All posts in Articles by Dr. Tucker

Muscle Imbalance

Combinations of muscle weakness and tightness cause musculoskeletal pain. The most difficult part of treatments are to the muscles that become inhibited, (restrained, blocked, or suppressed) because this requires patients to perform exercise at home on there own. Muscle inhibition is common in the neck, low back, and extremities.

Inhibition refers to the inability of a muscle to contract fully on demand. This inhibition is a neurological response and manifests particularly at the extreme ranges of motion – when the muscle is contracted fully. A muscle may have strength at the mid-range, but be very weak when moved into a shortened position; this creates instability at the joint. When the body senses instability, other muscles tighten up as a form of protection. To improve these muscle and joint imbalances I expect my clients to perform the exercises that I prescribe as part of my treatments.

Inhibitied muscles usually generate hypertonicity/tight muscles in adjacent regions of the body (low back & hip, neck & shoulders)). In other words, the relationship between weak and tight muscles is reciprocal. Inhibition is frequently found in muscles resulting from injury, inflammation or pain and that inhibition or weakness leads to reciprocal facilitation of its antagonist(s) muscles.

When a muscle has been over-stressed or over-worked, the result is altered feedback from the nervous system. This causes a reduced capability for the muscle to contract, from the instability through full physiological range. The end result is an inability for the muscles to properly stabilize joints. This is a major point that I want you to understand. I teach you stability (strength) exercises to train the weakened muscles to hold the joints in place again.

Again, please understand, hypertonicity in a muscle leads to blockage(s) or weaknesses in other muscles close by. Inhibited (weak) muscles are capable of spontaneous strengthening when the inhibitory reflex is identified and remedied (most commonly through joint or soft-tissue manipulation).

Muscle hypertonicity/tightness/spasm generates inhibition in surrounding regions of the body, and so spasm is treated first using the Deep Muscle Stimulator, warm laser, manipulation and deep soft tissue massage therapy.

The inhibited (weak) muscles are treated with exercise, rocker boards, wobble boards, and other tools. I prefer to teach clients bodyweight exercises, resistance band exercises, stability ball maneuvers and kettlebell training.

I pay a lot of attention to posture because the postural muscles tend to be short, tight and usually hypertonic. This is why some times I will teach you to stretch, and other times I will teach you to strengthen your muscles.

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Laser

Laser therapy gives consistent clinical results, with changes that are noticeable in just a few office visits. Laser effects the tissues to produce positive results such as faster wound healing and pain reduction. It is one of the best modalities to help relieve acute and chronic pain and repair injured/damaged tissue.

Just as photosynthesis creates energy for plants, the absorption of the laser light photons by cells in your body causes increased production of cellular energy to improve the rate and quality of healing.

Some of the effects include increased levels of endorphins and anti-inflammatory benefits.

Applicable conditions of laser therapy
1. Low back pain
2. Wound healing
3. Dermatological conditions
4. Temporo-mandibular Joint Dysfunction
5. Frontal and maxillary sinus inflammation
6. Rotator Cuff injuries (shoulder pain)
7. Epicondylitis (elbow pain)
8. Small joints of the hands
9. Trigeminal Neuralgia
10. Bell’s Palsy
11. Neck pain

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Anti-inflammatory Diet

Regarding the Anti-inflammatory Diet: The whole point of the avoid list is to remove as much of the inflammatory foods and commonly allergenic foods to give the body a much needed rest and hopefully begin to rejuvenate. This is similar to an allergy elimination technique. For example, you know that wheat & dairy products are everywhere and one of the most allergic foods. These foods need to be eliminated first.

I have my patients follow the anti-inflammatory diet for a month and then add 1 food every few days. If eggs ( I also know they are a perfect protein food) are what you miss the most… make it the first thing to try. Patients find this sooo easy to do themselves.

I want my clients to feel responsible and enpowered to take charge of their own health using nutrition. Each day I hear new clients come in and share with me their disappointing stories of things they have already tried. After they have been on my anti-inflammatory diet program for a month (sometimes sooner), they come to find out they had an exaggerated immune reaction (IGG). Clients get the message quickly without any nagging from me. Please don’t think I’m going to be upset with you for not following the diet to a tee. I love watching patients teach themselves their own lessens.

This is an example of one of the product protocols I use to help ‘miracles’ occur in my patients.

Choice 1: Ultraclear/Advaclear 28 day from Metagenics. This is a great maximum bang for the detoxing buck.

Choice 2: Xymogen OptiCleanse GHI, Mitochondrial Kit 28 day cleanse. Both have simple directions.

I keep track of patients progress using the body composition analysis. I personally evaluate and work with each patient to ensure weight loss progress.

Chronic pain patients can have slower pogress….sometimes several years and patience is the hardest thing to do. I look for the slow and steady slope with my chronic pain patients.

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About Gymstick

by Jeffrey H. Tucker, DC, DACRB

My background is in Chiropractic, helping people get out of acute and chronic pain. I have spent twenty five years in private practice teaching clients how to decrease pain and improve their health. It has been a great job, and it is something I see myself going for the rest of my life and career.

About fifteen years ago I started taking a post graduate program at my Chiropractic College to pursue my first passion, which was musculoskeletal rehabilitation. I continued to work as a Chiropractor, but I started including more exercise therapy and nutritional therapy into my practice. In essence, I strive to become a Wellness Consultant rather than just dealing with people in pain.

Many of my clients are not ready for the gym yet and need a program that could transition them to the gym. Many of them get injured while working out and training. Sometimes clients have to take a step backward to move forward and sometimes their voyage is not so much about discovery as rediscovery of lost flexibility, strength or speed. I developed a progression of core exercises that I was teaching to my patients to help them get out of pain, create muscle balance, symmetry and strength. Eventually, I started teaching an exercise class at Dance Studio No.1 in west Los Angeles. Many clients needed a class to progress to stronger levels. I started teaching with the intention of preventing future back problems and prepare them to get into better shape and fitness. The people that came for help in improving their fitness levels for everyday life really liked the way that I presented things. So, I have continued with this program over the past four years.

