Author Archives: artefact_admin

Demystifying the Treatment of Strain/Sprain Injuries of the Lower Back, Part 2

Part 1

Examination and Treatment of Low Back Pain

To properly diagnose and treat a low back syndrome, a detailed history, a thorough examination, and an understanding of the pain-sensitive structures and postural and phasic muscles in the lumbopelvic region are necessary.

History

Taking a detailed history is one of the most important aspect of an examination. The practitioner has to find the various clues from the patient’s history and then piece together the exact cause(s) of the patient’s low back pain. Some of the following questions are good to ask the patient: What was the date of onset of your low back pain? Was there a particular incident which caused your low back pain? Did you have a sudden onset of low back pain, or did the pain come on gradually? What exacerbates your low back pain complaints? Is this the first time you have suffered from low back pain?

The examiner should ask about past surgeries, accidents, serious illnesses or blood in the urine. Affirmative answers to these questions may be red flags of possible tumors, infections or visceral disorders, and warrant a referral to a primary doctor.

Observation

As patients walk into the examining room, their gait should be carefully evaluated during the stance and swing phase for muscular imbalances. Do they have a toe in or toe out gait? This may reveal possible medial or lateral hamstring tightness. Do they have a gluteus medius gait? Patients with this type of gait will tilt the entire torso over the midstance femur and will reveal weakness of the gluteus medius musculature. Do they have a gluteus maximus gait? This type of gait will reveal weakness of the gluteus maximus musculature in which the patient’s entire torso will hyperextend over the pelvis during early stance phase.10

Do these patients have a decreased stride length? This may reveal tightness of the hamstrings and hip flexor musculature. Do they have an antalgic lean or favor one leg over the other? When the patients are in the static position, the practitioner should observe for a sway back or lordotic posture. The sway back patient will have a flat lower back with an increase in the posterior curve of the thoracic and thoracolumbar region. Patients will usually complain of pain in the thoracolumbar junction. This posture develops as a result of weak hip flexors and lower abdominal musculature. Patients with a lordotic posture will have an increase in the anterior curve of the low back, caused by tightness of the psoas and erector spinae musculature and weakness of the abdominal and gluteus maximus musculature. Patients with a lordotic posture will usually complain of pain across the low back.

Muscle Testing and Orthopedic Tests

Contract-relax-antagonist-contract stretching of the hamstrings, quadriceps, hip flexors, external rotators and abductor musculature bilaterally is not only effective in treating low back pain, but is also an effective tool in revealing the various muscular imbalances which may be the cause of the pain. Muscle testing hip extension may reveal improper firing sequences as a result of weakness of the gluteus maximus musculature. Double leg raising and lowering and trunk curl sit-ups are useful in evaluating psoas and abdominal musculature strength.

Patients with weak abdominals when lying supine with their legs extended and raised 90 degrees will prematurely arch their back when lowering their legs to the ground. Wilson’s test is useful for revealing tightness in the rectus femoris, psoas and tensor fascia latae musculature. Some of the other useful orthopedic tests are Ober’s test; Trendelenberg’s test; sit-and-reach test; Nachlas’ test; Ely’s test; Valsalva’s test; Kemp’s test; and straight leg raising test. Lower extremity deep tendon reflexes and motor and sensory tests of the lower extremities should be conducted. If Valsalva’s test, Kemp’s test and straight leg raising test continue to test positive, and the patient’s complaints of radicular symptoms in their lower extremities continue, then a referral to a neurologist or an orthopedic surgeon for an evaluation would be warranted.

Treatment

Keys to Treating Low Back Strain/Sprain Injuries

1. Control pain.

2. Increase flexibility of the lumbopelvic musculature.

3. Increase strength of the lumbopelvic musculature.

4. Body must be trained to do certain motions.

5. Decrease emotional stress/depression.

In my treatment protocol, #1-4 will be addressed. Feldenkrais and Thomas Hannah relaxation techniques would be useful for #5 if necessary. Both of these doctors explain how emotional stress can cause voluntary reactions to become involuntary. This can lead to sustained contracture of the erector spinae musculature. The goal is to become aware of this and train your body to regain voluntary control of these reflexes, thereby relaxing the low-back musculature.11

There are three phases of healing: acute phase (1-2 days); repairative phase (2 days – 6 weeks); and a remodeling phase. As soon as the patient with a strain/sprain low-back injury can tolerate range-of-motion exercises, acute therapy should commence to promote a more efficient healing process during the reparative phase.

A recent book on repetitive motion disorders published by the American Academy of Orthopaedic Surgeons cites a histologic study in which Nirschl proposed that overuse syndromes are not an inflammatory process but instead represent failed repair of disrupted connective tissue. Supporting this theory were biopsy samples from tendons of patients with epicondylitis that showed disorganized collagen; pale, haphazardly arranged mesenchymal cells; an excessive amount of matrix tissue; and vascular buds with an incomplete lumen and insufficient elastin. This disorganized mesenchymal tissue has poor potential for healing. Based on these observations, a reasonable goal for healing would be to stimulate an inflammatory mediated process with appropriately oriented fibroblasts (laying down parallel fibers in the tendons, which would increase their strength) and to reduce the amount of matrix tissue through the use of appropriate exercises.12

Mooney states that active release techniques (ART* soft-tissue management system) “is a promising new deep-tissue technique for treating cumulative trauma disorders.”12 A practitioner skilled in this technique can palpate fibrotic lesions in the injured tissues. A fibrotic lesion will predispose this region to hypoxia, ischemia, and will result in a trigger point region with improperly oriented fibroblast fibers. To effectively treat this lesion, the practitioner will trap the lesion, and the patient will take the tissue from its shortened to elongated position. The goals for using this technique are to break up the lesions to allow the muscle to regain its proper length and strength, and to decrease painful symptoms.13When the muscle is properly treated and soft tissue motion is restored, the next goal for treatment is to free up joint motion. Manipulation will be used to free up joint fixations in the lumbar and sacroiliac region.

It has been demonstrated that meniscoids are present in the zygapophysial joints of the spine and contain innervation by C fibers. It seems reasonable that they might become entrapped between the opposing joint surfaces, and gapping of the joint might release the entrapped meniscoid, resulting in enhanced function. More recently, it has been postulated that stress on the capsule of the involved joint alters the afferent nerve traffic from the type I mechanoreceptors so that central control of motion cannot determine the joint’s spatial relationship. This alteration in neural control is postulated to affect the length and tone of the segmentally related muscles, further restricting normal joint movement.6

A high-velocity, low-amplitude thrust technique will cause a 1/8″ gapping at the joint and will free up joint motion. ART and manipulative procedures are very effective treatment tools which free up soft tissue and joint restrictions in the low-back region.

Teaching patients with low back pain a daily effective stretching routine that they can conduct at home will speed up the process of healing and will also prove useful in the prevention of low-back pain after treatment is ended. Using a flex-band 15-20 minutes per day to stretch the hip flexors (see Figures 1.1A and 1.1B), hamstrings (see Figures 1.2A and 1.2B), external hip rotators and abductors (see Figure 1.3), adductors (see Figure 1.4), erector spinae musculature (see Figure 1.5) and quadriceps (see Figure 1.6) will enhance the recovery process.

beg_iliopsoas
Figure 1.1A
Figure 1.1B
gen_ham
Figure 1.2A
Figure 1.2B
gen_ham2
lat_ham
Figure 1.3
Figure 1.4
fmedial_ham
erector_spinae
Figure 1.5
Figure 1.6
quadricep

I find a high compliance rate with flex bands, mainly because of their convenience. They allow you to do more range-of-motion exercises. Exercise balls tend to have a low compliance rate.They are effective tools, but they are too inconvenient and difficult to store at home.

Strength training for the lumbopelvic region should also commence with emphasis placed on strengthening the abdominal musculature, gluteus maximus musculature and quadricep musculature.

Combo therapy is a modality which may prove beneficial in speeding up the healing process of a low back strain/sprain injury. Combination therapy is an effective modality in which the electric muscle stimulation machine is connected to the ultrasound machine, allowing one to direct electric muscle stimulation and ultrasound through the ultrasound head. Ultrasound therapy in a continuous mode is effective for heating localized areas of deeply placed tissues. The effect of heat at a therapeutic level may induce muscle relaxation. Vasodilation also has a direct effect on removal of metabolites, which further decrease muscle excitability and allow relaxation. Electrical muscle stimulation may be used to maintain or gain range of motion and to break down or stretch adhesions. Indirectly, it may also influence pain, particularly when the pain is secondary to muscle spasm.14

Conclusion

Having an understanding of the anatomical and physiological structures of the low back and combining that with a strong biomechanical knowledge of the mechanisms which can cause low back pain are essential for a proper diagnosis of this condition. However, even though one has an understanding of the structures in the low back, the diagnosis can be confusing because of multilevel innervation and the instances where several conditions contribute to the low back syndrome.

Manipulation and ART are two effective tools in freeing up soft tissue and joint restrictions. In this author’s opinion and clinical experience, a low back strain/sprain injury can be appropriately treated when combining ART, a flexibility program utilizing flex bands, and a proper strengthening routine.

