Chronic Neck Pain

Managing Chronic Neck Pain: Screening and Exercise Protocols

By Jasper Sidhu, BSc, DC

Recent guidelines and other research have shed light on some of the effective treatment strategies for chronic neck pain.^1-2

In addition to spinal manipulation, exercise is a key recommendation; however, it appears that exercise for chronic neck pain is being underutilized by the chiropractic profession.³ Traditional rehabilitation strategies have focused primarily on muscle strength and endurance through high loads.

However, most of the exercises that are designed to provide favorable outcomes can be accomplished in a typical chiropractic treatment room with specific, gentle exercise strategies. Initial rehabilitation goals are to address muscular imbalances that can be a contributing factor in the development of chronic neck pain. Let's focus on how to develop an effective screening process and initiate an appropriate exercise program to resolve patients' pain.

Deficits in Motor Control of the Neck Flexor Muscles

With respect to muscular imbalances, research has identified deficits in motor control of the deep (longus colli and longus capitus) and superficial (SCM and anterior scalenes) neck flexor muscles, which results in reduced activity of the deep flexors and overactivity of the superficial flexors.^4-6 Furthermore, the deep flexors also display reduced isometric endurance.⁷Research has shown that those with chronic neck pain have a delayed activation responseof the deep flexors associated with voluntary arm movement.⁸

Since the deep cervical flexors are important for support of the cervical lordosis and joints, the cervical spine can be vulnerable to reactive forces from arm movements. Altered movement patterns of these muscles has also been demonstrated in patients with chronic headaches.⁹Adding a training program that addresses these muscular imbalances to conventional therapy has been shown to significantly reduce headache frequency, intensity and duration.¹⁰ This muscular imbalance has also been implicated in poor sitting posture, which can be responsible in the development and perpetuation of neck pain symptoms.¹¹ One study showed that exercises targeted at training these muscles demonstrated an improved ability of the neck pain patients to maintain a neutral cervical posture during prolonged sitting.

Screening for Muscle Imbalances and Endurance Deficits

Screening for muscular imbalances and endurance deficits is the first step to prescribing an appropriate exercise program. There are several methods in achieving this. Let's take a look at two of them, the cranio-cervical flexion test (CCFT) and the cervical flexion test (CFT).

Cranio-Cervical Flexion Test: The CCFT involves the use of a pressure biofeedback device that can provide valuable feedback on the amount of pressure a patient applies. This involves inflating the pressure feedback tool to 20 mm Hg. The patient then tucks in their chin ("yes nod") for 10 seconds in five incremental stages of difficulty, increasing the amount of pressure by 2 mm Hg increments. One study comparing the performance of this test between subjects with and without chronic neck pain showed that those with neck pain achieved a median pressure of 24 mm Hg, while those with no neck pain had a median pressure of 28 mm Hg.¹²

Once a patient demonstrates an inability to perform the test to normal values, they are instructed to use the pressure biofeedback device to train their muscles at various incremental levels of pressure, starting at 22 mm Hg and progressing to 30 mm Hg. They are trained to sustain a contraction for a 10-second duration at the highest level they can accomplish without pain or loss of the correct cranio-cervical flexion action. At this level, the goal is to perform 10 repetitions, gradually building up to higher level of pressure.

Cervical Flexion Test: The other way to screen a patient is to use the CFT. While a patient is in a supine position on the table, ask them to tuck their chin in and lift their head off the table. They should try to maintain this position. The test can be graded on a 12-repetition maximum ability. If the patient's head shakes, there may be increased fatigue. If the chin juts upward, it suggests overactivity of the SCM and scalene muscles, indicating a muscular imbalance.

Screening for Neck Pain: The Cervical Flexion Test. If the patient can tuck their chin, lift their head off the table and maintain the position (or do multiple repetitions without fatigue or head shaking), the test is normal (right image). If the chin juts upward, it suggests overactivity of the SCM and scalene muscles, indicating muscular imbalance (left image).

Once a patient is identified as having muscular imbalances, the patient is taught to lift the head off the table for 12 repetitions, with fatigue being the indicator to finish each repetition. The patient can then progress to three sets of 12 repetitions, building to three sets of 15 and finally three sets of 20 repetitions. The goal is to increase endurance of the cervical musculature, in addition to maximizing proper motion.

The question that arises is whether one screening technique is better than the other. One study compared these two exercises on cranio-cervical flexor muscle performance. Results showed that there was no significant difference between the techniques.¹³ However, the study was limited primarily to mild neck pain. Experience also shows that those with more severe neck pain may not be able to perform adequate chin tucks while lifting their head off the table. If a patient is unable to achieve this, start them on chin-tuck exercises in a seated position, progressing to incline positions that reduce the effects of gravity until the patient is able to perform the 12-repetition max. Either way, the goal of increasing muscle performance can be obtained through both methods.

The Seated Chin Tuck. As with the lying test, this is a good exercise (left image = starting position; right image = tucked position) for strengthening the neck musculature. Inability to perform the exercise properly may indicate abnormal fatigue of the neck flexor muscles.Another important consideration is that the CCFT can be utilized for elderly patients, since their performance in the test may be different than those who are younger. A study comparing elderly versus younger patients found there was a greater shortfall from the target pressures of all stages of the test. Being aware of this discrepancy will allow the clinician to progress the elderly patient much more carefully.

Add Neck-Pain Exercise Protocols to Your Practice

As current guidelines indicate exercise as a recommendation for chronic neck pain, more and more clinicians can begin integrating simple exercise protocols within their practice. The CCFT is an effective screening and treatment tool that addresses muscular imbalances. Once the muscular imbalances are addressed, rehabilitation can progress to isometric exercises utilizing resistance bands and full-body conditioning programs that also address the scapulothoracic areas. Integrating these exercise protocols into your treatment program will increase patient recovery and address chronic neck pain as a multi-factorial condition.