There are two distinct yet interdependent muscle systems in the body, the stabilization system (stabilizers = local muscle) and the movement system (mobilizers = global muscle). Both the local and global muscle systems must integrate together for efficient normal function. Neither system in isolation can control the functional stability of body motion segments (vertebrae and bones). The stabilizers assist postural holding, anti-gravity, and joint stability (support) function. These are prone to inhibition and weakness. The mobilizers assist rapid accelerated movements like we use when training with Kettlebells. The mobilizers are large and superficial muscles (the ones we see on our body). They provide range of movement, and produce high force or power. The mobilizers are prone to over activity and tightness. Once a movement segment has lost functional stability and has developed abnormal compensatory motion, stabilizing structures (both connective tissue and contractile) around these joints become less stiff and more flexible, more lax and have more “give” thus making these segments at risk of abnormal stress and strain.

There are specific indications for low load training of the muscle system. Clients will present with mild discomfort to intense pain during normal daily functions; unguarded movements cause sharp pain; they have very specific pain and/or stiffness in muscles and joints; symptoms associated with static positions and postures (sitting, standing and lying). Some clients come knowing they have unstable backs; some have a history of bad backs. The name of my exercise program is Progressive Body Movement (PBM). PBM is actually a priority system of building strength and flexibility. It’s a very rational method for getting people out of pain, and keeping them out of pain by creating spinal stability and strength.

Many of my clients need to learn what exercises they can do without hurting themselves. As soon as they would start yoga, or Pilates or weight training exercises, they would get a flare up in there low back, shoulder or neck. They had become afraid to exercise because they always hurt themselves afterwards. These clients needed to exercise just so they could get ready to exercise. I learned how to progress people from low load body weight exercises to bands and free weights and Kettlebells.

My tag line is, “We were all given a lifespan, let’s create a healthspan.”

My clients enjoyed the way that I was teaching because it was very much back to old school stuff, low tech floor work, bands, balls, and bodyweight maneuvers. I don’t use any fancy gadgets or machines. I progress them to free weight and Kettlebells. They really liked that, and I made it fun for them.

The key to helping clients and what you can do on your own is practice form before function, and uni-planar motions before multi-planar motions. I have learned to see simple compensations when evaluating client’s movement patterns. I use isolation for innervation of the system and to improve function. But, isolation is great for testing & rehab, not training.

We need to physically train the stability muscles. Strengthening exercises alone will not likely affect the timing and manner of recruitment of muscles during functional activities. With proper stability it makes using heavy weights such as Kettlebells safer and enhances performance.

Recently, a band exercise device called the Gymstick has come in to my rehab and wellness practice. I was in San Francisco at a workshop on the hip, being taught by a British instructor. I asked him if he had any new equipment that he was using in his rehab facility. He said that they were doing a lot of creative exercises with a device called the “Gymstick” and that it was great for core training.

So, when I got home I did my research and ordered the Gymsticks on-line. When they came I started using it for five to ten minutes as part of my own workouts. The Gymstick came with a visual poster of exercises, and I ordered a DVD. I liked it so much I ordered more for my clients and to use in my classes. My clients and students really like it. So, I thought, “I want to become a distributor of this and create an opportunity for groups of people to have Gymstick classes.”

I have been to many workshops and conferences over the years. I have heard some of the best trainers and coaches in the U.S. and none of the presenters I met ever mentioned the Gymstick. It is popular in Europe and just not known here in the United States yet.

To have a great foundation for weight lifting I recommend band work as well. I recommend slow, low effort repetitions and only move through the range that the weak link can be actively controlled. Perform 20-30 slow repetitions or approximately 1- 2 minutes of a given exercise. Initially, when these low load exercises ‘feel’ difficult or high-perceived effort is used then it is likely that that muscles slow motor unit is inefficient and you need to do these maneuvers. If an exercise with body weight, Gymstick, or other bands looks easy and feels easy, then it means there is better facilitation of slow motor unit recruitment. It is best to do local muscle dominant recruitment (Gymstick) on different days than strength training days. This makes it a good tool for rest days.

I have personally taken it on to get the word out there and really promote Gymstick, and the way of training with them. In fact, I don’t feel like I have to sell Gymstick. They sell themselves. As soon as you get someone to come to a class, they are hooked. It’s amazing. The results are quick and fast for stretching, strengthening, and functional training!

One of my clients, she came into my program a size 12 and she’s an 8 now. She feels very happy wearing clothing she hasn’t fit into in a long time. She enjoys feeling healthier and more flexible.

Gymsticks are going to be a great tool for me to make a niche in the market and offer new classes among those training in Los Angeles. It has always been my passion and goal to educate people about diet, nutrition, body work, and training. Los Angeles is very much a Pilates and Yoga town. We have lots of hard core gyms as well. I applaud all of these, but I think the Gymstick offers a good balance for motor control training and increasing a muscle recruitment challenge, as well as improving flexibility, thus increasing the potential to generate force and power.

I am into minimal equipment and basics. I like floor work, Kettlebells, dumb bells and bands for overload training, power and endurance.

Why am I hoping to go to get people more into Gymstick and kettelbells or even body strength training, opposed to using machines? I have never been a proponent of weight machines. I encourage people to get off the machines and get into functional fitness where you are standing and you need to ground yourself and you need to use your core strength and stability. It’s NOT about sitting in a machine and pressing as hard as you can, because that’s not going to do anything except if you are sitting down and pressing against somebody. That’s not real life. Real life is: you’ve got to chase a child around a park or mall; you need to lift and carry heavy objects; and you have sit to long in awful chairs. Gymstick provides low load training and exercises that can optimize slow motor unit recruitment; efficiently teach you to really internalize your power and bring it out when you need to.

Gymstick will help you activate the deeper, more local muscles of the body that help you achieve increasing the segmental stiffness of the spine and decreasing excessive inter-segmental motion and maintaining muscle control during low load tasks and activities. In contrast, using the Kettlebells will help you achieve high physiological load. Both the local muscles and the outer muscles contribute to both stability and mobility roles. The combination of Kettlebells and Gymstick repetitions will help give you endurance and stamina. There is no longer a need to rely on machines, every training session can be done at home.

I think the combination of Gymstick and Kettlebells is so functional. Clients are creating their own drills that are sport specific.

“Gymsticks are here and you don’t know what they are right now, but I am an instructor and I will show you!” (See info for class schedule)

Dr. Jeffrey Tucker: “I have studied with some of the best teachers in the musculoskeletal and nutrition world. I continue to take post graduate courses and seminars and get some more certifications.” You can visit Dr. Tucker at www.DrJeffreyTucker.com where you can purchase the Gymstick he mentions.

