Headaches and the Unresponsive Atlas Subluxation

By Joseph D. Kurnik, DC

This situation presents itself clinically as a failure to most attempts for correction. The patient presents with suboccipital pain on the left or right side. There is often radiating pain into the left or right face, especially the forehead, temple, or eye region.

Examination by static, visual and motion analysis reveals a C-1/C-2 articulation that is fixated in rotation, and lateral flexion on the left side. This means that the left side of C-1, when rotated to the right, exhibits restriction. C-1 also is restricted in lateral flexion on the left. The right side palpates freely.

When the doctor tries to adjust the atlas from the left side, nothing happens: no sound, no release, no correction, and probable increased soreness. You try again, but the atlas remains tight and unmoveable, yet clearly a hypomobile fixation. The title of this article calls this a subluxation, but it is actually a subluxation and fixation. The atlas is clearly malpositioned, as determined by static and visual analysis. To confirm this, while the patient is supine, press over the atlas lying under the SCM, bilaterally. You can feel the more anterior position and resistance of C-1 on the right side. The left side of C-1 from the anterior will palpate with less resistance.

Stop banging on the atlas and go to the right side. Do not bang on the right side of C-1, which can be very dangerous under any condition. Evaluate the ability of the occiput on the right side to rotate to the left, laterally flex on the right, and extend during rotation to the left. A common finding in these C-1 unresponsive headaches is a right-sided occipital fixation pattern. Occasionally, you may encounter a left-sided occiput rotation fixation. The most common finding with unresponsive left C-1 problems and responsive C-1 left fixations is a right-sided fixation of occiput on C-1.

You can encounter some combination of occipital problems involving rotation, lateral bending and extension. With one adjustment, you can free all the restriction problems just by incorporating correctional vectors to your corrective thrust. To rectify the extension or backward nodding problem, incorporate occipital extension in your thrust, combined with rotation. If you do not combine extension with rotation, correcting extension alone will be very difficult and can feel like you are punching the patient.

The result of correction to the occipital fixation dysfunction will be a release to atlas motion, overall cervical increased movement, and a gradual reduction in symptoms. "Migraine" type headaches often are associated with this right-sided occipital fixation pattern. Even if C-1 is responsive to adjusting on the left side, you commonly still encounter the right-sided occipital fixation. You also may encounter a simultaneous lateral bending and extension hypomobile fixation at C-2/C-3 level. You may correct this with a simultaneous contact at the occiput and C-2. The corrective thrust induces some rotation, lateral bending, and extension simultaneously. The rotation is not full, rotation and does not take C-2 to completion, which is necessary. C-2 will tend to favor rotation from right to left, and full rotation of C-2 from right to left can exacerbate the headache.

In summary, I advocate the following forms of analysis: 

• visual analysis, especially supine; observe position of SCM tissue bilaterally;
• static palpation while supine to the posterior and anterior aspects of the cervical spine bilaterally;
• static palpation of each cervical level arteriorly/posteriorly (joints and segments); extend palpation (tissue challenge); then push on tissues to feel for resistance. You will be surprised when you combine the palpation and challenge to anterior and posterior elements.
• motion palpation applied to the arterior/ posterior sides of the cervical spine in the supine position. This is easier and has more clear results than doing it seated. In this procedure, you have to bring each cervical segment and joint to tension, and beyond, with posterior and anterior contacts. There are two ways to do this, but a description of the technique has to be a separate article.
• Motion palpation to the anterior and posterior aspects of the occiput.

I guarantee that if you take the time to be more thorough in your palpatory examination of the cervical spine, you will become more accomplished in your diagnosis and understanding of cervical mechanics and patterns, including the occiput. Even beyond this, you will discover things that you have been doing wrong and must to change. You will be surprised at what you find if you force yourself to become more thorough, examining every angle of motion. You may not agree with my findings. You may say, "I've been practicing for 20 years and have had no problems, so why should I change?" Just try to be more thorough and see for yourself. 

LUMBAR BACKWARD

Lumbar Backward Bending and Its Effect on Discs

By Warren Hammer, MS, DC, DABCO

A very useful procedure for helping evaluate lower back and extremity pain is McKenzie's "centralization" phenomenon.¹ I have often found that when a patient is put into repeated end-range motions, mostly in extension and sometimes in lateral bending, the distal peripheral pain will retreat toward the originating spinal location.

Donelson et al.² evaluated chronic low back patients with backward bending, performed diagnostic disc injection (discogram) to provoke pain, and followed up with MRI. They concluded that patients whose pain centralized had discogenic pain with a functionally competent annulus; patients whose pain remained peripheral had discogenic pain with a much higher incidence of outer annular disruption and a possible "breached annular wall and an incompetent hydrostatic mechanism."

The exact reason why backward extension may reduce pain is still not definitely known. Sometimes lumbar flexion will reduce peripheral pain. It is known that the outer third of the annulus fibrosus is innervated. Coppes et al.³ found more extensive disc innervation in severely degenerated lumbar discs compared with normal discs. It is well accepted that discs can be the source of back pain without nerve root involvement. Both an inflammatory or chemical disturbance has been implicated, along with excessive mechanical deformation of damaged or sensitized disc tissue.⁴

Reasons given for the reduction and centralization of pain during backward bending include the anterior migration of nuclear tissue and the reduction of forces acting on pain-sensitive tissues, since extension may transfer compressive forces from the disc's vertebral body unit to the apophyseal joints so that nuclear pressure is reduced. Repeated extension movements in vivo have been shown to increase the height of the spine possibly by unloading the disc and permitting rehydration.⁵ During extension, the vertebrae may pivot around the apophyseal joints and unload the disc.

A question arises about lumbar extension, since extension also causes a transfer of load from the anterior annulus and nucleus to the posterior annulus, which is a major source of disc pain. The answer may be that patients with degenerated discs have reduced disc height and a damaged annulus or endplate. In extension, the zygapophyseal joints resist compressive forces on the spine, especially when the disc is narrowed. With increased disc degeneration, the posterior annulus would be stress shielded by the neural arch so that the posterior annulus became relatively unloaded in the extended posture.

Adams et al.⁴ concluded that pain relief would be anticipated only in those patients whose painful discs can be stress shielded by the neural arch in extension, which also relates to factors such as disc height and the "precise shape of the neural arch." If stress to the posterior annulus is not protected by the neural arch, this may explain why backward bending would increase pain.