References

1. Gross AR, et al. Conservative management of mechanical neck disorders: a systematic review. J Rheumatol, May 2007;34(5):1083-102.
2. Haldeman S, et al. The Bone and Joint Decade 2000-2010 Task Force on Neck Pain and Its Associated Disorders: Executive Summary. Spine, February 2008;33(4S):S5-7.
3. Freburger JK, et al. Exercise prescription for chronic back or neck pain: who prescribes it? Who gets it? What is prescribed? Arthritis Rheum, February 2009;61(2):192-200.
4. Falla D. Unravelling the complexity of muscle impairment in chronic neck pain.Man Ther, August 2004;9(3):125-33.
5. Johnson V, et al. Alterations in cervical muscle activity in functional and stressful tasks in female office workers with neck pain. Eur J Appl Physiol, June 2008;103(3):23-64.
6. Falla DL, et al. Patients with neck pain demonstrate reduced electromyographic activity of the deep cervical flexor muscles during performance of the craniocervical flexion test. Spine, October 2004;29(19):2108-14.
7. Jull GA, et al. Clinical assessment of the deep cervical flexor muscles: the craniocervical flexion test. JMPT, September 2009;31(7):525-33.
8. Falla D, et al. Feedforward activity of the cervical flexor muscles during voluntary arm movement is delayed in chronic neck pain. Exp Brain Res, July 2004;157(1):43-8.
9. Fernandez-de-las-Penas C, et al. Performance of the craniocervical flexion test, forward head posture, and headache clinical parameters in patients with chronic tension-type headache: a pilot study. J Orthop Sports Phys Ther, February 2007;37(2):33-9.
10. Van Ettekoven H, Lucas C. Efficacy of physiotherapy including a craniocervical training programme for tension-type headache; a randomized clinical trial.Cephalalgia, August 2006;26(8):983-91.
11. Falla D, et al. Effect of neck exercise on sitting posture in patients with chronic neck pain. Phys Ther, April 2007;87(4):408-17.
12. Chiu TT, et al. Performance of the craniocervical flexion test in subjects with and without chronic neck pain. J Orthop Sports Phys Ther, September 2005;35(9):567-71.
13. O'Leary S, et al. Specificity in retraining craniocervical flexor muscle performance. J Orthop Sports Phys Ther, January 1997;37(1):3-9.

 Tibiofibular Joint

Proximal Tibiofibular Joint Dysfunction

By Manuel Duarte, DC, DABCO, DACBSP, CSCS

Patients who complain of lower extremity pain and dysfunction are commonly seen in chiropractic practice. General diagnoses of the lower extremity often fall into general categories of either traumatic or overuse etiologies.

Traumatic injuries have a clear mechanism of injury, leaving the doctor to decide type and degree of tissue damage based on clinical history and examination. Overuse injuries often involve a mechanism of repetitive activities, which have the effect of stressing the involved tissues to the point at which breakdown occurs faster than the body can repair.

Mechanism of Overuse Injuries

In the overuse mechanism, there is often an underlying deficit in the body structure or function leading to an overload situation. Forces can accumulate, not be properly dissipated or be misdirected into areas not intended to handle the load. Injury may occur secondary to the structure not being able to meet the demands placed upon it. For example, a runner with knee pain may be engaged in too much activity too early in training. (A general rule for runners is to not increase mileage more than 10 percent per week.) The patient could cut down on overall mileage and give the body enough rest and nutrition to recover before the next training session.

Overuse combined with biomechanical faults will almost certainly create an overuse injury.⁵During running, each leg repeatedly absorbs loads equaling 1.5 to 5 times body weight. It has been suggested that repetitive loading of this type and the associated impact shocks cause microtrauma to the underlying tissues and may eventually cause enough damage to impair function. The use of cushioned or shock-absorbing insoles has been suggested to reduce the impact forces associated with running.⁴

Common overuse injuries related to this repeated microtrauma include conditions such as plantar fascitis, medial tibial stress syndrome and metatarsalgia. As such, part of a reasonable treatment plan could involve decreasing mileage and offering the patient a custom-made, shock-absorbing orthotic to decrease impact forces.

Involvement of the PTF Joint

The posterolateral surface of the tibia and the head of the fibula form an arthrodial articulation known as the proximal tibiofibular (PTF) joint. The capsule surrounding the PTF joint, although reinforced by anterior and posterior ligaments, is thicker anteriorly. The popliteus tendon helps to reinforce the posterior aspect of the capsule as it crosses the joint. At the biceps femoris insertion, the proximal fibula is integral in providing lateral stability of the knee.

There are three distinct movements that occur between the proximal tibia and the fibular head: anteroposterior glide, superoinferior motion and rotation. The ability of the PTF joint to withstand longitudinal or axial stresses is a direct function of its anatomy. The proximal aspect of the fibula seems best able to undergo tensile and torsional stresses. Compressive forces appear best managed distally, where the interosseous membrane ensures lower leg function by actively involving the fibula in load transference. The fibula has been shown to bear one-sixth of axial loading on the leg, with a key role in dissipating torsional stresses produced by ankle motion.

The PTF joint acts primarily to reduce torsional stress at the ankle, minimize lateral bending of the tibia and decrease weight-bearing torsion.¹ Abnormal force accumulation and altered biomechanics or trauma frequently affect a joint that, when injured, can contribute to chronic pain and considerable disability. It is my opinion that the PTF joint is an underappreciated and infrequently diagnosed cause of chronic leg and foot pain.

Disruption of the PTF joint has been considered a rare injury. Usually it is an isolated injury, although certain underlying pathological conditions may predispose the proximal end of the fibula to dislocate in a small number of patients.² Although dislocation of the tibiofibular joint is considered rare, subluxations and biomechanical faults at this joint are common enough to be considered in every clinical case of lateral knee pain and neurological findings of numbness and tingling in the lateral leg and dorsum of the foot. It has been my experience that this is especially common in active individuals, particularly athletes.

There are two basic types of tibiofibular joints: horizontal and oblique. Horizontal joints have a fibular articular surface that is usually circular and planar (or slightly concave in some cases) and that articulates with a similar planar-circular surface on the tibia. These articular surfaces are under and behind a projection of the lateral edge of the tibia, which provides some stability by preventing forward displacement of the fibula.

The second type of tibiofibular joint is oblique. In general, the more oblique joints have the least area of articular surface. Because this type of joint is less able to rotate to accommodate torsional stresses than a horizontal joint, it may subluxate and dislocate more frequently.

Anterolateral subluxation is the most common subluxation of the PTF joint that occurs during athletic activity, especially actions involving violent twisting motion. This subluxation is best discerned by clinical examination, which will reveal a prominent mass over the lower anterolateral knee joint.

