Leg Pain Sciatica 

Leg Pain Sciatica

Slipped disc... an analogy 

Leg pain sciatica usually, like the common cold, starts insidiously. Ignored, a cold may go through this process:Cold > Influenza > Bronchitis > Pleurisy > Pneumonia > Death

The process can usually be stopped at any stage with the appropriate treatment. Neglected, the disease process marches remorselessly on.

In the lumbar spine

In the lumbar spine, every case is different, yet the same:

Low Back Pain, LBP >>>

> LBP + tingling in the leg

> LBP + leg pain 

> LBP + neurological signs, like a foot drop

> The true hernia: no or very little back pain + severe leg pain, and possibly in extreme cases loss of bladder control. 

Research shows that 5% of sciaticas proceed to intractable pain within six months. Please don't assume you will be in the 95%! Tracking the progression of leg pain is done using the slump test for sciatica.

TIP:

You can and perhaps should always consider home treatment for lower back pain, but if it goes down your leg... then it's time to find a good chiropractor. Find a good Chiropractor ...

There are two kinds of antalgias: you may lean towards the painful side, or away . They are quite different.

Those who lean "towards" the painful side, if they are smart and listen to their chiropractor, will get better much quicker, but the chance of relapse is greater if they will not accept that, like the "away from" type, the disc will take 6-8 weeks to heal.

If the man in the picture had pain on the LEFT SIDE, and he is leaning towards the RIGHT SIDE, then he has the 'away from' kind. They take longer to come straight, but have a better chance of complete healing.

Antalgia is serious. It is often the prelude to a nasty leg pain sciatica that wends its way down the weary leg. Follow your doctor's instructions, but my advice is to stay at home at least until you can stand up straight. Don't sit, alternate between lying (with a cushion under your knees) and walking. Move onto your side as your back dictates, with the cushion between your knees. During the day, get up at least every hour and walk around. Research shows that too much bed rest is not helpful.

If you've come to this website because you're a bookworm, then you may enjoy this short story from Frog in my Throat. This story is all about an antalgia, in an amusing setting.BIG TOE ... Meet Jack!

But a neglected antalgia often leads to a leg pain sciatica, with tingling and pain spreading down the leg.

Tip

Bernard Preston's rule is: If you are in the Pisa sign then you shouldn't be at work. Don't sit, don't bend, and try very hard not to sneeze. A quick nose blow will usually stop a sneeze.

Depending which disc has been effected the leg pain sciatica may go down the back of the leg to the side of your foot, or down the side of your leg and over the big toe, or onto the top of your thigh.

Classically, there are four important grades. I add a fifth.

1. Back pain only.
2. Back pain spreading down into the leg.
3. Back pain, leg pain with first increased sensation and if neglected, ominously, numbness.
4. Back pain, leg pain with crippling weakness.
5. In the true hernia, there is less back pain, but the leg becomes a fire of pain. The bladder may be affected.
I could add a sixth.

6. Death. Balderdash you say. Sensationalism. I have a close relative who died after her seventh lower back and upper leg pain operation, aged 42. It happens. (She never consulted me!)

What is a "Lumbar Facet"?

Between the bones of the lumbar spine (the vertebrae) there are three joints:

1. A disc joint that is a sort of shock absorber.
2. Two facet joints.

On either side, between the disc joint and the facet joint lies the foramen where the nerve exits from the spine. That's where the drama begins.

Help for sciatica pain

These are the facet joints, fairly healthy ones. They control how far you can bend and twist your spine. In particular they determine how far you can extend your spine. Those girls have healthy facets! Extension - backward bending - doesn't cause pain obviously. But if and when they pinch the nerve there is help for sciatica pain.

Here you can see the relation between the facet on one side, the foramen with its nerve, and the disc...

What is Arthropathy?

We quacks like to use big words to impress you! Like "lumbago". Sounds impressive. It's just "sore back" in Latin, nothing more!

Try breaking big medical words down into their constituent parts:

Arthr-opathy

• Arthr simply means to do with a joint and is the root of the word arthritis. Arthr-itis. An itis (inflammation) of an arthr (joint)
• opathy simply means "a condition of". Sometimes if we want to sound really impressive and scare you we would say "a disease of". Don't be frightened of that word "dis-ease". It simply means a "lack of ease."

So, arthropathy simply means a condition to do with a joint. In this instance, a lumbar facet joint causing lower back pain and possibly leg pain.

So lumbar facet arthropathy is simply a condition  of the lumbar facets; some would call it a disease.

Mostly, it's an osis not an itis. It's essentially non inflammatory, so taking NSAIDs certainly won't help. in the other hand lumbar facet arthritis may be inflammatory, but even then we chiropractors are not in favour of Non Steroidal Anti Inflammatory Drugs except perhaps for a very short period for severe pain as they have such nasty side effects. 

Sometimes an arthropathy may become highly inflammatory; like, gout, America's fastest growing disease. Hospitalisations have increased by 400 percent in the last 20 years. Whilst this remains unproven it's most likely since the change from butter to margarine and omega 6 rich seed oils in the mid seventies.

There are other less common inflammatory arthritides caused by example by bowel disease; avoid all wheat products if you have colitis. Joint infections, diabetes and a particularly nasty one where the nerve to a joint becomes inflamed can all affect the mechanical parts of the body.

But most lumbar facet arthropathy is non inflammatory. In one sense it's a normal part of aging; like grey hair. As the facets joints get older wear and tear sets in, and they get thicker. Extension of the spine gradually becomes more limited.

Lumbar facet arthropathy

Nope, this is not a porn page. There are some very strange people in this world. Like my cousin who sent me this picture, and then said that, if I blog it, then I'm a dirty old man. Hmph. Maybe, but anyway I couldn't resist it.