Despite these observations, why lumbar extension may or may not relieve pain remains a mystery.

References: 

1. McKenzie RA. The Lumbar Spine: Mechanical Diagnosis and Therapy. Waikanae, New Zealand; Spinal Publications, 1981.
2. Donelson R, Aprill C, Medcalf R, Grant W. A prospective study of centralization of lumbar and referred pain. A predictor of symptomatic discs and annular competence. Spine1997;22(10).
3. Coppes MH, Marani E, Raph T, et al. Innervation of "painful" lumbar discs. Spine1997;22(20).
4. Adams MA, May S, Brian JC, et al. Effects of backward bending on lumbar intervertebral discs: relevance to physical therapy treatments for low back pain. Spine 2000;25(4).
5. Magnusson ML, Aleksiev AR, Spratt KF, et al. Hyperextension and spine height changes.Spine 1996;21.

MYOFASCIAL PAIN SYNDROME

Myofascial Pain Syndrome Presenting as Chronic Pelvic Pain

By Nancy Martin-Molina, DC, QME, MBA, CCSP

A.S. is a 44-year-old woman with a two-year history of lower abdominal pain. Her menses were regular, of six to seven days' duration, but had become progressively heavier over the past two years, which was attributed to fibroids.
She reported a recent six-month history of lower back pain that worsened one week before menses and continued throughout the menstrual cycle. She obtained modest relief from nonsteroidal anti-inflammatory drugs.

On initial presentation, she reported marked fatigue and constant pain in the lower back and the right lower quadrant of the abdomen. The pain was worse with physical activity. She denied any urologic or neurologic symptoms, but did complain of a recent increase in intestinal gas and bloating. She had declined a colonoscopy from an internist. She later developed difficulty arising from bed because of back pain and right leg pain. There is no loss of bowel, bladder, or sexual function. She works in data entry and does a lot of sitting, which she reports "causes her pain after prolonged seated activity."

The patient's medical history includes uterine fibroids, lower back and abdominal sensations of pressure, and constant mild pain that had been attributed to the fibroids. An immediate total abdominal hysterectomy and bilateral salpingo-oophorectomy had been recommended, which she declined. She reported history of previous trauma to the region in a vehicular accident 15 years ago, but denied significant residual effects other than joint stiffness. She takes no medications.

Examination revealed an ill-appearing woman complaining of severe pain in the right lower abdominal quadrant and the lumbosacral region. Physical examination was negative, except for moderate lower abdominal tenderness to deep palpation. She was afebrile; her white blood cell count and differential were normal; and her red blood cell count was borderline low with a slight increase in MCV and MCH. Ferriten and percent saturation confirmatory serum studies were obtained and tested positive for chronic anemia. Laboratory diagnostics ruled out hypothyroidism and folic acid deficiency.

She could forward flex to 70 degrees without pain and exhibited a positive Minor's sign on arising, with complaints of localized low back pain. The patient was without paresthesias, muscle weakness or hyporeflexia to indicate any specific nerve root involvement. Magnetic resonance imaging of the spine was the diagnostic test of choice to rule out neurologic disease when the situation warranted.

Range of motion of her hips and joints in the lower extremities does not reproduce her pain. The distal vascular exam is normal. She presents with a functional right short leg. Palpable trigger point bands, purposeful withdraw, and referred pain were demonstrated on digital examination of the thoracolumbar iliocostalis, gluteus medius and quadratus lumborum. Chiropractic assessment yields joint fixation of T10-12, L1-L2 vertebrae and pelvis. Postural examination revealed a head-forward, round-shouldered posture that maintained the pectoral muscles in a shortened and digitally painful position.

Radiographic weightbearing imaging studies were performed to evaluate her lumbar spine. The curvature was somewhat hypolordotic. There was mild loss in disc height of the fifth lumbar and first sacral levels.

Incidental findings: Fergerson's gravational line falls anterior to the sacrum. There were proliferative osteophytes and mild traction spurring demonstrated at the first and second lumbar intraspinous levels. There was laterolisthesis of the spinous processes accompanied by pelvic declination. The acetabuli and hip joint spaces were well-maintained. The bone density and soft tissue structures were unremarkable. There was no evidence of any gross pathology, congenital findings or obvious fracture.

Impression: spondylosis and postural changes.

Discussion: Myofascial Pain Syndrome (a hyperirritable spot within a taut band of skeletal muscle or fascia) This case illustrates the typical clinical findings of myofascial pain syndrome (MPS) presenting as chronic pelvic pain. Although the patient does have mild mechanical low back pain, her major difficulties are related to the chronic pelvic pain disorder.

Clinical Features

There are seven clinical features of MPS due to trigger points (TPs) that warrant discussion. First, there is the exquisite local tenderness of the TP that is well explained by sensitization of the nerve endings of group III and group IV muscle nociceptors. Substances known to make tissues sensitize include bradykinins, prostaglandins, histamine and leukotrienes. Awad biopsied a tender nodular area in the muscles of 10 subjects. Electron microscopy showed discharging mast cells and blood platelets, each of which is a source of histamine and serotonin. Mense et al. discovered that group III and IV muscle nociceptors are most responsive to bradykinins. The afferent nerves of these muscle groups are also capable of generating nerve action potentials that can lead to the referral of pain, and autonomic phenomena to areas some distance from the TP.

Third, there is a palpable band that is characteristic of myofascial pain and helps localize the involved muscles. Of valuable objective clinical identification is the local twitch response of the taut band associated with the TP. The rope-like sensation produced on digital examination of the involved muscle fibers at the TP can be explained by contracture.

Clinically, the patient will experience pain whenever tension is placed on the taut band muscle fibers. There is a perceived weakness without atrophy, and increased fatigability, that may be explained by localized shortening of a group of muscle fibers, and can be expected to cut off local circulation of the capillaries in the TP zone strong enough to produce localized tissue hypoxemia. This leads to an energy crisis that also explains the more rapid onset of fatigue in muscles afflicted with active TPs compared to muscles free of TPs. This may also offer a reasonable explanation as to why leaving the afflicted muscle in a contracted (shortened) position (i.e., while sleeping at night or prolonged seated activity) initiates pain. Patients often report being aware of pain within a specific muscle group upon awakening in the morning.

