Piriformis Syndrome -- Part II

By Warren Hammer, MS, DC, DABCO

Part I (June 21, 1991 issue of "DC") covered the piriformis syndrome with regards to anatomy, pathology, symptomatology, and diagnosis. This article will consider the variety of manual treatments for the condition.

The pathology of the syndrome governs the manual approach. The piriformis is inflamed, spastic, contains trigger points and, if at all chronic, has connective tissue adhesions.

Pelvic evaluation, especially of the sacrum and iliac bones, must be performed for specific adjustment of the area.

Palpation for active trigger points in the area is necessary. Travell¹ divides the piriformis in thirds from its origin to insertion and presses for trigger points. She states that the main trigger is in the lateral third near the greater tuberosity. The medial portion of the muscle may refer pain to the buttock and ischium, but does not refer pain down the lower limb like the gluteus medius. The lateral third may refer pain to the buttock and posterior thigh. The patient lies on the pain-free side with the upper thigh flexed and adducted over the table. The patient may add to the stretch by resting his arm on the thigh. The stretch and spray method may be used.

In the chronic situation, friction massage may be applied to the most tender portion in a direction perpendicular to the fibers.

The piriformis may be manually stretched² by standing on the opposite side of the prone patient's involved piriformis. The clinician reaches across and places the heals of his hands at a right angle to the piriformis, with the arms extended. The doctor leans with his body weight perpendicular to the long axis of the piriformis. Within a few minutes the muscle should relax.

Edwards³ describes a Nimmo-like technique in which the patient lies on the normal side with flexion of the hip and knees of the painful side. The clinician presses his elbow into the tendinous insertion near the greater trochanter using 40 to 60 pounds of pressure, 8 to 12 times, for 10 seconds each. The patient should feel rapid relief of pain. The procedure may have to be repeated two times a week for two to three weeks. Te Poorten⁴ has a similar method as Edwards except while he holds pressure on the piriformis he stretches the piriformis by pulling the leg externally, which internally rotates the hip.

Evjenth and Hamberg⁵, Muhlemann, and Cimino⁶ stretches a right piriformis with the patient supine and the doctor on the patient's right side. The right hip and knee are flexed about 60 degrees and the right foot is brought onto the lateral side of the left leg. The DC grips the ventral/lateral side of the right knee with the right hand and adducts (stretches the piriformis) the right thigh. The patient is then asked to isometrically contract laterally against the doctor's right hand. This position is held for at least seven seconds provided there is no pain, or with less resistance for 10 to 30 seconds if there is pain on contraction. The patient is told to relax while the doctor attempts to further stretch the muscle. If this is too painful the patient can actively move the thigh more into the stretched position (adduction). The patient is then asked to resist against adduction in order to stimulate his antagonists. The new position should be maintained for at least ten seconds and the entire procedure repeated a few more times.

References 

1. Travell, J.G.; Daitz, B. Myofascial Pain Syndromes: The Travell Trigger-Point Tapes. Myofascial Pain Syndromes of the Low Back and Hip. Baltimore, Maryland; Williams & Wilkins Electronic Media.
   
   
2. Steiner, C.; Staubs, C.; Ganon, M.; Buhlinger, C. Piriformis syndrome: Pathogenesis, diagnosis, and treatment. J. of Amer Osteopathic Association 1987; 87:318-323.
   
   
3. Edwards, F.O. Piriformis syndrome. Academy of Applied Osteopathy Yearbook 1962; 39-41.
   
   
4. Te Poorten, B.A. The piriformis muscle. JAOA 1969; 690:150-160.
   
   
5. Evjenth, O.; Hamberg, J. Muscle Stretching in Manual Therapy. Volume I, The Extremities. Alfta, Sweden: Alfta Rehab Forlag 1985; 97.
   
   
6. Hammer, W.I. Functional Soft Tissue Examination and Treatment by Manual Methods: The Extremities. Gaithersburg, Maryland: Aspen 1991.

Piriformis Syndrome: Part I

By Warren Hammer, MS, DC, DABCO

The patient with an unrelenting sciatica may be suffering with a piriformis syndrome. This syndrome is considered an entrapment neuropathy caused by pressure on the sciatic nerve by an enlarged or inflamed piriformis muscle.
The sciatic nerve can be compressed between the swollen muscle fibers and the bony pelvis.¹ Pace and Nagle²estimated that 45 of 750 cases referred to their back clinic were treated for this syndrome. They found that the condition was six times more prevalent in women than men. Because this syndrome is not common it is often overlooked and needless surgery may result. Wyant³states that the functional test for piriformis syndrome should be a routine part of the physical examination of all patients presenting with lower spinal backache. Besides backache, the piriformis muscle contracture and associated adhesions has been related to radiating pain from the sacrum to the hip joint over the gluteal region to the posterior thigh, coccydynia,⁴dyspareunia, male impotency5, and oblique axis rotation of the sacrum with its effect on the total spine up to the atlanto-occipital region.⁵

According to Gray⁶ and Freiberg⁷ the piriformis arises from the anterior sacrum between the second to fourth anterior sacral foramina, from the margin of the greater sciatic foramen and from the anterior surface of the sacrotuberous ligament, the anterior sacrospinous ligament and the capsule of the sacroiliac joint. Freiberg states that the piriformis is the only muscle that bridges the sacroiliac joint. The piriformis passes through the greater sciatic foramen (the upper part of which it fills) and inserts by a rounded tendon into the upper border of the greater trochanter.

Pecian⁸ examined 130 human specimens to determine the anatomical relations of the sciatic nerve and the piriformis. He found that in 6.15 percent of the cases the peroneal part of the sciatic nerve passes between the tendinous parts of the piriformis and a pinching of the nerve can occur. He found at least five other variations of the sciatic nerve in relation to the piriformis muscle. He concluded that when the nerve passed between the tendinous portion of the piriformis the nerve would more likely be pinched during passive medial rotation of the thigh which stretches the piriformis, causing the nerve to be pressed against the extended piriformis. In this case, resisted testing of the piriformis or ordinary active piriformis contraction would separate the tendinous portion of the piriformis surrounding the sciatic nerve and would not compress the nerve.