References

(includes references from parts I and II)

  1. British Medical Journal April 26, 1997;314:7089, p. 1225.
  2. Fordyce W. Nursing Homes. International Publishing Group, 1996, p. 32.
  3. Cailliet R. Low Back Pain Syndrome, 4th edition. Philadelphia: Davis Company, 1988, pp. 22-24, 76-103.
  4. Cramer G, Darby S. Basic and Clinical Anatomy of the Spine, Spinal Cord, and ANS. Mosby-Year Book, Inc., 1995, pp. 205-217, 251-271, 355-370.
  5. Greenman P. Principles of Manual Medicine, second edition. Baltimore: Williams & Wilkins, 1996, pp. 146-147, 449-456.
  6. Lewit K. Manipulate Therapy in Rehabilitation of the Locomotor System, second edition. Butterworth-Heinemann Ltd., 1991, pp. 14-32, 126.
  7. Kendall F, McCreary E, Provance P. Muscle Testing and Function. Baltimore: Williams & Wilkins, 1993, pp. 133-176, 350-354.
  8. Janda V. Muscle strength in relation to muscle length, pain and muscle imbalance. In: Harms-Rindahl K (ed.) Muscle Strength. New York: Churchill Livingstone, 1993.
  9. Robbins. Robbins’ Pathologic Basis of Disease, fourth edition. Philadelphia: W.B. Saunders Company, 1989.
  10. Michaud T. Foot Orthoses and Other Forms of Conservative Foot Care, Newton, MA, 1997, p. 181-191.
  11. Hanna T. Somatics. Addison-Wesley Publishing Company, Massachusetts, 1988, p. 42-95.
  12. Mooney V. The Journal of Musculoskeletal Medicine 1998, p. 11-18.
  13. Leahy M. Improved treatments for carpal tunnel. Chiro Sports Med 1995; Williams & Wilkins, p. 6-9.
  14. Reid DC. Sports Injury Assessment and Rehabilitation. New York: Churchill Livingstone Inc., 1992, p. 31-64.

Additional information was gathered from the following sources:

  • Liebenson C. Rehabilitation of the Spine. Baltimore: Williams & Wilkins, 1996.

Part 1

Demystifying the Treatment of Strain/Sprain Injuries of the Lower Back, Part I

Part 2

Joshua Dubin,DC,CCSP

Abstract:

A majority of the American population has suffered from low-back pain at some point in their adult lives. Prolonged rest used to be the mode of treatment for lumbar strain/sprain injuries, but this form of treatment leads to atrophy of the lumbopelvic musculature and ongoing low back dysfunction. This author’s goals of treatment for a low back strain/sprain injury are to control pain, restore soft tissue and joint function, and prescribe a good strength training and flexibility program for the lumbopelvic region.

The focus of this paper will be to describe the perception of low back pain; explain the postural and phasic muscles of the low back; detail the biomechanics of the lumbar spine and pelvis when bending forward and returning to the neutral standing position; depict four distinct situations which can predispose an individual to low back pain; and then explain this author’s examination protocol and treatment plan for low back strain/sprain injuries.

Key words: low back pain, rehabilitation, Flex Band ®, chiropractic, lumbar, A.R.T.

Introduction

Low back pain is common in the general population, affecting more than 60 percent of people at some time in their lives and often causing appreciable disability.1 According to an article in a 1992 issue of Business and Health, the average per employee nonspecific back pain disability costs among 12 diverse businesses were $1,000 in direct costs, $800 in hidden costs (lost productivity, temporary replacement hiring, bookkeeping, etc.), and $400 in disability costs for a total of $2,200 per employee.2

This paper will discuss four distinct situations which predispose one to low back pain; normal stress on an unprepared normal low back; normal stress on a deconditioned normal low back; sudden excessive stress on a normal low back; and normal stress on an abnormal low back. A rational strategy for the prevention and treatment of low back pain will be presented.3

Perception of Pain

Nociceptors are receptors located near the skeletal muscles, ligaments, tendons, joints, and fascia of the low back region. An anatomic structure must be supplied by nociceptive nerve endings to be a cause of low back pain. There are four main sources of neural innervation to spinal structures: the ventral rami; the dorsal rami; the recurrent meningeal nerve; and the gray rami communicants of the sympathetic trunk. All of these nerves innervate structures which can be possible low back pain generators (see Table I).

Tissue damage causes a release of prostoglandins, histamine, bradykinin, potassium and serotonin, which stimulate and activate nociceptor nerve endings. Activated free nerve endings release substance P into the surrounding area, leading to the release of histamine from adjacent tissue cells. Group IV afferent fibers relay nociception through the dorsal root ganglion and transport neurotransmitters, substance P and calcitonin, to the dorsal horn of the spinal cord, where they synapse and release these excitatory neurotransmitters. Nociceptive information then travels from the dorsal horn of the spinal cord via the neospinothalamic or paleospinalthalamic ascending tracts to the thalamus. From the thalamus this information then travels to the cerebral cortex where pain is perceived.4 Ongoing pain will lead to faulty motion patterns which will result in cumulative trauma injuries to adjacent muscle structures.

Table 1: Possible Pain Generators in the Low Back

Ventral RamisPsoas musculature
Quadratus lumborum musculature
Intertransverse musculature
Dorsal Ramis

Multifidus, rotators, semispinalis
Zygapophyseal joints
Periosteum of posterior vertebral arch
Interspinous, supraspinous and intertransverse ligaments, ligamentum flavum
Erector spinae muscles

Recurrent Meningeal Nerve

Periosteum of posterior aspect vertebral body
Posterior aspect of disc
Posterior longitudinal ligament
Anterior aspect spinal dura mater

Gray Ramis Communicants Associated with the Sympathetic Trunk

Periosteum of anterior and lateral aspect vertebral body
Lateral aspect disc
Anterior aspect disc
Anterior longitudinal ligament

Phasic and Postural Muscles of the Lower Back

To effectively treat and understand the cause of low back pain, it is necessary to be familiar with the phasic and postural muscles surrounding the spine and adjacent structures. The phasic and postural muscles in the lumbopelvic region are listed in Table II.

Slow©twitch muscle uses oxidative metabolism and has a high capillary density, giving it its characteristic red color. The twitch speed is slow, and the function of these muscles is that described as being tonic or postural. Muscles that have high density slow-twitch fibers react to functional disturbance by shortening and tightening. Fast-twitch fibers use a glycolytic metabolic pathway, fatigue rapidly and have low capillary density that results in a white color. Muscles of this type are described as phasic in function and react to disturbance by weakening.5

Table II: Phasic & Postural Muscles in the Lumbopelvic Region

Phasic1. Abdominal oblique, transverse abdominal & rectus abdominal musculature
2. Gluteus maximus & medius musculature
3. Quadricep musculature
Postural

1. Iliopsoas musculature
2. Erector spinae musculature
3. Rectus femoral musculature
4. Quadratus lumborum musculature
5. Multifidus, rotators, semispinalis musculature
6. Hamstrings
7. Piriformis musculature
8. Iliotibial band & tensafascialata musculature

Precipitants of Low Back Pain

The first situation which can lead to low back pain is normal stress on an unprepared normal low back. This individual attempts to lift an object and underestimates or is unaware of the actual weight of the object. As a result, the lower back muscles are not prepared to protect the functional unit. A functional unit consists of two lumbar vertebrae, an adjoining disc, facet articulations, surrounding ligaments, muscles, fascia, and the nerve roots exiting at that level. Initially, the surrounding musculature contracts to protect the functional unit; however, when the applied force exceeds the maximum strength of the musculoligamentous unit, one gets a strain/sprain injury to the lower back.

The second situation which can lead to low back pain is normal stress on a deconditioned normal low back. A low back can be structurally normal, but not necessarily conditioned. Conditioned, or functionally normal, means the surrounding low back tissues have appropriate flexibility and strength to accomplish a particular movement without injury. A conditioned normal low back will be able to bend forward and return to the standing position with ease. However, a deconditioned low back is susceptible to a strain/sprain injury when put under ordinary stress. These two coupled motions of bending forward and returning to the standing position are dependent on the strength and flexibility of various muscle groups and will be discussed as movement 1 and movement 2 respectively.

Movement 1: Anterior Flexion of the Lower Back

The low back consists of five functional units. There is approximately 9 degrees of flexion allowed at each functional unit, allowing up to 45 degrees forward flexion. At 45 degrees the fascia, muscles and ligaments of the low back are taut and no more flexion is allowed without forward rotation of the pelvis. An endpoint of motion in forward flexion of the low back is that point at which a person bends forward and can go no farther (no pain). If the ligaments, fascia and muscles of the low back are not flexible, this endpoint of motion will be decreased and will result in a strain/sprain injury of the low back when attempting to bend forward to 45 degrees. In order to bend forward past 45 degrees, the pelvis has to rotate anteriorly. The anterior motion of the pelvis is dependent on the flexibility of the hamstrings and gluteus maximus musculature. If the hamstrings and gluteus maximus musculature are not flexible, the pelvis will be limited in anterior flexion. When this limited endpoint of forward flexion is exceeded, one will usually complain/suffer from an acute onset of low back pain.