When a patient complains of pain and tenderness of the proximal part of the fibula, there may be associated symptoms in the lateral popliteal fossa along the stretched biceps tendon. In this case, pain can be accentuated by dorsiflexing and everting the foot. There may also be transient paresthesias along the distribution of the peroneal nerve. Movement of the knee is usually painless, with a deficit in range a few degrees short of full extension. The biceps tendon may be in a muscular spasm or may be palpated as hypertonic. Upon observation, the fibular head will appear as a prominent lateral mass. A typical mechanism of anterolateral subluxation may be the following:

• inversion and plantarflexion of the foot that causes tension in the peroneal muscle group, extensor digitorum longus and extensor hallucis longus, resulting in a forward-subluxating force of the proximal end of the fibula;
• simultaneous flexion of the knee, relaxing the biceps tendon and fibular collateral ligament;
• concomitant twisting of the body, transmitting the twist along the femur to the tibia, causing a relative external rotatory torque of the tibia on the foot, which is already fixed in inversion.⁶

The combination of points two and three above springs the proximal end of the fibula out laterally, at which point the violently contracting muscles (point 1) pull the fibula forward.

Tibiofibular subluxations occur under traumatic conditions such as twisting athletic injuries, a slipping injury in which the patient lands with their knee flexed under their body, or parachute landings. Anterolateral subluxations can be sustained from a wide variety of sports activities such as football, soccer, rugby, wrestling, gymnastics, judo, broad jumping and skiing Posterolateral subluxations are usually associated with violent trauma to the knee, with the proximal part of the fibula being pushed posteriorly and medially.

Severe disruption of the anterior and posterior capsular ligaments of the tibiofibular joint, probably with a significant tear of part of the fibular collateral ligament, allows the biceps to draw the unsupported proximal part of the fibula posteriorly. This type of dislocation is invariably associated with a fracture of the tibial shaft. The literature describes a variety of proximal fibula subluxations. I have provided a complete list of them with a description of the extra vertebral adjustment for each as follows:

Superior Fibula Subluxation

Subluxation: A superior fibula subluxation often allows eversion sprain of the ankle. Typical features include tenderness about the fibular collateral ligament due to jamming, restricted inferior fibula joint play, and possibly a slight foot-drop sign.

Adjustment: Place the patient supine with the knee extended and hip flexed at about 45 degrees. Stand at the end of the table with the patient's foot placed on the anterior aspect of your thigh. Grasp the patient's ankle with your lateral hand, and take a web or capitate contact at the proximal aspect of the lateral malleolus. With your medial hand, overlap the wrist of your contact hand for stability. Apply traction and simultaneously make a short, inferiorly directed thrust to correct the malposition.

Inferior Fibula Subluxation

Subluxation: An inferior fibula subluxation can be the result of inversion ankle sprain and is often associated with tenderness about the collateral ligament of the fibula and restricted superior fibula joint play.

Adjustment: Place the patient in the lateral recumbent position with the affected side upward and the medial aspect of the affected foot resting relaxed on the table. Stand at the foot of the table in line with the longitudinal axis of the patient's affected leg. Apply a capitate contact with your medial hand against the inferior aspect of the lateral malleolus, with your lateral hand grasping your contact wrist for stability. Apply pressure and simultaneously make a short thrust directed superiorly along the vertical axis of the fibula to correct the malposition.⁷

Anterolateral Fibula Subluxation

Subluxation: An anterolateral fibula subluxation is often the result of lateral hamstring strain, inversion ankle sprain or trauma to the posterolateral aspect of the knee. It is characterized by lateral hamstring tendon tenderness, genu varum, excessive ankle pronation, and restricted posteromedial fibula motion.

Adjustment: Place the patient prone with the involved knee flexed. Squat at the end of the table (facing the patient) so that the patient's leg can rest on your shoulder for stability. Grasp the involved leg and interlace your fingers around the posterior aspect of the patient's leg proximally. Direct a pisiform contact with your cephalad hand against the anterolateral aspect of the fibular head. Apply traction and simultaneously rotate the fibula posteromedially to correct the malposition.

Posteromedial Fibula Subluxation

Subluxation: A posteromedial subluxation of the fibula often follows inversion ankle sprain, violent hamstring pull, trauma to the anterolateral knee and genu valgum.

Adjustment: Place the patient prone with the involved leg fixed. Squat at the end of the table (facing the patient) so that the patient's leg rests on your shoulder for stability. Grasp the involved leg and interlace your fingers around the posterior aspect of the patient's leg proximally. Apply a specific pisiform contact with your lateral hand against the medial aspect of the involved fibular head. Apply traction, and simultaneously rotate the fibula impulsively anterolaterally to correct the malposition.

Postero-Inferior Fibula Subluxation

Subluxation: The typical physical features of a postero-inferior subluxation of the fibula include pain at the fibula head, lateral collateral ligament pain at the ankle, lateral hamstring complaints, and restricted anterosuperior fibula joint play. This subluxation is often the result of inversion ankle sprain.

Adjustment: Place the patient supine with the affected knee flexed. Stand lateral to the involved limb with your cephalad hand with the popliteal fossa. Apply a thenar-pad contact against the fibular head. For leverage, grasp the anterior aspect of the patient's lower leg with your caudad hand. Apply oblique pressure with your stabilizing hand to flex the knee and push the leg superiorly, while simultaneously briskly lifting the fibular head anteriorly with your contact hand to make the correction.³

Following the adjustment, application of physiologic therapeutics such as ultrasound or interferential and ice can be applied at the doctor's discretion. For overuse injuries and to correct biomechanical faults, I recommend custom-made, flexible orthotics to provide patients with a balanced, symmetrical foundation and relieve postural stress.

When pain allows, the patient should begin active care stretching and strengthening muscles. During the initial phases of treatment and during stressful activities, a wrap or tape could be applied as necessary to maintain joint integrity.

