A Major Cause of Anterior Knee Pain

By Warren Hammer, MS, DC, DABCO

It is important to determine if anterior knee pain is from the local area or referred from a more proximal site. While pain could be referred to the anterior knee from the hip or spine, distal extremity complaints that can be palpated as local pain are most likely to be the site of the lesion, rather than being referred.

Most patients entering our offices, especially athletes, have more involvement of the patellofemoral area than the intra-articular tibiofemoral joint. The largest anterior structure of the knee is the patella, and most of the time, the anterior knee pain is related to the patellar articulation or the surrounding tissues.

While there are of course many possible causes of anterior knee pain, such as patellar tendinosis, quadriceps tendinopathy, coronary ligament fibrosis, and prepatellar bursitis, to name a few, a particular passive structure that supports the patellar and knee has been recognized as a major source of pain. It is the patellar retinaculum. According to Biedert and Sanchis-Alfonso,¹ free nerve endings, which besides detecting pain, heat and cold, also detect crude touch and pressure, have the highest density in the tendon of the quadriceps muscle and the second highest in the retinacular and patellar tendon. They feel that this is necessary since these tissues control acceleration, deceleration and rotation of the knee joint, and require high proprioceptive capability.

The retinacular, an important stabilizer of the patella, is composed of fibrous bands that form discrete ligaments attaching medially and laterally into the patella. Both sides of the retinacular help to keep the patellar in alignment. For example, as the knee flexes, the lateral retinacular bands that originate from the iliotibial band exert a normal posterolateral force on the patella. If the medial support of the patella becomes weakened over time, the lateral retinacular pressure will cause a lateral tilting of the patella, or if allowed to continue, eventual subluxation and even dislocation.

According to what is known as the "Law of Valgus," the lateral side of the knee, composed of the distal vastus lateralis, iliotibial tract and lateral retinaculum, is normally stronger and more fibrous than the medial forces, composed primarily of the distal vastus medialis obliquus (VMO) and the medial retinaculum. This explains why lateral compression syndromes develop in the knee, and why lateral release operations are often performed. A tight lateral retinaculum that tilts the patella causes increased pressure on the lateral facet and eventual adaptive changes in the patellar articular cartilage.

Kasim and Fulkerson² evaluated the patella retinaculum in 25 patients, 20 of whom had experienced failed surgery such as realignment of the extensor mechanism or a lateral release procedure, and continued to complain of postsurgical anterior knee pain. The 25 patients with anterior knee pain underwent retinacular excisions followed by muscle flexibility and strengthening. Twenty-two of the 25 patients (88 percent) noted moderate to substantial improvement.

The most prominent cause of anterior knee pain has been blamed on what is called patellar malalignment, and surgical techniques are used to realign the patella. Kasim and Fulkerson stated that the cause of malalignment and patellofemoral pain often involves excess pressure on part of the patella due to imbalance of the retinacular restraints, causing the malalignment. Therefore, if we can find restrictive knee retinaculum, it is important to treat it and determine if the malalignment and patella tracking improves - and more importantly, whether the patient's symptoms improve. In their study, the authors found specific painful areas of the retinaculum that they excised. Histological studies revealed that the painful retinaculum contained neuromatous degeneration of the small nerves of the painful tissue and degenerated fascia, with no inflammation. It sort of resembled tendinosis-type tissue.

An important evaluation for a tight lateral restraint is use of the patellar tilt and glide test. The medial side of the patella can be tilted inferiorly to open the lateral side, at which point palpation of the lateral side would reveal tenderness. The lateral patella could be pushed (glided) medially, and failure of the patella to displace medially more than 1 cm would indicate a tight lateral retinaculum. The patella articulation (cartilage) would be suspected if the examiner compresses the patella and gets a painful response when the patient is asked to contract the quadriceps.