Movement 2: Extension of Lower Back from Full Anterior Flexion to Normal Posture

When individuals are bent over in forward flexion, they should initially flex their knees to return to the neutral standing position. Flexing the knees will tense the quadricep musculature, which tenses the iliotibial band, which tenses the tensor fascia latae musculature and pretenses the gluteus maximus musculature. The gluteus maximus contracts and the pelvis derotates from its anteriorly rotated position. At the same time, the abdominal oblique and transverse abdominal musculature contract. This action tightens the fascia surrounding the erector spinae musculature and takes pressure off of the low back when returning to the upright position. The kinetic motion chain of movement 1 and movement 2 clearly indicate that weak abdominal musculature (abdominal obliques & transverse abdominals), weak gluteus musculature, weak quadricep musculature, tight erector spinae musculature and tight hamstrings are precursors to lower back injury.6

Having flexibility of the iliopsoas muscle (hip flexor) is also crucial in the prevention of low back pain. Contracture of the psoas muscle will inhibit the gluteus maximus musculature, thereby limiting derotation of the pelvis when returning to the neutral standing position, which will predispose the low back to injury. The psoas musculature originates from the lumbar transverse processes and inserts onto the lesser trochanter of the femur making this muscle a powerful hip flexor. However, if the psoas musculature is not conditioned properly and shortens from its its normal length, it will cause an individual to have a lordotic posture. A lordotic posture in a standing neutral position consists of an anteriorly rotated pelvis with an increased anterior curve of the lumbar spine. Usually an individual with a lordotic posture will have a protruding abdomen, especially if the abdominal musculature is weak. This lordotic posture will put undue stress on the erector spinae musculature and will lead to a repetitive motion injury to the lower back. An individual with a lordotic posture will complain of a gradual onset of low back pain which will increase with time if not treated appropriately.

An individual without a lordotic posture can also suffer from a repetitive strain to the lower back. Prolonged standing or sitting in a forward flexed position causes a repetitive strain to the erector spinae musculature, posterior longitudinal ligament, supraspinous ligaments, and fascia of the low back. This forward flexed posture also causes the nucleus pulposus to migrate posteriorly which may cause failure of the outer annular fibers of the disc. Mackenzie techniques are based on doing extension exercises to strengthen the erector spinae musculature of the lower back and preventing injury due to a repetitive or constant anterior flexion posture.3 It is important to strengthen the erector spinae musculature to a certain extent; however, it depends on the individual’s low back condition on whether this form of treatment is warranted. Florence Kendall states that:

People who have a lordosis often complain of having a “weak back.” The term is used because of the feeling of aching and fatigue in the low back, and because of the inability to lift heavy objects without pain. This type of back is mechanically weak and inefficient because of the faulty alignment, but low back muscles are not weak. The connotation of the word “weak” is that the back muscles are weak and in need of strengthening exercises. On the contrary: the muscles are strong, overdeveloped and short, and back extension exercises are contraindicated.7

In this author’s opinion, a good strengthening and flexibility program for all of the muscles surrounding the lumbopelvic region with more emphasis on flexibility training for postural muscles and strengthening exercises for phasic muscles should be implemented in a treatment plan for all low back pain patients. One must also be aware of the interrelationship of antagonistic muscles in the lumbopelvic region. A tight postural muscle will make it difficult to strengthen an antagonistic phasic muscle as indicated by Table III.6Electromyographic (EMG) data show that a tight erector spinae muscle will be active during its reverse action, trunk flexion, and thus inhibits the action of the agonist and the abdominals. After the erector spinae muscle has been stretched, not only does it relax during trunk flexion, but also a significant, spontaneous facilitation effect is seen in the abdominal muscles.8 An individual with weak abdominal musculature and tight erector spinae musculature would want to begin a daily erector spinae stretching routine, not only to stretch the low back musculature, but also to allow for proper strengthening of the abdominal musculature.

Table III: Antagonistic Postural and Phasic Musculature in the Lumbopelvic Region

Postural Musculature   Phasic Musculature
Tight psoas
>
Weak gluteus maximus
Tight erector spinae musculature
>
Weak abdominal musculature
Tight tensafascialata/quadratus lumborum
>
Weak gluteus medius musculature

The third condition which can lead to low back pain is a sudden excessive stress on a normal low back, such as a severe blow to the low back while playing a contact sport; auto accident; traumatic fall; or other acute traumas. Trauma-related injuries can cause a severe strain of the musculature surrounding the low back and can also extensively involve the ligaments, fascia, disc and nerve roots in this region. As a result, these injuries will take longer to heal than low back strain/sprain injuries not related to trauma.

The fourth condition which can lead to low back pain is a normal stress on an abnormal low back. An abnormal low back does not have integrity of the functional units and is, therefore, susceptible to low back pain under normal stress. Table IV lists several tumor and tumor-like processes, joint diseases and muscular disorders which decrease the strength of the functional unit and predispose these individuals to low back pain under normal conditions.9

Table IV: Abnormal Low Back Conditions

Tumor & Tumor-like Processes Muscular Disorders Joint Diseases
Metastatic carcinoma Muscular dystrophy Ankylosing spondylitis
Multiple myeloma (limb-girdle) Reiter’s syndrome
Osteosarcoma Myasthenia gravis Tuberculosis arthritis
Ewing’s sarcoma   Suppurative arthritis
Hodgkins lymphoma   Osteoarthritis
Osteoid osteoma   Osteoporosis

Editor’s note: Part II of “Demistifying the Treatment of Strain/Sprain Injuries of the Lower Back” will appear in the February 22nd issue of Dynamic Chiropractic.

References

  1. British Medical Journal April 26, 1997;314:7089, p. 1225.
  2. Fordyce W. Nursing Homes. International Publishing Group, 1996, p. 32.
  3. Cailliet R. Low Back Pain Syndrome, 4th edition. Philadelphia: Davis Company, 1988, p. 22-24, 76-103.
  4. Cramer G, Darby S. Basic and Clinical Anatomy of the Spine, Spinal Cord, and ANS. Mosby-Year Book Inc., 1995, p. 205-217, 251-271, 355-370.
  5. Greenman P. Principles of Manual Medicine, 2nd edition. Baltimore: Williams & Wilkins, 1996, p. 146-147, 449-456.
  6. Lewit K. Manipulate Therapy in Rehabilitation of the Locomotor System, 2nd edition. Butterworth-Heinemann Ltd., 1991, p. 14-32, 126.
  7. Kendall F, McCreary E, Provance P. Muscle Testing and Function. Baltimore: Williams & Wilkins, 1993, p. 133-176, 350-354.
  8. Janda V. Muscle strength in relation to muscle length, pain and muscle imbalance. In: Harms-Rindahl K (ed.) Muscle Strength. New York: Churchill Livingstone, 1993.
  9. Robbins. Robbins’ Pathologic Basis of Disease, 4th edition. Philadelphia: W.B. Saunders Company, 1989.

Part 2

Getting a Leg Up on Shin Pain

Download as pdf

by Joshua Dubin, DC, CCSP, CSCS, Rachel Dubin, DPT, Gregory Doerr, DC, CCSP

ABSTRACT:

Shin splints is an injury of the lower leg that often afflicts athletes. Generally, symptoms include pain on the anterolateral or posteromedial surfaces of the shin. There is a great deal of research on the treatment and prevention of shin splints, and based on extensive research, several hypotheses have been proposed for its pathophysiology; however, the exact cause of shin splints remains unknown. This paper explains the anatomy of the lower leg and biomechanics of gait. It presents possible etiologies and risk factors for shin splints, and it reviews options for treatment and prevention. Its conclusion, based on extensive literature review, reveals that most cases of shin splints respond favorably to conservative care. Such care generally includes home exercise, training and equipment modifications, and treatment by a skilled practitioner. However, in more advanced cases surgery may be necessary.

Introduction and History:

Shin splints is one of the most common exercise induced lower extremity injuries in athletes participating in activities that require prolonged or quick bursts of running and/or jumping.1 Such activities may include track and field, soccer, basketball, volleyball, basic military training, and long-distance running.7-11

During running each foot strikes the ground approximately 50-70 times per minute, or a total of 800 times per mile, with a force 2-4 times body weight.1,12 The muscles, tendons, and bones that support the lower extremity can usually adapt to such an increased work load if training progresses appropriately. However, the following risk factors may predispose to the development of shin splints by leading to increased ground reactive-forces acting on the lower extremity and/or a compromised musculoskeletal support structure: training errors, foot shape/biomechanics, poor conditioning, high body mass index, poor nutrition, and degenerative changes.1,13-16

Symptoms associated with shin splints may include pain over the anterolateral, or the distal two thirds of the posteromedial aspect of the shin.2-6 Usually, these symptoms are present with activity and alleviated with rest.7 However, if the athlete trains throughout pain and a proper treatment program is not initiated, the symptoms and severity of shin splints may progress.

In the 1900s shin splints was initially defined as any type of pain from the hip to the ankle.14 This broad definition seemed appropriate because treatments for lower extremity injuries were rudimentary and relatively ineffective. Throughout the last four decades medical research has led to advancements in understanding the causes, treatment, and prevention of sports injuries. The exact pathophysiology of shin splints remains unknown; however several possible etiologies have been studied.1,17,18

An understanding of the kinesiology, physiology, and anatomy of the lower leg, risk factors associated with shin splints, and a detailed history and physical examination may aid the practitioner in developing a proper treatment and prevention protocol.3,19,20 Most cases can be effectively treated with conservative care.1,21

Anatomy of the Lower Leg

figure1Long bones, such as the tibia, consist of an outer rigid layer. This external surface consists of several concentric rings of cortical bone that are surrounded by periosteum, a thin layer of dense fibrous connective tissue that is richly supplied by nerves and blood. The periosteum is anchored to the cortical bone by bundles of connective tissue “Sharpey fibers” (figure 1). The periosteum has several functions: it protects the underlying bone, participates in the repair and remodeling process of bone, and is the site of attachment for adjacent muscles. figure2Muscles consist of bundles of individual fibers (fasciculi) that are surrounded by endomysium, a thin delicate layer of connective tissue. The fibrocartilage strands of the periosteum intertwine with the endomysium of abutting musculature, creating an extensive origin of attachment. At these origins of attachment the underlying cortical bone is rough or thickened due to bone remodeling in response to traction exerted by muscles.22,23

figure3The tibia has three potential sites for attachments of muscles: a posterior surface, and anterolateral and medial surfaces that are separated by the anterior tibial crest. The soleus, flexor digitorum longus, and tibialis posterior musculature attach to the posterior surface of the tibia (figures 2A). The tibialis anterior musculature attaches to the anterolateral surface of the tibia (figure 2B). These muscles are contained within the superficial posterior, the deep posterior, or the anterior compartment of the leg (figure 3).3,6,24,25 The muscles surrounding the shin aid in coordinating movements of the foot and ankle and in reducing ground reactive forces.