Mizuguche⁹ felt that before the piriformis could aggravate the sciatic nerve there first had to be a preexisting tension on the sciatic nerve by scarring or arachnoiditis around the nerve roots secondary to laminectomy or some space-occupying lesion such as osteoarthritic spurs. He thought that ordinary walking would cause the piriformis to impinge the shortened nerve. A history of trauma to the sacroiliac or gluteal region has also been blamed¹⁰.

The straight leg raise may be positive due to a contracted piriformis muscle. In a study by Freiberg and Vinke¹¹ on 10 cadavers it was found that after raising the leg 25 degrees, the sacrotuberous ligament becomes taut because of its attachment to the ischial tuberosity and the hamstrings. A contracted piriformis muscle which originates off the sacrotuberous ligament also tightened during the SLR.

The functional tests for a piriformis syndrome is naturally based on the function of the piriformis muscle. One of the main reasons for muscle testing is to determine if a muscle is painful. Since the piriformis muscle is an external hip rotator when the hip is in extension and an abductor when the hip is in flexion,⁹ external hip rotation should be tested with the patient supine with the legs hanging off the table edge at the knees. The patient then attempts to push his leg medially against resistance. The abduction test for the piriformis could be tested with the patient sitting facing the examiner. The patient attempts to abduct the knee against resistance.² The patient will complain of pain and possible weakness due to the pain. There may be pain when the patient sits or squats due to external rotation of the thigh and hip.⁵ Passive internal rotation of the thigh with the patient supine could also aggravate the condition. Pressure on the piriformis by way of rectal or vaginal examination may reproduce the symptoms.³ A positive "piriformis sign" due to piriformis contracture may be seen by the persistent external rotation of one lower extremity when the patient is supine. A contracted piriformis may result in a functional short leg.⁵ The symptoms of female pain during coitus (dyspareunia) could be due to the externally rotated hips, but female pain and male impotency is also attributed to piriformis compression of the pudendal nerve and blood vessels.⁵ 

According to Retzlaff et al.,⁵ on the side of the piriformis contracture the sacral base will be rotated anteriorly and examination of a prone patient will show a deepened sulcus on that side. The apex of the sacrum will appear posterior on the opposite side at the level of the posterior inferior illiac spine (oblique axis rotation of the sacrum). This may cause rotoscoliosis of the lumbar spine and increased lumbar lordosis which may effect the function of the whole spine. Digital pressure over the piriformis may refer pain along the complaint area.

Part II will discuss a variety of conservative treatments for this syndrome.

Warren Hammer, M.S., D.C., D.A.B.C.O.

Editor's Note:

Dr. Hammer will conduct his next soft tissue seminar on -----date ------ in ----- place -----. You may call 1-800-327-2289 to register.

Dr. Hammer's new book, Functional Soft Tissue Examination and Treatment by Manual Methods: The Extremities, is now available. Please see the Preferred Reading and Viewing list on page xx, part #T126 to order your copy.

References 

1. Jankiewicz JJ, Hennrikus WL, Houkom JA: "The appearance of the piriformis muscle syndrome in computed tomography and magnetic resonance imaging: a case report and review of the literature." Clin Orth & Rel Res:262,205-209.
   
   
2. Pace JB, Nagle D: "Piriformis syndrome." West J Med 24:436, 1976.
   
   
3. Wyant G: "Chronic pain syndromes and their treatment: III. The piriformis syndrome." Can Anaesth Soc J. 26:305, 1976.
   
   
4. Thiele GH: "Tonic spasm of the levator ani, coccygeus and piriformis muscles." Trans Am Pract Soc 37:145-155, 1936.
   
   
5. Retzlaff E, Berry AH, Haight AS et al. "The piriformis muscle syndrome." J AM Osteopath Assoc 73:799-807.
   
   
6. Gray H: Anatomy of the Human Body. 26th ed. Philadelphia: Lea & Febiger, 1956:541.
   
   
7. Freiberg AH: "Sciatic pain and its relief by operations on the muscle and fascia." Arch Surg 34:337m 1937.
   
   
8. Pecian M: "Contribution to the etiological explanation of the piriformis syndrome." Acta Anat (Basel) 105:181-186, 1979.
   
   
9. Mizughuchi T: "Division of the piriformis muscle in the treatment of sciatica." Arch Surg 111:719-722, 1976.
   
   
10. Robinson D: "Piriformis syndrome in relation to sciatic pain." Am J Surg 73:356-358, 1947.
    
    
11. Freiburg AH, Vinke TA: "Sciatica and the sacroiliac join." J Bone Joint Surg 16:126, 1934.

Evaluating the Elbow

By Deborah Pate, DC, DACBR

Injuries to the elbow are common in childhood. The history and clinical examination are essential for ruling out fracture; proper views of the elbow are indispensable to determine the extent of the injury.

Lateral and anteroposterior views usually are sufficient to rule out a fracture, with the exception of a fracture of the radial head. A supplemental radial head-capitellum view can be very helpful. The anteroposterior projection usually suffices to demonstrate injury to the lateral epicondyles, the olecranon fossa, the capitellum, the trochlea, and the radial head. This view also demonstrates the relationship of the forearm to the central axis of the arm, known as the carrying angle. Normally, the long axis of the forearm forms a valgus angle of 15 degrees with the long axis of the arm (Figure 1).

In children it is essential to recognize the four secondary ossification centers of the distal humerus: the capitellum, the medial and lateral epicondyles, and the trochlea. The usual order in which these centers appear and the age at which they become radiographically visible are important factors in the evaluation of injuries to the elbow in children. Displacement of any of these centers serves as a diagnostic indicator of the type of fracture or dislocation. For instance, the medial epicondyle always ossifies before the trochlea. If radiographic examination in a child between four and eight years of age reveals a bony structure in the region of the trochlea (before this center should appear), and shows no evidence of the ossification center of the medial epicondyle, it must be assumed that the ossification center of the medial epicondyle has been avulsed and displaced into the joint. (Figure 2)

The lateral view of the elbow also is important for evaluating the joint space, the olecranon process, and the anterior aspect of the radial head. It is limited, however, in the information it can provide, particularly with respect to the posterior half of the radial head and the coronoid process, because of the overlap of bony structures.