Current clinical and research evidence indicates that the TP phenomenon begins primarily as a neuromuscular (histochemical) dysfunction resulting from muscle overload. Active TPs then can progress at an unpredictable rate to a dystrophic phase and demonstrate pathological changes.

MPS is a condition that is treatable by eliminating the specific trigger points that are the immediate cause of pain and correcting those factors that predispose to recurrence. Metabolic, endocrine, toxic, inflammatory and other systemic disorders can stress muscle and impair its ability to heal. The most common systemic factors associated with MPS are hypothyroidism, folic acid and iron insufficiency. Subclinical hypothyroidism is often overlooked because its symptoms are subtle, including widespread multiple TPs, cold intolerance, and fatigue. Iron is essential for the conversion of T4 to the active form of T3 thyroid hormone. Cholesterol is often elevated, and hyperactivity, while an unexpected sign, is often present and caused by constant body movement in an attempt to generate body heat. The most useful test is the highly sensitive thyroid stimulating hormone assay. A level in the upper range of normal should lead to further clinical correlation.

Patients with lowered folic acid levels feel cold and have lower cholesterol levels in contrast to hypothyroidism, which is accompanied by headaches, disturbed sleep and restless leg syndrome. Measurement of serum folate, serum vitamin B12 and red blood cell folate gives the most complete assessment of folate status. Iron deficiency is often seen in patients with MPS, usually women in premenopause that have inadequate iron stores. Consuming NSAIDs may lead to depletion of iron stores. Among systemic illness, fibromyalgia is sadly, too often confused with MPS.

Of special concern in these pelvic pain patients is the evolving disc herniation of the lumbar spinal segments. By exerting pressure over the dorsal afferent spinal nerve roots, the evolving disk herniation can produce a pain syndrome before any development of pain typically associated with radiculopathy, e.g., radiating pain and/or numbness of extremity occurs. Early close clinical monitoring of neurological status is warranted.

The chiropractic profession has long utilized manual treatment of MPS, most commonly in addressing the mechanical factors that include structural inadequacies, such as the short leg syndrome, postural stresses, and ultimately, correction of the vertebral subluxation complex. Additionally, many chiropractic practitioners, often at pre-adjustment, utilize digital ischemic compression of the TP for 15-30 seconds, rhythmic percussion of the TP at about two-second intervals to provide a counter-irritant to disrupt the TP and Ultrasound, or electrical stimulation heat application to stimulate endorphin production. Personally, I find that chiropractic adjustments prior to the administration of physiotherapy can significantly shorten the treatment plan duration.

A.S was treated 22 times over a 12-week period under my direction. Conservative chiropractic treatment included high-velocity thoracic, lumbar and pelvic adjustments. Percussor therapy, ultrasound with trigger-point head, and myofascial release with digital ischemic pressure was utilized. Finally, she was taught to recognize activities that would aggravate the pain and to distinguish the TP distribution. A stretch-conditioning muscle program was prescribed for use at a local gym.

Early in the course of care, she was given a referral for gynecological consultation and examination, and was consequently treated concurrently with a local OB/GYN. My medical colleague's report showed upon pelvic examination, a tender cervix and uterus, with tender adnexa as well. No palpable masses were detected. Pelvic ultrasonography was also negative for any mass. This patient's exam had yielded benign uterine fibroids, secretory endometrium, and ovaries with no pathologic change. She was instructed that the total abdominal hysterectomy and bilateral salpingo-oophorectomy that had been previously recommended was, in all likelihood, years away from any clinical consideration. She had a moderate number of white blood cells on a vaginal saline wet prep and was treated with a short-term trial of antibiotics. She received iron supplementation for three months, B12 injections twice weekly for one month, and six sessions of intravaginal electrical muscle stimulation of the levator ani muscle groups to disrupt active TPs.

In working closely with OB/GYN medical practitioners, I have discovered about 30 percent of their patients with pelvic pain belong in my practice; conversely, some of my patients in their practices. This recognition has afforded mutual respect, opportunity for co-referrals, and mutual cooperation when it comes to patient care.

References 

1. Gatterman MI. Disorders of the Pelvic Ring. Chiropractic Management of Spine-Related Disorders. Williams & Wilkins, 1990; 7: 112-127.
   
   
2. Gerwin RD. The management of myofascial pain syndromes. Journal of Musculoskeletal Pain (The Haworth Press, Inc) Vol. I, No. 314, 1993, pp. 83-94.
   
   
3. Travell JG, Simmons DG. Myofascial Pain and Dysfunction: The Trigger Point Manual.Williams & Wilkins, 1992.
   
   
4. Simmons DG. Myofascial pain due to trigger points. International Rehabilitation Medicine Association, IRMA Monograph Series Number 1, Nov 1987.
   
   
5. Travell JG, Simmons DG. Myofascial origins of low back pain. Postgraduate Medicine, Low Back Pain, Part I, Vol. 73, No 2, February 1983.
   
   
6. Rubin, D. Myofascial trigger point syndromes: an approach to management. Arch Phys Rehabil Vol. 62, March 1981.
   
   
7. Travell JG, Rinzler SH. The myofascial genesis of pain. Postgraduate Medicine Vol. II, No. 5,May 1952.
   
   
8. Kraus H. Evaluation and treatment of muscle function in athletic injury. Amer Journal of Surg, Vol. 98, September 1959.
   
   
9. Awad EA. Interstitial myofibrositis. Arch Phys Mid 54:449-453. 1973.
   
   
10. Mense S. Nervous outflow from skeletal muscle following chemical noxious stimulation. J Physiol 267:75-88, 1977.

Pelvic Unleveling

By Kim Christensen, DC, DACRB, CCSP, CSCS

The most useful method of determining pelvic unleveling is to involves examining the patient in normal, upright posture. This eliminates much of the confusion surrounding this topic and simplifies treatment decisions. 
Whenever we check a patient on the treatment table, whether prone or supine, errors of positioning are introduced (and are very difficult to exclude).

Measurements of pelvic balance obtained in the non-weightbearing position have been found to be very unreliable.¹ In a relaxed, upright posture, these confounding factors are not present. Accurate clinical and radiographic determinations are then possible,² and effective chiropractic care can proceed.

Determining Anatomical Sources

When evidence of pelvic unleveling has been identified in the standing position, efficient treatment depends on the anatomical source of the misalignment. Either the pelvis or the lower extremities must be the cause of the biomechanical imbalance. If it is the pelvis, treatment will need to be directed to this region. When the cause is in the lower extremities, successful care can be expected only with evaluation and correct treatment of the foot, ankle or leg asymmetry. Since the lower extremities provide the foundation and support for the pelvis during standing and walking, it is not surprising that they can have a profound effect on the alignment of the pelvis and spine.