Biomechanics of the Lower Leg during Ambulation

figure4There are two main phases to a running gait, a stance phaseand a swing phase. During the stance phase the foot contacts and adapts to the ground. The swing phase begins when the stance leg lifts off the ground. Most sport-related injuries can be attributed to repetitive ground reactive forces during the stance phase of gait.26 The stance phase of gait consists of the following sub-phases:

  • initial contact, when the foot of the swing leg initially contacts the ground.
  • loading response, beginning shortly after initial contact as the foot begins to adapt to the ground.
  • early midstance, when the contralateral swing leg is midline with the body and distributes the body weight over the stance leg.
  • late midstance, starting when the foot of the stance leg changes from a mobile adaptor that absorbs ground reactive forces to a more rigid lever that prepares the foot for toe-off.
  • terminal stance, beginning shortly after heel-lift and ending with toe-off (figure 4).27,28,29

figure5Throughout loading response and into early midstance, the foot goes through a series of transformations coined “pronation,” allowing the lower extremity to be more efficient in absorbing ground-reactive forces. Pronation of the foot and ankle consists of the following movements:

  • 1. The heel bone turns outward (everts), and the medial longitudinal arch (instep arch) lowers toward the ground.
  • 2. The tibia approximates to the toes (ground reactive dorsiflexion).
  • 3. The forefoot turns outward (abducts) (figure 5).

Normal range of pronation is four degrees of heel eversion and twenty degrees of ground reactive dorsiflexion. Pronation of the foot and ankle should end before late midstance as the foot prepares for toe-off.27,28,30

figure6Shortly after the foot strikes the ground the muscles attaching to the anterior and posterior aspect of the tibia contract eccentrically; the muscle fibers elongate as tension is produced in an attempt to decelerate a particular motion. The soleus, tibialis posterior, and the flexor digitorum musculature have points of origin on the posterior aspect of the tibia. They contract eccentrically during loading response and into midstance to decelerate pronation. Shortly after initial ground contact, the tibialis anterior muscle contracts eccentrically to decelerate foot slap as the forefoot descends towards the ground (figure 6).24,32

Under normal circumstances, the musculoskeletal support structures of the lower extremity can adapt to these repetitive eccentric loads. However, training errors, structural abnormalities, and other factors may predispose to excessive eccentric loads placed on the lower leg musculature, resulting in anterolateral or posteromedial shin splints. The exact pathophysiology of shin splints is unknown; however, research has come up with several hypothetical causes.

Possible Etiologies of Shin Splints

Traction Periostitis/Periostalgia

Current research supports the hypothesis that posteromedial shin pain in runners may be caused by excessive eccentric contractions of the superficial and deep posterior compartment muscles that originate on the tibia. Training that does not allow for proper adaptation of the musculoskeletal support structures of the lower leg, due to increased workloads, may lead to inflammation or degenerative changes to the surrounding fascia (fasciitis) or to the periosteum (periostitis/ periostalgia).2,6,26 Currently, medial tibial stress syndrome (MTSS) is the most common term to describe posteromedial shin pain thought to be caused by periostitis or periostalgia.1,19

Anterolateral shin pain has been linked to repetitive eccentric contractions of the tibialis anterior musculature. Downhill running accentuates a more pronounced foot slap, predisposing to fatigue of the tibialis anterior musculature, which may result in anterolateral shin pain due to a similar mechanism of injury as MTSS.14 This paper will define this condition as “anterior tibial stress syndrome” (ATSS).

Bone Stress Reaction

Bone remodeling of the tibia in response to increased work loads commences approximately five days after stimulation.2 Two types of cells are active in bone remodeling: osteoblast cells and osteoclast cells. Osteoblast cells produce new bone, while osteoclast cells react to increased stress by reabsorbing bone. Following bone reabsorption, osteoclast cells secrete osteoid, which is uncalcified bone. Osteoid calcifies into new bone after interacting with calcium and phosphate ions. These adaptations should result in a stronger more rigid skeletal support structure. However, it may take ninety days for the reabsorbed bone to be replaced by mature strong bone.14 Overtraining may lead to a higher ratio of bone reabsorption by osteoclast cells as compared to the production of new bone by osteoblast cells. This may result in a compromised porous skeletal support structure, which is susceptible to a bone stress reaction.1,10,11 Bone stress reactions may include microfractures, or in the more advanced stages a stress fracture. The tibia is the most common location of stress fractures in athletes,19,33,34 and most stress fractures occur four to five weeks after the onset of new exercise.12

The treatment of posteromedial or anterolateral shin splints in minor injuries is similar whether the etiology is traction periostitis/periostalgia or bone stress reaction.1,19 The initial history and physical examination should focus on discovering possible risk factors. Treatment and prevention of shin splints should include steps to eliminate or minimize these risk factors.

Risk Factors Associated with Shin Splints

Risk factors for shin splints are intrinsic (within self) and extrinsic (external to self). 6, 36

Table 1

Intrinsic Risk Factors Extrinsic Risk Factors
Lower limb structural abnormalities
• pes planus (flat foot, which may lead to excessive pronation)
• pes cavus (high arch, which may limit pronation and ability to absorb shock)
Training progression
• inappropriate intensity, frequency, or duration of training
• hill training that does not progress gradually
Poor Conditioning
• overweight (body mass index > 30 kg/m2)
• insufficient muscle endurance
• insufficient muscle strength
• limited flexibility
Gear
• unsuitable footwear
Female Triad
• osteoporosis
• amenorrhea
• eating disorder
Training surface
• hard uneven ground
Age related changes
• especially noticeable after 4th decade of life
Type of sport
• activities that involve repetitive running and/or jumping
History
• previous stress fractures

1,2,4,10,11,14-16,19,22,33-36,38

A detailed history and physical examination can aid in discovering risk factors that may have contributed to the development of shin splints. Most risk factors are correctable or can be minimized, aiding in the treatment and prevention of future episodes.

Training Guidelines

Recommendations for frequency, duration and intensity of training runs:1,29,39,40

Aerobic Conditioning, 70-80% maximum heart rate (Max HR=220-age):

This level of training is recommended for gradual adaptation to work loads with both cardiovascular conditioning and connective tissue adaptation. Initially, long-distance runners should establish a training base of 4 miles per run at this low intensity level. A progressive training schedule may include a frequency of 4 runs in a 7-day period, generally consisting of 3 shorter runs (each approximately 4-6 miles) during the week, and 1 longer run during the weekend.41 It is recommended that the weekly training mileage should not be increased by more than 10% per week. Based on marathon training logs and personal experience, the duration of the long run is usually increased by an increment of 2 miles per week or every other week, and he intensity should continue at the aerobic conditioning pace. After a proper training base is established, the short duration training runs can be conducted at an increased intensity level.

Anaerobic Conditioning, 80-90% maximum heart rate:

This training is below lactate threshold, the point after which blood lactate rises rapidly, leading to increased ventilation (speaking to a training partner becomes difficult) and eventual muscle fatigue. Anaerobic conditioning training should include a 5 minute warm up, followed by a 15-20 minute duration at the anaerobic conditioning level, then a 1 mile recovery run at the aerobic conditioning pace, followed by another 15-20 minute run at the 80-90% level. Anaerobic training makes running at a submaximal lactate pace easier over a prolonged duration. Ideally, the marathon pace should be conducted slightly below the lactate threshold. Towards the end of the race, “the last kick,” the pace can be increased.

Aerobic Capacity Training (intervals), 90-95% maximum heart rate:

This training is a vigorous challenge to the athlete’s aerobic and anaerobic capabilities, and stimulates slow twitch and fast twitch muscle fibers. This pace should only be maintained for 6-9 minutes, followed by a 4-5 minute recovery run at a slow pace. Aerobic capacity training runs elevate the lactate threshold and condition the body to deal more efficiently with oxygen debt and muscle fatigue.

Other Training Tips:

Add uphill training gradually. Running uphill should be conducted at a slower pace because of increased energy expenditure due to increased arm and shoulder action, and hipflexor and knee lift. Uphill running also predisposes to an increased eccentric strain on the posterior calf musculature. Downhill running should be limited because of increased risk and limited benefits.40,42

Change running shoes every 300-500 miles (approximately every 3-4 months). A sneaker loses approximately 50% of its ability to absorb ground reactive forces after 300-500 miles.1,19,37,43,44

Modify training. Add exercises such as swimming, bicycling, and using an elliptical machine on non-running days, or while recovering from an injury. For prevention of injury, the older athlete (after 4th decade of life) may limit running on pavement.1,4,11,30,45

Implement an eccentric strength training program for the lower leg musculature. This program can aid in the treatment and prevention of injury.76 Standing and seated calf raises strengthen the gastrocnemius, soleus, and the intrinsic musculature of the foot. A dorsiflexionassisted resistive device, resistive tubing, or a cable machine strengthens the tibialis anterior and extensor musculature of the leg.1,4,30,35,43,46,47 The strength training program should address the whole lower kinetic chain.4 Squats eccentrically strengthen the quadriceps, hamstrings, and gluteal musculature; romanian deadlifts eccentrically strengthen the latter two muscles. Abduction, adduction, and hip extension exercises can be conducted with a cable machine or tubing.48 Based on my training experience, this lower extremity routine should be conducted at a frequency of one time per week, usually on a Tuesday, Wednesday, or Thursday, if the long run is conducted on a Saturday or Sunday.