The lateral view in children can be used to assess possible joint luxation or fracture. The distal humerus in children has an angular appearance resembling a hockey stick, the angle of which normally measures approximately 140 degrees. Loss of this configuration occurs in a supracondylar fracture. If a line were drawn along the longitudinal axis of the proximal radius, it should pass through the center of the capitellum. If a line were drawn along the anterior cortex of the distal humerus extending downward through the articulation, it should intersect the middle third of the capitellum. (Figure 3)

Disruption of this relation serves as an important indication of the possible presence of fracture or dislocation. Finally, regardless of the age of the patient, displacement of the normal positions of the fat pads of the elbow also provides a useful diagnostic clue to the presence of fracture. Normally, the posterior fat pad, which lies deep in the olecranon fossa, is not visible on the lateral view. When it becomes visible and the anterior fat pad appears displaced (the positive fat pad sign), evaluation for a fracture mainly of the radial head should be undertaken.

This information should be useful in the evaluation of the elbow, particularly in children. If there is any question as to fracture, reasonable precautions should be taken to avoid any possible permanent damage to the elbow.

References

Greenspan, Adam. Orthopedic Radiology, 1988.

Deborah Pate, D.C., D.A.C.B.R.
San Diego, California

Editor's Note:

Dr. Pate's book, Case Studies in Chiropractic Radiology is now available through MPI's Preferred Reading and Viewing list. Please see pages xx, Part #T123 for further information on how to order your copy. 

A) For the AP view of the elbow, the forearm is positioned supine on the cassette. B) The film in this projection demonstrates the medial and lateral epicondyles, the olecranon fossa, the capitellum, and the radial head. C) The secondary centers of ossification of the distal humerus usually appear in the following order: capitellum at one to two years, the medial epicondyle at four years, the trochlea at eight years and lateral epicondyle at ten years. 

(A,B) Displacement of the ossification center of the medial epicondyle secondary to the fracture may mimic the normal appearance of the ossification center of the trochlea (C). 

(A) For the lateral projection of the elbow, the forearm rests on its ulnar side on the cassette, with the joint flexed 90 degrees. (B) In children, the normal position of the capitellum relative to the distal humerus and proximal radius is determined by the position of the capitellum intersected by two lines: A line (a) coincident with the longitudinal axis of the proximal radius passes through the center of the capitellum, and a line (b) parallel to the anterior cortex of the distal humerus intersects the middle third of the capitellum. Disruption of this relation indicates the possible presence of abnormality.

Figure 4: For the radial head-capitellum view of the elbow, the patient is seated at the side of the table, with the forearm resting on its ulnar side, the elbow joint flexed 90 degrees, and the thumb pointing upward. The central ray is directed toward the radial head at a 45 degree angle to the forearm.

Management of the Frozen Shoulder (Adhesive Capsulitis)

By R. Vincent Davis, DC, PT, DNBPM

Frozen shoulder is a clinical entity, rather than a pathological entity. It may be the sequelae of rotator cuff lesions, the arthritides, idiopathic etiology, or fractures and dislocations. It is most commonly found when disuse of the joint is coupled with a "periarthritic personality" and low pain threshold exhibited in the clinical history. 
The acute phase should be considered when painful limitation of the glenohumeral joint becomes less painful as a result of increasingly limited motion of the joint. The subacute phase presents with some restriction of joint motion but with pain which presents in excess relative to the clinical findings. The chronic phase involves absence of pain with an immobile shoulder and scapulothoracic motion, rather than joint motion.

Clinically, this entity progresses from pain resulting from vasospasm and includes muscle spasm as a mechanism to limit otherwise painful motion in a patient presenting with extremity abduction in dependent position. This pathophysiology enhances venous stasis, congestion, vasospastic anoxia and leads to an edematous, proteinaceous exudate with inevitable fibrosis. Fibrosis progresses to adhesions of the osteofibrous case.

Although prevention is the best approach to this process, following acute trauma to any of the shoulder soft tissue, moist cryotherapy is applied. This author uses contrast therapy with cryotherapy as the final agent applied. As soon as the initial symptoms of acute inflammation are resolved, active use of the arm and glenohumeral joint with full range of motion will prevent progression of this entity. During this exercise period, moist heat as an infrared gel pack, or hydrocollator packs, are used to prepare for exercise procedures.

In the absence of trauma, and/or if the patient is poorly compliant and of the periarthritic personality with low pain threshold, moist warm infrared therapy is appropriate, especially using a shoulder wrap in which the entire shoulder region is wrapped with the device. Make certain to guard against thermal damage to the patient. Thirty minutes of application is sufficient to provide for reflex vasodilation. Immediately following each warm infrared application instruct the patient in appropriate range of motion exercises within their tolerance limit.

If the patient presents with subacute or chronic findings, the therapy must be intensive and includes the same initial moist warm infrared therapy followed by pulsed hydrocortisone/lidocaine phonophoresis of low wattage and then interferential current therapy using the Davis procedure. During, and immediately following all modality application, range of motion exercises must be attempted. This therapy assumes the absence of any large concretions as well as complete cuff tears which are surgical problems. This author opposes manipulation of the joint under anesthesia for many reasons, having witnessed this procedure as a surgical technician many times.

The patient should be encouraged to practice good postural habits avoiding the mechanical deficit involved in the "droopy shoulder" habit. In order to establish and maintain full range of motion of the joint rhythmic stabilization exercises are mandatory. Using an active resistive approach to this procedure may effectively substitute and circumvent any need for manipulative reduction of the joint. After achieving full range of motion of the joint, daily exercises are mandatory to avoid exacerbation. Contrary to popular opinion, this author has seen a limited number of recoveries from this clinical entity and absence of residual disability or limitations of motion is uncommon. Proper treatment, initiated early in the process, with intensive management and avoidance of progression of the lesion remains the best regimen.

References

Anderson, W.A.D. Pathology, 3rd ed. Mosby.

R. Cailliet. Shoulder Pain. F.A. Davis.

Davis, R.V. Therapeutic Modalities for the Clinical Health Sciences, 1st ed., 1983. Copyright -- Library of Congress TXU-389-661.

Griffin, J.E.; Karselis, T.C. Physical Agents for Physical Therapists, 2nd ed. Springfield: Charles C. Thomas 1982.

Krusen; Kottke; Ellwood. Handbook of Physical Medicine & Rehabilitation, 2nd ed. Philadelphia: W.B. Saunders Company 1971.

Krupp & Chatton. Current Medical Diagnosis & Treatment, 1980. Lange

Schriber, W.A. A Manual of Electrotherapy, 4th ed. Philadelphia: Lea & Feibiger 1975.