References

1. Bressler H, Deltoff M. Proximal tibiofibular joint dysfunction: an overlooked diagnosis.Chirop Sports Med, 1988;2(2).
2. Ogden JA. Subluxation and dislocation of the proximal tibiofibular joint. J Bone Joint Surg, 1974;56:145-54.
3. Schafer RC. Knee and Leg Trauma. 1997.
4. O'Leary K, Vorpahl KA, Heiderscheit B. Effect of cushioned insoles on impact forces during running. J Am Podiatr Med Assoc, Jan/Feb 2008;98(1).
5. Quinn E. Checklist for Running Overuse Injuries. About.com: Sports Medicine.
6. Ahmad R, Case R. Dislocation of the fibular head in an unusual sports injury: a case report. J Med Case Reports 2008;2:158.
7. Hatzokos I, Drakou A, Christodoulou A, et al. Inferior subluxation of the fibular head following tibial lengthening with a unilateral external fixator. J Bone Joint Surg, 2004;86:1491-6.

Functional Integrity of the Pelvis & Hips: Gluteal Activation Enhances Athleticism and Injury Prevention

By Chris Feil, DC and William E. Morgan, DC

For most athletes, success is largely dependent on optimal functioning of the gluteal muscles (gluteus maximus, medius and minimus), and functional integrity of the hips and pelvis. Unfortunately, functional training and evaluation is not well-understood by many practitioners and athletes. Appropriate gluteal activation and pelvic-hip control is not only important to the rising number of cross-fitness devotees for generating maximal athletic power; it is also important to virtually every chiropractic patient. In addition to generating athletic power, proper hip function is valuable in the prevention of injuries to the knees, hips, pelvis and lower back. The cross-fitness activities of squatting, cleans, kettlebell swings, tire flipping, medicine ball tossing, and sprinting are all multi-joint movements that require hip involvement. Let's discuss methods to maximize proper hip motion and form during these activities.

Many in modern society have what Stuart McGill, PhD, calls "gluteal amnesia."¹ Dr. McGill has identified that when athletes [or any of us] lose the ability to engage our hips during athletic activities or exercises (such as cross-fitness programs), this adversely affects performance and increases the likelihood of injury. What Dr. McGill calls "gluteal amnesia," we might identify as loss of functional hip integrity: essentially the loss of the normal volitional ability to move one's hips through their range of motion with appropriate muscle activation.

In addition to muscular inhibitions, other factors that may contribute to motion dysfunctions are soft-tissue contractures or restrictions and articular fixations. While chiropractic adjustments may directly affect these restrictive lesions, knowledge of gluteal activation is also required to teach patients how to properly activate these muscles.

Function of the Gluteus Maximus

The gluteus maximus (GM) is the largest muscle of the body, and it is the major driver in lifting, throwing, swinging, pushing and running (particularly when sprinting and running hills). The GM originates at the crest of the pelvis, the dorsal sacral ligament, along with some fibers that originate from the thoracodorsal fascia. The [distal] insertions attach to the femur and to the iliotibial band. The GM helps stabilize the sacroiliac (SI) joints by causing force closure, essentially forming a self-bracing, protective compressive force to maintain the alignment and reduce shear forces on the SI joint. The GM attachment to the sacral ligaments may aid in pelvic stability due to active ligament tightening by gluteal contraction.²

The late professor Vladimir Janda associated decreased GM control in his theory of lower cross syndrome.^3-4 This muscle imbalance is associated with the pelvic posture variation calledanterior pelvic tilt. Observing anterior pelvic tilt during a postural examination of a patient should provoke you to further screen for gluteal dysfunction.

The gluteal muscles are the primary extensors of the hip, but hip extension is only part of their role in true athletic function. The muscle fibers of the GM are oriented diagonally, sloping laterally and caudally from their origin. With this orientation, the GM muscles contribute to external rotation and abduction of the thigh. Both hip extension and thigh external rotation are the "concentric" motions of the GM muscle.

It is important to remember that muscles have two contractile functions: concentric contractions (muscle shortening) and eccentric contractions (muscle lengthening). Eccentric muscle contraction is actually more powerful and more efficient than concentric contractions. The eccentric function of the GM muscle will limit and control hip flexion and thigh internal rotation.

Because of its fiber orientation, the GM serves as a primary muscular shock absorber for the hip and knee joint. Just as the hydraulic shock compresses and dampens the load in a car, the GM dissipates the forces in the athletic movements of jumping, landing, and lateral agility motions by eccentrically absorbing forces and limiting movements endangering joints of the lower extremities.⁵ The link between GM dysfunction and uncontrolled valgus and internal rotation motions of the knee has particular clinical significance and will be discussed in greater detail in an upcoming article.

Tremendous loads can be transmitted through the acetabulofemoral joint if the force is not dampened by the adjacent muscles. This shock absorption function is important to understand in a culture in which so many degenerative hip disorders occur. As many desk-bound workers with inadequate GM control participate in cross-fitness programs, they are unknowingly placing themselves at greater risk for osteoarthritis in their hips.

Figure 1: Squat Functional Screen: Passing. Normal lumbar lordosis, posterior travel of hips, varus knee position, and limited anterior travel of knees.Initiating Movement at the Hip and GM Activation

Elite power-lifters are able to squat more than 1,000 lbs injury-free through very purposeful activation of the GM and maximizing hip motion with the hip hinge.⁶ The term hip hinge refers to truncal motion in which the lumbar spine is fixed in a neutral lordosis and all motion occurs at the acetabular joint, not the spine.

An ideal squat begins by securing the toes and heels firmly on the floor. The lumbar spine should be fixed or "locked" into a neutral lordosis throughout the squatting motion. While descending, the buttocks should travel back and down; using a stool, gym ball, or chair as a target may be beneficial in learning this motion pattern. A wide stance is preferred, and the participant should be mindful not to allow the knees to travel forward.

Purposely engage the GM throughout the squatting motion both during decent and ascent; the use of an elastic exercise band around the thighs will help the patient to consciously engage the GM. The ascent phase of a squat reverses the motion groove of the descent phase. It should also be noted that the patient needs to stiffen the core during hip hinges and squatting

The Squat as a Functional Screen for Gluteal Activation

Inspecting a patient's ability to squat is a practical method for clinical screening of the lumbo-pelvic-femur chain. While the patient performs repetitive squatting motions, analyze the three main components of gluteal involvement: hip extension, flexion and external rotation.

Figure 2: Squat Functional Screen - Failures. Anterior knee travel, valgus knee position, and loss of lumbar lordosis.