Stretch. Static stretching and ballistic stretching have both been shown to increase flexibility of the lower extremity.49,50 I have found a post-workout stretching routine to be helpful in decreasing cramping and muscle soreness, especially after a long duration training run or bike ride.

Introduce pre-season conditioning. Pre-season conditioning that includes a plyometric program can jump-start the process of bone remodeling and prepare the lower extremity support structures for elevated eccentric work loads.2,6,14,15,26,51,76

It should be emphasized that every athlete needs to be addressed individually. Generic marathon training schedules are helpful, however they may need to be modified for each individual to maximize gains and minimize injury. An experienced trainer may aid the athlete in achieving goals by tailoring a training program and re-assessing progress based on training logs and exertion levels.

Following the above training advice may prevent injury. However, additional treatment and training modification may be necessary for the athlete who experiences shin pain. The discouraged athlete will usually seek care when an injury makes training impossible.

Diagnosing Shin Splints

To properly diagnose the athlete’s condition, the treating physician will take a detailed history and examination to discover the onset and location of pain and attributed risk factors. Palpation may reveal diffuse tenderness over the distal two thirds of the posteromedial aspect of the shin (MTSS) or the anterolateral aspect of the shin (ATSS).16,19,37 However, palpation that reveals the following may be a red flag for bone-stress reaction:

  • focal tenderness localized to bone
  • swelling
  • warmth / redness
  • inability to train due to severe pain at the localized sight.14,17,19

Plain film radiographs (x-rays) are routinely taken of the leg in patients with shin pain. This baseline study may reveal a periosteal reaction, callus formation, or a radiolucent line that are common findings of a bone stress reaction or frank stress fracture. Radiographs may also rule out other pathological conditions such as an osteoid osteoma, osteosarcoma, or Ewing’s sarcoma. However, bone stress reactions are usually not visualized on radiographs until the 2nd to 6th week post injury/initial complaints of symptoms.1,21,35,52 “The sensitivity of early fracture detection by radiography can be as low as 15%, and follow up radiographs may demonstrate diagnostic findings in only 50% cases.”16 More advanced studies may be needed for further evaluation, such as an MRI (magnetic resonance imaging test) or a BS (bone scan). These studies are more sensitive in detecting bone pathology earlier in the stage of injury, and they aid clinical judgment in regards to a gradual return to sport specific training. Such gradual returns may require a longer period of modified rest, immobilization, or corrective surgery for more advanced cases of bone stress reactions.1,10,53

Treatment of shin splints

Goals of therapy include the following:

  • reduce pain and promote healing.
  • incorporate pain-free modified training to maintain fitness.
  • correct or minimize risk factors.
  • gradually re-introduce pain-free activity.
  • develop realistic additional training goals.

Severity of symptoms and level of injury are generally scored on a four-grade system:

Grade 1: Pain is present at the end of the workout but is minimal.

Grade 2: Pain is present during the workout but does not affect performance.

Grade 3: Pain during the workout affects performance but dissipates when the workout ends.

Grade 4: Pain does not allow participation in sport and is present during activities of daily living.1

Usually, the athlete will seek treatment when pain hinders performance. The initial goals of therapy are to promote healing and reduce pain and inflammation. The following initial treatments may be useful:

Inflammation reduction

Use of nonsteroidal anti-inflammatory medications per prescription, and application of a cold pack to the shin for twenty minutes on, one hour off, repeated throughout the day can reduce inflammation. Use of iontophoresis with dexamethasone may also decrease inflammation.1,19,56

Ultrasound and electric muscle stimulation combination therapy

The therapy can restore normal muscle tone, aid in the healing process, and reduce pain.1,10,19,32,57,58

Manual adjustments to the ankle and foot

Adjustments free-up joint motion of the talocrural, subtalar, and midtarsal joint articulations.57,59

Deep tissue procedures, such as the Graston Technique (manual therapy that utilizes specially designed devices) and Active Release Technique (a patented manual therapy technique)

figure7Procedures break up scar tissue and restore soft tissue motion (figures 7A,7B). There is considerable clinical procedures in treatment of strain/sprain injuries.60-63 Myofascial techniques have been shown to stimulate fibroblast proliferation, leading to collagen synthesis that may promote healing by replacing degenerative tissue with a stronger and more functional tissue.45,65

Phototherapy, such as low-level laser therapy or infrared light

Phototherapy decreases inflammation, increases the speed of tissue healing, and decreases pain.58,64

The above treatments may reduce pain and inflammation, and may speed the body’s normal healing response. However, time is a primary factor in recovery: Approximate return to pre-injury strength for bones, ligaments, muscles, and tendons can range from 12 weeks, 40-50 weeks, 6 weeks-6 months, and 40-50 weeks respectively.1,19

During the initial treatment phase – for more severe Grade 2, Grade 3, and Grade 4 injuries – athletes can maintain cardiovascular fitness with modified training. For example, a runner should cycle or swim at a pain-free level.1,12,19

There are no exact studies indicating when to re-introduce sport-specific training; however, the following may be a useful guideline: If there are no time-specific training goals, cease sport specific activity for 2 weeks, and maintain cardiovascular fitness with modified training. After 2 weeks of modified training and conservative therapy, re-introduce pain-free running on a soft track or treadmill, at approximately 50% of the pre-injury intensity and duration. Then, increase the duration of the training runs by 10% each week. It is hopeful that the pre-injury duration can be reached in 5-6 weeks. Athletes should cease running if they experience pain. A brief period of modified training and resumption of pain-free running at a lower intensity and shorter duration may be necessary. The intensity of the training should progress appropriately only after the pre-injury duration is obtained.37,19

Depending on the duration of the athlete’s most recent pre-injury training run, my recommendations for return to activity may vary with the above guidelines. Usually the duration of the initial training run would be 2-4 miles, conducted on a treadmill, at a speed of 10 minute/mile (very slow for most athletes). If the athlete can conduct 2-3 of these traning runs without pain, we would create a program, based on the above guidelines, for achieving time-specific goals.

Before re-introducing sport-specific training, the following methods may reduce the workload placed on the musculoskeletal support structure of the lower leg that are present due to intrinsic risk factors:

  • Buy proper running shoes. A pes cavus foot structure may benefit from a cushioned sneaker. The sneaker liner can be removed and replaced with a cushioned insole. The rearfoot varus, pes planus valgus, and forefoot varus foot structure may benefit from a motion-control sneaker.66
  • Use appropriate arch supports as necessary. A semirigid orthosis with a medial arch support, no higher than five-eighths of an inch, can limit excess or prolonged pronation.1,2,27,28,35,67-70
  • Tape the foot. Taping can limit pronation.57,71,72
  • Temporarily use a quarter-inch or three-quarter inch heel lift.

Temporary use can limit compensatory pronation caused by ankle equinous. As range of motion of the talocrural joint in dorsiflexion improves with therapy, the heel lifts can be removed.1,28,68

  • Apply a shin sleeve or strapping. Sleeves and strappings can add support for leg muscles.
  • Obtain nutritional advice. A dietitian can calculate caloric burn rate and develop a meal plan for healthy weight loss, maintenance, and proper nutrition.19
  • Obtain medical examinations Primary physicians or gynecologists can rule out deficiencies common in athletes, such as low estrogen, ammenorhea, or low bone density.
  • Train for flexibility Increasing flexibility can reduce compensatory pronation due to ankle equinous, and the posterior calf musculature can be stretched.1,35,43,73,74

The treating physician needs to continually re-evaluate the athlete during the course of therapy. If the athlete has time-specific goals, is not responding to conservative care, or symptoms re-appear when sport-specific training is re-initiated, a BS or MRI may be needed. In addition, treatment of slow healing stress fractures may require immobilization with casting or a walking boot for approximately 3-8 weeks.4,10 Pain-free modified training can maintain the athlete’s cardiovascular fitness, and sanity, during this period. Once union of the stress fracture is evident on repeat imaging studies, and pain is not present with ambulation, sport-specific training can be gradually re-introduced.

If non-union of the stress fracture is present on repeat imaging studies after 4-6 months of immobilization and rest, surgery may be necessary. Surgery may include intramedullary nailing, cortical drilling, or excision and bone grafting.1,4,33,75 In recalcitrant cases of MTSS, surgery may include fasciotomy of the posteromedial superficial and the deep fascia of the tibia.1 Posteromedial fasciotomy may aid in alleviating the pull of the soleus and deep posterior calf musculature of the leg on their insertions on the tibia, as well as decreasing pain due to denervation of the periosteum.37,19 Post-fasciotomy studies have indicated good results in regards to reduced shin pain, however many athletes are not able to return to full sport specific training levels.35,75

Conclusion:

Shin splints is one of the most common lower leg sport-related injuries. Risk factors include training errors, foot structure abnormalities, high body-mass index, age-related degenerative changes, poor conditioning, and inadequate calcium intake or estrogen levels. Most cases of shin splints can be treated successfully with conservative care. Conservative treatment includes the following:

  • reduction of pain and inflammation
  • modified training to maintain cardiovascular fitness
  • modifications to gear, such as obtaining new running shoes
  • implementation of a strength and flexibility program
  • correction of training errors
  • a pain-free gradual return to sport-specific activity
  • nutritional counseling or hormonal therapy

If the injury does not respond to conservative care, or there is a time-specific training goal, a BS or MRI may be beneficial in the early detection of stress fractures or other pathologies. Other treatment options for recalcitrant shin splints may include prolonged immobilization with pain-free modified training, surgery to promote bone-union, or a fasciotomy.