Determination of Causal Factors

Whether the pelvic unleveling originates in the pelvis or the lower extremities, the cause must be either an anatomical asymmetry or a functional imbalance. Anatomical sources include growth asymmetries, anomalies and postfracture discrepancies. Functional problems encompass subluxations and biomechanical imbalances. Since these two categories are treated very differently, they must be separately identified. Here are the details of these causes in the two regions:

In the Pelvis

Anatomical asymmetry: A very small percentage of patients will demonstrate pelvic unleveling caused by a growth asymmetry or an old fracture of an ilium. The innominate bones can develop with a substantial difference in height, although this is rare. Luckily, it also is the least likely to cause symptoms. For sedentary patients, an ischial lift (a wedge under the "sit-bone" of the smaller side) can prevent problems from developing when seated for long periods. For most patients, standard chiropractic care of biomechanical problems in the spine and pelvis is sufficient.

Functional imbalance: Much more common in the pelvis is a biomechanical source of pelvic unleveling: sacroiliac joint subluxations. This condition can be caused by work postures, recreational habits, or even a broken-down chair at home. Muscle imbalances are frequently part of this syndrome, the most common being weakness of the hip extensor muscles. Tightness of a psoas muscle, or shortening of the hamstrings from excessive sitting, can also contribute to pelvic unleveling. An "antalgic" posture, in response to acute pain and inflammation of the lower spinal joints, often results in a difference in height of the iliac crests.

Treatment should include specific stretches targeted to shortened muscles, with strengthening and stabilizing exercises for weak or poorly coordinated muscles. Specific adjustments of the pelvis and lumbar spine are necessary to regain normal pelvic biomechanics and full function of the region.

In the Lower Extremities

Anatomical asymmetry: Some patients have a difference in the anatomical components of the lower extremities, which results in pelvic unleveling. This may be the result of a fracture of the tibia or femur that healed with persisting shortness, but much more likely is a simple growth asymmetry. In fact, it is quite amazing that most of us have no significant difference in the length of our legs. Somehow, most legs grow to an equal length at adulthood. Those that end up with a difference in length over 9 mm (measured while standing) have a higher incidence of low back pain.³ Athletes and those who spend a lot of time on their feet may develop chronic symptoms with 5 mm, or even just 3 mm of discrepancy.⁴

Functional imbalance: The most commonly seen cause of pelvic unleveling is loss of support from the foot, in particular due to collapse of the medial arch. When the arch drops (excessive pronation), the leg rotates medially and the femur head drops, causing an unlevel pelvis. Excessive pronation may occur from a young age through lack of development of the arch, but most commonly it occurs in later years when the ligaments that support the arches undergo plastic deformation. Since this process usually happens gradually over many years, there is often no significant foot pain. The patient with this condition begins to develop chronic low back and pelvis problems, but doesn't any foot symptoms. The doctor of chiropractic must always have an index of suspicion and include a lower extremity postural exam in the evaluation of most new patients. When there is evidence of pelvic unleveling, investigation of the feet and ankles, along with inspection of shoe wear patterns, is necessary.

Lift vs. Orthotic

It is very important to recognize the functional short leg, since providing a lift instead of an orthotic is likely to perpetuate the associated sacroiliac subluxations.⁵ There is no reliable information on the radiographs to differentiate between these conditions. A pelvic tilt, a lower sacral base, and a femur head discrepancy may indicate a lower extremity source, but not whether it is an anatomical or functional short leg. The clinical postural exam with lower extremity screening is the only way to make this determination. If there is any doubt, the safest approach is to fit the patient with flexible, custom-made orthotics initially. If there is a persisting pelvic tilt after wearing the orthotics for several weeks and receiving chiropractic adjustments, a heel lift can easily be added to the orthotic for complete correction.

Conclusion

Once pelvic unleveling has been found in a patient, effective treatment can be planned. The first step is to differentiate whether the source of the imbalance is in the pelvis or the lower extremities. This may require accurate, standing radiographs taken without projectional distortion. A determination of anatomical asymmetry or functional imbalance will then help guide treatment. Most commonly, the lower extremities do not provide the necessary support for the pelvis. In many cases, orthotic support for foot pronation, knee rotation or femur angulation is needed. Those few patients with a true anatomical leg length discrepancy will need to be supplied with the appropriate lift. The cost of additional time required to determine the source of the pelvic unleveling will be repaid in more effective chiropractic care and longer lasting adjustments. The gratitude of patients who have finally found a doctor interested enough to individualize their treatment will help build a tremendous practice. This level of service ensures a great future for chiropractic, no matter what the insurance companies say or do.

References 

1. Woerman AL, Binder-MacLeod SA. Leg length discrepancy assessment: accuracy and precision in five clinical methods of evaluation. J Orthop Sports Phys Therap 1984; 5:230-238.
2. Friberg O, et al. Accuracy and precision of clinical estimation of leg length inequality and lumbar scoliosis: comparison of clinical and radiological measurements. Int Disabil Studies1988; 10:49-53.
3. Giles LGF, Taylor JR. Low back pain associated with leg length inequality. Spine 1981; 6:510-511.
4. Subotnick SI. Limb length discrepancies of the lower extremity; the short leg syndrome. J Orthop Sports Phys Therap 1981; 3:11-16.
5. Rothbart BA, Estabrook L. Excessive pronation: a major biomechanical determinant in the development of chondromalacia and pelvic lists. J Manip Physiol Therap 1988; 11:373-379.

Patellofemoral Pain Syndrome and Epicondylitis: Myofascial Treatment

By Guy Hains, DC

Patellofemoral pain syndrome (PFPS) is a common cause of knee pain.¹ In fact, it is the most often diagnosed disease of the knee in orthopaedic and physiotherapy clinics.² Once it starts, PFPS becomes chronic and seriously limits physical activities in adults.³ Surgery for PFPS is costly and has not been shown to be useful.⁴

The patient who suffers from this condition feels pain at the anterior knee level, at the peripatellar and retropatellar regions, especially when they squat, go up or down the stairs, or sit down for a long time (cinema sign).^5-6 The termchondromalacia is still used, but most experts agree that the two conditions differ.^5-7

Etiology and Diagnosis

Certain authors theorize that PFPS is caused by a degeneracy of the cartilage, but it is well-known that cartilage has no nerve cells, and that many people have no pain even if the cartilage is substantially altered, while others have a lot of pain with normal cartilage.