R. Vincent Davis, D.C., B.S.P.T., D.N.B.P.M.E.
Independence, Missouri

 Subluxation Complex

Proof of the Subluxation Complex

By Jesse Jutkowitz

I recently came across a medical monograph by Alf Breig M.D., that the profession should find interesting. It is a sequel to two other monographs by the same author and gives objective medical and objective scientific proof of the subluxation complex. 
The most recent work is, Skull Traction and Cervical Cord Injury. The two previous works were, Adverse Mechanical Tension in the Central Nervous System, and Biomechanics of the Central Nervous System.

Claiming proof of the subluxation complex is a heady thought, but it is there and you do not have to stretch to see it. The subluxation complex will have to undergo some expansions and some deletions, but that is how theory is improved. It is amazing how well D.D. Palmer did with what he had to work with.

Firstly, one must note that when nerve tissue is impinged upon, it stretches axially (along its length). This is noted in all three of the above references and objectively in live subjects as well as fresh cadavers and canines. Next, nerve tissues that are stretched to a certain very small extent (noted in the text as "perhaps only imperceptibly lengthened") are extremely liable to lose their conductivity. "This has been verified by, among others, neurological surgeons¹, who have observed that critical tension of nerve fibers abolishes their conductivity and that their conductivity can be restored by relaxation of the fibers, as long as they are basically undamaged." This passage is from the most recent monograph but is referenced in the previous two as well as in many other papers on anatomy and physiology. (I did not do a literature search for this article, but I have been exposed to literature by Dr. Grace Jacobs, Ph.D. confirming this fact since my second year at Northwestern Chiropractic College).

So far, we have found, objectively, that pressing on a nerve stretches the nerve and reduces its ability to carry nerve impulses (conductivity).

The next major fact contributing proof to the subluxation complex theory is the entire thrust of Dr. Breig's objective experimentation which is that ventroflexion of the spinal column stretches the nerve tissue in the spinal cord and nerve roots (especially where there are firm attachments of the nerve tissue and meningeal sheaths to the spinal column at the occipitocervical spine region craniad and the lumbar spine-sacrum caudad), resulting in reduced conductivity, leading to neurological symptoms and damage to nerve tissue in the central nervous system. Dorsiflexion (extension) of the spinal column (not hyperextension) relaxes the nerve tissue of the brainstem, spinal cord (pons cord tract), and nerve roots relieving the axial stretching of the neurons returning normal conductivity of nerve impulses, which relieves the symptoms and neurologically induced dysfunction. Here we have Palmer's chiropractic, no?

Now we have, objectively, from Dr. Brieg's work: Pressing on a nerve stretches the nerve; stretching the nerve reduces its ability to carry nerve impulses (conductivity); and if the nerve is not damaged, taking the stretch off the nerve will relieve the symptoms and restore normal nerve function.

This means that any biomechanical problems that increase spinal flexion, thus increasing axial stretch on nerve tissue, will usually cause neurological symptoms or make them worse. Anything done to relieve the flexion and stretching will relieve the symptoms and restore normal nerve function where there is no permanent damage to the nerves themselves. This is subluxation complex theory.

Now comes a big problem. What happens when subluxations are reduced?

Because flexion of the column and cord is what causes stretching or tension on cord nerve tissue and the nerve roots, it is a reduction in flexion of the entire spinal column that must be a result of a reduction or correction of a subluxation complex. This is not a local effect. This is an entire spinal column and pelvis effect. The definition of a subluxation as a vertebra out of place relating to the vertebra above it and the vertebra below is a start, but that definition is inadequate. A proper definition must include spinal column flexion as well as spinal cord and nerve root stretching to fit the biomechanical facts. For all those attempting to eliminate full spine x-ray, I give notice that you are throwing away the main proof of the chiropractic subluxation theory.

I propose a definition of a subluxation or subluxation complex -- a vertebra slightly out of place that causes spinal column, cord, and nerve root flexion causing stretching of nerve tissue including the entire or local areas of the pons cord tract and nerve roots resulting in direct or indirect neurological symptoms. This definition fits the biomechanical and clinical facts. If you have something better that fits the facts, submit it.

Do subluxations cause the spinal column to lengthen? Do subluxations cause spinal flexion?

These are things that need to be researched on a full spine level. Dr. Breig writes about changes in spinal length visible on x-ray. As much as "one centimeter increase in length in the cervical spine alone" (sectional x-ray, not full spine), resulting from traction, causes not only cervical nerve root neurological symptoms but also objective lumbar nerve root neurological symptoms including objective loss of sensation, bladder control, and paresis. When the traction is released and the cervical spinal length is again measured on x-ray, it has shortened, allowing the spinal cord tissue to relax. Usually within a day or two, patients regain bladder control, sensation, and strength in both the arms and legs -- objectively noted and documented in many cases. However, the x-rays are mostly cervical x-rays. What happens in the lumbar spine and pelvis? These are areas for investigation by chiropractors.

Do you know what happens to the length of a person's spine when he sits compared to when he stands? A fairly clear full spine lateral view may be taken using the Bolin filter system but on most occasions a separate cervical lateral view will be needed for trabecular patterns.

What happens after one adjustment? Two? Ten? Twenty? There is currently a research project involving chiropractors, radiologists, and medical orthopedists: People are examined using MRIs. Some are adjusted and some are not. The MRI then is redone and examined for change. Virtually none of the adjusted patients have changed in the measurements. (It is a one set technique).

Doing the same type of investigation myself, using full spine radiography in place of MRI, the only significant finding I can demonstrate has been a very notable change in the length of the spinal column as measured with an opsiometer on George's line from Fergason's sacral base angle line to the occipital base line. Do this investigation yourself. Some of you will find the spinal length decreases, some will find it increases. Does this mean what you did increased the tension on the cord and nerve roots and made things worse? Some of you will find no effect.

As you can surmise from the above discussion, one of the things chiropractic needs and has always needed is an objective measure by which to judge chiropractic. I think Dr. Breig has provided a valid objective measure -- spinal length.

In Adverse Tension in the Central Nervous System, which is a manual for surgically setting the cervical spine in slight extension to slacken the pons cord tract, as well as researched and objectively documented explanation of the effect on neurological tissue, Dr. Breig identifies cord myelopathies, rhizopathies, neurogenic urinary incontinence, respiratory insufficiencies, cerebral palsy, various neurogenic painful spasticities, even multiple sclerosis and amyotrophic lateral sclerosis (ALS) as all being successfully treatable by spinal cord relaxation. The implications for chiropractic are enormous but objectivity in spinal length and spinal length changes by chiropractic adjustment must be established.