A key point in assessment is the initiation of hip movement before knee flexion or ankle dorsiflexion. The knee should remain in a varus position throughout the squatting motion. The lumbar lordosis should remain unchanged during the entire squat. (Figure 1) Early anterior knee translation (Figure 2a), a valgus knee angle (Figure 2b), and a flexed lumbar spine (Figure 2c) are failures for the squat functional screen.

Figure 3: Squat Functional Screen - Palpation. The clinician provides challenge by applying medially directed pressure on the knees while the patient performs a squat.The examiner should palpate the GM for activation throughout the movement of both ascending and descending phases of the squat. In addition to palpating the GM, activation of the gluteus maximus can be tested by applying medial pressure to the knees. If the GM is engaged the examiner will note springy, firm resistance. With proper GM function, it should be difficult for the examiner to push the squatter's knee into a valgus position. (Figure 3) With practice and patience, you will be able to identify motion defects and provide precise recommendations for improving motion patterns.

Athletes performing cross-fitness feats of strength, agility, and endurance with functional impairments can expect to have reduced levels of performance and increased occurrences of injury and infirmity. Gluteal activation and properly functioning hip mechanics are fundamental components of proper motion and maximized athletic performance. Cross-fitness devotees with impaired gluteal/hip function can expect diminished performances and increased risk of injury. An astute clinician should be able to observe a cross-fitness athlete's squat and discern gluteal function and activity, correcting those at risk before injury occurs.

References

1. McGill S. Low Lack Disorders: Evidence-Based Prevention and Rehabilitation, 2nd Edition. Champaign: Human Kinetics, 2007:110-112.
2. Wilson J, et al. A structured review of the role of gluteus maximus in rehabilitation. New Zealand Journal of Physiotherapy, 2005;33(3):95-100.
3. Bullock-Saxton JE, Janda V, Bullock MI. Reflex activation of gluteal muscles in walking.Spine, 1993;18(6):704-8.
4. Morris CE, Chaitow L, Janda V. Functional Examination for Low Back Syndromes. In: Morris C. Low Back Syndromes: Integrated Clinical Management. McGraw-Hill, 2006:347.
5. Boling MC, Padua DA, Creighton RA. Concentric and eccentric torque of the hip musculature in individuals with and without patellofemoral pain. Journal of Athletic Training, 2009;44(1):7-13.
6. Liebenson C. The hip hinge. Journal of Bodywork and Movement Therapies, 2003;7:151-152.

The Lumbar Spine & Low Back Pain in Golf

By Shawn Thistle, DC, BKin (hons), CSCS

The Study

Title: The Lumbar Spine and Low Back Pain in Golf: A Literature Review of Swing Mechanics and Injury Prevention
Authors: Gluck GS, Bendo JA, Spivak JM
Authors' Affiliations: University of North Carolina, Department of Orthopedic Surgery, New York University School of Medicine, NYU Hospital for Joint Diseases, The Spine Center
Publication Information:Spine Journal, September/October 2008;8:778-88.

Overview

Golf is a unique sport that is growing tremendously around the world.

It can be played regardless of age, gender, or skill level (through "handicapping"). Between 1970 and 1990, the reported number of golfers in the United States alone more than doubled to 23 million. By the year 2000, there were more than 25 million golfers and 14,000 courses in the U.S. The World Golf Federation expects 55 million golfers by the year 2020.

Manual therapists should be aware that roughly 33 percent of golfers are over the age of 50, and this number will surely grow. These numbers all indicate the growing potential for a rising health care burden of the sport.

Golfers are prone to a number of injuries, with low back pain (LBP) being one of the most common. It is estimated that LBP accounts for 26-52 percent of golf-specific injuries. It is also estimated that up to 30 percent of touring professional golfers play injured at any one time. This study discusses the existing theories and literature surrounding the mechanics of a golf swing as they pertain to low back injury and the prevention and rehabilitation of potential golf-specific LBP.

Forces on the Spine During a Golf Swing

It is well-known that axial twisting is a risk factor for LBP - the golf swing combines this motion with compression, lateral bending and anterior/posterior shear. This combination of motions (compression, torsion and lateral bending) are also known risk factors for disc herniation. Kinematic studies have revealed that during a golf swing, the lumbar spine can sustain compressive loads of up to eight times body weight (about 6100 ± 2400N in amateurs and 7584 ± 2400N in professional golfers). As a comparison, similar studies on NCAA football linemen revealed compressive forces of ~8600N while hitting a blocking sled, and cadaveric studies have revealed that disc prolapse can occur at loads of ~5800N. Facet joints resist ~50 percent of shear; a golf swing has been shown to produce anterior/posterior shear forces of 596 ± 514N. (Loads of 570 ± 190N are able to produce pars interarticularis fractures in cadaver studies.)

The Golf Swing

Perfecting a golf swing is no simple task. In fact, it is one of the most complex athletic skills. The swing itself can be broken into four major components: backswing or takeaway, forward swing, acceleration with ball strike, and follow-through. There are two general stylesof golf swing: modern and classic.

The "Modern" Golf Swing:

• Emphasizes a large shoulder turn with minimal hip turn.
• The restricted hip turn is accomplished by keeping the front foot planted flat on the ground throughout the swing.
• This method maximizes shoulder-hip separation, and is thought to quietthe lower body and increase the chance of striking with a square club face.
• This separation angle is known as the "X-factor" - measured via lines drawn through the axial orientation of the hips and shoulders at the end of backswing.
• This swing can be problematic, as it causes increased lateral bend (also called the "crunch factor") and exaggerated hyperextension on follow-through (also known as the "reverse C" position), which can lead to overactivation of the spinal extensor muscles.