The patellar grinding test is considered to be the most specific for PFPS.^8-9 It is done with the patient's leg in extension; the examiner grasps the patella with one hand on the other, and applies a compressive pressure on the patella vertically into the patellofemoral joint space.^{5, 9-10} The test is positive if it causes pain.

The grinding test has to be performed delicately at the beginning, gradually augmenting pressure to the patient's tolerance. The greater the pain, the more serious the condition. This test is frequently positive even in asymptomatic patients; it is only past a certain level of irritation that the symptoms appear.

The most common causes of PFPS are overwork, bad alignment of the patella and trauma.^11-12 For example, an office worker decides to redo a wooden floor. For three days in a row, they kneel and/or squat, and a few days later the symptoms appear.

Treating PFPS With Ischemic Compression

The present author carried out a randomized trial on PFPS.¹³ The aim of this trial was to test the efficacy of 15 myofascial therapy treatments using ischemic compressions directly to the knee in 38 patients suffering from chronic PFPS. The experimental group (27 patients) received treatment directly to the knee, while the control group (11 patients), received ischemic compressions to the trigger points (TrPs) localized in the hip muscles.

The patellar grinding test was used with a scale from 0-5 to quantify the pain present; the test was performed by another chiropractor who did not participate in the treatments.

Intervention: When the TrPs were located under the patella, treatment was like the examination: the patella was crushed in the hyperirritable foci (1 or 2); the pressure was very light at the beginning and gradually increased to patient tolerance. Then the pressure was kept up for 8 seconds without moving.

When TrPs were found (one or two) at the peripatellar level, they were treated with thumbtip pressures in a 90 degree angle. The 8-second pressure was to patient tolerance and repeated at each visit until elimination, or in this trial, within 15 treatments. In all cases of PFPS, there are TrPs under the patella (retropatellar), but not necessarily at the plica level (peripatellar).

My hypothesis is that passive and oriented mobilization of the patella was an ischemic compression on the TrPs located under the patella. The ones at the peripatellar level were treated directly with thumbtip pressure. TrPs may be located in muscles, ligaments, tendons, fasci and articular capsules.¹⁴

Results of this trial demonstrated a decrease in the irritation with the patellar grinding test. After 15 treatments, the treatment success rate was 60 percent in the experimental group versus 28 percent in the control group. In the experimental group, there was still a 43 percent amelioration six months later.

The aim of these treatments should be the complete elimination of all the TrPs. Often, right after the first few treatments, there is great improvement. As well as patellofemoral pain syndrome, many patients have TrPs somewhere around the knee, so it is best to treat all the problematic areas, especially the ones pinpointed by the patient. At the site indicated, every square centimeter should be examined attentively with thumbtip pressure.

Some patients have edema at the anterior part of the knee; normally, this will vanish while taking care of the PFPS. In obese patients, the knee may be deformed with calcium deposits and hyperirritation, mostly at the interior part of the knee (osteoarthritis), at the level of the meniscus and at the lower insertion of the vastus lateralis and medialis muscles. All these irritations can be treated with ischemic compressions and these patients, even those with major problems, can be significantly helped. A good way to treat the inside of the knee is to have the patient lie on the symptomatic side while you apply an 8-second thumbtip pressure vertically on each TrP.

Pain at the interior or exterior meniscus, with or without tears, can be treated with very good results using ischemic compressions. Examination with magnetic resonance has shown that 67 percent of people over age 65 have tears of the meniscus without any symptoms.¹⁵ Surgery may be warranted when there is a tear plus misplacement of the meniscus and the knee cannot be extended.

Epicondylitis: Overview and Treatment

Lateral epicondylitis, also known as tennis elbow, is the most common elbow problem in adults. Normally it is produced by an accumulation of microtraumas causing inflammation and degeneracy of the musculotendinous tissue attached to the epicondyle. This problem may be extremely debilitating, even with regard to the performance of normal daily activities.^16-17

Occupational activities that necessitate repeated forced dorsiflexion of the forearm, and jobs involving radial deviation with the arm in supination, such as plumbing and computer work, may cause stress at the extensor muscles of the wrist. This can result in degenerative changes to the common tendon of these extensors at their point of attachment on the lateral epicondyle of the humerus. As the name suggests, is often seen in tennis players.^18-19

In a trial by Hay²⁰ on epicondylitis, four weeks of anti-inflammatory medication proved no more effective than placebo. For Ollivierre,¹⁶ cortisone injections may attenuate the symptoms, but they cause degeneracy, weakness and sometime a rupture of the musculotendinous unit. Surgery may be useful in less than 5 percent of cases of lateral epicondylitis.²¹

The treatment I use with this condition is as follows: With the patient supine, stretch their arm along their body, applying an 8 second thumbtip pressure on the trigger points (TrPs) localized along the extensors muscles and at the epicondylitis. These TrPs may be very sensitive, so you should proceed delicately at the beginning, gradually augmenting the pressure to the patient's tolerance. The extensor muscles are attached to the epicondyle and descend for 8 centimeters along the radius.

Another approach may be used concurrent to the aforementioned treatment. The TrPs may be treated with the patient kneeling on the floor, perpendicular to the table, their forehead resting on the asymptomatic arm. Stretch the arm along the table with the hand in pronation. The TrPs may then be reached easily; an 8-second pressure on each will normally produce evident amelioration within six treatments, in my experience.

In cases of medial epicondylitis, the irritation is on the inside of the humerus. The TrP may be reached with the patient's hand supine.

Every patient has some irritation at these sites, but the symptoms will appear only above a certain level. Sometimes it is useful to check for pain when you press the elbow directly from posterior to anterior. If this mobilization produces pain, an 8-second pressure, repeated until the hyperirritability is gone, may affect the overall elbow function. Chronic medial or lateral epicondylitis may need 10-20 treatments before resolving.