Treatment of choice is the Graston technique (see image left), since the instruments can be used to penetrate and release the retinaculum. The practitioner could open up the lateral side by pressing down on the medial side of the patella to reach more areas (not shown). Friction massage can also be attempted. All of the peripatellar retinaculum should be evaluated for tenderness and restriction. It is necessary to treat and evaluate the retinaculum with the patient supine and the knee extended, to allow freer motion of the patella while it is out of the trochlea sulcus. Stretching and strengthening of the related areas should also be part of the procedure.

References

1. Biedert RM, Sanchis-Alfonso V. Sources of anterior knee pain. Clin Sports Med2002;21:335-347.
2. Kasim N, Fulkerson JP. Resection of clinically localized segments of painful retinaculum in the treatment of selected patients with anterior knee pain. Am J Sports Med2000;28(6):811-814.

The Stepping Test: A Useful Tool for Cervical Rehabilitation

By Donald Murphy, DC, DACAN

The "stepping test" was first developed by Fukuda¹ as a test of vestibular function. More recently, the test has been shown to greater reflect somatosensory function than that of the vestibular system.^2-4 Gordon et al.^2,3 had subjects who were negative for the stepping test walk on a rotating treadmill for two hours and found that upon retesting them, the stepping test became positive. 
They felt that this could only have resulted from an alteration in the central nervous system (CNS) program for stepping. This was caused by a change in somatosensory input from the locomotor system induced by walking on the rotating treadmill.

There was no stimulation of the vestibular apparatus in these experiments, because the head remained stationary while the subjects walked on the rotating treadmill. Fukushima and Hinoki⁴ had normal subjects perform the stepping test while they wore, alternately, cervical collars and lumbar corsets. They found that while the cervical or lumbar spine was restrained, the stepping test became positive. Their conclusion was that interruption of the afferentation from the mechanoreceptors in the spinal muscles led to alteration of the tonic neck and lumbar reflexes, resulting in rotation of the body while stepping.

How Is the Test Performed?

The test is performed by having the patient stand with eyes closed, arms outstretched and wearing ear muffs. The patient marches in place at the pace of a brisk walk while keeping the eyes closed (Figure 1). The doctor observes for any rotation that takes place. Rotation of 30 degrees or more is considered a positive test. The significance of the test is that it suggests the presence of either faulty kinesthetic sense or tonic neck reflexes (or both). In the low back pain patient, a positive test is likely a reflection of either faulty kinesthetic sense or faulty tonic lumbar reflexes.

What Is the Clinical Utility of the Test?

I have used this test for several years and have found it to be quite useful in decision- making in rehab. Experiments are ongoing at my center investigating its full utility. The alterations results of these studies may alter and enhance its use in years to come, but this is how I use it.

The test detects alterations in the motor program for stepping, part of the primitive program of gait. These result from disruption of the normal processing of afferent information from the locomotor system. Abnormal processing likely results from dysfunction of the joints, muscles, and/or skin and fascial. The theory of faulty movement patterns states that this abnormal afferentation can cause a change in the program for certain movements.5 If the faulty movement pattern becomes "fixed" in the CNS, i.e., if a plastic change in the nervous system in which the program for that particular movement becomes accepted by the CNS as "normal," correcting the afferentation may not be enough to correct the program. In this case, rehabilitation may be required to retrain the CNS in creating another plastic change, in which an attempt is made to restore the faulty program to normal.⁶

Let's take the example of a patient with chronic headaches. The exam reveals joint dysfunction at C0-C1; myofascial trigger points in the suboccipital muscles (which reproduce the pain); hypertonicity of the right sternocleidomastoid; and a positive stepping test. The initial outline of treatment may be manipulation to the C0-C1 segment, ischemic compression to the suboccipital muscles, and postisometric relaxation to the right sternocleidomastoid. Is sensorimotor training necessary in this case? Perhaps, but in the interest of saving time, it may make more sense to treat the peripheral dysfunction (which would have to be done anyway) and recheck the stepping test to see if the gait program has been corrected as a result of the manual treatment provided.