My classes have progressed to a more general fitness population that wants to have a more challenging work out. They know that I push them quite hard, but with what I call “my watchful eye” making sure that they maintain good form. They know that I want them to succeed at their goals. Whether their goal is to get out of pain from a sports injury, loss weight, or to become fit, I am going to give them my undivided attention in getting them their safely and uninjured, but I don’t expect anything less than one hundred percent of their effort.

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Injury with Low-Speed Collisions

by Jeffrey H. Tucker, DC, DACRB

Can pain and dysfunction develop from a low-velocity collision without attendant injury? “Low-speed” impact refers to 1-2 miles per hour and goes up to 20-25 mph. “Moderate speeds” are 25-40 mph and “high speeds” are 40 mph and over.

Jackson16 and States13 estimate that 85 percent of all neck injuries seen clinically result from automobile crashes, and of those due to such collisions, 85 percent result from rear-end impacts. Morris reported that rear-end impacts of as little as five mph can give rise to significant symptoms.17 The dynamic and vehicle factors that contribute to rear-end collision injury are:

  • vehicles involved
  • speed differential
  • vehicle weight
  • location of impact
  • direction of impact
  • head restraint location
  • seat failure
  • seat back angle
  • seat back height

Wiesel states that approximately 10 percent of the occupants of the stricken vehicle in rear-end automobile collisions will develop whiplash syndrome.10 Approximately 10-15 percent of patients suffering from cervical soft tissue injuries following motor vehicle accidents fail to achieve a functional recovery.

Emori and Horiguchi state: “Whiplash, in some cases, persists for years but usually no obvious symptoms show up with radiological or other quantitative diagnostic techniques.”9 Our present technology does not permit precise identification of deranged soft tissues.

Research quoted by White and Panjabe11 states that an eight mph rear-end collision may result in a two g force acceleration of the impacted vehicle and a five g force acceleration acting on the occupant’s head within 250 msec of impact. (One g equals an acceleration of approximately 32 ft./sec.) Car crashes happen in literally one/two eye blinks. The point is that the head and neck experience more g forces than the car in low-speed impacts.

Kenna and Murtaghsay state: “It is wrong to assume that maximum neck injury occurs in a high-speed collision; it is the slow or moderate collision that causes maximum hyperextension of the cervical spine. High-speed collisions often break the back of the seat, thus minimizing the force of hyperextension.”21

A major dilemma exists for the auto manufacturer, insurance companies, and the consumer of autos. Each would like the vehicle to provide the maximum protection for the occupant with the minimum material damage to the vehicles during a collision. Stiffer cars with spring-like rear bumpers that increase the rebound have less damage costs, however the occupant experiences an increased neck snap and the potential for greater injury. When a car gets struck from the rear by another auto, the very first thing that happens is the struck car is accelerated. The occupant of the struck care experiences higher speeds as it attempts to “catch up” with the car. Navin and Romilly state: “This relative movement of the head to the shoulder during the rebound is the likely cause of neck injuries as this is the point at which dynamic loading of the neck will be maximum.”8 They conclude: “Of major concern to researchers is the lack of structural damage present below impact speeds of 15 kmh. This indicates that the bumper system is the predominant system of energy absorption between the impact and the occupant. It was also observed that deflection of the seatback tends to pitch the occupant forward, with the shoulder displacement leading the head. This relative head to shoulder motion is the likely source of whiplash injury.”

Research has shown that high impact forces are transmitted directly to the occupant in low-speed impacts and that the vehicle does not begin to crush until impact speed exceeds 15 or 20 mph.1,13 Severy1 demonstrated a 10 mph impact produced total collapse of only 2 1/2 inches in the rear structures of the impacted vehicles. Therefore, minor property damage does not necessarily equate to minor injury. The most important question is not, “What is the damage to the vehicle?” but, “What was the acceleration to the vehicle that you were in?” Injury will occur because of the acceleration differences between the different inertial parts of the occupant’s body, especially from the person’s head, versus trunk inertial acceleration differences.

Navin and Romilly have demonstrated that, “Rear vehicle impacts between 5-12 mph indicate that some vehicles can withstand a reasonably high speed impact without significant structural damage. The resulting occupant motions are marked by a lag interval, followed by a potentially dangerous acceleration up to speeds greater than that of the vehicle.”8

Severy1 demonstrated conclusively that seemingly harmless low-speed rear-end collisions were capable of producing damaging forces to the head and neck. Severy and associates recorded head accelerations as great as 11.4 g. Most research evidence suggests that the major injuries are due to the hyperextension phase of the cervicothoracic spine.

Factors that Influence the Extent of Injury

Headrests are the best protection in rear-end collisions. However if the headrest is set too low, the head is able to roll over the top of the headrest, producing even more hyperextension.2

Emori’s experiments were to simulate relaxed necks of unexpected passengers in struck vehicles. Without a headrest, the neck extension can become almost 60 degrees, which is a potential danger limit of whiplash at collision speeds as low as two mph.9

The exact position of the head at the moment of impact is important to know. If the head is turned, the injury will be greater on the side it is turned to. When head rotation is present, the pattern of tissue injury is potentially more severe.19

A surprise collision will usually cause more injury because the ligaments will be injured more than the muscles. When a person knows they are going to be struck, they will tense up the muscles and therefore injure the muscles first. MacNab states: “In impacts up to 15 mph the right front seat passenger stands in greater danger of injury than does the driver, because the driver can brace himself to some extent by holding onto the steering wheel.”14

Common predisposing factors include degenerative joint disease and spinal stenosis. The potential for injury is increased because the neck is less resilient.

The seatback stiffness requires investigation. The harder/stiffer the seatback the less forward acceleration and therefore the less injury. The less stiffer the seatback the more forward acceleration and therefore the risk of increased injury.

Jackson states: “The belt has very little if any deterring effect on the cervical spine as the head and neck continue forward motion. Even the addition of a shoulder harness will not relieve but will only increase the forces which must be absorbed by the head and neck, although such a harness may prevent contact injuries.”12 Seat belts save lives by preventing occupants from going through the windshield, but they contribute to the neck injury.

The Office of the Chief Scientist (London), Department of Health and Social Security, had this comment regarding seat belts in 1985: “We predicted an increase in the case of two injuries: sprains of the neck and fractures of the sternum. Both were confirmed. The other apparent increase in a major injury which was not predicted was abdominal injuries of organs other than the kidney and bladder.”