Then I got to wondering whether you get dirty old women?

What these pretty young women do display is a healthy lordosis; that's the curve in the lower back, seen from the side. These are quite normal. When you have lumbar facet arthropathy, you wouldn't be able to lie like that. It would give you lumbago and perhaps also pain radiating down the leg; the part the lower limb affected depends on which nerve is pinched.

The sciatic nerve comes from the lower lumbar spine and travels down the back of the thigh, outer calf and the foot.

The femoral from the mid to upper lumbars passes to the front of the thigh and inner lower leg.

What is a lordosis?

Viewed from the side, the spine has three normal primary curves. Two of them, in the neck and lower back, are called a lordosis. It is concave posteriorally. Absence of this curve is always potentially serious.

Is the Facet Syndrome a Myth?

By Warren Hammer, MS, DC, DABCO

What is a "Lumbar Facet"?

Between the bones of the lumbar spine (the vertebrae) there are three joints:

1. A disc joint that is a sort of shock absorber.
2. Two facet joints.

On either side, between the disc joint and the facet joint lies the foramen where the nerve exits from the spine. That's where the drama begins.

Lumbar facet syndrome is a very convenient diagnosis for mechanical low back pain (LBP). The signs^1,2 of a classic facet syndrome are: pain on lumbar hyperextension and decreased range of motion in any plane but especially in extension and rotation, local facet tenderness, absence of neurologic deficit or root tension signs; on lumbar flexion there may be relief, and straight-leg raising may or may not be normal.

Pain is usually of a deep aching variety and may extend to the buttock, hip, and even below the knee but not into the foot. But most of these symptoms and signs may also refer to pain of discogenic origin.²

"The function of the lumbar apophysial joints is to allow limited movement between vertebrae and to protect the discs from shear forces, excessive flexion, and axial rotation."³

Structures in the lumbar spine that receive a nerve supply are the zygapophysial joints, the ligaments of the posterior elements, the paravertebral muscles, the dura mater, the anterior and posterior longitudinal ligaments, and the intervertebral disks.⁴ It becomes clear that functional tests cannot specifically stress the facet joints. Firmly holding the patient's hips and pelvis, and asking the patient to bend forward to determine if relief occurs, to help pinpoint a facet involvement or creating pain on lumbar extension versus flexion cannot specifically incriminate a facet since all of the tissues mentioned above will also be stressed. While the facet joints are part of the picture of mechanical LBP, and chiropractic adjustments move zygapophysial joints, there are, of course, many other factors to be considered as to the reason patients experience relief from adjustments.

Unfortunately, at our present state of knowledge, the diagnosis for LBP or for that matter any diagnosis incriminating a mechanical cause for LBP (as differentiated from, for example, a herniated disk compressing a specific nerve) is speculative. Nachemson states that "although today there is a better understanding of pain, the pathomechanism of low back pain is unknown."⁵ He goes on to state that orthopedic surgeons who operate on patients with ill-defined back syndromes should realize that rarely are diagnoses scientifically valid, nor is the effectiveness of surgery proven by acceptable clinical trials.

While most authorities agree that the facet joint capsule has free nerve endings and is a probable source of pain, according to Jackson² and others,^1,6 the "diagnostic capabilities for testing the presence of a facet syndrome have been proven invalid."

A common method for diagnosing lumbar pain are diagnostic blocks where an anesthetizing agent is injected to determine if pain is relieved. According to Jackson,² who examined the literature and has performed three separate studies of his own regarding the injection of facet joints, the facet is not a common or clear source of significant pain and the facet syndrome is not a reliable clinical diagnosis.²

While many studies involving facet injection have been favorable, Jackson states that there are very few randomized controlled prospective studies. He states that the facet joint can only hold about 1-2 ml and many studies using more than that amount rupture the capsule and spreads the anesthetic to outlying areas. Jackson² in one study evaluated 390 patients with facet joint injections. He found that patients with more pain on lumbar extension and rotation did not get more pain relief after facet injection. He concluded that more than 90 percent of the patients with the signs of facet syndrome, did not respond better to facet injection.

Jackson² quotes a study by Lorenz et al.,⁷ which demonstrates that the upper lumbar facets L2-L3 in the lumbar neutral and extension positions have higher compressive loads than the L4-L5 level. He uses this argument to prove that facets are not primary sources of pain since clinically most back pain occurs in the lower L4-L5 levels. Of course he does not mention the fact that due to greater disk degeneration at the L4-L5 level the pressure on the L4-L5 facets will increase accordingly.⁸

I suppose since no one at the present time can pinpoint the exact source of pain in the mechanical low back problem, it is easy to prove that no one location is the source of the pain. For years there has been an argument between the disk and the facets as the main source of pain. Until someone can definitely prove that the facet is not a principle cause, I, for one, will be using facet syndrome as a plausible diagnosis.

References 

1. Lippitt AB: The facet joint and its role in spine pain management with facet joint injections. Spine, 9:746-750, 1984.
   
   
2. Jackson RP: The facet syndrome, myth or reality? Clin Orthop., 279:110-121, 1992.
   
   
3. Adams MA, Hutton WC: The mechanical function of the lumbar apophysial joints. Spine 8:327-330, 1983.
   
   
4. Bogduk N, Twomey LT: Clinical Anatomy of the Lumbar Spine. New York, Churchill Livingston, 1987.
   
   
5. Nachemson AL: Newest knowledge of low back pain: a critical outlook. Clin Orthop, 279:8-20, 1992.
   
   
6. Butler D, Trafimow JH, Andersson GBJ, et al: Discs degenerate before facets. Spine, 15:111, 1990.
   
   
7. Lorenz M, Patwardhan A, Vanderby R: Load-bearing characteristics of lumbar facets in normal and surgically altered spinal segments. Spine, 8:122-130, 1983.
   