Theoretically, restoring normal joint and muscle function in this case would normalize mechanoreceptive input from those structures. This may be enough to normalize the gait program. If, after a reasonable amount of time to correct the peripheral dysfunction, the stepping test becomes negative, it is not likely that further treatment with sensorimotor training will be necessary. If, however, correction of joint and muscle dysfunction is made and the stepping test remains positive, there is a likelihood that the faulty program for gait has become fixed in the CNS. Further intervention in the form of sensorimotor training will be necessary.

Sensorimotor training would be the rehabilitation method of choice in this case because it allows the practitioner to induce a bombardment of the CNS with mechanoreceptive signals from the locomotor system while the patient in standing on one leg on a wobble board, a position that mimics the stance phase of gait. This, theoretically may allow the CNS to make another plastic change in the gait program, more toward normal.

The stepping test can be used as a tool to demonstrate the presence of a faulty gait-related program and to determine whether the treatment and rehabilitation is doing the job of correcting the problem. Of course, outcome measures that reflect pain intensity, such as a Visual Analogue Scale or Numerical Rating Scale, and the degree of disability the patient is experiencing as a result of the problem, such as the Neck Disability Index or Headache Disability Inventory,7 will also be necessary to assess whether the correction of the faulty program is successful in helping bring about meaningful change in the patient's clinical status.

Efficiency is of the utmost importance for effective treatment and rehabilitation of patients in the busy practice environment. Any test or procedure that I can find that allows me to save time while enhancing my ability to help my patients is of tremendous value. The stepping test is a clinical evaluative procedure that does not take a great deal of time to administer, but provides the practitioner with information that he or she can use in making decisions with regard to whether additional rehabilitative measures are required and on which methods (e.g., sensorimotor vs. stabilization) the greatest focus should be placed.

References 

1. Fukuda T. Statokinetic Reflexes in Equilibrium and Movement.Tokyo: University of Tokyo Press, 1984.
2. Gordon CR, Fletcher WA, Jones GM, Block EW. Is the stepping test a specific indicator of vestibulospinal function? Neurology 1995;45:2035-2037.
3. Gordon CR, Fletcher WA, Jones GM, Block EW. Adaptive plasticity in the control of locomotor trajectory. Exp Brain Res 1995;102:540-545.
4. Fukushima H, Hinoki M. Role of cervical and lumbar proprioceptors during stepping: an electromyographic study of the muscular activities of the lower limbs. Acta Otolaryngol(Stockh) 1985; Suppl 419:91-105.
5. Murphy DR. Dysfunction in the cervical spine. In: Murphy DR (ed.) Conservative Management of Cervical Spine Syndromes. New York: McGraw-Hill, 2000:71-104.
6. Janda V, Va Vrova M. Sensory motor stimulation. In: Liebenson C (ed.) Rehabilitation of the Spine: A Practitioner's Manual. Baltimore: William and Wilkins, 1996:319-328.
7. Yeomans SG. Outcomes management of cervical spine complaints. In: Murphy DR (ed.)Conservative Management of Cervical Spine Syndromes. New York: McGraw-Hill, 2000:329-356.

Thoracic, Lumbar, Sacroiliac and Hip Joint Relationships

By Joseph D. Kurnik, DC

Mechanical and functional examination of the spine and sacroiliac joints can be approached in the following ways: 

1. static palpation
   
   
2. motion palpation
   
   
3. visual analysis
   
   
4. x-rays
   
   
5. instrumentation
   
   
6. other methods

I use the first four methods on the list, with most emphasis on the first three methods of analysis.

If the patient presents with low back and/or hip complaints, I follow these procedures: 

1. standing ranges of motion;
   
   
2. deep tendon reflex testing, if motion/sensory signs are present;
   
   
3. dermatone testing if motor/sensory signs are present;
   
   
4. seated motion, static, and visual examination of the SI joints and spine;
   
   
5. prone motion, static, and visual examination of the SI joints and spine;
   
   
6. hip joint examination if hip complaints are present.