Clemens and Burrow20 report that any shoulder restraint mechanism in front-end collision increases the degree of cervical flexion, with potential for injury.

The car fender or bumper is designed to avoid or reduce damage in a low-speed collision. It is not a safety device to prevent or reduce injuries to people in the car. The government requires bumpers on passenger cars to prevent damage to the car body and parts, such as headlights, tail lights, grille, hood and trunk latches, at barrier impact speeds of up to 2 1/2 mph. This is equivalent to a five mph crash into a parked vehicle.

Injuries Sustained

Myofascial structures can be stretched; asymmetric increase in muscle tension can develop, causing altered joint movement; the facets can become affected, and posture altered.

MacNab did whiplash type research with monkeys and was able to describe these injuries:3 slight muscle tears of the sternocleidomastoid ruptures; ruptures of the longus colli; retropharyngeal hematoma; esophageal hemorrhage; cervical sympathetic plexus lesion; tearing of the anterior longitudinal ligament.

Dunn and Blazer7 concluded: “The most injurious head deflection in an acceleration injury is hyperextension. Even though sustained in low-velocity, rear-end collisions, this acceleration injury can produce forces significant enough to produce musculoligamentous tears with resultant hemorrhage and even disk disruption and avulsion fractures of the vertebral bodies. In addition, the integrity of the apophyseal joints may be violated.” They also conclude that in head-on collisions (flexion injuries): “In low- velocity flexion accidents, because the chin strikes the chest when the full range of physiologic flexion has been reached, minimal damage occurs.”

Prognosis

If present, degenerative changes should be noted as they may affect the prognosis. A claim of aggravation of a known pre-existing injury may occur after a low-speed impact.

Hohl4 and Hohl and Hopp5 found that complaints of interscapular pain, upper extremity pain, and numbness carried a poor prognosis, as did findings of a sharp cervical curve reversal, or restricted motion at one level on flexion/extension radiographs. Greenfield and Ilfeld15 also noted that shoulder pain and arm and hand pain indicated slower progress toward recovery, and that if upper back pain and interscapular pain present, a longer and more intensive treatment program was needed.

Norris6 found that the presence of objective neurological signs, significant neck stiffness and muscle spasm, and/or pre-existing degenerative changes adversely affected the outcome.

Hohl did a seven year follow-up after injury of patients without previous x-ray evidence of disc disease and found that 39 percent had developed degenerative disc disease at one or more disc levels since injury.4

Discussion

We enjoy the thrill of driving bumper cars travelling at approximately 1-2 mph without a head restraint and without adequate seat belts at amusement parks. We like the feel of speedy roller coasters that whip our head and neck, and push our body to provide a sense of increased g forces. And if we should experience soreness or discomfort after these rides we have the ability to continue to go on and have fun the rest of the day. We relax and tell ourselves that it will go away. And so it could be with many of our patients involved in low-speed, low-impact collisions. The doctor must reinforce to the patient that it will go away. If the pain doesn’t go away we must be able to discuss the mechanisms of injury and substantiate the presence of injury/illness.

Insurance companies and the general population have a skeptical attitude about these types of cases. Television commercials are polluting the juries viewpoint and the public is frustrated with the cost of insurance premiums. Ask people what they think of rear-end collisions, jury awards, and attorneys. They will respond with a different value than 10-15 years ago.

We need to make sure that patients are being sincere in their complaints. Credibility on the patient’s side is very important. The issues of the low-dollar damage amount and low speed will come up. The doctor has a credibility image to maintain as well. Adjustors will look at the doctor’s records and the treatment plan; insurance companies want to see a treatment plan. The important issues are the type of treatment, the cost of treatment and the length of time. The diagnosis is not indicative of the extent of the injury. Reports to the adjustor should supply the diagnosis and prognosis. At this point it does not appear that the insurance industry cares that chiropractic can substitute for more expensive care.

The key to documentation is showing that the patient is receiving benefit from the treatment (getting pain relief and improving functional capacity). Documentation must justify the treatment for the injury. It must show that treatment was actually rendered, and substantiate the injury by detailing the subjective and objective findings on the examination; justify treatment by showing decreases in pain and suffering; increasing recovery time; decreasing the likelihood of complications; increasing the function of the person during the recovery.

References

  1. Severy DM, Mathewson JH, Bechtol CO. Controlled automobile rear- end collisions, an investigation of related engineering and medical phenomena. Can Serv Med J, 1995;11:727.
  2. Ewing C, Thomas DJ. Human head and neck response to impact acceleration. Navel Aerospace Medical Research Laboratory Monograph, #21, Aug. 1971.
  3. MacNab I. Acceleration injuries of the cervical spine. J Bone Joint Surg, 1964;46A:1797-1799.
  4. Hohl M. Soft tissue injuries of the neck in automobile accidents. J Bone Joint Surg, 1974;56A:1675-1682.
  5. Hohl M. Hoop E. Soft tissue injuries of the neck: II. Factors influencing prognosis, abstracted. Orthop Trans, 1978;2:29.
  6. Norris S. The prognosis of neck injuries resulting from rear-end vehicle collisions. J Bone Joint Surg, 1983;65:9.
  7. Dunn EJ, Blazer S. Soft tissue injuries of the lower cervical spine. Instructional course lectures, Am Academy of Ortho Surgeons, 1987;36:499-512.
  8. Navin FP, Romilly DP. An investigation into vehicle and occupancy response subjected to low-speed rear impacts. Proceedings of the Multidisciplinary Road Safety Conference VI, June 5-7, 1989, Fredericton, New Brunswick.
  9. Emori RI, Horiguchi J. Whiplash in low-speed vehicle collisions. Vehicle Crash-Worthiness and Occupant Protection in Frontal Collisions. Society of Automotive Engineers, Feb. 1990.
  10. Wiesel SW, Fetter HL, Rothman RH. Neck Pain. Charlottesville, VA. The Michie Co., 1986, pp 10-26.
  11. White AA, Panjabi MM. Clinical Biomechanics of the Spine, New York, JB Lippencott, 1978, pp 153-158.
  12. Jackson R. The Cervical Syndrome. Springfield, IL. Charles Thomas Co., 1977.
  13. States JD, Korn MW, Masengill JB. The enigma of whiplash injuries. Proceedings of the 13th Annual Conference of the Amer. Assoc. for Auto. Med., 1969.
  14. Rothman RH, Simeone, FA. The Spine, 2nd edition. W.B. Saunders Co., p. 648.
  15. Greenfield J, Ilfeld FW. Acute cervical strain: evaluation and short-term prognostic factors, Clin Orthop 122:196, 1977.
  16. Jackson R. Crashes Cause Most Neck Pain. Amer. Med. News, Dec. 5, 1966.
  17. Morris F. Do head restraints protect the neck from whiplash injuries? Archives of Emergency Medicine, 1989, 6:17-21.
  18. Rutherford W, Greenfield T, Hayes HR, Nelson JK. The medical effects of seat belt legislation in the UK. Dept. of Health and Social Security, Office of the Chief Scientist, Research Report #13, 1985.
  19. MacNab I. The “Whiplash Syndrome.” Orthop Clin North Am 1971;2:389-403.
  20. Clemens HJ, Burrow K. Experimental investigations on injury mechanisms of the cervical spine at frontal and rear-end vehicle impacts (from the German). Acta Ortho Unfall-Chir, 1972;75:116-45.
  21. Kenna C, Murtagh J. Whiplash, Australian Family Physician, June, 1987; 16:6.
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The Psoas and Iliacus: Functional Testing