Let me close with a passage from Dr. Breig's Skull Traction and Cervical Cord Injury and comment that it indicates how valuable chiropractic can be if measured objectively.

In a disorder with such alarming symptoms as those in ALS, it would seem especially inappropriate to delay the simple surgical measure of keeping the neck fixed in slight extension while awaiting the approval of an ethics committee. When, therefore, a woman in her 50s was admitted to a hospital in Nancy, France, some years ago, suffering from ALS and cervical myelopathy, we followed the above programme and performed the cervicolordodesis (CLD) operation, where the cervical lordosis is fixed, relaxing the spinal cord and brainstem nerve tissue. Within a few days not only was her spasticity diminished and urinary incontinence reduced, but her swallowing was also clearly facilitated. Some weeks after this operation we were informed that this patient continued to improve; however, we subsequently learned that she had died some months later after having been treated at a physiotherapy institution with -- among other measures -- forcible forward bending of her neck.

Dr. Breig notes that medical people are looking for enzymatic disturbances with ALS and multiple sclerosis, which has also been successfully treated by CLD and well-documented when the evidence is that these conditions are mechanical in origin.

"Mechanical origin" -- this should be music to chiropractic ears.

Which college will institute a research program that uses the simple expedient of measuring objectively, on radiograph, the length of the spinal column preand postadjustment and then correlate that with objective changes in function and changes in symptomatology? This would seem to be an inexpensive yet vitally important finding for chiropractic that could be run in the school clinics. Most of the histological and mechanical work on nerve tissue itself has already been done by Dr. Breig and others.

Which technique of reducing subluxations is the most effective? Does motion palpation identify subluxations as opposed to compensations? Does physiotherapy help chiropractic adjustments? Which technique is the most effective? Which is least effective? This research is neither expensive nor difficult and is easy to duplicate, so let's get busy.

When taking lateral full spines views, let the patients relax since you want them in the position where the spinal column is working as the primary support structu

Management of Rotator Cuff Syndrome

By R. Vincent Davis, DC, PT, DNBPM

The rotator cuff of the shoulder is a musculotendinous cuff which is composed of muscular fibers of the supraspinatus, infraspinatus, teres minor, and subscapularis muscles. These muscular fibers blend with and reinforce the capsule of the shoulder joint. 
The etiology of this form of omodynia involves a tear in the fibers of one, or more, of these muscles and presents clinically with shoulder pain which is aggravated by motion and results in impairment of normal range of motion. Since a minor stress can easily cause a partial or complete tear of tissue already impaired by degenerative changes, these clinicopathologies are relatively common. Ischemically induced changes in such degenerative lesions predispose these tissues to stress tears due to their friability.

Typically, the history presents with an acute, severe pain of a "tearing" type with a 6 to 12 hour pain-free interval followed by the gradual return of pain and increasing intensity. If the examination reveals the presence of arm abduction, the tear is probably incomplete. In the absence of arm abductability, or the presence of the "drop arm test," the tear is probably complete and the patient should be referred for orthopedic surgical consult.

Treatment regimens for rotator cuff syndrome are controversial. Each physician, regardless of discipline, is influenced and guided by the training and education received relative to treating such pathologies. The following is recommended by this author.

Initially, cryotherapy should be administered following any episode of trauma admitted by the patient as heat therapy superimposed upon acute trauma is contraindicated. The shoulder should be placed in a sling but not fixed to the chest cage. This will provide reduced motion, but avoid immobilization which may predispose to adhesive capsulitis (frozen shoulder).

Following about 72 hours of cryotherapy involving 20 minute exposures to moist cryotherapy, begin pulsed phonophoresis (as often as time and circumstance will permit) with 2.5 percent lidocaine ointment combined with the oil coupling agent directing the sound beam directly over the site of the lesion, and if palpable, over the general area of the "tuft" of the tear. If trauma history is absent in this episode, cryotherapy is disregarded and pulsed lidocaine phonophoresis is commenced including the shoulder sling. Phonophoresis should be set for low intensity, 0.75 W/cm2 maximum, for 8 to 10 minutes, and may be necessary at least once daily for several days until pain allows for beginning of active abduction exercises with the arm in the sling. This procedure is continued so long as pain is present when performing the active abduction exercise.

With the absence of pain during active abduction, the sling is removed and the patient is instructed to begin "walking the wall" with his fingers. If pain reappears with the introduction of this exercise, interferential current therapy is commenced using the Davis procedure. Since pain is a product of stretching shortened soft tissue components, it is to be expected.

All exercises are performed with care initially and then gradually increased in strength and intensity as physiologically tolerated.

The Davis procedure my be performed several times daily, if necessary. The object of the exercises is to come as close as possible to pain-free circumduction of the shoulder joint.

In the absence of any traumatic episode in the history, treatment may include the application of shorthwave diathermy. This author recommends its use prior to performing pulsed lidocaine phonophoresis and should be limited to no more than 20 minutes at each therapy using the triple drum electrode. The purpose of this deep heating agent is to enhance hyperemia in periarticular tissue, thereby attempting to alter the effect of ischemic soft tissue degeneration.

References

Cailliet, R. Shoulder Pain. F.A. Davis 1987.

Davis, R.V. Therapeutic Modalities for the Clinical Health Sciences, 1st ed., 1983. Copyright -- Library of Congress TXU-389-661.

Griffen, J.E.; Karselis, T.C. Physical Agents for Physical Therapists, 2nd ed. Springfield: Charles C. Thomas 1982.

Hoppenfeld Physical Examination of the Spine and Extremities. Appleton, Century, Crofts 1987.

Krusen; Kottke; Ellwood. Handbook of Physical Medicine & Rehabilitation, 2nd ed. Philadelphia: W.B. Saunders Company 1971.

Schriber, W.A. A Manual of Electrotherapy, 4th ed. Philadelphia: Lea & Feibiger 1975.

Paravertebral Autonomic Plexus?