In the examination of the lumbar spine in the seated position, it is often difficult to test the mid-to-upper lumbar spine. Often, it may appear to be normal or hypermobile in movement, especially in extension. If, however, the patient is examined prone, the mid-to-upper lumbar and lower thoracic regions take on a different appearance. Unsuspectingly, mid-to-upper lumbar and lower thoracic problems may emerge.

Exerting posterior to anterior pressure at consecutive segments from L-5 to T-12 most often reveals a hypomobile (fixation) region. The usual levels of fixation are L-2, L-1, and T-12. Among these, L-1/L-2 is most often hypomobile in the posterior to anterior direction. It is often coupled with rotation spinous right and a right lateral flexion hypomobile dysfunction. Again, this fixation region is easy to miss with the patient seated, because of the overall give of the lumbar spine.

The effect of the upper lumbar or lower thoracic extension fixation (in possible combination with other thoracic extension fixations) is increased L-5/S-1 stress. This is caused by reactive compensatory increased extension; a spinous right rotation pattern may also be palpable. If you miss the upper lumbar problem, you could easily be led to believe that this was solely an L-5/S-1 problem. The reaction to the L-5/S-1 stress can be a unilateral or bilateral AS fixation, involving counter-nutation and lumbosacral stabilization. Attempts to adjust L-5 or either ilium may be met with no success, or mild joint releases and relief of symptoms. If, however, the upper lumbar extension fixation is released; then the L-5/S-1 fixation and both AS ilium fixations may spontaneously clear.

There may be one or two other thoracic extension (with coupled rotation and lateral bending disorders) fixations contributing similarly and simultaneously to the L-5 and sacroiliac disorders. In other cases, adjusting the upper lumbar and thoracic dysfunctions will partially clear the L-5 and SI joint fixations, and an L-5 correction (due to a secondary L-5 fixation) will be required to release completely the remaining SI joint AS dysfunction. The L-5 correction may involve an adjustment and/or flexion traction.

There is a relationship of the upper lumbar or lower thoracic dysfunction to hip joint problems. It may be neurological or secondary to overstress from the loss of sacroiliac motion. With the AS fixation the hip joint is the only source of locomotion during hip flexion. With normal SI joint function, there is coordinated hip and SI motion during hip flexion. With the loss of ilium motion in the PI direction, there is increased wear and tear in the hip joint proper, because it is the only joint being used in that area during hip flexion. This process also may lead to gluteal, quadricep, hamstring, groin, and knee disorders.

Correction of the upper lumbar disorder can be accomplished according to the technique utilized. Keep in mind that an L-5 dysfunction with a probable LP listing may be present, as well as the upper lumbar problem. It is easiest and most successful to vary the techniques for correction of each level.

To attempt a side-posture correction at L-1 and L-5 is more difficult than doing an incline adjustment at L-1 and a side posture at L-5. I use a specially constructed incline table (similar to the Pettibon style) to do most lower thoracic and upper lumbar adjustments. It is usually an easier and more effective way to adjust the extension restrictions at the lower thoracic and upper lumbars. Supine corrections may be used, but this is more difficult than seated incline adjusting. Prone adjusting at these levels is met usually with patient resistance and anxiety. In the seated incline style, you may also slightly flex the region to be adjusted, especially if inflamed, in order to slightly disengage the facet joints and make an easier correction.

Try monitoring the SI joints yourself with static and motion palpation, pre- and postadjusting to upper lumbar and/or lower thoracic fixations. You may be surprised to see improvement in SI joint functioning with your upper lumbar and lower thoracic corrections

Patellafemoral Pain Syndrome: An Associated Disorder or Medical Problem?

By Joseph D. Kurnik, DC

There is no clear consensus in the literature concerning the terminology, aetiology and treatment for pain in the anterior part of the knee. The term 'anterior knee pain' is suggested to encompass all pain-related problems.