REFERENCES

1. Reid DC. Sports Injury Assessment and Rehabilitation. New York: Churchill Livingston Inc., 1992.

2. Yates B, White S. The incidence and risk factors in the development of medial tibial stress syndrome among naval recruits. The American Journal of Sports Medicine 2004; 32(3):772-780.

3. Hislop M, Tierney P. Anatomical variations within the deep posterior compartment of the leg and important clinical consequences. Journal of Science and Medicine in Sport 2004; 7(3):392-9.

4. Wilder RP, Sethi S. Overuse injuries: tendinopathies, stress fractures, compartment syndrome, and shin splints. Clin Sports Med 2004; 23:55-81.

5. Magnusson HI, Westlin NE, Nyquist F, Gardsell P, Seeman E, Karlsson MK. Abnormally decreased regional bone density in athletes with medial tibial stress syndrome. American Journal of Sports Medicine 2001; 29(6):712.

6. Herring K. A plyometic training model used to augment rehabilitation from tibial Fasciitis. Current Sports Medicine Reports 2006; 5(3):147-54.

7. Batt ME, Ugalde V, Anderson MW, Shelton DK. A prospective controlled study of diagnostic imaging for acute shin splints. Medicine & Science in Sports & Exercise 1998; 30(11):1564-1571.

8. Thacker SB, Gilchrist J, Stroup D, Dexter Kimsey C. The prevention of shin splints in sports: a systematic review of literature. Medicine & Science in Sports & Exercise 2002; 34(1):32-40.

9. Korpelainen R, Orava S, Karpakka J, Siira P, Hulkko A. Risk factors for recurrent stress fractures in athletes. The American Journal of Sports Medicine 2001; 29:304-310.

10. Jensen J. Stress fracture in the world class athlete: a case study. Medicine & Science in Sports & Medicine 1998; 30(6):783-787.

11. Tommasini SM, Nasser P, Schaffler MB, Jepsen KJ. Relationship between bone morphology and bone quality in male tibias: implications for stress fracture risk. Journal of Bone and Mineral Research 2005; 20(8):1372-1380.

12. Wall J, Feller JF. Imaging of Stress Fractures in Runners. Clinics in Sports Medicine 2006; 25:781-802.

13. Sommer HM, Vallentyne SW. Effect of foot posture on the incidence of medial tibial stress syndrome. Medicine & Science in Sports & Exercise 1995; 27(6):800-804.

14. Noakes T. The Lore of Running (4th Edition). Illinois: Human Kinetics, 2003; 803-816.

15. Shaffer RA, Rauh MJ, Brodine SK, Trone DW, Macera CA. Predictors of stress fracture susceptibility in young female recruits. The American Journal of Sports Medicine 2006; 34(1):108.

16. Spitz D, Newberg A. Imaging of stress fractures in the athlete. Radiologic Clinics of North America 2002; 40:313-331.

17. Bhatt R, Lauder I, Finlay DB, Allen MJ, Belton IP. Correlation of bone scintigraphy and histological findings in medial tibial syndrome. British Journal of Sports Medicine 2000; 34:49-53.

18. Magnusson HI, Ahlborg HG, Karlsson C, Nyquist F, Karlsson MK. Low regional tibial bone density in athletes with medial tibial stress syndrome normalizes after recovery from symptoms. American Journal of Sports Medicine 2003; 31(4):596.

19. Edwards PH Jr, Wright ML, Hartman JF. American Journal of Sports Medicine 2005; 33:1241.

20. Bennell K, Crossley K, Jayarajan J, Walton E, Warden S, Kiss SZ, Wrigley T. Ground reaction forces and bone parameters in females with tibial stress fracture. Medicine & Science in Sports & Exercise 2004; 36(3):397-404.

21. Aoki Y, Yasuda K, Tohyama H, Ito H, Minami A. Magnetic resonance imaging in stress fractures and shin splints. Clinical Orthopaedics 2004; 421:26-267.

22. Weineck J. Functional Anatomy in Sports, Second Edition. St. Louis: Mosby-Year Book, 1990.

23. Wheater PR, Burkitt HG, Daniels VG. Functional Histology. New York: Churchill Livingstone, 1987.

24. Banks AS, Downey MS, Martin DE, Miller SJ. Foot and Ankle Surgery. Philadelphia: Lipincott Williams & Wilkins, 2001.

25. Clemente CD. Anatomy: A Regional Atlas of the Human Body (3rd Edition). Baltimore: Urban & Schwarzenberg, 1987.

26. Richie D, DeVries H, Endo C. Shin muscle activity and sports surfaces. Journal of the American Podiatric Association 1993; 83(4):181-190.

27. Michaud TC. Foot orthosis and other forms of conservative foot care. Newton MA: Thomas C Michaud, 1997.

28. Donatelli RA. The biomechanics of the foot and ankle, 2nd Edition. Philadelphia: F.A. Davis, 1996.

29. Norkin CC, Levangie PK. Joint Structure and Function: A Comprehensive Analysis (2nd Edition). F.A. Davis, Philadelphia 1992.

30. Banks AS, Downey MS, Martin DE, Miller SJ. Foot and Ankle Surgery. Philadelphia: Lipincott Williams & Wilkins, 2001.

31. Inman VT. Human Locomotion. Can Med Assoc J. 94:1047, 1996.

32. Chleboun GS, Busic AB, Graham KK, Stuckey HA. Fascicle length change of the human tibialis anterior and vastus lateralis during walking. Journal of Orthopaedic & Sports Physical Therapy 2007; 37(7):372-379.

33. Larson CM, Traina SM, Fischer DA, Arendt EA. Recurrent complete proximal tibial stress fracture in a basketball player. The American Journal of Sports Medicine 2005; 33(12):1914.

34. Pozderac RV. Longitudinal tibial fatigue fracture: an uncommon stress fracture with characteristic features. Clinical Nuclear Medicine 2002; 27(7):475-478.

35. Fredericson M, Wun C. Differential diagnosis of leg pain in the athlete. Journal of the American Podiatric Medical Association 2003; 93(4):321-324.

36. Reinking MF, Austin TM, Hayes AM. Exercise-related leg pain in collegiate cross-country athletes: extrinsic and intrinsic risk factors. Journal of Orthpaedic & Sports Physical Therapy 2007; 37(11):670-678.

37. Kortebein PM, Kaufman KR, Basford JR, Stuart MJ. Medial tibial stress syndrome. Medicine & Science in Sports & Exercise 2000; 32(2):S27-S33.

38. Taunton JE, Ryan MB, Clement DB, McKenzie DC, Lloyd-Smith DR, Zumbo BD. A retrospective case-control analysis of 2002 running injuries. British Journal of Sports Medicine 2002; 36:95-101.

39. Smurawa T. Overuse injuries curb triathlon preparation efforts. Biomechanics 2006; 13(5).

40. Martin DE, Coe PN. Better Training for Distance Running (2nd Edition). Champaign, IL: Human Kinetics, 1997.

41. Higdon H. Hal Higdon’s Marathon Training Guide. www.halhigdon.com/marathon/Mar00novice.htm. Accessed March 14, 2008.

42. Armstrong RB, Ogilvie RW, Schwane JA. Eccentric exercise-induced injury to rat skeletal muscle. Journal of Applied Physiology 1983; 54(1):80-93.

43. Roxas M. Plantar fasciitis: diagnosis and therapeutic considerations. Alternative Medicine Review 2005; 10(2):83-93.

44. Messier SP, Edwards DG, Martin DF, et al. Etiology of iliotibial band friction syndrome in distance runners. Medicine & Science in Sports & Exercise 2995; 27(7):951-960.

45. Dyck D, Boyajian-O’Neill L. Plantar Fasciitis. Clinical Journal of Sports Medicine 2004; 14(5):305-309.

46. Friden J, Sfakianos PN, Hargens AR. Muscle soreness and intramuscular fluid pressure: comparison between eccentric and concentric load. Journal of Applied Physiology 1986; 61(6):2175-2179.

47. Allen RH, Gross MT. Toe flexors strength and passive extension range of motion of the first metatarsophalangeal joint in individuals with plantar fasciitis. Journal of Orthopaedic & Sports Physical Therapy 2003; 33(8):468-78.

48. reference for squats-muscle activity

49. Witvrouw E, Mahieu N, Roosen P, McNair P. The role of stretching in tendon injuries. British Journal of Sports Medicine 2007; 41:224-226.

50. Witvrouw E, Mahieu N, Danneels L, McNair P. Stretching and injury prevention. Sports Med 2004; 34(7):443:449.

51. Chmielewski TL, Myer GD, Kauffman D, Tillman SM. Plyometric exercise in the rehabilitation of athletes: physiological responses and clinical application. Journal of Orthopaedic & Sports Physical Therapy 2006; 36(5): 308-319.

52. Ruohola JPS, Kiuru MJ, Pihlajamaki HK. Fatigue bone injuries causing anterior lower leg pain. Clinical Orthpaedics and Related Research 2006; 444:216-223.

53. Gaeta M, Minutoli F, Vinci S, Salamone I, D’Andrea Letterio, Bitto L, Magaudda L, Blandino A. High-resolution CT grading of tibial stress reactions in distance runners. American Journal of Radiology 2006; 187:789-793.

