing trochanteric bursitis, and would possibly rule out sciatic pathology. Of course, the bursa and tendon complex is then palpated to confirm diagnosis. To treat trochanteric bursitis, myofascial release and active release technique should be an important part of the treatment protocol.

Most of the common pathology of the upper gluteals is related to poor maintenance of the muscles and prolonged sitting and keyboard work. Use of the opposite hand with repetitive stress has been shown to cause constant firing of these gluteals to stabilize the pelvis, especially if optimum postural mechanics are not observed. Prolonged driving is a freqent cause of gluteal pain and aggravation of TrP pathology as the right foot is held in a fixed position over the gas pedal and the gluteals are engaged but immobile. Prolonged standing without movement, as in waiting in line, especially if the feet are placed close together, reducing the base of support, may also be a key aggravating factor. Prolonged sitting on a fat wallet, of course, is always suspect in aggravation and perpetuation of TrPs. To release the gluteus minimus, which is deep to the gluteus medius and the upper edge of the gluteus maximus, manual release in stretch may be easier than finding the TrPs with a needle. The anterior fibers are held in stretch by lying on the uninvolved side, flexing the opposite hip to stabilize the pelvis, and extending and adducting the thigh over the edge of the table. The patient is then moved to the other edge of the table and the thigh of the leg to be treated is flexed about 30 degrees with the leg off the edge of the table to laterally rotate the hip. To needle the TrPs, the patient is propped in comfortable positions and the physician palpates deeply, noting the direction of pressure that elicits the referred pain or maximum tenderness. A number of TrPs can be found in the muscle, under the PSIS, from the upper buttocks around to GB29. Deep needling is often necessary and the physician should insert slowly as the pelvic bone lies deep to the muscle. Contact with the bone may be irritating momentarily, and also ruin the tip of the needle, in which case, one should remove the needle and use a new needle without an irritating bent needle point.

When there are TrPs in the gluteals and/or piriformis, sleep posture can easily aggravate them. A stable bolster, such as a buckwheat hull tube, should be used to elevate the affected leg in a side-lying posture. This also takes mechanical stress off of the lumbosacral joint and SI. A pillow between the legs is often recommended, but is problematic, as many people move their legs in deep sleep and the pillow position may change to one that is irritating for the muscles and joints.

The tensor fascia latae, or TFL, like the gluteus minimus, may mimic the common hip pathology of trochanteric bursitis, and may also produce a pattern of lateral thigh pain that is mistaken for sciatic pathology. The TFL is referred to by Travell and Simons as the "surreptitious accomplice" because this muscle is often not the focus of the symptom pathology but is important as a contributor to symptoms. The TFL functions to assist hip flexion, abduction and medial rotation, but primarily acts to stabilize during gait and control movement. Stabilization of the pelvis, hip and knee are dependant on healthy TFL function. Patterns of myofascial pain are usually difficult to localize but affect the hip and lateral thigh. Since the innervation of the muscle is from the L4-S1 and a branch of the superior gluteal nerve, problems impinging these nerves may result in poor TFL firing and weak response in the responsibilities of stabilizaation, causing overload strain. Prolonged sitting, which immobilizes the muscle in a shortened position may also contribute to the activation and perpetuation of trigger points. Release of the TrPs is best accoomplished with the patient prone and the knee passively flexed and the hip laterally rotated. If the thumb is on the belly of the muscle, palpable stretch and location of the TrP is evident. The Iliotibila band TrP, approximately GB31, may be stretched and palpated by lying the foot over the opposite calf and using the left thumb to palpate. Needling may be performed in this position, or may be performed in a side-lying position with the leg propped in hip extension and lateral rotation, or may be perfomed with the patient supine. Needling with the patient supine is easiest, but a small riser under the pelvis, and dangling of the leg off the table to achieve lateral hip rotation and knee flexion may be necessary to stretch the TFL.