By excluding anterior knee pain due to intra-articular pathology, peripatellar tendinitis or bursitis, plica syndromes, Sinding Larsen's disease, Osgood Schlatter's disease, neuromas and other rarely occurring pathologies, it is suggested that remaining patients with a clinical presentation of anterior knee pain could be diagnosed with patellofemoral pain syndrome (PFPS). Three major contributing factors of PFPS are discussed: (1) malalignment of the lower extremity and/or the patella: (2) muscular imbalance of the lower extremity: and (3) overactivity.

The above excerpt was the opening statement of a review article in Sports Medicine, October 28(4): 245-262, authored by Roland Thomee, Jesper Augustsson and Jon Karlsson.

The article identified the pathologies that can generate anterior knee pain: 

• cartilage damage;
• menisci, ligament and capsular damage;
• sequelae after patellar fracture, dislocation or subluxation;
• sequelae after knee surgery;
• quadriceps tendinitis;
• iliotibial band friction syndrome;
• pre-and infrapatellar bursitis; and
• pesanserinus bursitis.

The authors made it clear that medical science does not have an answer as to the causes of anterior knee compartment syndrome not arising from the preceding pathologies. They do speculate nonpathologic causes as being related to lower extremity misalignment, muscular imbalance of the lower extremity, and overactivity.

With regard to misalignment, it is well known that foot pronation or supination will change patella stress and possibly position. With regard to muscle imbalance, it is known that hypertonic quadricep status will cause increased tension at the pre and infra patellar regions, as well as increasing patellar compression against the underlying articular cartilage. Overactivity in conjunction with patellar subluxation, stress or compression will naturally lead to increased potential for anterior knee complaints -this is common sense.

A few interesting questions or issues arise within this milieu of statements: 

1. How does the position of chiropractic compare with that of medicine in identifying causes and treatment of PFPS?
   
   
2. Are pathologies previously identified isolated pathologies, or are they the result of the stresses of muscle imbalance and patellar misalignment?

With regard to the first issue, there is a monumental difference in understanding and potential for treatment. This past statement may sound dramatic and sensational, although it is not intended to be so. In the field of traditional medicine, what will be done to remedy muscle imbalance and patellar subluxation? Ultrasound, exercise, stretching, electrotherapy, splinting, etc.? These will help to improve muscle imbalance, but to what extent and for how long? In the field of chiropractic, there exists the same therapeutic approaches. Both professions, therefore, incorporate therapies, exercise, and sophisticated rehab techniques. It seems, however, that PFPS has not been treated and rehabilitated with significant success by either profession. I can only suggest that approaches to treat PFPS are more similar than dissimilar by both professions (excluding exceptional therapies like applied kinesiology and other unique and non-traditional approaches).

It is my observation that chiropractic is missing a unique opportunity to move ahead of this stalemate and therapeutic position, by viewing PFPS as a spinal and sacroiliac-associated disorder rather than as an isolated extremity disorder.

In previous articles for DC, I have tried to present some facts, premises, ideas, and hypotheses concerning the following relationships:

1. Relationships between the spine and sacroiliac functioning: 

1. that occiput and spinal dysfunction can and do cause SI adaptation dysfunctions:
   i.) AS ilium fixations (sacral counter-nutation).
   ii.) PI ilium fixations (sacral nutation).

2. With AS ilium fixations, muscle imbalances do occur: 

1. gluteal hypertonicity and irritation
2. hip flexor hypertonicity and irritation
   i.) proximal flexors-iliopsoas
   ii.) distal flexors-rectus femoris, gracilis, adductor magnus
3. knee extensors-rectus femoris

These muscle groups, because of their hypertonicity, have become contracted and shortened; thus pulling at origin and insertion points.