By Deborah Pate, DC, DACBR

Anterior disc herniations and concentric bulges are difficult to document as clinically significant. Radiographically a mild bulge of the discal annulus is considered clinically not significant. 
There are patients, however, with disc bulges and correlative symptomatology. It is this type of case that becomes difficult to defend, when all radiographic and orthopedic findings are within normal limits. It becomes the task of the treating doctor to defend the patient. For example, I recently reviewed a case of a patient who had lower back pain and intermittent right leg pain. The leg pain was vague and did not follow any particular dermatomal or scleratomal pattern. The computerized axial tomography (CAT) scan demonstrated mild concentric annular bulging of the L1 and L2 discs, which measured only 2 mm. This radiographic finding is considered within normal limits. The patient underwent a magnetic resonance imaging (MRI) and there was no evidence of degenerative disc disease and again there was only minimal disc bulging at the L1 and L2 levels. Orthopedic and neurologic findings were negative. As the evaluator, I gave the patient a diagnosis of intervertebral disc syndrome. The case went to arbitration. Needless to say, I was anxious to defend the patient but felt I needed some means of defending my diagnosis. I would like to share with you some material that might help in the defense of some of these types of cases.

We are all aware of the fact that the annulus is innervated. It is the manner in which the disc is innervated that is the basis for the vertebrogenic pain caused by the injured disc. In the lumbar spine, somatic fiber originating for the recurrent meningeal nerve supply the posterior longitudinal ligament, the meninges, the blood vessels, the posterior extent of the outermost fibers of the annulus fibrosus, a portion of the periosteum of the vertebral bodies, and the underlying bone. In addition, a small branch from the ventral ramus of the somatic spinal nerve root directly innervates the posterolateral aspect of the vertebral body and adjacent tissues. Injury to any of these structures will incite well-circumscribed local somatic pain.¹ Afferent pain fibers to the paraspinal sympathetic ganglia have been identified innervating the anterior and anterolateral disc and paravertebral structures including the anterior longitudinal ligament, the periosteum of the vertebral body, and the vertebral body itself.² There is also a major sympathetic ganglion which joins the recurrent meningeal nerve.³ Therefore, the entire periphery of the disc is supplied with afferent sympathetic fibers.³ 

Schematic diagram of innervation of anterior spinal canal and structures of anterior aspect of spinal column (modified from 15-17): 1 = nucleus pulposus; 2 = annulus fibrosus; 3 = anterior longitudinal ligament/periosteum; 4 = posterior longitudinal ligament/periosteum; 5 = leptomeninges; 6 = epidural vasculature; 7 = filum terminale; 8 = intrathecal lumbosacral nerve root; 9 = ventral root; 10 = dorsal root; 11 = dorsal root ganglion; 12 = dorsal ramus of spinal nerve; 13 = ventral ramus of spinal nerve; 14 = recurrent meningeal nerve (sinuvertebral nerve of Luschka); 15 = autonomic (sympathetic) branch to recurrent meningeal nerve; 16 = direct somatic branch from ventral ramus of spinal nerve to lateral disk; 17 = white ramus communicans (not found caudal to L2); 18 = gray ramus communicans (multileval irregular lumbosacral distribution); 19 = lateral sympathetic efferent branches projecting from gray ramus communicans; 20 = paraspinal sympathetic ganglion (PSG); 21 = paraspinal sympathetic chain; 22 = anterior paraspinal afferent sympathetic ramus(i) projecting to PSG; 23 = anterior sympathetic efferent branches projecting from PSG; 24 = lateral paraspinal afferent sympathetic ramus(i) projecting to PSG. (Note: Afferent and efferent sympathetic paraspinous branches/rami may be partially combined in vivo.)

Because of the embryologic origin and anatomic pathways of the autonomic system, the conscious perception of somatogenic pain may result in appropriate localization of the symptomatology and the involvement of autonomic reflex functions. However, in general the pain is referred to the region corresponding roughly to the somatic distribution of the afferent fibers of the spinal nerve with which the afferent sympathetic fibers enter the spinal canal.³

The referred pain produces a nonspecific pain perceived in the low back as diffuse, deep, dull, and aching. This pain may also be referred to the lower extremities, however, it does not follow at dermatomal or scleratomal pattern. 

This symptomatology has been referred to as the somatoautonomic syndrome.³ Further research is needed to aid in the recognition of this common but frequently misdiagosed problem.

References 

1. Edgar, M.A.; Ghadilly, J.A. "Innervation of the Lumbar Spine." Clin Orthop 1976; 115:35-41.
   
   
2. Jackson, H.C.; Winkelman, R.K.; Binkel, W.H. "Nerve Endings in the Human Lumbar Spinal Column and Related Structures." J Bone and Joint Surg (Am) 1966; 14:475-489.
   
   
3. Jinkins, J.R.; Whitemore, A.R.; Bradley, W.G. "The Anatomic Basis of Vertebrogenic Pain and the Autonomic Syndrome Associated with Lumbar Disc Extrusion." AJR June 1989; 152:1277-1289.

Lumbar Supports: A Cause of Myofascial Pain

By John Lowe, MA, DC

Several years ago, a young woman consulted me for severely sensitive skin from her waist down. This symptom had appeared a few hours after she climbed out of bed and bent over to stretch her low back.

My examination of her suggested that her symptoms were related to lesioned disks. I ordered an MRI, and the radiologist told me that her 3rd and 5th lumbar disks were herniated. I fit her with an elastic lumbar support to minimize axial compression of her lower lumbar spine.¹She had no pain that first day, but when she returned the next day, she had a persistent aching in her low back and upper buttocks. She woefully resolved "I guess it has to get worse before it gets better."

As is my custom, I palpated the muscles that classically refer to her areas of complaint. Several irritable trigger points (TPs) infested the muscles, and when I pressed them, her pain flared. She then told me that after wearing the support for a couple of hours, her lower back began to ache. The aching was tolerable, though, so she left the support on. The support had compressed and activated dormant TPs in the underlying myofascia, like a purse strap activates TPs where it cuts into the crest of a trapezius.²

A few minutes of ultrasound focused into the TPs stopped her pain. I advised her, "Wear the support only when it's imperative that you sit or stand for more than brief periods." And in case the TPs began referring again, I taught her how to desensitize them.

After this experience, I watched other patients to whom I gave lumbar supports. In some cases, the supports activated the TPs the way they had in the young woman. Each of these patients had active TPs in the muscles that make up the fleshy walls of the lateral and posterior torso. (See Figure 1)

Lumbar supports can be a valuable adjunct to the protective muscle contractions that accompany many spinal conditions.3 But as I looked back over the years I'd given patients lumbar supports, I realized that I should have screened patients for TPs likely to be activated by the support.