References

1. Crossley K, Bennell K, Green S, McConnell J. A systematic review of physical interventions for patellofemoral pain syndrome. Clin J Sport Med, 2001;103-10.
2. McMullun W, Roncarati A, Koval P. Static and isokinetic treatment of chondromalacia patella : a comparative investigation. J Orthop Sport Phys Ther, 1990;12:256-66.
3. Kannus P, Natri A, Paakkala T. An outcome study of chronic patellofemoral pain syndrome : seven year follow-up of patients in a randomized controlled trial. J Bone Joint Surg (Am), 1999;81(3):355-63.
4. Sandow MJ, Goodfellow JW. The natural history of anterior knee pain. J Bone Joint Surg(Am), 1985;67:36-38.
5. Garrick JG. Anterior knee pain (chondromalacia patella). Phys Sportsmed, 1989;17:75-84.
6. Hilyard A. Recent development in the management of patellofemoral pain. The McConnel program. Phys Ther, 1990;76:559-65.
7. Kelly MA, Insall JN. Historical perspective of chondromalacia patellae. Orthop Clin N Am,1992;23:517-21.
8. Dehaven KE, Dolan WA, Mayer PJ. Chondromalacia patella in athletes. Am J Sports Med,2002;7:5-11.
9. Meyer JJ, Zachman ZJ, Kiating JC. Effectiveness of chiropractic management for patellofemoral pain syndrome's symptomatic control phase: a single subject experiment. J Manip Physiol Ther, 1990;13(9):539-49.
10. Dryburg DR. Chondromalacia patella. J Manip Physiol Ther,1987;11(3):214-17.
11. Dixit S, Difiori JP, Mines B. Management of patellofemoral pain syndrome. Am Fam Physician, 2007;75:194-202.
12. Fulkerson JP. Diagnosis and treatment of patients with patellofemoral pain. Am J Sports Med, 2002;30(3):447-56.
13. Hains G, Hains F. Patellofemoral pain syndrome managed by ischemic compression to the trigger points located in the peri-patellar and retro-patellar area: a randomized clinical trial.Clin Chiro, 2010;13:201-209.
14. Travel JG, Simons DG. Myofascial Pain and Dysfunction; The Trigger Point Manual, 1st Edition, Volume 2. Baltimore: Williams and Wilkins; 1992:6.
15. Greis PE, Bardana DD, Holmstrom MC. Meniscal injury: basic science and evaluation. J Am Acad Orthop Surg, 2002;10(3):168-76.
16. Ollivierre CO, Nirschl RP. Tennis elbow, current concepts of treatment and rehabilitation.Sports Med, 1996 Aug; 22(2).
17. Ciccotti MG, Charlton WPH. Epicondylitis in the athlete. Clin Sports Med, 2001;20(1).
18. Olancher KD, Halbrecht J, Louri GM. Medial and lateral epicondylitis in the athlete. Clin Sports Med, April 1996;15(2).
19. Kushner S, Reid DC. Manipulation in the treatment of tennis elbow. J Orth Sports Phys Ther, 1986;7(5):264-72.
20. Hay E, Paterson S, Lewis M. Pragmatic randomised controlled trial of local corticosteroid injection and naproxen for treatment of lateral epicondylitis of elbow in primary care. Brit Med J, October 1999.
21. Kraushaar BS, Nirschl RP. Tendinosis of the elbow (tennis elbow). J Bone Joint Surg,1999;81-A(2).

SHOULDER

Get That Shoulder to Move: Restoring Internal Rotation

By Justin Hildebrand, DC

How many times have you mobilized, performed ART, Graston, FAKTR and PIR, and stripped a patient's posterior capsule, yet on re-exam, discovered it was still blocked? Internal rotation (IR) of the shoulder is commonly diminished in overhead athletes (e.g., baseball pitchers), as well as the general population.

A decrease in IR can often be attributed to overactive or shortened infraspinatus or teres minor muscles, and joint dysfunction due to capsular contraction of the posterior shoulder ligaments. This loss of mobility is so common that the term glenohumeral internal rotation deficit(GIRD) is used to describe it.

Verifying Capsular Tightness

Checking passive IR at 90 degrees of abduction is standard procedure. IR should measure 75-85 degrees. According to Neumann,¹ posterior capsule restriction is associated with anterior displacement or decentration of the humeral head during internal rotation. He also states that tension in the infraspinatus can limit the amount of slack in the posterior capsule due to its attachment to the capsule.

Dashottar² describes that to properly check for capsular tightness, the glenohumeral (GH) joint must be placed in flexion and IR; and conversely, while checking for muscular tightness, the GH joint should be placed in extension. This implies that placing the patient supine with the shoulder in 90 degrees abduction and checking passive IR does not distinguish capsular versus muscle dysfunction.

Chiropractors and manual therapists must look at what is causing the loss of IR and properly treat it. If manual techniques are applied and re-examination still shows a decrease in IR, decentration or neurological tightness of the joint must be examined.

"Neurological tightness" refers to tightness due to CNS factors and will not likely change without decreasing tonicity in tonic muscles, activating phasic muscles and creating maximum load-bearing in joints. If one aspect is ignored, then the neuromuscular strategy will not be efficient and the CNS will choose the most convenient pathway to perform the activity.

Treatment Considerations

When the shoulder joint is decentrated, the muscles are not allowed to work synergistically and compensation occurs. The posterior capsule will continuously appear shortened, as will the infraspinatus and teres minor. We must activate the pelvic and respiratory diaphragm to create stability of the lumbar spine; create elongation of the spine to activate the deep stabilizing system (deep neck flexors, multifidus, intersegmental vertebral muscles, transverse abdominis, and obliques); and centrate the shoulder and hip joints to allow for synergy of the stabilizers and prime movers. By recruiting the abdominal canister and the stabilizing system of the spine, the correct CNS program can be activated, proper joint kinematics exercised and IR restored.

Commonly, the "sleeper stretch" is used to lengthen the posterior shoulder and increase internal rotation. With the patient in a seated position, this stretch mimics the Hawkins-Kennedy test for shoulder impingement. Performing the sleeper stretch induces GH joint impingement.³

Setup (top) and performance (bottom) positions for the RT2 Supported exercise to increase shoulder IR.Reinhold recommends having the patient place the scapula flush on the ground, in the scapular plane, to decrease the load and faulty biomechanics placed on the shoulder during the sleeper stretch. However, I suggest eliminating this stretch and using the concepts of "Reflex Turning 2" as described by Vojta.⁴

In a small cohort (n=11) of healthy, young-adult chiropractic students, an average of 11.5 degrees of increased GH internal rotation was observed after performing the "RT2 Supported" exercise. All participants demonstrated an immediate increase in range of motion ranging from 1-21 degrees. Based upon this pilot study, future research is planned to look at both the short-term and long-term effects of this exercise protocol.