The "Classic" Golf Swing:

• Aims to reduce the X-factor by raising the front heel of the foot during the backswing to increase hip turn, shortening the backswing, or a combination of the two.
• A small set of data indicates that a reduced backswing does not have a detrimental effect on club-head velocity or ball-contact accuracy, although further study is needed to confirm this.
• This reduces the separation between the shoulders and hips, thereby decreasing torque on the lumbar spine.
• This swing emphasizes a balanced, upright form that also serves to reduce the crunch factor.
• The end of this swing is characterized by an erect "I" finish with balanced shoulders.
• Case reports have indicated that this type of swing can reduce the incidence and recurrence of LBP; however, more research is required.
• The Crunch Factor and Further Points of Interest
• The crunch factor, although lacking clinical evidence to support its relevance, is defined as the product of lumbar lateral bending angle and rotational velocity. Further research is required to elucidate the utility and relevance of this measure.
• One epidemiologic and radiographic study of elite golfers¹demonstrated that 55 percent of subjects had LBP, and those with LBP had significantly greater "trailing-side" vertebral body and facet arthritis when compared to age-matched controls.
• One study² showed that golfers with LBP consistently exceed their trunk rotation during swings compared to rotation in neutral posture at a controlled speed. This "supramaximal" rotation may cause excessive strain on viscoelastic structures surrounding the spine.
• In general, amateur and professional golfers utilize the "modern" swing in an attempt to maximize power and distance.
• Other common golf injuries include medial epichondylalgia (also known as golfer's elbow), hook of hamate fractures, rotator-cuff pathology, extensor pollicis brevis/abductor pollicis longus tenosynovitis, and knee injuries (which may not be as common, but can be severe - just ask Tiger Woods!).

Differences Between Amateurs and Professionals

• Professionals practice constantly with a consistent swing, leading to overuse injuries.
• Amateurs do not play as frequently, and often demonstrate multiple inconsistencies in their swing, leading to injury resulting from poor mechanics.

Lumbar Stabilization During the Golf Swing

• EMG studies performed on golfers have indicated that similar muscles are involved in stabilization during a golf swing as in various other athletic tasks - namely the internal/external obliques (IO/EO), quadratus lumborum (QL), erector group (spinae/multifidi), and rectus abdominus (RA).
• Specifically, during a golf swing the muscles most active are: contralateral EO, ipsilateral IO and latissimus dorsi, QL and RA.
• In general, the takeaway phase has the lowest overall muscle activation, while the forward swing/acceleration has the highest.
• Studies have indicated that the gluteus maximus is a critical stabilizer of the hip during the golf swing, and contributes significantly to power generation during the swing.

Treatment, Conditioning and Prevention Strategies

• There is a paucity of golf-specific literature in these areas.
• In a small collection of case studies on LBP in golfers, training with the "classic" swing method, in combination with general trunk muscle stabilization exercise (McGill/Queensland), was recommended. However, the contribution of swing modification to symptom resolution cannot be conclusively outlined yet.
• Some evidence suggests that lack of lead hip flexibility is associated with LBP in a small group of professional golfers.³
• There is also some low-level evidence that golfers who stretch/warm-up for 10 minutes before playing have a lower risk of sustaining injury.

Conclusions and Practical Application

The relation of golf to LBP will surely be the focus of a growing amount of research moving forward, assuming the sport continues to grow at its current pace. Manual therapists should stay abreast of this literature so we can assist golfers in their conditioning and maintenance programs for the sport, and also to manage any injuries that may arise while considering the specific demands of the sport and its participants.

References

1. Sugaya H, et al. Low back injury in elite and professional golfers: an epidemiologic and radiographic study. In: Farrally M, Cochran A, Eds.Science and Golf III: Proceedings of the World Scientific Congress of Golf. Champaign, Ill.: Human Kinetics, 1999: 83-91.
2. Lindsay D, Horton J. Comparison of spine motion in elite golfers with and without low back pain. J Sport Sci 2002;20(8):599-605.
3. Vad VB, et al. Low back pain in professional golfers. Am J Sports Med 2004;32:494-7.

CranioSacral Therapy Alters Brain Functioning: A Clinical Overview

By John Upledger, DO, OMM

While head of the clinical psychophysiology service at McLean Hospital - the largest psychiatric teaching hospital at Harvard Medical School - Paul Swingle, PhD, FCPA, RPsych, was asked to consult on a research project conducted by an osteopath at the New England Medical School who wanted to determine the effect CranioSacral Therapy (CST) had on the brain activity of a patient and therapist during a typical session.

"At the time, I dismissed CranioSacral Therapy as pure bunk," said Dr. Swingle, now a clinical psychoneurophysiologist in Vancouver and a highly respected biofeedback practitioner. Nonetheless, he agreed to measure the brain activity during the treatment session. "What I found startled me," he said. "With all the necessary experimental controls in place, I saw a marked change in alpha brainwave amplitude that immediately coincided with the CranioSacral Therapy. I didn't know exactly what the technique was, but the results so impressed me that I promptly enrolled in a class."

That was over four years ago. Since then, Dr. Swingle has used CS in his neurotherapy practice to help modify brain functioning to treat a wide range of disorders. "During treatment sessions I obtain EEG measurements. Some of the most important brain effects I've witnessed include a marked increase in theta and alpha brainwave amplitude in the back of the brain associated with the induction of a still point." Dr. Swingle's discovery was consistent with my early findings at Michigan State University when I was first developing CST, and with studies conducted by Dr. Elmer Green, formerly of the Menninger Clinic and Hospital in Topeka, Kan.

"Slow wave (i.e., theta) deficiency in the occipital region is associated with poor stress tolerance, sleep disturbance, racing thoughts, generalized anxiety, and vulnerability to substance addiction," said Dr. Swingle. "Neurotherapy that focuses on restoring this deficit is strongly enhanced with still-point induction."

Currently, Dr. Swingle treats children with involuntary movement disorders and seizure disorders. A major component of his protocol is to "increase the sensory motor rhythm over the sensory motor cortex [roughly across the top of the head from the tips of the ears]. The sensory motor rhythm is represented by brainwave activity between 13 and 15 cycles per second. When made stronger with brainwave biofeedback, it results in increased seizure threshold and reduced involuntary body movements," he notes. The increased brainwave amplitude Dr. Swingle has witnessed with CST is associated with "calm and passive attentiveness."

He has also reported an increase in the important sensory motor rhythm when a thoracic release is performed. To illustrate, he performed still point inductions on six patients with closed head injury and one with attention deficit disorder. "The effect of the still point was an increase in theta amplitude from a low of 6.2 percent to a high of over 80 percent," he reported. "Such changes in theta amplitude can have profound effects on brain quieting."