Now before giving a patient a lumbar support, I palpate the muscles the support will squeeze. When a patient's muscles harbor irritable TPs, I give what has become standard advice: "Use the support only when the benefits from wearing it are worth the myofascial pain that it may induce." I desensitize potentially troublesome TPs before the patient straps on the support; this reduces the risk of the support stimulating myofascial pain.

I tell the patient, "Test how tightly you can wear the support without pain. If it causes moderate pain, have someone massage the spots (which I marked with indelible ink) and then soothe them with moist heat. If the support causes severe pain, stop wearing it even if you have to stay recumbent most of the time."

Patients like the young woman, seldom blame the support for aggravating their condition. Some of them parrot her statement about symptoms getting worse before getting better. Or they say things like, "I guess this aching is just part of having a herniated disk." I dispel these erroneous notions. "The support is the culpret," I explain. "But when you understand how to use it properly, it can help you get well." In the meantime, the other symptoms patients suffer will be a pure reflection of their primary problem, unclouded by iatrogenic myofascial pain. 

References 

1. Cailliet, R.: Low Back Pain Syndrome. F.A. Davis, Philadelphia, 1981, p. 125.
   
   
2. Travell, J.G. and Simons, D.G.: Myofascial Pain and Dysfunction: The Trigger Point Manual. Baltimore, Williams and Wilkins, 1983, p. 198.
   
   
3. Lowe, J.C.: The lumbar corset: an adjunct to protective constrictions. Anabolism: Journal of Preventive Medicine, 6:(2)5, 1987.

Patellar Malalignment, Part III

By Warren Hammer, MS, DC, DABCO

In this article on patellofemoral (PF) problems we will deal with the rationale of treatment based on our static and functional examination described in part I and II. The main purpose of the PF examination was to determine if the patellofemoral dysfunction was localized to the structure (abnormal femoral sulcus and patella contours determined by x-ray, abnormal patella height due to length of patella tendon causing alta or baja, genu valgum or varum) or secondary dysfunction due to peripheral problems such as atrophy or tightness of the tissues that insert into the patellar: vastus medialis obliquus (VMO), iliotibial band, vastus lateralis, tightness of the retinaculum or abnormalities originating from the hip to the feet. 
Mann¹ states that an intensive conservative six- month treatment program should be attempted before surgical intervention.

All of the biomechanical insults found on the examination discussed in the previous article require treatment if possible. It was stated that structural problems such as excessive genu valgum or femoral anteversion could only be treated from a compensatory point of view such as stretching or strengthening involved muscles or using orthotics. Correcting the flexibility of muscles such as the hamstrings, quadriceps, tensae fascia lata, gastrocnemius, hip abductors, medial and lateral hip rotators were mentioned.

Probably, the most significant muscle relating to patellar function is the VMO. As previously stated, the sole function of this muscle is to act as a medial stabilizer to the patella. There is normally more of a tendency for increased lateral knee forces on the patella. There is a normal valgus Q angle in which the pull of the quadriceps on the patella is directed slightly lateral. The knee normally has a more prominent lateral condyle to help the patella resist these lateral forces.

There should be a dynamic balance between the medial and lateral forces that stabilizes the patella throughout its range of motion. The EMG activity between the vastus lateralis and VMO are almost equal, especially in the last 30 degrees of extension,³ although it has been found in patients with PF problems that the vastus lateralis fires before the VMO. The end extension range is probably the range where the knee requires most control by quadriceps contraction,⁴because during the last 20 degrees of extension the patella cannot depend on receiving the complete stabilization of the femoral sulcus. It is at this range that the quadriceps are performing their chief function as an eccentric decelerator. It is apparent that weakness of the VMO or tightness of the lateral retinacula will have an adverse effect on patella tracking. Abnormal tracking creates increased chondral changes. The VMO due to its location will be the first to show atrophy; it is also indicative of general quadriceps weakness, not only isolated VMO weakness.⁵ If found to be weak or atrophied (see previous article), just strengthening this muscle often relieves many PF problems.

Before discussing the exercise procedures regarding the PF area, it is important to understand the effect of compression forces on the patella (patellofemoral joint reaction force) at different ranges of knee motion. There are two sources of patellofemoral compression. One is due to the forces exerted by the quadriceps and the other is the force exerted by increasing the acuteness of the knee angle between the patellar tendon force and the quadriceps tendon force.⁶ Both of these forces are increased with knee flexion of 90 degrees. As the angle of flexion increases the force increases. Therefore most of the exercises recommended for PF problems are never performed near the 90 degree knee flexion position.

Henry⁷ feels that excessive progressive resistance exercises with the knees more than 45 degrees of knee flexion can produce retinaculitis or tendinitis. The usual exercises are straight leg raises, short arc terminal knee extension (patient sitting with pillow under the knee and extending from 20 to 0 degrees), and isometric quadriceps setting (patient contracts knee muscle holding knee in as straightened position as possible). A specific exercise for the VMO is a diagonal straight leg raise with the patient sitting on a table with thigh and leg flat (outstretched). The extremity should be positioned slightly lateral to the midline and the foot should be externally rotated. The patient lifts the straight laterally rotated extremity up and across the midline as if the knee were going towards the opposite shoulder. Besides strengthening the medial quadriceps, the hips flexors, adductors, and hip rotators are also exercised. Eventually weights can be added.

Hanten and Shane⁸ show that the VMO can be selectively strengthened by performing hip adduction exercises alone since the VMO originates off the tendon of the adductor magnus and somewhat off the tendon of the adductor longus muscle. They feel that a "strong VMO originating from weak adductors would serve only to draw the adductor tendons toward the patella, having no effect in reducing the lateral malalignment."⁸ Patients can be given a home exercise for the VMO. With the leg extended the patient pushes the patella laterally while attempting to contract the medial quadriceps. Patients can also push and hold the patella in a lateral to medial position to stretch the lateral retinaculum.