An Exercise to Increase GH Internal Rotation

The following details setup and performance of the "RT2 Supported" exercise, as presented by Rich Cohen and based on concepts in movement development seen in the works of Vojta. This exercise activates the abdominal chains. Perform as follows. [See images for setup and performance presentations.]

Setup:

1. Have the patient lie on their side, stacked on the shoulder with their down arm at 90 degrees of flexion at the shoulder and elbow. The downside arm will now be in a centrated position.
2. The bottom leg should be slightly bent and the top leg placed in the 90-90 position. The top leg should now be centrated. If centration is not obtained, place a support under the bent knee.
3. The patient should be lying directly on the shoulder and their head should be supported without any lateral flexion or rotation.
4. Place the upside hand on the medial epicondyle and instruct the patient to push down while pronating the downside arm.
5. Instruct the patient to attempt to lift themselves off the ground onto their elbow.
6. Patient should hold for a 10 second count and repeat 10 times.

Notes:

• Elongation of the spine is key and activation of the lower scapula stabilizers should be felt.
• The neck muscles, levator scapula and trap should be quiet.
• If the exercise seems easy, make sure the top leg is raised to 90 degrees.
• If the exercise seems too difficult, try pushing down harder on the elbow.

Vojta's protocol loads the humeral head, which allows one to roll into a crawling position. This facilitates the raising mechanism of pectoralis, lateral rotators, and abductors of the shoulders. Reflex Turning 2 exercises can help activate the abdominal chains, which will increase the rotation of extremities by restoring the elongation of the spine and the cross-chain patterns of the abdominals.⁵ Incorporating these principles will likely help restore CNS programming and joint centration, and decrease glenohumeral internal rotation deficits.

References

1. Neumann DA. Kinesiology of the Musculoskeletal System: Foundations for Rehabilitation. St. Louis, MO: Mosby Elsevier, 2010.
2. Dashottar A. "Posterior Shoulder Tightness Measurements: Differentiating Capsule, Muscle and Bone." Dissertation, Ohio State University, 2012.
3. Reinold M. "3 Reasons Why I Don't Use the Sleeper Stretch and Why You Shouldn't Either." MikeReinold.com, July 11, 2011.
4. Votja V, Peters A. Votja's Principle. Praha: Grada Publishing, 1995.
5. Cohen R. "Introduction to Reflex Locomotion According to Vojta." Lecture, 2010.

Flexion-Intolerant Lower Back Pain (Part 2): Exercise Rehab

By Marc Heller, DC and Phillip Snell, DC

One of the things that has puzzled us for years is the presentation of the flexion-intolerantpatient. We have realized there is a large overlap with sacroiliac indicators.

In acute lumbar pain, the SI often twists, subluxes, goes haywire. The patient will often have a short leg, the ASISs are not level; there are trigger points in the glutes. This can be a red herring: You can chase the SI, but if the patient continues to irritate their flexion-intolerant lumbar spine, they won't get better.

Many patients with flexion-intolerant pain are misdiagnosed, often for years. The family doc will tell the patient they strained their back. The PT or chiropractor will often tell the patient their pelvis is twisted or out of line. Unless the person has obvious disc signs, such as antalgia or sciatica, the disc component is often missed.

What do we suspect is happening? What does pain do to the musculature? Any pain that affects the lower back will shut down the multifidi, and upregulate the erector spinae and the quadratus lumborum. Any pain in the lower back, hips or pelvis will create gluteal amnesia (inhibited glutes) and upregulate the hip flexors, such as the rectus femoris and TFL.

The bird dog. For additional exercise images and several demonstration videos, read the app version of this article.What does this muscular pattern do to the pelvis? If the muscular imbalance is more prominent on the right side, it will create an anterior rotation of the right ilium relative to the sacrum. The hip flexors are attaching to the front of the right ilium and pulling it forward. The erector spinae is attaching to the right posterior iliac crest and pulling it forward. The inhibited multifidi are not doing their job of nutating the sacral base forward, so the lumbosacral area tends to not extend properly.

This is a hypothesis, an idea why the sacroiliac ends up in the forward-rotated, loose-pack, unstable positioning. We don't know for sure. We just know we see many patients who fit the flexion-intolerant picture, many of whom are misdiagnosed and poorly treated.

Rehabbing the Flexion-Intolerant Back

Treating the flexion-intolerant patient is primarily about rehab. Once flexion intolerance has been identified, self-care includes graded exercise progressions with the goal of long-term improvement.

As the flexion-intolerant pattern encompasses the disc-injured back, many clinicians are overly cautious about exercise and recommend excessive activity restriction. Similarly, many patients may be reluctant to embark on an exercise program, as they have previously had major flare-ups or re-injury with exercise.

The trunk raise. For additional exercise images and several demonstration videos, read the app version of this article.An astute clinician can provide guidance by teaching the patient how to move sustainably without pain, and how to progress exercises wisely to reduce risk for re-injury. Moreover, when the patient understands the injury pattern, they can make educated choices on their own in the future to avoid potentially harmful exercises. Spine researcher Dr. Stuart McGill has written one of the best texts on this topic, Ultimate Back Fitness and Performance.

The following recommendations borrow from the rehab works of Robin McKenzie, Craig Liebenson, Gray Cook, and Pavel Kolar and add the strength training expertise of Pavel Tsatsouline, Dan John and others to offer a graded exercise program with acute and chronic considerations. We will introduce four key components of self-care for flexion intolerance:

• Pain management with movement
• Correction of the spinal hinge
• Building endurance in spine stabilizers
• Improving mobility in key restriction areas

Step 1: Pain Management With Movement

In line with the empowering approach of Robin McKenzie, repetitive end-range loading of extension may allow for quick, self-directed pain management for not only peripheral sciatica symptoms, but also for back pain. In assessment, once a seated slump test, SLR, and/or other signs suggest flexion intolerance, prone extensions to the elbow position can be performed several times to gauge the response to extension loading.

If the patient feels no change in pain or feels only slightly improved, continued performance of the extensions can make an equivocal case become clearer. In chronic cases, it may be necessary to trial the provocative flexion movement for 10-20 repetitions to see if this aggravates the pain.