   
8. Dunlop RB, Adams MA, Hutton WC: Disc space narrowing and the lumbar facet joints. J Bone Joint Surg, 66B:706-710, 1984.

Meralgia Paresthetica

By Brad McKechnie, DC, DACAN

Meralgia paresthetica is a painful condition attributed to entrapment or injury to the lateral femoral cutaneous nerve at the site where the nerve leaves the pelvis. The patient with meralgia paresthetica may complain of a dull ache, itching, numbness, tingling, or burning sensation over the lateral and anterolateral thigh.^1-6 The pain associated with this condition may vary in intensity from mild to very severe and frequently occurs following activity with relief following rest. 
The lateral femoral cutaneous nerve originates from the posterior division of the L2 and L3 nerve levels and is a pure sensory nerve.^1,6Following emergence from the intervertebral foramina of L2 and L3, the nerve traverses the abdomen, first making an appearance at the lateral border of the psoas muscle, and then passing obliquely across the iliacus muscle toward the anterior superior iliac spine. The nerve then exits the pelvis just medial to the anterior superior iliac spine by traversing the fibers of the inguinal ligament.¹ The nerve is tightly surrounded by the tendinous fibers of the inguinal ligament at this point and makes a right-handed bend to change direction from a horizontal course in the pelvis to a more vertical course in the lateral and anterolateral thigh.^1,3Various hypotheses have been formulated for the cause of this condition based on the anatomical relationship between the lateral femoral cutaneous nerve and the structures associated with the inguinal region:⁶ 

1. The nerve may be angulated or compressed against a sharp edge of fascia as it pierces the iliac fascia prior to exiting the pelvis beneath the inguinal ligament.
2. The nerve may be subjected to friction where it is wedged between the attachment of the inguinal ligament with the ASIS.
3. The nerve may pass through the tendinous fibers of the inguinal ligament and be pinched at this site.
4. The nerve may be compressed as it crosses the iliac crest or may be compressed within the substance of the sartorius muscle or tensor fascia lata muscle.

Numerous factors may contribute to mechanical damage of the lateral femoral cutaneous nerve as it exits under the inguinal ligament, such as obesity, constricting garments or girdles, direct pressure on the thigh in the region of the nerve, postural alterations, or increased demands placed on the abdominal muscles secondary to pregnancy or marching.^1,2,3,4,6 Meralgia paresthetica affects men more than women due to possible occupational considerations and may be bilateral in approximately 25 percent of cases.^1,2 Clinically, the history may reveal that the pain is potentiated by extension and relieved by flexion, as well as being aggravated by long periods of standing or walking.^1,2 Physical examination may reveal a sensory loss taking the form of a reduction of tactile sensation in the distribution of the lateral femoral cutaneous nerve.

Drawing depicts the sensory field for the lateral femoral cutaneous nerve.

These findings may be accompanied in three-fourth of cases by a tender spot over the inguinal ligament that is two finger widths medial to the anterior superior iliac spine.1,6 Symptoms may also be aggravated by clinically reproducing hip extension through orthopedic tests such as Nachlas' test.¹

In diagnosing meralgia paresthetica, care should be taken to rule out intraspinal, retroperitoneal, abdominal, or pelvic pathologies, diabetes mellitus, and L3 disc prolapses.^1,3,5,6Clinically, the L3 disc prolapse may produce alteration of the patellar reflex. In contrast, the reflex will not be altered in meralgia paresthetica.⁵

Most cases of meralgia paresthetica will respond to conservative care. Modalities that may prove helpful in the treatment of this condition may include ultrasound, electrical stimulation, or transverse friction techniques to break up possible adhesions affecting the lateral femoral cutaneous nerve at the inguinal region. Postural alterations and functional spinal problems should also be addressed in the management of this condition.

References 

1. Mumenthaler M: Neurology. Thieme-Stratton, Inc., New York, 1983.
2. Sunderland S: Nerves and Nerve Injuries, ed 2. Churchill-Livingstone, New York, 1978.
3. Turek SL: Orthopedics: Principles and Their Application, ed 4. J.B. Lippincott, New York, 1984.
4. Mohr JP: Manual of Clinical Problems in Neurology, ed 2. Little, Brown and Company, Boston, 1989.
5. Kramer J: Intervertebral Disc Disease: Causes, Diagnosis, Treatment, and Prophylaxis. Year Book Medical Publishers, Chicago, 1981.
6. Bradley WG, Daroff RB, Fenichel GM, and Marsden CD: Neurology in Clinical Practice: The Neurological Disorders. Butterworth-Heinemann, Boston, 1991.

The Carpal Tunnel Syndrome

By Deborah Pate, DC, DACBR

Carpal tunnel syndrome (CTS) is a relatively common, chronic, and disabling condition. This syndrome is typically characterized by nocturnal hand discomfort, finger paresthesias in the median nerve distribution, and thenar muscle atrophy.

This condition is most frequently caused by compression of the medial nerve in the carpal tunnel. This disorder occurs most often between the ages of 30 and 60 and is two to five times more common in women than men. The dominant hand is affected frequently; however, 32 to 50 percent of cases occur bilaterally.

Anatomically, the carpal tunnel is formed by all the carpals of the wrist, which is deepened by the tubercles of the scaphoid and trapezium on the radial side and by the pisiform and hook of the hamate on the ulnar side. This concavity is converted into a tunnel by the tough flexor retinaculum which stretches between the tubercle of the scaphoid and ulnar styloid. The eight flexors of the fingers, the long flexor of the thumb, and the median nerve all share the space in the tunnel.