3. These hypertonic muscles can cause: 

1. hip complaints - hip is compressed between flexors and extensors
2. groin complaints - strain at hip flexor origin and insertion
3. ischial complaints - hamstring origin tension
4. quadricep, hamstring, hip flexor, gluteal complaints - hypertonic, contracted, and strained status
5. knee complaints, anterior and posterior - hip flexor/leg extensor tension and shortening
6. ankle/foot complaints

4. Properly correcting the SI disorders can spontaneously correct and clear the associated complaints listed above. These are in the form of AS ilium fixations, which are most often reactions to lumbar and thoracic disorders.

5. If spinal/sacroiliac abnormalities and their associated disorders exist long enough, the correction of the spine/SI malfunctioning may not be possible. However, they set up the need of for more complete and longer-lasting resolution of associated disorders through other therapeutic approaches. (stretching, rehab. techniques, electrotherapy, myofascial release, ultrasound etc.).

6. I am advocating a more thorough consideration of viewing certain nonspinal problems, like PFPS, as associated disorders. That is, disorders such as PFPS can have an origin in spinal and sacroiliac dysfunction. The treatment for such associated disorders must include, primarily, correction of the spinal and sacroiliac dysfunctions.

Hypermobility Syndrome

By Warren Hammer, MS, DC, DABCO

Have you ever had a patient complain of recurring pain in numerous joints, or respraining of a particular (wrist) joint, who may or may not express an inflammatory picture, and has been to many other doctors without a definite diagnosis or helpful treatment? This patient may be suffering with a hypermobility syndrome (HMS).

Because other conditions may express joint hypermobility, and can be excluded by laboratory testing, HMS becomes a diagnosis of exclusion. Two conditions that definitely have joint hypermobility and are connective tissue disorders are Ehlers-Danlos and Marfan syndrome. These two conditions exhibit hyperelastic skin, hernias, lenticular abnormalities and abnormal body proportions. ¹ Other conditions exhibiting hypermobile joints are rheumatoid arthritis, osteogenesis imperfecta, systemic lupus erythematosus, poliomyelitis, myotonia congenita, and some neurological conditions.

HMS patients have a gender-influenced dominant trait with an abnormality of type I collagen. The condition is more common in females. Type I collagen is the most common collagen and is contained in tendons, ligaments, joint capsules, skin, demineralized bone and nerve receptors.¹Hypermobility of joints and spine is due to abnormal laxity of ligaments, joint capsules and intervertebreal discs. Back patients with symptoms who do not develop osteoarthrosis or disc degeneration usually experience spontaneous improvement with increasing age, thus losing their juvenile hyperlaxity. This usually occurs between 30 and 40 years of age. In HMS patients, too much activity causes pain.

Hypermobility per se is a state, not a disease, but it may lead to generalized arthralgia or localized symptoms (frequent ankle sprains, knee effusions, dislocations of the shoulders and recurrent episodes of back pain). Pain can occur even after minor strains, especially in young women.² HMS patients, besides having hypermobile joints, have decreased joint position sense, making them more vulnerable to minor damage. Reduced sensory feedback may lead to biomechanically unsound limb positions being adopted. This mechanism may allow acceleration of degenerative joint conditions, and may account for the increased prevalence of such conditions seen with HMS subjects.³

HMS patients have more osteoarthritis; increased nerve compression disorders;⁴chondromalacia patellae; excessive anterior mandibular movement;⁵ mitral valve prolapse;⁶uterine prolapse; and varicose veins.² Larsson⁷ et al., state that patients with HMS who have a sedentary job have increased spinal pain.

Criteria for the diagnosis of HMS are: 

1. passive thumb apposition to touch the forearm;
   
   
2. passive little finger hyperextension of more than 90 degrees;
   
   
3. elbow hyperextension of more than 10 degrees;
   
   
4. knee hyperextension of more than10 degrees;
   
   
5. forward flexion of the trunk with the knees straight and the palms of the hands resting flat on the floor.

HMS is usually diagnosed in individuals who can perform three or more of these tests.⁸ Some clinicians include excessive ankle dorsiflexion and foot eversion in the criteria for HMS.