The importance of neuromuscular reeducation and targeted stretch and exercise in the treatment protocol for myofascial pain syndromes

Often, instruction given to the patient that is targeted, succinct and to the point is crucial in the overall treatment success. One example is in the treatment of degenerative knee disorders. Myofascial release of the muscles that stabilize, as well as the muscles below the knee that wrap around the joint and frequently are the main cause of pathology, such as the gastrocnemius and tibialis posterior and anterior, are important to the success of treatment of the complex joint of the knee. Other key contributors that wrap the knee include the TFL and hamstrings. Stress imbalances of the pelvic girdle, low back, hip and foot can also be significant contributors to pathology. But if the targeted strengthening and toning of the stabilizing quads is not taught to the patient, success may never be realized. Even modern medicine has now come to realize the importance of thes strategies, as evidenced from this article in the New York Time, Health: http://www.nytimes.com/2009/02/03/health/nutrition/03exer.html. Targeted strengthening of the quads involves isolating each of the vastus muscles with leg position, and strengthening each individually according to the need of the muscle. The number of repetitions is determined by the patient and should not exceed the limits of the muscles. When sufficient tone is achieved in all of these muscles, especially the vastus medius, the knee is supported in activity and repeated strain does not set back the course of rehabilitation.

This same principle is applied to all treatment protocols in myofascial pathology. Without a simplified and direct instruction in postural mechanics, targeted stretch and exercise, your success in treatment may be eliminated by the strain injuries that the patient continues to experience in activities of daily living. Seminars in these neuromuscular reeducation techniques will hopefully be the subject of future CEU seminars.

What is neuromuscular reeducation exactly? CPT 97112 is defined as "Therapeutic procedure, one or more areas, each 15 minutes; neuromuscular re-education of movement; balance; coordination; kinesthetic sense; posture; and proprioception." When the physician instructs the patient in the kinesthetically correct methods of postural mechanics, targeted stretch and targeted exercise, with correct postural balance, coordination, proprioception and kinesthetic sense, this is neuromuscular reeducation. When the physician uses this time to merely assist or direct the patient performance of therapeutic exercise, range of motion, or flexibility, it is described differently, and is coded as CPT 97110, Therapeutic Exercise. Neuromuscular re-education is thus concerned with the correct instruction of the patient in body mechanics and focus of attention onto the targeted muscle, or other tissue, as well as the focus of the patient in the reflex of breathing technique concerning muscle relaxation, postural stresses, and a holistic approach to using self-administered therapies to achieve cessation of repetitive postural stress injury at work or during activities of daily living. Myofascial release techniques of focused contract and release and reciprocal inhibition also are considered re-education, as is active release technique. Myofascial release is thus integrally tied to neuromuscular re-education, and is most successful when coupled in every treatment session. CPT 97112 should use the -59 modifier to signify use of a mutually exclusive procedure such as chiropractic manipulative treatment, CPT 98942, in the same treatment session, but not when performing myofascial release and soft tissue manipulation, CPT 97140, in the practice of the Licensed Acupuncturist.

Information Resources

  1. A pretty complete explanation of myofascial syndrome and pathophysiology that relates the trigger point pathology to acupuncture is available here in a research article from the University of California Irvine - unfortunately, like many of these informative articles that would support such Complementary Medicine, it was taken down - one has to ask why so many of these types of articles are censored on the internet: http://www.acupunctureinmedicine.org.uk/servearticle.php?artid=382
  2. A comprehensive paper on supersensitivity denervation and the neuropathic aspects of myofascial pain syndrome is presented here - this too, was unfortunately taken down: http://www.www.northwestims.com/Bonica-Chapter.pdf This was published in Bonica's Management of Pain, Third Edition, John D. Loeser, MD, et al, Lippincot and Wilkens. A bit of th text is available today at this site: http://www.istop.org/myofascialpain.html

Anatomical drawings should always be considered in context. Actual anatomy varies from body to body, and the anatomical drawings approximate the midrange of anatomical variance. The physician must rely on physical exam and palpation to be accurate in therapy, and must consider the anatomical variations when using a sense of anatomy in analysis of diagnosis. Modern diagnosis in musculoskeletal medicine is primarily application of one's knowledge of anatomy and physiology, and one's analytical skills must not be overlooked when utilizing standards of differential diagnosis.