1. The local entrapment of the median nerve within the carpal tunnel can be classified into three groups:

a. The decrease in the size of the carpal tunnel due to bony or soft tissue changes such as misalignment of the carpal bones, fractures, dislocation, and hypertrophic osteophytes of fibrous scarring.

b. An increase in the volume of the normal content of the carpal tunnel. This can be due to occupational hypertrophy of the muscles and tendons in the carpal tunnel which is not uncommon in dentists, tennis, golf players, typists, factory workers, and persons confined to wheelchairs. Synovial proliferation due to arthritis, tenosynovitis, edema due to congestive heart failure, and amyloid in patients in dialysis are other less common causes for an increases in the content of the carpal tunnel.

c. Space-occupying lesions such as lipoma and ganglion cysts that also cause entrapment of the median nerve within the carpal tunnel.

2. Systemic diseases also will cause neuritis affecting the median nerve, most commonly patients with diabetes; seven percent of patients with CTS have diabetes.

3. The third cause of CTS has been labeled as iodiopathic, in fact 50 percent of patients with CTS have an unknown etiology. CTS has also been found in association with menopause and late trimester pregnancy.

The diagnosis of CTS until recently has been mainly empirical. Present diagnostic parameters include clinical history, clinical signs, and nerve conduction studies which can be equivocal. Imaging modalities prior to magnetic resonance imaging (MRI) have been in most circumstances non-contributory, with the exception of osseous lesions, such as fractures and osteophytes. Likewise, the choice of conservative or surgical treatment is largely empirical.

The reason for the success or failure of conservative treatment is poorly understood, possibly because the exact cause for the symptoms is generally not established prior to treatment. The role of MRI in the evaluation of carpal tunnel syndrome is presently not definitive because the parameters for conservative and surgical treatment have not been established.

Unfortunately for our patients, there is no generally accepted guide for when a patient should undergo surgery. Many times the patient undergoes surgery whenever the orthopedist feels the patient hasn't responded to conservative care. If there is no demonstrable cause of pressure on the median nerve, then conservative management should be the preferred treatment. Reasons for the failure of surgical treatment or recurrences of symptoms could be due to delayed treatment, inadequate incision of the flexor retinaculum, postoperative scar or neuroma, or a growing space-occupying lesion within the carpal tunnel. The diagnosis and treatment of CTS could be made substantially more objective with the use of MRI.

The location, swelling, and constriction of the median nerve can be easily assessed with MRI. Edema and fluid in tendon sheaths can also be seen with MRI. Ischemic necrosis of bone, incisional neuroma, and fat within the carpal tunnel can also be demonstrated. MRI can be used to assess the etiology of the patient's symptoms permitting a more rational choice of treatment options directed toward the etiology. Posttreatment MRI examination could also serve as a useful means in predicting the success or failure of a given treatment.

Diagnosing a Meniscus Tear

By Warren Hammer, MS, DC, DABCO

This article is written with the idea of attempting to diagnose by physical examination whether a meniscus tear is present. Often patients complain of vague knee pain which most tests do not detect and the cause is a degenerated, torn meniscus. 
There is no one reliable test that specifically says that a meniscus is torn. Strobel and Stedtfeld list 20 tests that may indicate that a meniscus tear exists.¹ They state that the percentage of a correct diagnosis is between 60-95 percent. If there is an associated anterior cruciate ligament deficiency, a lateral meniscus tear can only be diagnosed by physical examination in eight percent of the cases and a medial meniscus tear in 32 percent of the cases.² "In patients with a chronic anterior cruciate ligament tear of more than three years' duration, tears of both menisci are very common."²

In order to understand meniscus testing, it is important to appreciate some of the functional aspects of the meniscus. Most meniscus tests usually create a positive response from the patient due to a "compression or entrapment of the meniscus between the femur and tibia."¹ It is important to understand that one function of the menisci is to limit extreme knee flexion and extension. In extreme knee extension during the screw-home motion, the menisci are forced anteriorly and the anterior horns of the menisci block further extension. In full flexion, the posterior horns of the meniscus are driven posteriorly and block knee flexion.³ As the knee flexes, the menisci move posterior partly due to the contraction of the semimembranosus and popliteus which attach to the posterior medial and lateral menisci respectively. Contraction of the quadriceps by its effect on the patellofemoral mechanism pulls both menisci forward with knee extension.³ Therefore, during meniscus testing, if the pain or snapping occurs near maximum knee flexion, the posterior horns are probably involved, and if the pain or clunk occurs toward knee extension, the middle to anterior portion of the meniscus is probably involved. Ellison⁴ describes testing for a tear of the anterior horn by having the standing patient internally and externally rotate on an extended knee.