54. Hod N, Ashkenazi I, Levi Y, Fire G, Drori M, Cohen I, Bernstine H, Horne T. Characteristics of skeletal stress fractures in female military recruits of the Israeli Defense Forces on bone scintigraphy. Clinial Nuclear Medicine 2006; 31(12):742-749.

55. Love C, Din AS, Tomas MB, Kalapparambath TP, Palestro CJ. Radionuclide bone imaging: an illustrative review. Radiographics 2003; 23:341-358.

56. Pellecchia GL, Hamel H, Behnke P. Treatment of infrapatellar tendonitis: a combination of modalities and transverse friction massage versus iontophoresis. J Sports Rehabil 1994; 3(2):35-145.

57. Hyde T. Conservative management of sports injury. Baltimore: Williams & Wilkins, 1997; pp477-82.

58. Gum SL, Reddy GK, Stehno-Bittel L, Enwemeka CS. Combined ultrasound, electrical muscle stimuation, and laser promote collagen synthesis with moderate changes in tendon biomechanics. Am J Phys Med Rehabil 1997; 76(4):288-96.

59. Young B, Walker M, Strunce J, Boyles R. A combined treatment approach emphasizing impairment-based manual physical therapy for plantar heel pain: a case series. The Journal of Orthopaedic & Sports Physical Therapy 2004; 34(11):725-33.

60. Walker JM. Deep transverse frictions in ligament healing. Journal of Orthopaedic & Sports Physical Therapy 1984; 6(2):89-94.

61. Brosseau L, Casimiro, Milne S, et al. Deep transverse friction massage for healing tendonitis. Cochrane Database Syst Rev 2002; (4):CD003528.

62. Kvist M, Jarvinen M. Clinical histochemical and biomechanical features in repair of muscle and tendon injuries. Int J Sports Med 1982; 3 Suppl 1:12-14.

63. Roniger LR. Massage, strengthening reduce knee OA pain disability. Biomechanics 2007; XIV(2): 17-18.

64. Roniger LR. Research focus on lower limb pain brings relief. Biomechanics 2008; XV(1):21.

65. Leadhetter W. Cell matrix response in tendon injury. Clinics in Sports Medicine 1997; 11(3): 533-79.

66. Butler R, Davis I, Hamill J. Interaction of joint type and footwear on running mechanics. The American Journal of Sports Medicine 2006; 34(12):1998-2005.

67. Fillipou D, Kalliakmanis A, Triga A, Rizos A, Grigoriadis E. Sports related plantar fasciitis. Current Diagnostic and Therapeutic Advances. Folia Medica 2004; 46(3):56-60.

68. Sobel E, Levitz S, Caselli M. Orthoses in the treatment of rearfoot problems. Journal of the American Podiatric Association 1999; 89(5):220-33.

69. Landorf K, Keenan A, Herbert R. Effectiveness of different types of foot orthoses for the treatment of plantar fasciitis. Journal of the American Podiatric Association 2004; 94(6):542-49.

70. Kogler G, Veer F, Solomonidis S, Paul J. The influence of medial and lateral placement of orthotic wedges on loading of the plantar aponeurosis: an in vitro study. Journal of Bone & Joint surgery 1999; 81-A(1):1403-1413.

71. Landorf K, Radford J, Keenan A, Redmond A. Effectiveness of low-dye taping for the short term management of plantar fasciitis. Journal of the American Podiatric Association 2005; 95(6):525-30.

72. Radford J, Burns J, Buchbinder R, Landorf K, Cook C. The effect of low-dye taping on the kinematic, kinetic, and electromyographic variables. Journal of Orthopaedic & Sports Physical Therapy 2006; 36(4):232-41.

73. Didiovanni B, Nawoczenski D, Lintal M, Moore E, Murray J, Wilding G, Baumhauer J. Tissue-specific plantar fascia-stretching exercise enhances outcomes in patients with chronic heel pain: a prospective randomized study. The Journal of Bone & Joint Surgery 2003; 85-A(7):1270-77.

74. Mahieu N, McNair P, DeMuynck M, Stevens V, Blanckaert I, Smits N, Witrouw E. Effect of static and ballistic stretching on the muscle-tendon tissue properties. Medicine & Science in Sports & Exercise 2007; 39(3):494-501.

75. Yates B, Allen MJ, Barnes MR. Outcome of surgical treatment of medial tibial stress syndrome. The Journal of Bone & Joint Surgery 2003; 85- A(10):1974-1980.

76. Woodley BL, Newsham-West RJ, Baxter GD. Chronic tendinopathy: effectiveness of eccentric exercise. British Journal of Sports Medicine 2007; 41:188-199.

77. Andrew JR, Harrelson GL, Wilk KE. Physical rehabilitation of the injured athlete (3rd Edition). Philadelphia, PA:Saunders, 2004.

78. Comfort P. Kasim P. Optimizing squat technique. Strength and Conditioning Journal 2007; 29(6):10-13.

Special thanks to Audrey Mahoney for creating the illustrations.

*To be published in BioMechanics, May/June 2008. ©2008 Dubin Chiropractic

Iliotibial Band Friction Syndrome

Download as pdf

ABSTRACT:

Iliotibial band friction syndrome (ITBFS) is an inflammatory, non-traumatic, overuse injury of the knee affecting predominantly long-distance runners. A home exercise program that includes a flexibility and strength conditioning routine and modified training recommendations can aid in the treatment and prevention of further injury. Most cases of ITBFS can be treated successfully with conservative therapy. Recalcitrant cases of ITBFS may require other interventions such as cortisone injections and/or surgery.

Iliotibial Band Friction Syndrome

Running has increased in popularity for cardiovascular fitness and sport over the last decade (1,2,3,4). It has been estimated that approximately 30 million Americans run for exercise (5). However, it has also been projected that one-half to two-thirds of those runners may sustain a non-traumatic repetitive strain injury at least once (5,6). Iliotibial band friction syndrome (ITBFS) is an inflammatory, repetitive strain injury to the knee that is particularly common in long distance runners (1,7,8,9,10). ITBFS may be caused by a multitude of factors including training errors, worn out running shoes, and/or lower leg misalignments (1,4,11,12,13,14,15,16). The main symptom of ITBFS is a sharp pain on the outer aspect of the knee that can radiate into the outer thigh or calf (17,18,19). Knee pain usually occurs at a particular distance of each training run, probably due to muscle fatigue (1,12), and is more pronounced shortly after the foot contacts the ground surface (20). Attempting to run throughout the pain will intensify the symptoms, eventually causing the athlete to shorten his stride or walk. The frustrated athlete, who may be training for a race, will not be able to progress his mileage appropriately. However, the despondent runner may be unreceptive to advice to temporarily discontinue running and initiate therapy, resulting in a more severe grade of injury. Pain may now be present with walking, exacerbated by walking up or down stairs, and a stiff-legged gait may be acquired to relieve symptoms (21). Based on clinical experience and as a recreational runner, I have identified several reasons why most athletes are unwilling to temporarily discontinue running: it is a time-efficient exercise; genuine friendships are formed in group training; no other cardiovascular exercise can beat the “runner’s high”; and the fear of not attaining his or her training goal. My experience and research studies show conservative therapy to be extremely successful in the treatment of ITBFS (8,22). A proper treatment protocol should include the following: inflammation reduction, pain-free training modification, flexibility and endurance strength training of the muscles surrounding the pelvis and thigh, and correction of faulty training habits (1,2,7,8,9,10,11,12,13,23,24).

IBFS2

The treating physician should have an understanding of the anatomy of the iliotibial tract, surrounding musculature of the outer thigh and pelvis, the extrinsic and intrinsic risk factors that predispose long distance runners to ITBFS, and the biomechanics of the ankle, tibia and knee during the stance phase of gait.

Anatomy of the Iliotibial Tract

IBFS3

Fascia is a sheath-like tissue that surrounds muscles and muscle groups. The fascia lata surrounds the hip and thigh. The iliotibial tract (ITT) is a lateral thickening of the fascia lata, originating from the iliac crest of the pelvis. The ITT continues down the outer third of the thigh, at the femur bone, passing over a protuberance called the greater trochanter. At the level of the greater trochanter, fibers from the gluteus maximus (GM) and Tensor fascia lata (TFL) musculature merge with the ITT posteriorly and anteriorly, respectively. Located between the ITT and greater trochanter is a bursa, a fluid filled sac that functions to decrease friction between two adjacent structures. The ITT attaches superficially to the fascia of the vastus lateralis musculature, and through passage of the intermuscular septum to the linea aspera, a linear ridge on the posterolateral aspect of the femur. As the ITT approaches the knee joint, it passes over a protuberance on the outer aspect of the femur, the lateral femoral epicondyle (LFE). A thin layer of fatty tissue is located between the ITT and LFE. As the ITT approaches the knee joint it splits into two structures, the iliopatellar band and a distal extension of the ITT. The distal extension of the ITT crosses the knee joint and attaches to Gerdy’s tubercle, a bump located on the proximal outer aspect of the tibia. The iliopatellar band migrates medially to join with the lateral retinaculum, a sheath-like tissue that attaches to the outer aspect of the patella (Figure 1,16,19,20,25,26,27,28,29,30,31). The distal extension of the ITT provides lateral stabilization to the knee joint through its attachment to the distal femur and the proximal tibia; the iliopatellar branch of the ITT aids in decelerating medial glide of the patella and leg flexion (32).

To properly diagnose, treat, and prevent ITBFS, a physician should understand the biomechanics of the ankle, tibia, and knee joint that this area undergoes during a typical running gait, and how these movements dynamically affect the ITT.