by Jeffrey H. Tucker, DC, DACRB

The psoas has segmental attachments posteriorly to all lumbar transverse processes, anteriorly at all lumbar vertebral bodies and to all lumbar discs except L5-S1 disc.1,2 Fibers that attach on the transverse processes are named the posterior fasciculi fibers. They range from approximately 3-5 cm in length. The fascicles that attach to the discs and bodies are called anterior. They are approximately 3-8 cm in length. The fascicles run inferolaterally to reach a central tendon, where they descend over the pelvic brim as it passes deep into the inguinal ligament and anterior to the capsule of the hip joint, sharing a common insertion with iliacus to the lesser trochanter of the femur.3 The tendon is separated from the pubis and the hip joint by a subtendinous iliac bursa. Along the pelvic brim, the lateral fibers of the iliacus and the fibers of the psoas come together. This is referred to as the conjoint tendon of the psoas major and the iliacus. Because the psoas muscle attaches to the anterior portion of the transverse processes of all lumbar vertebra and intervertebral discs, it can contribute to mechanical lumbo-pelvic-hip dysfunction and pain.

Proximally, fibers of the diaphragm and psoas are inter-related. The diaphragm’s medial arcuate ligament is a tendinous arch in the fascia of the psoas major. Distally, the psoas fascia is continuous with the pelvic floor fascia, especially the pubococcygeus.2

Based on his anatomic studies, Bogduk does not believe the attachment of the psoas muscle has a long enough level to act as a prime flexor of the lumbar spine. Bogduk’s analysis indicates that in the standing erect posture the psoas exerts an extensor moment on the upper lumbar spine and a flexor moment on the lower segments. The major forces acting on the lumbar spine are compression and anterior shear forces. The psoas has a primary stability role at the lumbar spine for axial compression and it has minimal movement function on the lumbar spine.4

Local Stability Function Local Stability Dysfunction
Muscle stiffness to control segmental translation.

No or minimal length change in function movements.

Anticipatory recruitment prior to functional loading provides protective stiffness.

Activity is continuous and independent of the direction of movement.

Uncontrolled segmental translation.

Segmental change within cross-sectional area.

Altered pattern of low threshold recruitment.

Motor recruitment timing deficit.

In 1998, Dangaria and Naesh demonstrated that there is a significant decrease in the cross-sectional area of the psoas at a segmental level in patients with sciatica. The study determined there is an association between wasting of psoas and multifidus muscles observed on MRI scans in patients presenting with unilateral low back pain.

They took 50 consecutive patients presenting to a back pain triage clinic with unilateral low back pain lasting more than 12 weeks. They found the cross-section area of the psoas major was ipsilaterally decreased in unilateral lumbar-disc herniation. The reduction in the cross-section area (CSA) is positively correlated with the duration of continuous sciatica, rating of pain, self-reported function and the presence of neural compression.7

The results and data analysis compared the CSA between the symptomatic and asymptomatic sides. There was a statistically significant difference in the CSA between the sides. There was a positive correlation between the percentage decrease in CSA of the psoas on the affected side and with the rating of pain, reported nerve root compression and the duration of symptoms. Hodges also had reported on an association between decrease in the CSA of multifidus and the duration of symptoms.

Atrophy of multifidus has been used as one of the rationales for spine-stabilization exercises. They concluded the evidence of coexisting atrophy of the psoas and multifidus suggests that a future area for study should be selective exercise training of the psoas.

Exercises: Clients who do not suffer from an isolated psoas or iliacus muscle with a local stability dysfunction (meaning the muscle is allowing joint instability) can perform the following bodyweight exercises:

  • Perform sit-ups with the hips and knees flexed. The iliopsoas participates as strongly during sit-ups with the hips and knees flexed as when they are extended.
  • Perform push-ups. The psoas is activated more than the abdominals during push-ups.
  • Seated hip flexion. Maximum activity of the psoas occurs with resisted hip flexion. This maneuver can be performed with the use of resistance bands (seated or supine).

Also, make sure the client maintains a neutral lumbar spine. However, if compression and shear are the sources of your client’s pain, avoidance of these three exercises is necessary. Selective exercise training, described as low-load exercises would be indicated.

Yoshio, et al., concluded that the primary role of the psoas major was for lumbar stability and that the psoas major contributed very little to hip flexion. He explained that the primary role for the psoas major is at the hip for stability. This was achieved through maintaining the femoral head in the acetabulum.8 The psoas can be said to be clinically deficient if it fails to segmentally hold the vertebrae in place at the level of pain in patients who have segmental lumbar dysfunction (hypermobile segments).

Low-load exercise facilitation of psoas is directed to the spinal neutral postures and segmental axial compression and spinal rotatory control, not hip flexion movements. Specific segmental psoas facilitation will improve lumbar segmental control.5

Action of psoas: The local stability role of psoas is to longitudinally pull the head of the femur into the acetabulum, with the spine fixed and supported in neutral alignment to produce axial compression along its line of pull.