Patients with HMS may complain of symptoms from ages 3 to 70, which usually affect multiple joints over the years. "They typically lack the positive laboratory findings found in rheumatologic disorders and, in the absence of acute trauma, lack the radiologic changes, inflammation, swelling and decreased mobility typical of orthopedic pathology."¹ Unless they have specifically stressed a particular joint and created an inflammation, HMS patients do not respond to anti-inflammatory medication.

HMS patients must be educated about their body mechanics, posture and activities. Activities may have to be modified. Even splints, braces and taping may have to be used to protect vulnerable joints. ¹ Movement of the joints in the end-ranges should be discouraged. Stretching muscles rather than joints should be emphasized. Guided progressive strengthening exercises and balance boards for proprioceptive stimulation are recommended.

References: 

1. Russek LN. Hypermobility syndrome. Phys Ther 79(6), 1999.
2. Nef W, Gerber NJ. Hypermobility syndrome. When too much activity causes pain. Schweiz Med Wochenschr 128(8),1998:302-10.
   
   
3. Hall MG, Ferrell WR, Sturrock RD, hamblen DL, Baxendale RH. The effect of the hypermobility syndrome on knee joint proprioception. Br J Rheumatol 34(2), 1995:121-5.
   
   
4. El-Shahaly HJA, El-Sherif AK. Is the benign joint hypermobility syndrome benign? Clin Rheumatol. 10(19), 91:302-307.
   
   
5. Buckigham RB, Braun T, Harinstein D 5. A, et al. Temporomandibular joint dysfunction syndrome: a close association with systemic joint laxity (the hypermobile joint syndrome). Oral Surg Oral Med Oral Pathol 72,1991:514-519.
   
   
6. Grahame R, Edwards JC, Pitcher D, et al. A clinical and echocardiographic study of patients with the hypermobility syndrome. Ann Rhem Dis 40,1981:5 41-546.
   
   
7. Larsson LG, Mudholkar GS, Baum J, Srivastava DK. Benefits and liabilities of hypermobility in the back pain disorders of industrial workers. J Intern Med. 238, 1995:461-67.
   
   
8. Beighton P, Solomon L, Soskoine CL. Articular mobility in an African population. Ann Rheum Dis 32, 1973:413-418.

Neuromyofascial Pain Syndromes

By David BenEliyahu

Patients often present with complaints of numbness, parasthesias, and tingling in the upper or lower extremity. Many times it is not spinal nerve irritation but rather a peripheral entrapment.
Many peripheral entrapments in the extremities are often due to a muscle "tunnel syndrome." Peripheral nerves often traverse through muscle or ligamentous tunnels. For example, the median nerve passes between the two heads of the pronator teres muscle; the sciatic nerve passes under the piriformis, and the ulnar nerve passes through the heads of the flexor carpi ulnaris muscle. Tunnel syndromes can result from myofascial trauma such as in car accidents causing overstretch injury to muscle and/or fascial structures; repetitive motion injuries; and sports injuries. Trauma often will promote the formation of adhesions, which by neural compression can restrict intraneural blood flow or tether the nerve. Tractional injuries or force can cause internal neural ischemia with resultant interruption in axoplasmic transport. Four mechanisms by which myofascial entrapment of peripheral nerves can occur include: 

1. direct compression between fibers of a hypertonic muscle;
   
   
2. direct compression between muscle and an unyielding fascial sheath;
   
   
3. direct compression between bone and hypertonic muscle;
   
   
4. traction caused by adhesions.

NEUROMYOFACIAL

1. Thoracic Outlet 

1. Scalenes syndrome: The brachial plexus and subclavian vessels are susceptible to entrapment between the anterior and middle scalenes. Patients will typically present with pain and tingling in the upper extremity across the C8/T1 distribution. Numbness is often seen in the hand and forearm. Ischemic symptoms can be seen as well with coldness of the hand and changes in skin color and temperature. Adson's test may be positive.
2. Pectoralis minor or hyperabduction syndrome: The neurovascular bundle gets entrapped between the pectoralis minor and the coracoid process. Hyperbduction often reproduces the symptoms, and Wright's or Roo's tests are often positive.