Strobel and Stedtfeld¹ feel that examiners should learn three to five meniscus tests and use them on every patient since individual tests by themselves are inconclusive. For example, the validity of individual tests shows that Apley grinding test is 46 percent accurate, painful hyperextension 43 percent, Steinmann I sign 42 percent, and McMurray test only 35 percent. Interestingly, the most reliable sign is palpatory tenderness on the meniscus at the joint line (60-80 percent). According to Kapandji⁵, rotating the tibia internally will cause the medial portion of the meniscus to move anteriorly. The opposite will occur with tibial external rotation. Kromer¹ puts his finger tip in the joint line at the tender area and percusses the finger with his middle finger as in percussing the chest wall in order to elicit tenderness. Sometimes a local swelling may appear on the joint line which may be a meniscal cyst. This usually occurs on the lateral meniscus. Fifty percent of cysts coexist with a meniscal tear.¹

Three excellent tests to learn besides palpating for tenderness are: 

1. McMurray: Patient is supine with the knee flexed completely on the flexed hip. Examiner rotates foot externally and slowly extends the knee while creating a varus force with the other hand on the medial knee. An attempt is made to reproduce the painful snap which the patient may be complaining of. This is supposed to be putting pressure on the medial meniscus tear from the medial femoral condyle, but another test called Fouche's sign contradicts this conclusion. In Fouche's test the tibia is internally rotated to stress the medial meniscus. The theory behind this test is that as the tibia is slowly extended from the flexed position, the meniscus moves anteriorly and "almost catches between the femur and tibia before abruptly slipping back posteriorly, producing a snap."¹ This test is considered almost pathognomonic for a posterior meniscal tear.
   
   
2. Steinmann I Sign: With the knee near extension, the examiner can forceably rotate the tibia in external or internal rotation and slowly flex the knee. The forced rotation moves the meniscus in such a way as to stretch it anteriorly and compress it posteriorly. As the knee is slowly flexed with rotation, painful tears may be elicited at various sites. It is thought as with the McMurray test that lateral rotation of the tibia stresses the medial meniscus and medial rotation stresses the lateral meniscus.¹
   
   
3. Steinmann II Sign: Since the meniscus moves posteriorly with knee flexion and anteriorly with knee extension, if you palpate a tender meniscus in the joint line and slowly flex the knee, the portion palpated will probably lose its tenderness if a meniscus is involved. If the tenderness remains during knee flexion, the problem might be due to a collateral ligament lesion.

In tests such as McMurray and Steinmann I, it is important to first rule out collateral ligament sprain since these tests involve rotation and twisting which may aggravate the injured ligament giving a false positive meniscus lesion.

According to Clancy⁶, as far as palpation for meniscal pain in the joint line is concerned, medial meniscal injury usually causes posterior medial joint line pain and mild medial joint line pain, while lateral meniscus injuries usually cause midlateral pain rather than posterolateral pain. Isolated anterior medial pain is usually not a sign of a meniscal tear since anterior horn tears represent less than one percent of meniscus tears.

While manipulation of the knee has been successful in releasing a locked knee due to an acute torn meniscus, often times conservative treatment is disappointing. Longitudinal tears that occur near the periphery of the meniscus where there is adequate circulation will heal⁷, since the peripheral meniscal blood supply is capable of producing a reparative response similar to other connective tissue. To aid the circulation, deep heat (diathermy) may also help if healing is to occur. But to really know the status of a meniscal tear, arthrography, arthroscopic evaluation or MRI is often necessary.

In an acute situation, it is difficult to immediately determine if the meniscus is involved, especially if there is associated collateral ligamentous sprain. If the meniscus is the primary injury, effusion may not occur until the next day. The knee usually gives way and locks in extension, but unless the patient remembers that he could not immediately extend the knee after the injury, loss of extension could be due to hamstring spasm, pain or hemarthrosis due to other causes. While this article is emphasizing the meniscus, it is important to be able to evaluate the knee for ligamentous instability and other problems including the patellofemoral joint.

A patient with a chronic degenerative meniscus tear may complain of catching or grinding or may only complain of intermittent pain at the joint line. Occasionally, meniscus testing and other tests may reveal no symptoms at all. By having the patient perform deep knee bends, the meniscus may loosen so testing can be validated.

References 

1. Strobel M, Stedtfeld HW: Diagnostic Evaluation of the Knee. New York: Springer-Verlag, pp 166-182, 1990.
   
   
2. Henning CE, Lynch MA, Glick KR: Physical Examination of the Knee: in Nicholas JA, Hershman EB: The Lower Extremity and Spine in Sports Medicine. Vol I, St. Louis: CV Mosby, pp 765-800, 1986.
   
   
3. Renstrom P, Johnson J: Anatomy and biomechanics of the menisci. Clinics in Sports Med., 9:523-538, 1990.
   
   
4. Ellison AE: Athletic Training and Sports Medicine. Chicago: American Academy of Orthopedic Surgeons, 1985.
   
   
5. Kapandji IA: The Physiology of the Joints. New York: Churchill Livingstone, 2: 1970.
   
   
6. Clancy WG: Evaluation of acute knee injuries in: Finerman G: Symposium on Sports Medicine, The Knee. St. Louis: CV Mosby, 185-193, 1985.
   
   
7. Weiss C, Lundberg M, Hamberg P, et al: Non-operative treatment of meniscal tears. J Bone Joint Surg, 71A: 811-822, 1989.

Management of Adhesions of the Scapulothoracic Interface -- Scapulocostal Syndrome

By R. Vincent Davis, DC, PT, DNBPM

The scapulothoracic interface anatomically constitutes only a potential space between the anterior surface of the scapula and the posterior aspect of the respective costal margins. This potential space is occupied primarily by myofascial components. 
Upper extremity motion commonly involves the movement of the scapula on the posterior thoracic cage, and to minimize the coefficient of friction resulting from such motion, the interface is lubricated by a serous fluid.

Following trauma to the soft tissue components of the scapulocostal interface, traumatic edema is formed. Irrespective of where it occurs in the body tissues, the presence of inflammatory edema is the antecedent to adhesion formation. This is a well-recognized clinicopathological process. If allowed to progress, such adhesions formation will inevitably result in loss of motion of the scapula on the respective thoracic cage. Such loss of motion then complements pathological progression of this lesion to one of complete adhesive myofascitis of the scapulothoracic interface. This is, of course, an exquisitely painful clinicopathology.