Training of psoas: This can be practiced side-lying, incline sitting, supine, prone or standing; for example, while supine with the lumbar lordosis passively supported in neutral by the patient’s hands, a folded towel and the legs comfortably apart. If side-lying (with the dysfunctional side up), both legs are flexed with the spine and pelvis in neutral alignment in terms of tilt and rotation. The top leg is supported horizontal, with the spine, pelvis and upper trunk all neutral. Have the client shorten the leg or “pull the hip into the socket” or “suck the hip into the socket.” This will create a barely perceptible movement and yet will be felt by the client. This can be performed for 10-second holds and 10 repetitions.

Testing of the iliacus and hip capsule: Have the client stand against a wall, with heels (feet) apart, and shoulders and head touching the wall. Normal is the ability to posterior tilt to touch the small of the back against the wall. If the client cannot posterior tilt by flattening their back onto the wall with the feet apart and the hips and knees straight, but can do so with knees bent and the hip flexed, the restriction could be shortened iliacus or the anterior hip capsule. By bending the knees and unlocking the hips, this unloads the tension from the iliacus and the anterior hip capsule and allows the pelvis to posterior tilt.

Iliacus/hip capsule correction: The abdominal and gluteal muscles are contracted to posterior tilt the pelvis and flatten the back onto the wall. While maintaining the posterior tilt and flat-back position, the knees are slowly straightened (hips extended) to slide the body up the wall.

At the point that the back cannot be held on the wall, cease sliding up and actively restabilize onto the wall. Hold this position for 20 to 30 seconds, and repeat the maneuver three to five times. To isolate the right or left side of a weak iliacus muscle, ask the client to raise one leg at a time while maintaining a flat back against the wall. If an asymmetry exists, spend time on the weaker side.

Clinical application to this information is that the “overhead bilateral arm pull” test, as used in the Sacro-Occipital Technique (SOT) to test for a short or tight psoas, does not often correlate to the modified Thomas test.

Hip flexor muscle-length tests are performed by using the modified Thomas test.

Test: Patient is supine, with buttocks at the end of the table. The patient flexes one knee and holds the knee to the chest with both arms. The free leg hangs down to the floor. The position of the lumbar spine is flat on the table, not arching into extension or flexion.

Observe: If the patient has tight hip flexors, the thigh/hip will rest in some flexion or the lumbar spine will extend to allow the leg to rest on the bed. The modified Thomas test assesses the hip flexors, rectus femoris, quads and ITB muscle lengths. Patient is in the same position as the Thomas test, but should start by standing at the end of the bed and roll back onto it with one knee held to the chest while the other leg dangles off the end of the bed. Check that the lumbar spine is not extended.

Observe the degree of the hip flexion. If above neutral, either hip flexors or rectus femoris are tight. To differentiate, ask the patient to extend their knee. If it falls into more hip extension, the rectus femoris is tight. Also observe for increased tautness in the rectus femoris.

Check relative position of abduction/adduction at the hip and observe lateral structures. The thigh should lie in the neutral position, as if the client was standing. An abducted position indicates that ITB could be tight. On visual analysis, the ITB may present a groove in the lateral thigh. This would support overactive/tight ITB findings.

Check the knee flexion. Ask the patient to flex their knee further. A normal muscle length in quads will allow 90 degrees or more of knee flexion in this position. Watch for compensatory hip flexion. Tibial position also can indicate tightness in the ITB, especially in the distal components. It will be in external rotation if tight. Check the position of the tibial tubercle.

Another take-home value from this article: The supine straight-leg raise used for nerve tension signs also is affected by iliopsoas activity.

Test: Patient performs an active straight-leg raise test (utilizing hip-flexor muscles). Positive for neural tension is radicular pain into the leg before 60 degrees of hip flexion.

Retest: At the point of symptoms, the therapist supports the weight of the patient’s lower extremity while instructing the patient to totally relax their musculature. If the symptoms are alleviated or eliminated, this finding suggests the problem is the effect of shear or compression on the spine from the contraction of the hip flexors and not a true entrapment of the nerve (tethered nerve).

References

  1. Bogduk N, Pearcy M, Hadfield G. Anatomy and biomechanics of psoas major. Clinical Biomechanics, 1992;7:109-19.
  2. Gibbons SGT. A review of the anatomy, physiology and function of psoas major: A new model of stability. Proceedings of: The Tragic Hip: Trouble in the Lower Quadrant. 11th Annual National Orthopedic Symposium. Halifax, Canada. Nov 6-7, 1999.
  3. Gibbons SGT. The model of psoas major stability function. Proceedings of 1st International Conference on Movement Dysfunction. Edinburgh, Scotland. Sept 21-23, 2001.
  4. Bogduk N, Pearcy MJ, Hadfield G. Anatomy and biomechanics of psoas major. Clin Biomech, 1992;7:109-19.
  5. Review course notes: Comerford and Mottram, 2001.
  6. Barker KL, Shamley DR, Jackson D. Changes in the cross-sectional area of multifidus and psoas in patients with unilateral back pain: the relationship to pain and disability. Spine, Nov. 15, 2004;29(22):E515-9.
  7. Dangaria TR, Naesh O. Changes in cross-sectional area of psoas major muscle in unilateral sciatica caused by disc herniation. Spine, 1998;23(8):928-31.
  8. Yoshio M, Murakami G, Sato T, et al. The function of the psoas major muscle: passive kinetics and morphological studies using donated cadavers. J Orthop Sci, 2002;7:199-207.
  9. Christensen K. Neuromobilization Course, May 2007.
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Tensor Fascia Latae and Iliotibial Band – Functional Evaluation

by Jeffrey H. Tucker, DC, DACRB

The tensor fascia latae (TFL) acts through the iliotibial tract by pulling it superiorly and anteriorly. It assists in flexing, medial rotation and abduction of the hip and extension of the knee joint. The TFL arises from the anterior part of the outer lip of the iliac crest, the lateral aspect of the anterior superior iliac spine and the upper part of the anterior border of the iliac wing. Keep in mind that in addition to arising from the iliac crest, the iliotibial band (ITB) attaches into the posterior gluteus maximus muscle in the back. When the TFL and gluteal muscles contract, they increase tension on the band. Often, one muscle dominates the movement pattern causing an imbalance to occur, which may lead to injury. When a muscle imbalance exists, some muscles are short (overactive) and others are long (underactive).1-7

Muscle length imbalance (or muscle weakness) is a common occurrence that occurs in the synergistic muscles in the hip:

Flexors: The TFL becomes short and the iliopsoas becomes a long and/or weak muscle.