  1. anatomy of the primary low back muscles of concern in myofascial syndromes, the quadratus lumborum overlying the psoas at the approximate level of L2-3; the psoas minor would be a thin ropy muscle on the anterior belly of the psoas major, on the approximately 80% of individuals with this anatomical feature: http://www.bartleby.com/107/illus388.html
  2. anatomy of the low back muscles, the QL, psoas minor, and iliacus, from an anterior view, with the TrPs located in the bellies of the muscles at approximately L1-2: http://www.bartleby.com/107/illus430.html
  3. anatomy of the lumbosacral and femoral nerve plexus; to the right, the unmarked psoas and QL are seen to overlie the major nerve plexus as well as to potentially impinge the femoral cutaneous nerve to contribute to neuropathy of the lower extremity, typically referred to with a catch-all term 'sciatica': http://www.bartleby.com/107/illus824.html
  4. anatomy of diaphragm and its relationship to the quadratus lumborum and psoas major at the level of L1-3; since the QL and psoas also attach to the 12th rib, chronic postural strain in office work, with loss of correct diaphragmatic breathing, may lead to chronic contracture of the diaphragm affecting low back pathology: http://www.bartleby.com/107/illus391.html
  5. anatomy of the piriformis and gluteus minimus underlying the gluteal maximus (cut away); the sciatic nerve may take one of 3 routes through, under, or atop the piriformis, causing various types of sciatic irritation; note the relationship of the greater trochanter anatomically to find the TrPs: http://www.bartleby.com/107/illus434.html
  6. anatomy of the inguinal ligament, which overlies the femoral outlet and the psoas hip flexor, and is of concern in Meralgia Paresthetica, or thigh pain with paresthesia, when chronic myofascial syndromes contribute to calcification and inflammatory irritation of the ligament, which chronically irritates the femoral nerve plexus: http://www.bartleby.com/107/illus394.html
  7. anatomy of the inguinal ligament again, and its relationship to the tensor fascia lata (TFL) as well as the fossa ovalis under the inguinal ligament, where the femoral outlet and the nerve plexus emerges into the thigh, part of the cause of the Meralgia Paresthetica, along with nerve irritation deep to the anterior superior iliac spine (ASIS): http://www.bartleby.com/107/illus431.html
  8. anatomy of the Femoral nerve plexus and cutaneous femoral nerve under the inguinal ligament and through or over the iliopsoas; the pattern of numbness and weakness seen in Meralgia paresthetica is clearly demonstrated: http://www.bartleby.com/107/illus827.html
  9. anatomy of the piriformis muscle in relation to the coccygeus, the primary cause of myofascial strain perpetuating coccygodynia, or coccyx pain, in occupational injuries; often the contributing myofascial problems must be treated before progress can be achieved; xie of GB34 and GB35 is also effective: http://www.bartleby.com/107/illus404.html
  10. anatomy of the lower leg, with the key pathological muscles, the tibialis anterior, extensor digitorum, and peroneals forming a complex with TrPs close together: http://www.bartleby.com/107/illus437.html
  11. anatomy of the foot, demonstrating how the tibialis anterior will dorsiflex and invert, or supinate the foot, while the adjacent peroneals will plantar flex and evert, or pronate the foot: http://www.bartleby.com/107/illus441.html
  12. anatomy of the lower leg, with the soleus underlying the gastrocnemius; the main soleus TrP is located approximately at LV5 on the medial aspect, and can contribute to diverse pathologies, including typical runner's strain or medial tibial sprain, as well as chronic stiffness of the low back and spine: http://www.bartleby.com/107/illus438.html
  13. anatomy of the lower leg, with the tibialis posterior and popliteus muscles, frequent contributors to chronic knee pain; the main tibialis posterior TrP is located near SP9 on the medial aspect: http://www.bartleby.com/107/illus439.html
  14. Use of the treatment codes for myofascial release and neuromuscular re-education should be bundled, with 15 minutes spent on each aspect of treatment, but use of the -59 is appropriate when combining the 97112 NMR code with the chiropractic manipulation of the spine. Here is the government guideline: http://www.cms.hhs.gov/NationalCorrectCodInitEd/Downloads/modifier59.pdf