Dr. Swingle has reported these findings at various North American conferences. According to Dr. Swingle, children undergoing sensory motor rhythm training strongly benefit by a CST sequence of still point followed by sphenoid, thoracic and occipital releases. In terms of brainwave activity, this CST regimen results in increased amplitude of occipital theta frequencies (mental quieting) and of the sensory motor rhythm (body quieting). "The quieting often occurs immediately," he added, "and parents usually report a marked, sustained improvement."

Once a skeptic, Dr. Swingle now strongly advocates the use of CST as part of neurotherapeutic treatment of many disorders. The synergistic effect of these modalities results in "efficient and permanent remediation of many disorders associated with anomalous brain functioning."

CranioSacral Therapy and Scientific Research, Part II

By John Upledger, DO, OMM

Roppell, Retzlaff and I successfully demonstrated live sutural contents and rhythmical cranial bone and sutural motion, I began working with biophysicist and bioengineer Zvi Karni, PhD, DSc. He was a visiting professor from the Technion-Israel Institute of Technology in Haifa, Israel, where he chaired the biophysics department. He initially joined me to prove that I was crazy in my concept that "energy" was passed from one person to another during a hands-on treatment session (later named CST). After closely observing my treatment sessions, we theorized how we could best investigate. I became his student in biophysics, and he became my student in clinical manual medicine and biology. He gave me reading assignments in classical and quantum physics followed by pop quizzes; I gave him insight into the strange hands-on approach I was using.

Dr. Karni and I worked intensively for about three years, after which he was recalled to Israel. He arranged for me to go there the following summer as a visiting professor at Technion, where he introduced me to Professor Nachansohn, MD, the director of the Loewenstein Hospital, Ra'anana, the country's principal neurological rehabilitation hospital. I studied in the hospital's coma ward. After examining numerous comatose patients, I discovered that their craniosacral rhythms, as monitored in the paravertebral regions, were not present at the level of spinal cord injuries and below. With 100 percent accuracy, I was able to tell doctors the precise level of spinal cord injury in each patient, with no clue other than the loss of palpable craniosacral rhythm. This was truly a "blind" study, with eight to 10 very skeptical neurologists observing constantly.

During our years together at Michigan State University (MSU), Dr. Karni and I decided that we would look at the human body as an insulator bag made up of skin and mucous membranes full of electrical-conductor solution. We hypothesized that the conductor solution would undergo voltage changes in response to energy changes that occurred in the body as I did my treatments. In order to measure such millivoltage changes, Dr. Karni built what he called a modified Wheatstone bridge. The instrument algebraically added the millivoltage deflections in both the positive and negative directions at any given instant from a determined baseline. Thus, we could see millivoltage changes in patients as they occurred.

We began this series of experiments by applying electrodes on the midline of each patient's anterior thigh, three inches above the superior border of the patella. The grounding electrodes were placed upon the dorsum of each foot on the anterior midline over the tarso-metatarsal junctions. We also monitored cardiac activity through a V-2-placed electrode, and we tracked pulmonary/respiratory activity by placing sensitive strain-gauge and band apparatuses around the thoracic cage at the level of the juncture of the manubrium sterni with the xiphoid bone. Circumferential variations in thoracic-cage volume reflected breathing activity. These four measuring devices were then plugged into a polygraph that recorded the heart rhythm, breathing activity, and total-body millivoltage changes.

Dr. Karni monitored the readings on polygraph paper. Initially I told him what was happening as I initiated treatment techniques or patient changes occurred, and he noted the comments on the polygraph paper at appropriate locations. After a while, he was making accurate patient observations by simply monitoring changes in the polygraph recordings. We treated more than 150 patients this way and collected what seemed like miles of data. By demonstrating correlations in total-body electrical potential, we again confirmed the activity of what we called the craniosacral system.

As all of these laboratory studies were taking place, my colleagues and I conducted two clinical inter-rater reliability studies on children. I developed a 19-parameter evaluation protocol used to rate the level of mobility for various bones of the skull and sacrum. The first study was carried out on 25 nursery-school children examined by myself, one of two other cranial osteopaths, and a student assistant. The four of us evaluated the children independently, and reported our findings on each parameter to an independent research assistant. No one had any knowledge of the other's findings until after an independent statistician completed the statistical analysis. The percentage of agreement between the examiners varied from 72 percent to 92 percent, with the allowed variance of 0-0.5 percent. Once again, these findings supported the existence of a craniosacral system and sutural movement.

Still not satisfied, I went on to use the same examination protocol on 203 grade-school children. I personally evaluated the children with no knowledge of their histories. I then reported my findings to a research assistant who faithfully recorded them. An independent statistician then collected information from each child's school file, along with historical data from parent interviews. He correlated my findings with the data he recovered, and reported a very high level of agreement between the craniosacral examination findings and learning behavior; seizure problems; head injuries; hearing problems; and even obstetrical problems.

The study, because of its scientific design, obviated the possibility of random agreement. The results showed that standardized, quantifiable craniosacral system examinations represent a practical approach to the study of relationships between craniosacral system dysfunctions and a variety of health, behavior and performance problems. Other researchers have performed similar studies related to psychiatric disorders and symptomatology in newborns. Again, most of this work has been published. This is but a small portion of the research that has been done to prove the efficacy of therapy upon the craniosacral system.

Today, there are close to 100,000 CranioSacral Therapists around the world - and even more reports of patients helped by its noninvasive techniques. I find it odd that this information counts for nothing in the eyes of some skeptics who continue to proclaim the craniosacral system a fantasy. In any case, the craniosacral system will continue to exist and be used therapeutically with essentially no risk.