Hip abductors: The TFL becomes short; the posterior gluteus medius becomes long (and/or weak).

The difference in the length of two synergistic muscles contributes to compensatory joint motion and the development of movement impairment. The weak muscle (iliopsoas or posterior gluteus medius) usually is associated with pain in the muscle belly, which is noted upon contraction or with palpation. The long muscle (iliopsoas or posterior gluteus medius) synergist will cause the pain to usually occur during hip-joint motion because the pain generator is the faulty control of the head of the femur in the acetabulum. The gluteus medius is the primary frontal-plane stabilizer of the hip. When it’s underactive, the TFL, adductor and the opposite quadratus lumborum (QL) become overactive.1

Shortened muscles over time can become structurally short and mechanically incapable of lengthening to an appropriate level.1-7 Long muscles can become structurally long and incapable of shortening to an appropriate level.5,6 When muscles are incapable of firing correctly, compensation occurs, and this will alter joint motion from its normal path.

If you have been performing the overhead squat maneuver (described in previous articles), you will notice that the knees can drift inward or outward on the descent. The TFL is implicated as being overactive in both the knee moving inward and outward, which may seem to be a contradicting statement. The movement at the knee depends if the foot is in the open or closed chain. In the open chain, the TFL is a major abductor of the femur and is noted as being overactive when the gluteus medius and/or maximus are underactive.1,13,14 The gluteus medius and/or maximus have been shown to be prone to underactivity when the lack of activity leads to synergistic dominance or overactivity of other muscles.1,9,14 Overactivity (synergistic dominance) of the TFL, piriformis and biceps femoris can all stem from or lead to underactivity of the gluteus medius/maximus because they are each a functional synergists to the gluteal complex.1,9,14

In the closed chain, the knee could move inward if the TFL is overactive doing the squat evaluation. The TFL (and the soleus, lateral gastrocnemius, biceps femoris) attaches to the lower leg and has the ability to produce external rotation of the lower leg.13,14 The TFL (and the adductor complex, biceps femoris [short head], and lateral gastrocnemius) affects either the femur and/or the lower leg. When overactive, these muscles can cause altered knee position.14 In conjunction, the medial hamstrings (particularly at the knee), gracilis, popliteus, medial gastrocnemius, and the gluteus medius and/or maximus are muscles which, when underactive, will allow the femur to adduct (internally rotate) and/or the lower leg to abduct (externally rotate).14

The TFL (and biceps femoris [short head] and lateral gastrocnemius) crosses the knee joint (tibiofemoral joint) laterally. When overactive, as compared to the medial structures, it laterally pulls the femur and lower leg closer together in the frontal and transverse planes.14 Without adequate medial support, the knee is virtually pushed inward, resulting in the “knee-inward” compensation during the squat assessment.

The TFL, bicep femoris (long head), piriformis, gluteus minimus and medius all have an effect on the femur and when overactive can cause the knees to move outward during the overhead squat assessment.14

Common Stresses

Intrinsic Factors/Causes of TFL-ITBS

  1. Tightness in the TFL-ITBS. This is detected by performing the modified Ober’s test. The client is positioned in side-lying, with the unaffected side down. The pelvis and spine in neutral alignment and the bottom leg flexed for support. The uppermost leg is extended (although the leg may be flexed as much as 10 to 15 degrees, and the test still will be valid) and needs to be above the horizontal. The hip is laterally rotated and extended, as far as no lumbar extension occurs. Tell the client to actively flatten the waist towards the floor and actively hold the leg in slight abduction and lateral rotation. The knee is not locked and the foot is relaxed. The client is then instructed to slowly lower the leg towards the floor until the iliotibial band hangs on the greater trochanter and cannot lower any further. The key to an accurate test is not letting the pelvis move, either into lateral tilt, anterior tilt or rotation. As the leg lowers, the hip should not flex or medially rotate. It’s essential to maintain the laterally rotated position of the hip. Ideally, the leg should lower into at least 10 to 15 degrees adduction (approximately two to three inches above the floor for females and one to two inches above the floor for males) without loss of proximal control of the pelvis or hip. The iliotibial band lacks extensibility if the leg does not adduct sufficiently.
  2. Myofascial restrictions in the hip and thigh musculature, which will increase tension on the band. The iliotibial band is not sensitive to mechanical stretch. The iliotibial band only becomes sensitive to mechanical stretch in the presence of inflammatory pathology. The client will describe fascial inflammation as “burning outer-thigh pain.” Manual palpation can detect tension in the band. Visual postural analysis reveals a deep groove along the iliotibial band when it’s tight. With the client in the Modified Thomas test position, the tensor fascia latae is tested by adducting the horizontal thigh until the pelvis moves. This should be 15 to 20 degrees. Iliotibial band tightness is confirmed by restricted passive extension/adduction of the thigh with the knee flexed to 90 degrees.
  3. Weakness in hip abductors (common in distance runners).
  4. Weakness or poor control of knee muscles.
  5. Dominance of anterior hip muscles, (TFL) over posterior hip muscles (gluts). Tight hip flexors cause the pelvis to rotate while walking. This leads to one side of the abdominals and one side of the gluteus medius shutting down.
  6. Excessively flat feet or high arches. Poor instep strength is a cause of Achilles tendon inflammation and chronic knee pain from the iliotibial band attachment at the knee.
  7. Bow legs or knock-knees.
  8. Leg-length inequality.
  9. Limited ankle ROM. During the overhead squat if the feet/toes externally rotate, this is usually associated with decreased ankle dorsiflexion and lateral gastrocnemius muscle tightness. During the overhead squat, when you observe the feet turn out, you likely may observe knee valgus (inward knee movement) due to increased hip adduction muscle activity. This must be resolved through mobilization, inhibition and muscle-lengthening procedures before moving up the kinetic chain. The biceps femoris (short head) and TFL also can cause the lower leg to abduct which can perpetuate eversion of the foot/ankle.14

Extrinsic Factors/Causes of TFL-ITBS

  1. Training errors (e.g. excessive mileage, sudden increase in mileage, sudden increase in intensity of training, too much hill work, running on crowned roads).
  2. Worn-out running shoes. Top runners replace their running shoes every 250 to 300 miles. I’ll see clients who wear shoes up to 500-plus miles.
  3. Overstriding.
  4. Failing to warm up or cool down.