Michele and Eisenberg call attention to fatigue associated with habitually faulty posture which exerts tension on the deep cervical fascia and respective musculature. This results in dull, aching pain in the posterior cervical region with pain radiating to the occiput, medial border of the respective scapula, and down the arm and forearm on the ulnar aspect of the hand. This pain complex may also radiate along the vertebral border of the scapula to the region of the fourth and fifth ribs posteriorly. Exquisite tenderness is a common clinical finding near the insertion of the levator muscles into the vertebral border of the scapula with a sensation of stiffness in the region of the shoulder girdle.

The differential diagnosis should rule out the cervicobrachial syndromes and generalized disorders such as polymyositis and fibromyositis. Diagnostic evaluation should include, but not be limited to, performance of the Apley test, the scapular wing test, the passive and active motion tests to rule out muscle weakness and intra-articular causes of reduced range of motion (ROM). If the respective scapula and thoracic cage move in unison rather than one upon the other, this constitutes a prominent clinical feature of this syndrome. The subscapularis, latissimus dorsi, teres major, rhomboid minor and major, serratus anterior, supraspinatus, and trapezius are all muscles implicated in the clinical features of this lesion.

Although treatment of the lesion involves some controversy, this author recommends the following therapeutic regimen. Apply interferential current employing the Davis procedure ("DC", November 15, 1988) placing the electrodes approximately one inch peripheral to the respective scapula. The object of this electrode placement is to ensure that the resulting interference pattern is located within the potential space of the scapulothoracic interface, as much as possible. For best clinical results, the IFC device should deliver a rectangular waveform with an average 25 microsecond pulse width and a beat frequency of approximately 120 Hz. In my experience, these electrical parameters will allow for the clinical application of as much as 60 to 70 ma of IFC to be applied. The major percentage of patients treated in this manner experienced an anesthetic effect from the IFC application.

It is possible to enhance this clinical process by pre-empting this IFC application with shortwave diathermy. SWD should result in an increase in the passive congestion in this area which should increase the hydration of these tissues with electrolytes. NMSC is, of course, an electrolyte mediated tissue stimulus.

The patient should be placed in a loose sling following treatment to reduce their tendency to use these components without arresting such motion. Correction of faulty posture by exercise and improved postural habits should be included in this regimen. Treatment may be administered every other day for several weeks, if necessary.

Failure of this regimen to restore painless scapulocostal motion will probably require consultation with an orthopedic surgeon for possible reduction of existing adhesions under anesthesia.

References

Arch. Phys. Med. Rehabil. 49:383, 1968.

Davis RV: Therapeutic Modalities for the Clinical Health Science, ed 1. Copyright -- Library of Congress, TXU-389-661, 1983.

Griffin JE, Karselis TC: Physical Agents for Physical Therapists, ed 2. Springfield: Charles C. Thomas, 1982.

Krupp and Chatton: Current Diagnosis and Treatment. 533: Lange 1980.

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

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

Activities of Daily Living (ADL) Considerations in Cervical Acceleration/Deceleration (CAD) Trauma

By Arthur Croft, DC, MS, MPH, FACO

In the early stages of treatment of CAD injuries, patients should be seen at sufficient frequency to ensure adequate inflammation control and pain control. Naturally, this routine is a burden on the patient who then must make allowances for travel time and time in our offices. 
And, as the physician sees the patient frequently during this time, he will often falsely assume that the patient fully understands all of the implications of his injury and the subsequent healing process. An extension of this assumption of comprehension is that patients should know which activities at home or at work may be harmful or should be avoided, and which should be modified in some way. Not only are these assumptions incorrect; they are negligent. In fact, we should not even assume that patients will make logical inferences in all ADL situations after receiving only one or two examples from us. For example, we may caution our patients about working with a forward-head posture since this places unnecessary strain on the cervical musculature. Yet, the patient may then spend three hours reading War and Peace that evening in bed with the head flexed acutely against the headboard and wonder why his neck hurts so much the next morning.

We see our patients frequently during the early phases of treatment, but in fact we are with our patients for only a small fraction of the day. The remaining 23-1/2 hours are spent in pursuits of work, leisure, and in sleep that are beyond our view but not our influence. This is why ADL advice is so important. Patients can unknowingly nullify or undo all of our best therapeutic efforts in this period.

What ADL? The logical choice for ADL recommendations is within the first few treatments. Patients are usually so overwhelmed by their report of findings, initial treatment, and advice about ice, rest, etc., that it is wise to wait until their second or third visit to give them advice about ADL which, by itself, is a lot of information.

Who should give the advice? In our clinic it is given by our associate doctors. We arrange special nightly meetings once or twice a week where patients are encouraged to bring their family.

The associate doctor on duty that day gives the lecture to patients of all other doctors and associate doctors in our group.

If you are a solo practitioner it might be more practical to devote extra time to one or two treatment sessions and give advice on ADL at that time. Alternatively, it might suffice to make a videotape to give to patients or simply to give out a pamphlet outlining your recommendations.

Chiropractic assistants (CAs) can also provide ADL advice although patients are generally more compliant with the doctor's advice. This is especially true in cases where the CAs knowledge of biomechanics and healing is limited or when CAs appear young and inexperienced.

Contents: A good deal of information needs to be relayed to the patient. Naturally, sufficient time allowances need to be made for this and, since our retention rate is usually only a fraction of the material presented, reinforcement is important. This can be accomplished in part by the doctor and staff on subsequent visits, but it may also be helpful to provide the patient with a check-off list of "dos" and "don'ts" or some type of summary of your recommendations on ADL.