2. Pronator Teres

The median nerve can get entrapped between the humeral and ulnar heads of the pronator teres muscle. The patient will complain of pain and tingling in the palmar and dorsal aspect of the hand, palm and fingers.

Patients will perceive motor impairment at the thumb and finger flexors, which is a distinguishing factor between carpal tunnel syndrome(CTS) and pronator teres syndrome(PTS). CTS involves mostly the thenar muscles, whereas PTS involves the wrist and finger flexors as well. Resisted muscle testing of the pronator teres provokes the pain, as can Tinel's tap or digital pressure over the pronator teres.

3. Flexor Carpi Ulnaris

This muscle tunnel syndrome represents entrapment of the ulnar nerve between the humeral and ulnar heads of the flexor carpi ulnaris muscle.

Patients complain of pain, muscle weakness and parasthesias . Tinel's tap and digital pressure can reproduce the pain. Froment's sign may be seen in long-standing cases.

4. Radial Tunnel Syndrome

This syndrome is often misdiagnosed as chronic lateral epicondylitis, because patients complain of lateral elbow pain at the forearm. Stretching the supinator muscle will often provoke the symptoms as well as resisted supination. Resisted middle finger flexion will increase the pain as well. The radial nerve enters the radial tunnel in a fibrous arch between the brachialis and brachioradialis muscles. Further distal, the nerve splits. The posterior interosseous nerve goes through the arcade of Frohse under the supinator.

5. Piriformis Syndrome

The sciatic nerve typically passes under the piriformis, but in some cases will pass through it. Hypertonicity in the priformis can occur due to several factors. Sacroiliac or pelvic pathomechanics can cause piriformis spasm/trigger points, as can lumbar discopathy or radiculopathy. Symptoms include buttock pain, hip pain, positive Lasague's sign, increased pain on internal rotation, decreased pain on external rotation, sensory hypesthesia over the S1/2 dermatomes , and diffuse motor weakness. Pain in the sacral or gluteal region is the most constant symptom.

Treatment of Neuromyofascial Pain Syndrome

Many treatment techniques that can be used alone or in combination to reverse the effects of neuromyofascitis. 

1. Ischemic compression: Often referred to as "Nimmo," digital pressure over the trigger point or use of a taut band is applied for about 5-6 seconds and slowly released, being repeated three times.
   
   
2. Postisometric relaxation: Also known as "contract - relax," the patient isometrically contracts the muscle against resistance for about five seconds; then the patient stretches in the opposite direction. This is repeated progressively.
   
   
3. Spray and stretch: Developed by Travell and Simons, a vapocoolant spray is used. The patient stretches the muscle progressively. One may use ice massage to accomplish the same thing.
   
   
4. Active myofascial release: Developed by Leahy and Mock, there are four phases of releasing tension/adhesions in the taut bands. Phase III entails digital pressure over the adhesion, while the muscle is passively stretched. Phase IV entails the same thing except with active motion.
   
   
5. Manipulation of associated joint dysfunction/subluxation: Sacroiliac adjustments in the case of piriformis syndrome, first rib, C7/T1 adjustments in TOS cases, etc.
   
   
6. Exercise rehabilitation and stretching: This is a key component to successful resolution and recurrence of the problem.

References

1. Pecina MM. Tunnel Syndromes. CRC Press, 1997.
   
   
2. Perle S. Chiropractic management of peripheral neuropathy. Topics Clin Chiro 1999;6(4):6.
   
   
3. Feinberg. Nerve entrapments at the elbow. Topics Clin Chiro 1999;6(4):20.
   
   
4. McDaniel and Khodadi. Pronatoe teres syndrome. Topics Clin Chiro 1999;6(4):51.
   
   
5. Nordhoff LS. Motor Vehicle Collision Injuries. Aspen, 1996, p.40-42.

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 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.