It has been found that the rectus femoris shows greater EMG activity during straight leg raises than during quadricep sets while the vastus medialis, gluteus medius, and biceps femoris showed greater activity during quadricep sets than during straight leg raises.⁹ Quadriceps setting generates 40 percent more EMG activity in the VMO than during straight leg raises (SLR). Reilly and Marten¹⁰ feel that compression of the patella on the femur normally occurs with the load coming from above and most exercises are performed with the load distal to the knee. Hughston¹¹ feels that the extensor mechanism is used as an extensor of the femur on the fixed tibia so that increasing the extensor strength by extending the tibia on the fixed femur is not functional. He feels that climbing hills is probably one the best exercises (providing knee flexion does not go past 50 degrees). With distal loading of the foot for quadriceps strengthening from flexion to extension, maximum forces with free weight are between 60 and 20 degrees,⁹ a range that is not recommended.

Beckman et al.,¹² feel that all of the above exercises which are of the open kinetic chain type are not as functional as the closed kinetic (weight bearing type). They therefore recommend lunges (dueling position), stair downs (walking down stair exercises stressing the weight bearing knee) and partial squats (bilateral and unilateral), all of the above never flexing the knee more than 50 degrees flexion. Palpate the patella for crepitus when the patient does partial squatting so that the exercise is only performed in the noncrepitus range. Partial squat exercises are important during the first 10 to 30 degrees of flexion when the quadriceps are working at their chief function of deceleration. The patella should also be evaluated and treated for loss of joint play.

In any acute PF problem it is important to reduce swelling before initiating strengthening type exercise because a swollen knee reflexly inhibits quadriceps contraction, causing atrophy and weakness.¹³ Attempting quadriceps strengthening when there is effusion and pain is a waste of time and effort. PF rehabilitation protocol by Brunet and Stewart¹⁴ includes isometric quad sets of 50 per hour, followed by straight leg raises (SLRs), eight sets of 10 lifts three times per day. The SLR are done with the noninvolved knee flexed to 90 degrees with foot next to outstretched involved knee. Patient contracts the knee muscles and raises involved leg up parallel with the uninvolved thigh. Patient holds for three seconds, lowers leg and rests for three seconds. Patient rests for one minute after each set of ten lifts. As soon as leg lifts become easy, free weights are added from one to fifteen pounds and added as soon as patients state that they are no longer fatigued.

Stationary biking could be used passively at first by using the good knee only. Later it can be used progressively by decreasing the seat height or increasing the pedaling force.

To decrease pain during exercise and walking, to increase the surface area of patella contact, to create a more even distribution of load, and to allow the muscles inserting into the patellar to function properly, the patella can be taped into a neutral position. It is necessary to take into consideration patella rotation based on which direction the inferior pole is rotated, lateral or medial tilt, medial or lateral glide towards the condyles, and finally superior and inferior tilting of the opposite poles.^12,15. Depending on the abnormal directions, the patella is taped towards the normal position. For a laterally positioned patella, tape from lateral border of patella and pull the tape medially. If the patella is tilted, tape from the middle of the patella and pull the tape (i.e., medially) to lift the lateral border of the patella. Taping also helps to influence the dynamic control of the patella. A Palumbo or Camp brace can also be used to help control the patella position during rehabilitation.

In conclusion, patella malalignment is the chief functional stress underlying may PF problems. A forceful quadriceps contraction on a malaligned patella eventually results in excessive chondral wear. Strobel and Stedfeld¹⁶ state that "chondromalacia" should not be used as a diagnosis since it is really a "pathoanatomic and morphologic presentation of the cartilage." They feel that due to the complex nature of many PF problems that the best term would be "femoropatellar pain syndrome."

References 

1. Mann, R.A. "Biomechanics of the Foot and Ankle." In Mann R (ED): Surgery of the Foot, 5 ed. St. Louis, Mosby 1986.
   
   
2. Hammer, W.I. Functional Soft Tissue Examination and Treatment by Manual Methods: The Extremities. Gaithersburg, Maryland, Aspen 1991.
   
   
3. Reynolds L., Levin, T.A., Mediros, J.M., et al. "EMG Activity of the Vastus Medialis Oblique and the Vastus Lateralis in Their Role in Patellar Alignment." Am J Phys Med 1983; 62:61-70.
   
   
4. Delitto, A., Lehman, R.C. "Rehabilitation of the Athlete with a Knee Injury." Clin in Sports Med 1989; (8) 4:805-840.
   
   
5. Lieb, F.J., Perry J. "Quadriceps Function: An Anatomical and Mechanical Study Using Amputated Limbs." J Bone Joint Surg. 1968; 50A:1535-1548.
   
   
6. Frankel, V.H., Nordin M. Basic Biomechanics of the Musculoskeletal System. Philadelphia, Lea & Febiger 1989.
   
   
7. Henry, J.H. "Conservative Treatment of Patellofemoral Subluxation." Clin in Sports Med 1989; (8) 2:261-278.
   
   
8. Hanten, W.P., Schulthies, S.S. "Exercise Effect on Electomyographic Activity of the Vastus Medialis Oblique and Vastus Lateralis Muscles." Phys Ther 1990; (70) 9:561-565.
   
   
9. Soderberg, G.L., Minor, S.D., Arnold, K., et al. "Electromyographic Analysis of Knee Exercises in Healthy Subjects and In Patients with Knee Pathologies." Phys Ther 1987; 67: 1691-1696.
   
   
10. Reilly D., Martens, M. "Experimental Analysis of Quadriceps Muscle Force and Patellofemoral Joint Reaction Force of Various Activities." Acta Orth Scand 1972; 43:126.
    
    
11. Hughston, J.C. "Patellar Subluxation." Clin Sports Med 1989; 8:153-161.
    
    
12. Beckman M., Craiig, R., Lehman, R.C. "Rehabilitation of Patellofemoral Dysfunction in the Athlete." Clin Sports Med 1989; (8) 4: 841-860.
    
    
13. deAndrade, J.R., Grant, C., Dixon, A.S. "Joint Distension and Reflex Muscle Inhibition in the Knee." J Bone Joint Surga 1965; 47A: 313-322.
    
    
14. Brunet, M.E., Stewart, G.W. "Patellofemoral Rehabilitation." Clin Sports Med 1989; (8) 4:319-329.
    
    
15. Arno, S. The A Angle: A Quantitative Measurement of Patella Alignment and Realignment." JOSPT 1990; (12) 6:237-242.
    
    
16. Strobel, M., Stedtfeld, H.W. Diagnostic Evaluation of the Knee. New York: Springer-Verlag, 1990.