In general terms, we can describe the components of ADL advice by setting objectives or goals for the patient. By the end of the ADL session the goals are: 

1. The patient understands (in broad terms) the forces of the trauma and the need for care. He has a feeling for how the tissues were injured. Much of this will reinforce information given in your report of findings (ROF).
   
   
2. The patient understands (very generally) the healing process and why your care and advice are fundamental to achieving the best possible outcome.
   
   
3. The patient has an understanding regarding the need for rest, ice, work restrictions, and ergonomic considerations at work.
   
   
4. The patient has an understanding of the need for adequate nutritional status to provide a suitable environment for all stages of injury -- acute, regenerative, and remodeling.
   
   
5. The patient understands the importance of stretching, exercise, and home traction.

Of these components, numbers one and two should be covered in the ROF. This is also true of number four. We shall concentrate then on numbers three and five here.

It is universally agreed that a certain amount of rest (to an injured area) is necessary during the immediate post-injury period. Unfortunately, patients are, more often than not, reluctant to heed advice about rest, especially when it translates into time loss from work. And, when patients are at work during this phase of injury, it is unusual that they will use ice as prescribed for obvious practical reasons. Even the wearing of a cervical collar will often engender enough teasing or attention to discourage its use: all the more reason to keep the patient at home for a few days. The therapeutic reality of this critical window of opportunity cannot be overstated to the patient. When patients are pursuing legal remedies it might do to remind them that their non-compliance will be evident in the medical records and will likely create more than just therapeutic difficulties! For example, when a patient does not heed their doctor's advice regarding work restrictions, appointment times or schedules, home traction, etc., an effective defense strategy would be to suggest that the patient who is truly in pain would indeed have been compliant.

I usually recommend two to three days off work to ensure adequate rest, immobilization, and the use of ice and supplements. Therefore this recommendation is not based on the strenuousness of the work. In more severe injuries, this period will be extended depending on the patient's progress and the physical demands of the job. When light duty is available at work, it is always preferable to have the patient return as soon as possible. Work restrictions and ergonomic considerations include the following: 

1. Patients should test the size of an object before lifting. They should use mechanical devices when possible.
   
   
2. Repetitive movements such as lifting, pushing, pulling, sweeping, digging, bending or twisting should be limited or avoided (depending on the severity of the patient's condition). When possible, patients should attempt to alternate their activity by switching hands, changing their position or the position of their work.
   
   
3. Loads should be lifted and carried as close to the body as possible.
   
   
4. Weights carried primarily on one shoulder or one hip should be periodically redistributed or a backpack or other method can be used.
   
   
5. Activities involving prolonged static positions of the head, particularly rotation, lateral flexion or extension, must be avoided. Flexion more than 10-15 degrees should also be avoided if it is to be prolonged.
   
   
6. Working in a seated position with elbows unsupported should be avoided as it places significant strain on trapezius, scalene, and other frequently injured muscle groups.
   
   
7. Seated posture is very important. Patients should sit straight up and the chair should support their backs. An adjustable back is best and should allow approximately 10 to 15 degrees inclination;² high backs are best. The arms should be supported at 90 degrees, as should the thighs. The feet should be flat on the floor. The upholstery should be porous to allow heat dissipation. Swivel chairs on casters are preferable. Aside from providing comfort, a good chair will significantly reduce spinal stress.
   
   
8. Video display terminals (VDTs) commonly trap patients in static positions for long periods. In addition to factors mentioned above (#7), the hands should be directly over the keyboard. The carpal tunnel must not be compressed; again, this is prevented by adequate arm rests. Both the top of the monitor display and keyboard should be visible without head movement. A stand for reference material prevents unnecessary neck postures but should be varied from side to side throughout the day if possible. Alternatively, where this is not feasible, the stand and monitor can be spaced equidistant left to right so as to reduce neck rotation.
   
   
9. Telephone speaker-phones can be used to avoid holding the receiver between ear and shoulder -- a definite sin. Headsets are an alternative to this as are padded shoulder rests.
   
   
10. Using adequate light will prevent eye fatigue and craning the neck forward to see better. Also, if eyeglasses are necessary for close work they should be used. Bifocal glasses should not require excessive extension of the neck for close work.
    
    
11. Heavy headgear (helmets, etc.) should be replaced with lighter or more modern equipment when possible.
    
    
12. Posture must be stressed always. Any forward posture of the head results in an increased load on paraspinal muscles and spinal structure.

Home activities center on sleeping, relaxing, and recreation. With regard to the latter, every patient needs to be assessed based on their hobbies and sports. Usually these can be modified as needed. For example, with competitive racket sports, patients can spend a week or two just hitting balls for practice. More vigorous sports such as basketball, volleyball, soccer or rugby can't be modified, and some substitute activity can be suggested. Weight training can usually be modified by decreasing the intensity and exertion of the workouts (i.e., less weight).

Patients should be encouraged to sleep on a firm (but not too firm) mattress of sufficient size for two persons (king or queen). Cervical pillows are used in all cases. Stomach sleeping is to be discouraged, particularly in upper cervical involvement or when headache are a prominent complaint. To discourage this, patients can sew large bulky buttons on the fronts of nightgowns or pajamas. These are impossible to sleep on!

Many postures that patients are accustomed to assuming around the home -- slouching in the easy chair, lying on the couch with the head propped up by one arm, are comfortable but counterproductive. Patients must be advised to eliminate all cervical, thoracic and lumbar stress by maintaining good posture at all times -- even during relaxation.

Other activities placing undo strain on the neck or back should be curtailed -- carrying small children on the shoulders, for example. Last but not least are the instructions about home exercise, stretching, and traction.

References 

1. Croft AC: Whiplash: the Masters' Program. Module 3: Whiplash Treatment and an Introduction to TMJ. Coronado, Spine Research Institute of San Diego, 1992.
   