Functional Testing of the TFL

Have the client stand two to three inches from a wall with their feet together, with the sacrum and thoracic spine on the wall. The client should be able to contract the abdominal and gluteal muscles to flatten the lumbar spine onto the wall and hold it there. This test reveals the ability to self-correct a lumbar lordosis. If the client can’t posterior tilt the pelvis to flatten back on the wall, then the tensor fascia latae (TFL) and iliotibial band could be the cause. Have the client repeat the test with their feet shoulder-width apart. This unloads the TFL and IT band and enables the client to posterior tilt the pelvis to flatten back on to the wall. To correct this dysfunction, have the client repeat the test procedure with their feet shoulder-width apart, actively posterior tilting the pelvis and holding this position for 20 to 30 seconds and repeat the stretch three to five times. Over time, gradually bring the feet closer together. When the client can do it with their feet together have them rotate the hips out while actively posterior tilting the pelvis. A unilateral shortness of the TFL muscle can contribute to sacroiliac joint problems and restrict external hip rotation and extension. In terms of performance, it affects the swing phase of the leg during sprinting, because it causes the foot to swing out at toe-off and the foot to go medial and pronate at touchdown. This can be the cause of shin splints because of the rapid deceleration.

Treatment and Rehabilitation of TFL-ITB Syndrome:

Acute Phase

  1. Ice.
  2. Anti-inflammatory diet and supplements to reduce inflammation.
  3. Activity modification. Stop the perpetuating factors that caused the irritation.
  4. Sleep with a pillow between the knees to decrease tension on the ITB.

Subacute Phase

  1. Massage, myofascial release techniques.
  2. Address tight areas and trigger points. A foam roll is best for this.
  3. Stretch the TFL-ITBS. The Modified Thomas maneuver is one way to manually stretch the TFL-ITBS. I prefer teaching clients the “standing self-stretch” method. For the right TFL-ITBS, stand in a split-leg stance with the right leg behind the left in a full stride stance. Externally rotate the right foot, leg and hip and maintain weight on the right foot. Raise the right arm straight overhead with the palm facing forward. Place the left hand on the left iliac crest and push with enough pressure from left to right to feel the stretch. Stand with a “tall spine” and slightly rotate the left shoulder anterior. You may need to slightly extend your torso to gain a greater stretch sensation. Hold this pose for 20-30 seconds and repeat this maneuver two to three times. Performing a gluteal bridge with the toes raised with adduction gets a stretch to the TFL as well.

Strength and Stability Phase

  1. Bridging with single-leg raise. Repeat the movement up and down. Build up to one to two minutes of slow continuous movement.
  2. Clam shell. The aim is to strengthen the gluteus medius. Lie on your side with your hips stacked one on top of the other and your legs together with the heels connected. Extend your lower arm, palm up, so that you can rest your head. Now angle your stacked thighs forward 30 to 45 degrees, without changing the position of your spine, which must be still in a straight line from your head to your tail. From this position, pre-contract the gluteus medius and lift the top leg. In the beginning, allow the heels to stay in contact. Do not let the pelvis rotate forward or backward. Lift the thigh up from the hip to its maximum height. Hold it up for 10 seconds and slowly bring it back down. Repeat this 10 times.
  3. Standing with an elastic band around the knees, perform a single-leg/thigh abduction (one at a time) in a semi-squat position. Keep the big toe down on the ground. Build up to one to two minutes of continuous movement.
  4. Step downs. Step down from a 2” to 6” stable step very slowly.

References

  1. Sahrmann SA. Diagnosis and Treatment of Movement Impairment Syndromes. St. Louis: Mosby, Inc., 2002.
  2. Liebenson C. Integrated rehabilitation into chiropractic practice (blending active and passive care). In: Liebenson C, Ed. Rehabilitation of the Spine. Baltimore: Williams & Wilkins, 1996:13-43.
  3. Comerford MJ, Mottram SL. Movement and stability dysfunction – contemporary developments. Man Ther, 2001;6(1):15-20.
  4. Panjabi MM. The stabilizing system of the spine. Part I: Function, dysfunction, adaptation, and enhancement. J Spinal Disord, 1992;5(4):383-9.
  5. Kendall FP, McCreary EK, Provance PG, et al. Muscles: Testing and Function, with Posture and Pain. 5th ed. Baltimore: Lippincott Williams & Wilkins, 2005.
  6. Janda V. Evaluation of muscle imbalances. In: Liebenson C, Ed. Rehabilitation of the Spine. Baltimore: Williams & Wilkins, 1996:97-112.
  7. Sahrmann SA. Posture and muscle imbalance. Faulty lumbar pelvic alignments. Phys Ther, 1987;67:1840-4.
  8. Powers CM. The influence of altered lower-extremity kinematics on patellofemoral joint dysfunction: A theoretical perspective. J Orthop Sports Phys Ther, 2003;33(11):639-46.
  9. Janda V. Muscles and motor control in low back pain: assessment and management. In: Twomey LT, Ed. Physical Therapy of the Low Back. Edinburgh: Churchill Livingstone, 1987:253-78.
  10. Janda V. Muscle strength in relation to muscle length, pain, and muscle imbalance. In: International Perspectives in Physical Therapy VIII. Edinburgh: Churchill Livingstone, 1993:83-91.
  11. Edgerton VR, Wolf SL, Levendowski DJ, Roy RR. Theoretical basis for patterning EMG amplitudes to assess muscle dysfunction. Med Sci Sports Exerc, 1996;28(6):744-51.
  12. Richardson C, Hides J. Closed chain segmental control. In: Richardson C, Hodges P, Hides J, Eds. Therapeutic Exercise for Lumbopelvic Stabilization. A Motor-Control Approach for the Treatment and Prevention of Low Back Pain. Edinburgh: Churchill Livingstone, 2004:221-32.
  13. Neumann DA. Kinesiology of the Musculoskeletal System: Foundations for Physical Rehabilitation. St. Louis: Mosby, 2002.
  14. Vasilyeva LF, Lewit K. Diagnosis of muscular dysfunction by inspection. In: Liebenson C, Ed. Rehabilitation of the Spine. Baltimore: Williams &Wilkins, 1996:113-42.
  15. Fry AC, Smith JC, Schilling BK. Effect of knee position on hip and knee torques during the barbell squat. J Strength Cond Res, 2003;17(4):629–33. Exercise Specialist
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