Resources

• Frymann, V.M., Relation Of Disturbances Of Craniosacral Mechanisms To Symptomatology Of The Newborn: A Study Of 1,250 Infants, Journal of the American Osteopathic Association, 65:1059, June, 1966.
• Retzlaff E.W., et al, Nerve Fibers And Endings In Cranial Sutures Research Report, Journal of the American Osteopathic Association, 77:474-5, 1978.
• Retzlaff E.W., et al, Possible Functional Significance Of Cranial Bone Sutures, report, 88th Session American Association of Anatomists, 1975.
• Retzlaff E.W., et al, Structure Of Cranial Bone Sutures, research report, 75:607-8, February 1976.
• Retzlaff E.W., et al, Sutural Collagenous And Their Innervation In Saimiri Sciurus, Anat. Rec., 187:692, April 1977.
• Retzlaff E.W., Mitchell FL Jr., The Cranium and its Sutures, Germany: Springer-Verlag Berlin Heidelberg, 1987.
• Sperino, Guiseppi, Anatomica Humana, 1:202-203, 1931.
• Upledger, John E., The Reproducibility Of Craniosacral Examination Findings: A Statistical Analysis, Journal of the American Osteopathic Association, 76:890-9, 1977.
• Upledger, John E., Relationship Of Craniosacral Examination Findings In Grade School Children With Developmental Problems, Journal of the American Osteopathic Association, 77:760-76, 1978.
• Upledger, John E., Mechano-Electric Patterns During Craniosacral Osteopathic Diagnosis And Treatment, Journal of the American Osteopathic Association, 1979.
• Upledger, John E. and Jon Vredevoogd, CranioSacral Therapy, Eastland Press, Seattle, Calif., 1983.
• Upledger, John E., Craniosacral Therapy II: Beyond The Dura, Eastland Press, Seattle, Calif., 1987.
• Upledger, John E., SomatoEmotional Release And Beyond, UI Publishing, Palm Beach Gardens, Fla., and North Atlantic Press, Berkeley, Calif., 1990.
• Woods, J.M., and R.H. Woods, Physical Findings Related To Psychiatric Disorders, Journal of the American Osteopathic Association, 60:988-93, Aug. 1961.

CranioSacral Therapy and Scientific Research, Part I

By John Upledger, DO, OMM

I cannot count the number of times I have been told by well-meaning friends and harsh critics that CranioSacral Therapy (CST) should be investigated using scientific methods. Many people say CST would be a real boon to health care - if only there were more scientific proof.

I explained why I believe CST can never be adequately evaluated within the confines of the laboratory. In addition, many people don't realize that research has indeed been done. For you skeptics, I offer the following overview:

In the mid-1970s, I was approached by Michigan State University (MSU) to uncover the scientific basis for a premise put forth by William Sutherland, DO, in the 1930s: that the joints and sutures of the cranium do not fully ossify, as was once believed. From 1975 through 1983, I was a professor in the department of biomechanics at MSU's College of Osteopathic Medicine, where I led a team of anatomists, physiologists, biophysicists and bioengineers to test and document the influence of the craniosacral system on the body. Together we conducted research - much of it published - that formed the basis for the modality I went on to develop and name CranioSacral Therapy.

I first worked with neurophysiologist and histologist Ernest Retzlaff, PhD, to prove that under normal conditions, cranial sutures do not calcify before death. We studied numerous bone and suture samples taken from neurosurgery patients between the ages of seven and 57 years. Not only did these samples show living sutures completely free of calcification, but they were chock full of collagen and elastic fibers; arteries; arterioles; capillaries; venules; veins; nerves; and neuroreceptors.

After in-depth examinations, we demonstrated definitive potential for movement between the cranial sutures. Yet these results appeared to contradict anatomy-lab samples taken from cadavers whose skull sutures were calcified. These seemingly conflicting findings suggested that the calcification of skull sutures seen in preserved cadavers was due to postmortem changes and reactions to chemical embalming agents. Our findings supported those published in Anatomica Humanica by Italian professor Guiseppi Sperino, who noted that cranial sutures fuse before death only under pathological circumstances.

Once we saw the potential for motion in living sutures, our next step was to demonstrate that the motion we had hypothesized actually existed in the living skull. With the assistance of biophysicist Richard Ropell, PhD, we began using head (band) strain gauges on living subjects. These gauges demonstrated rhythmical expansion-contraction movements of the cranial circumferences at eight to 12 cycles per minute; however, there were other variables that could discredit these measurements as solid evidence of sutural movement, so we had measure the movements of one skull bone in relation to another. While we could not use humans for studies like this, we were able to use live monkeys from the university's pharmacology department.

In pain-free experiments, we anesthetized the monkeys and did minor surgery to cement an antenna directly to each parietal bone, about two centimeters lateral to the sagittal suture, and two centimeters posterior to the coronal sutures. We then wired these two 10-inch antennae so that we could broadcast a radio signal between them. In the recorded wavelengths, we discovered as the parietal bones moved independently of each other, the distances between antenna times changed. These changes demonstrated interparietal movement of about 12 cycles per minute. At one point, I placed a fingertip on the monkey's coccyx. With minimal pressure, I was able to stop the parietal bone motion.

Now we had evidence of a system that could move parietal bones rhythmically - and be stopped by pressure on the coccyx. This and a multitude of other factors caused me to deduce that the coccygeal pressure influenced the parietal motion via the hydraulic force of cerebrospinal fluid (CSF) moving through the dural membrane and myofascial system related to the spinal column and the cranium.

My first inkling that such a hydraulic system existed came some years earlier during a neck surgery I assisted. The lead surgeon had removed the spinous processes and part of the laminae of the middle cervical vertebrae (C4 and C5) in order to expose the meningeal dura mater and keep it intact. At that time, I witnessed a rhythmical rise and fall of CSF pressure at about eight cycles per minute. It became clear that a fluid pressure deep to the dura mater was causing its continual movement. This fluid had to be cerebrospinal, and its volume had to be increasing and decreasing cyclically. Why hadn't this phenomenon been noticed in surgeries before? The answer is surprisingly simple: In most cases, the dura mater was incised. (Fortunately, that's not always the case.) I recently received a letter from Professor Charles Probst, a prominent Swiss neurosurgeon. He reported seeing,

"... without any doubt, rhythmical spinal cord movements with a four to 10 cycle-per-minute rhythm. This rhythm is corresponding to that of cerebrospinal fluid, visible very well with the subarachnoid space being opened. All these movements have quite another frequency than those of the pulse-beat [heart] and respiration! This is all, I can tell you, based on our own experiences in about 20,000 neurosurgical operations (11,000 cranial, 9,000 spinal)."

In the case of lumbar-puncture procedures, when the needle enters the CSF compartment, the fluid enters the manometer via the needle and an elbow apparatus. When the fluid rises to its peak pressure, a valve is opened to take a specimen. It was generally assumed that the CSF specimen that was removed accounted for the reduction of pressure in the manometer. Any cyclic drop in fluid pressure was thus overlooked.