Once the flexion intolerance is clear, revert to the extension movements for corrective home exercise. A standard prescription of 5-6 reps, each lasting 30 seconds, may be performed 5-6 times daily. In severe cases, the sets of 5-6 reps can be performed as frequently as hourly.

Another option for pain control is decompression exercises, tested to see if they relieve pain or improve antalgic posture. This concept is outlined in several previous articles and also is presented in a YouTube video.

It is important to explain to the patient that extension exercise may help the pain, but does not correct the faulty movement problem. For that, we need to establish a different set of spine-sparing movements.

Step 2: Correcting the Spinal Hinge

Here is a simple way to frame the flexion-intolerant spine. The patient has a tendency to habitually hinge or bend forward in the lumbar spine when bending forward. Enough volume and intensity of this faulty movement can result in progressive failure of the inner layers of the annulus. This process can progress for some time with no apparent consequence, owing to the lack of innervation of the inner annular layers.

Once the torn layers progress to the innervated outer third of the annulus, the lumbar hinging that used to be well-tolerated begins to cause pain. Prolonged sitting with a rounded lumbar curve may also play a role in this. Tissue creep stretches the annulus and potentially makes it more vulnerable to injury.

Establishing a hip-hinge pattern is the correction and can be performed by teaching a "waiter's bow" or by using a dowel. This should be the prime objective in the first encounter, as no amount of passive pain management will be enough to help the patient from hurting themselves again when they try to get up from the treatment table.

Placing three fingers on L3-5 while the patient attempts the hip hinge will help the clinician feel the beginning of the hinge and stop the patient before they feel pain. The goal is to build on pain-free movement to reduce threat and improve function.

By using graded exposure to pain-free movement, we can start to "rewire" the altered pain processing in the chronic pain patient struggling with central sensitization. The patient now begins to feel empowered as they associate reduction in pain with the quality of their movement. Moreover, the feeling of pain with lifting now can even be educational at this stage, as the patient begins to relate the pain to less-optimal movement.

After the hip hinge is grooved, the next order of business is to apply that good-quality movement to getting things off the floor. We recommend using the box squat and the sumo deadlift. These should be taught and repeated to build confidence and reduce fear of performing daily tasks.

While we borrow from the gym for these patterns, the box squat is performed with body-weight only. We showed you a very similar exercise in the last article, titling it "sit to stand." It bears repeating. The goal is to affect a posterior weight transfer with the squat pattern to cue the glutes while the spine is maintained in a stable position. Ingraining this pattern allows for pain-free transitional movement when getting up and down out of a chair, etc.

In this first visit, if the patient is demonstrating the ability to get to a reasonable depth on their box squat, we can then progress them to the sumo deadlift pattern. Again, while we're using gym vernacular, the sumo deadlift is not done with heavy weight. A 20-35 lb. kettlebell is handy, as the handle is about a foot from the floor and the weight approximates the weight of a child or other commonly encountered weights with day-to-day activity.

At this stage, overcoaching the lumbar curve is appropriate to help assure that the patient does not lapse into the lumbar hinge. Later, we can back off that extreme lumbar lordosis to avoid facet, pars and hip injury. The patient is usually sent home at this point with instructions to utilize the more sustainable hip hinging, squatting and lifting strategies; and to manage pain with repeated lumbar extensions.

Step 3: Training Endurance in Maintaining a Neutral Spine

McGill's work has shown us that endurance of the lumbar stabilizers is more important than strength or power in those muscles. To help anchor the patterns discussed in the first treatment, we may now begin building better support for the "guy wires" of the spine. An analogy of the spine as a tower, supported by guy wires (the surrounding muscles) is sometimes helpful.

An important point must be made as we embark on these exercises to improve "core muscles." Many people with flexion intolerance may have previously undertaken a "core strengthening" approach that consisted of many sit-ups or crunches. Often they found that these exercises helped for a while, but then began to aggravate their back. While sit-ups and crunches will definitely build a robust set of abs, they do it at the expense of spine flexion.

We strongly advise abdominal exercises that maintain neutral. Think of the isometric and eccentric function of the abdominals as anti-extensors, rather than spine flexors. Plank-based abdominal exercises are imperative, but it is also important to attend to the lateral stabilizers and the extensors.

The following three exercises are performed with the same set / repetition and volume schedule: 10 seconds of work followed by 2 seconds of rest. We suggest a total volume of about 80 percent of perceived maximal effort each day until the patient is able to pass a lumbar functional capacity evaluation (FCE). [Click here to view a demonstration of the FCE].

Plank variations to address the abdominal muscles can be performed supine as McGill's trunk raise and/or in prone as a front plank on the elbows. On the trunk raise, make sure the patient does not come up too high from the floor to the point that hinging in the lumbar spine occurs.

Side planks can address the lateral spine stabilizers quite well. Instruct patients to raise their ribs as high from the floor as possible before lifting up and then push the floor away to keep the shoulder happy. If straight-leg position is too difficult, peeling back to bent knees is OK at first. They can build up to the straight-leg position.

For extensor muscles, care must be taken to not exceed tolerable compression loads generated by many exercises. The bird dog, performed with a very tightly held core, can be very rigorous. Tracing an imaginary square at the hand and foot allows a bit of perturbation challenge to the tightly held neutral spine.

Keep extremities rigid and don't let rotation occur at the pelvis. Have the patient push the floor away with the hand and keep the spine long. The essence of core is to keep the trunk still as the extremities move.

Step 4: Enhance Thoracic and Hip Mobility

Consistent with the "joint by joint" philosophy, the tendency to hinge in the lumbar spine area may be a reflection of poor mobility in the hips and thoracic spine. Spending time focusing on mobility in the inherently stiff areas helps to assure that during global movement patterns, the body isn't "requesting" mobility from the inherently stable lumbar spine.

We don't have room to describe this in detail, but a simple exercise to begin to address this is the thoracic sphinx. It is basically a pelvic tilt on all fours, modified to focus the movement into the thoracic spine.

We have given you an overview of how to start to rehab the flexion-intolerant back patient. We cannot overemphasize how important the rehab aspect is for these patients. Either do the rehab work or co-treat by referring out for rehab on these patients. These folks need our help.

The optimal approach is not repetitive steroid injections. Fusion surgery should be a last resort. The solution starts with simple exercises for pain control,  learning to move properly and safely, building core endurance, and increasing mobility above and below the lower back.