   
2. Abdel-Moty E, Khalil TM, Rosomoff RS, et al.: Ergonomic considerations and interventions. In Tollison CD, Satterthevaite JR (eds), Painful Cervical Trauma: Diagnosis and Rehabilitative Treatment of Neuromusculoskeletal Injuries. Baltimore. Williams & Wilkins, 1992.

Prudent Examination Procedures When TM Dysfunction Is Suspected

By Darryl Curl

Disorders of the temporomandibular joint may be frustrating for the practitioner, but they are rewarding to treat because these patients are veritably in need of help. Those with TMJ dysfunction comprise a significant portion of the population who suffer from head/neck pain.

This head/neck pain group make some 50 million office visits each year to seek help; they spend more than $400 million a year in over the counter pain relievers.

I'm asked two frequent questions: "What should a chiropractor look for during an examination that indicates a problem with temporomandibular joint or its associated structures?"; and "Which problems should be referred to a dentist." Let's answer this two-part question by addressing the examination first, after all this is where it all begins.

Where Do We Start?

The first question you should ask yourself before you enter the examination room is, "Who is most likely to have a TM disorder?"

Let me share some interesting facts with you. Estimates of the number of chronic head/neck pain suffers in this country vary, but seven out of 10 people suffer to a significant degree at some time or another from head/neck pains. Other studies report that 40-80 percent of the population has some degree of TM dysfunction. Moreover, the research data indicates that the most frequent/consistent complaint of patients with TM dysfunction is head/neck pain.

So far, all you can say as you enter the examination room is that there is a rather high likelihood that the person you are about to examine will have some degree of TM dysfunction in addition to their head/neck complaints. It is a start, but of no real clinical use, since these guidelines are too general.

Findings to Look for When Examining Active Range of Motion of the TM Joint

Gait analysis is a very informative clinical procedure. The inability of the mandible to undergo a normal gait cycle is a compelling sign suggestive of craniofacial disorders or temporomandibular disorders.^1,2

In the JMPT, 15(2), February 1992, I published a clinical paper, "The VROM Scale: A Method for Analysis of Mandibular Gait in a Chiropractic Setting." This paper presents a method of analyzing mandibular gait in a chiropractic setting that is consistent with what is known of the biomechanics and pathomechanics of the mandible and its articulations.

Amount of Opening: Limited opening can be a warning sign for discal derangements (internal derangements) and should not be taken lightly. It must yet be determined if the limitation is due to pain, soft, or hard tissue problems. Soft tissue causes are likely muscular (external derangements) and can be differentiated by a soft-end feel.

Be aware of hypermobility of the TM joint. These joints are likely to be unstable and may dislocate, adding even more damage to the already lax joint capsule. The normal range of maximum opening is 55 mm to 60 mm.

Direction of Opening: The normal opening path of a joint is straight down, with the midline staying true. If an opening deviation is seen, note when the deviation occurs. For example, early opening at 7-8 mm, early closing at 38-35 mm.

Protrusive Deviation: Again, the path should be straight with the midline staying true. Deviations in protrusion are usually indicators of internal derangements.

Lateral Excursions: When the patient is asked to move the jaw slowly from side to side (to the limit), note any pain or restriction. Measure the distances using the midline of the upper and lower teeth as a guide. The test suggests a TM disorder if there is pain or limitation and may indicate joint inflammation, muscular dysfunction, coronoid process impingement or internal derangement (such as an anteriorly positioned disc or discal adhesions).

Findings to Look for When Muscle Testing

Masticatory muscle testing is probably the most overlooked part of the examination. By far, most pain associated with TM dysfuncton is myogenous pain (e.g., myositis, intrinsic muscle spasm, muscle guarding, myofascial trigger points, tendinitis, etc.) Here are examples of two muscle groups commonly evaluated when screening for TM disorders.

Lateral Pterygoids: These muscles are primary opening muscles and can be tested by putting one hand under the chin and the other just above the external occipital protuberance (EOP). The patient opens the mouth slightly and the chiropractor applies a strong closing force to the chin. Be careful, because like the hamstrings, these muscles can cramp easily. Pain in the lateral pterygoid is often associated with internal derangement of the ipsilateral temporomandibular joint.

Closing Muscles: (Masseter, temporalis, and medial pterygoid) are tested by placing a thick gauze pad over the lower front teeth to protect the fingers that will pull the jaw down, while the other hand supports at the forehead. Be careful, a human's bite is very strong. Watch out for loose front teeth, caps, dentures, etc. Practically speaking, this test is difficult to do with everyone, so you may want to modify it with putting gauze pads between the back teeth and determining if the patient experiences pain when clenching. (No fingers please). Note the visual definition of the musculature, especially the masseter, when the clenching occurs. Hypertrophy suggests the person either bruxes or clenches.

Problems That May Be Related to Joint Noises

Joint noises are traditionally taken to be one of the classic signs of TM dysfunction. However, current research is altering this concept a bit. It seems as though there are some circumstances where joint noises can occur in an otherwise healthy joint.

Joint sounds are best determined by palpating the lateral TM joint capsule and "listening" while the patient moves the mandible. Sounds such as crepitus, popping, clicking, or squeaking may be heard. These sounds are usually not present in a healthy joint and their presence suggests some sort of internal derangement.

References 

1. Eversole L, Machado L: Temporomandibular joint internal derangement and associated neuromuscular disorders. J AM Dent Assoc, 110:69-79, 1956.
2. Schellhas K: Diagnostic criteria for intra-articular TM disorders. Community Dent Oral Epidemiol, 17:252-257, 1989.