Lower Leg Biomechanics with Running

IBFS5

Gait can be separated into two phases: the stance and swing phases. This discussion will focus on the stance phase, as it directly relates to ITBFS. During the stance phase, the foot contacts and adapts to the ground surface; during the swing phase, the leg accelerates forward and prepares for ground contact. The stance phase consists of initial contact, loading response, mid-stance, and terminal stance (33) (Figure 2). The ankle joint, tibia, and knee joint move in synchronicity during the individual stance phases, changing the lower extremity into a rigid lever for initial ground contact and toe-off, or a mobile shock absorber from loading response and into early mid stance (34).

Two tri-planar movements are particular to the ankle joint during the stance phase, supination and pronation. The ankle assumes a supinated position for stability during initial contact and in preparation for toe-off. Supination consists of calcaneal inversion (the heel is turned inwards), plantar flexion (the toes approach the ground surface) and adduction of the forefoot (the toes point toward the midline) (Figure 3). Ankle pronation occurs throughout loading response and into early mid stance, transforming the foot and ankle into a supple mobile adaptor that is efficient in absorbing ground reactive forces. Ankle pronation consists of eversion of the calcaneus (the heel turns outward), ground reactive dorsiflexion (the tibia moves forward over the foot) and abduction of the forefoot (the toes and forefoot turn away from the midline) (Figure 4) (2,35).

IBFS6

During initial contact the knee is flexed approximately 21 degrees (36), the ITT should be located anterior to the LFE, and the ankle is supinated (Figure 5). Throughout loading response and early midstance, the ankle pronates, the tibia internally rotates, the knee joint flexes beyond 30 degrees, and the ITT translates posterior to the LFE (Figure 6). From early midstance and continuing into terminal stance the ankle re-supinates, the tibia externally rotates and the knee re-extends (33).

It has been proposed that ITBFS is secondary to repetitive knee movement through an impingement zone of 30 degrees of leg flexion (9,10,17). This injury is most common in long distance runners because the activity involves repetitive leg flexion and extension approximately 800 times per mile (37,38). The onset of pain associated with ITBFS will cause an athlete to shorten his stride, thereby limiting leg flexion and minimizing friction of the ITT over the inflamed fatty tissue and periosteal layer of the LFE. This

IBFS7A

altered gait will temporarily allow the athlete to continue running, but may exacerbate the condition. A study performed on athletes who had acute or sub-acute clinical symptoms for ITBFS revealed MRI findings of fluid accumulation in the fatty tissue deep to the ITT (17,39,40). Secondary bursa or thickening of the ITT may be more common in chronic stages of ITBFS (41).

Repetitive flexion and extension of the leg through the 30 degree impingement zone may be one risk factor; however the causes of ITBFS are multifaceted. Other risk factors include training errors and structural misalignments.

Training Errors and Risk Factors for ITBFS

Training errors are contributory to most overuse running injuries. Properly progressed training programs allow the supporting structures of the pelvis and knee to adapt to increased stresses. Inappropriately increasing the intensity, duration, and frequency of the training runs, as well as incorporating hills on the training routes too soon, may overload the supporting structures of the knee, eventually leading to injury (2,8,9,11,12).

Structural misalignments that cause altered movement patterns of the ankle, tibia and knee joint can also be contributory to ITBFS. Knee movement occurs in 3 planes of reference: the sagittal plane, frontal plane, and transverse plane. Flexion and extension of the leg occur in the sagittal plane (Figure 7A). Frontal plane movements include varus (gapping of the lateral aspect of the knee joint) (Figure 7B), as well as adduction of the lower extremity towards the midline. Internal rotation of the tibia on the fixed femur takes place in the transverse plane (Figure 7C). Excessive repetitive movement patterns of the knee occurring in the sagittal, frontal, and transverse planes are risk factors for ITBFS (17,18,20,21).

IBFS7B

Studies have suggested two factors that lead to excessive adduction of the stance leg in the frontal plane, causing increased tension of the ITT: weakness of the muscles that abduct and support the pelvis, and running on cambered (arched) surfaces (20). Contraction of the gluteus medius, GM, and TFL occur predominately during the first 35% of stance (9). Long distance runners with ITBFS have weaker hip abduction strength in the affected leg compared with their unaffected leg (10). Fatigue and weakness of the GM, TFL, and gluteus medius may occur later during a run, resulting in an altered “Trendelenberg gait,” raised ipsilateral hip, and increased frontal plane adduction of the thigh and leg (1,42) (Figure 8). This modified gait has been shown to increase tension on the ITT and is a risk factor for ITBFS (1,20).

IBFS8

Pronounced adduction of the stance leg due to muscle fatigue leads to increased tension on the ITT that may initiate or exacerbate symptoms related to ITBFS.

Excessive internal rotation of the tibia in the transverse plane can also be caused by structural misalignments and can contribute to ITBFS. Anatomical misalignments such as rearfoot varus, forefoot varus, and pes planus may cause excessive or prolonged pronation of the ankle joint throughout the stance phase of gait. Abnormal pronation of the ankle joint may cause greater than normal internal rotation of the tibia, accompanied by increased tension on the ITT at its insertion point on Gerdy’s tubercle during each foot strike, predisposing to injury (1,12,38,43,44,45) (Figure 9).

Risk Factors for ITBFS

Extrinsic risk factors may include:

  1. Worn out running shoes. A sneaker loses approximately 50% of its ability to absorb ground reactive forces after 300-500 miles (14). The more worn out the shoe, the more ground reactive forces are transferred to the knee.
  2. Training programs that increase mileage or incorporate hills inappropriately. Weekly mileage should not be increased more than 5-10% per week to allow for adaptation of the muscles, tendons, ligaments and bone to increased stress (46,47,48).
  3. Running at an improper pace. Placing too much strain on untrained legs may lead to fatigue and injury. Long runs to improve aerobic conditioning should be slow, at 65-70% maximum heart rate. Anaerobic threshold training can be conducted with shorter runs at 85-100% maximum heart rate (46).
  4. Running on a cambered surface or slippery surface (11).

Intrinsic risk factors may include:

  1. Bow leg/genu varum (49)
  2. IBFS9

    Rearfoot and forefoot varum (50)

  3. Pes cavus/high arch. A pes cavus foot has limited ability in absorbing ground reactive forces, placing more stress on the knee joint.
  4. A prominent LFE and tight IT and TFL.
  5. Weak gluteus medius, GM and TFL (42).
  6. Tightness and weakness in the Quadriceps, ITT and lateral retinaculum. This may lead to excessive lateral tracking of the patella and decreased deceleration forces acting on leg flexion, leading to increased stress on the lateral stabilizing structures of the knee joint (47,51).

Diagnosing ITBFS

A physician can diagnose ITBFS and discover internal and external risk factors for the condition through a detailed history and physical examination. A history should include the following questions: What are your current symptoms? When did you first notice the injury? How have you progressed the frequency, duration and intensity of your weekly training runs? Do your training routes include hills or cambered surfaces? How old are your running sneakers? What are your training goals?

Two orthopedic tests that aid the doctor in diagnosing ITBFS are the Modified Ober’s test (Figure 10) (42,52) and Noble’s test (Figure 11) (15,17,52). The Modified Ober’s test is an assessment tool for evaluating tightness of the ITT and TFL. Initially the patient lies on the non-injured side. The doctor raises the upside hip and thigh into slight abduction, extends the thigh, and then allows the thigh to drop vertically into adduction. The doctor should stabilize the pelvis and thigh with one hand to prevent flexion of the pelvis and internal rotation of the thigh, movements that may lead to false negative findings. The Modified Ober’s test is positive for a tight ITT and TFL if the thigh does not descend to or beyond 10 degrees of the horizontal plane.

Noble’s test can be utilized to differentiate between ITBFS and other conditions that refer pain to the outside of the knee, such as bicipital tendonitis, popliteus tendonitis, lateral collateral ligament strain, lateral meniscal tear or cyst, and osteoarthritis (53,54,55,56,57, 58). The patient is instructed to lie on his back with his leg hanging off the side of the bench and his knee flexed to 90 degrees. The doctor places his thumb over the LFE and instructs the patient to extend his leg. As the patient extends his leg to approximately 30 degrees, the ITT translates anteriorly under the doctor’s thumb. If the patient complains of lateral knee pain that is similar to pain present while running, Noble’s test is positive for ITBFS.

IBFS10

The Creak test (17) is analogous to Noble’s test. During this orthopaedic test the athlete is standing and instructed to transfer his weight to the fully extended injured leg. He is then instructed to flex the injured leg to approximately 30 degrees. As the leg flexes to 30 degrees, the ITT would track over and posterior to the LFE. If lateral knee pain is present at approximately 30 degrees of leg flexion, the test is positive for ITBFS.

Further examination should include a strength and flexibility assessment of the musculature surrounding the thigh and pelvis, and observation of the athlete’s lower extremity biomechanics with standing and walking.

Therapies

Initial goals of therapy are to reduce swelling and inflammation. Pain-free modified training can then be implemented to improve strength and flexibility of the hip, thigh, and calf musculature, as well as cardiovascular fitness. The end goal is to return the athlete to a pain-free running routine. Grading the injury helps to determine the plan of treatment (7,43).

Grades of Iliotibial Friction Injuries and Phases of Tissue Repair and Treatment
Grade 1

Pain does not occur during normal activity, but generalized pain is felt about 1 to 3 hours after sport-specific training has ended. Tenderness usually resolves within 24 hours without intervention.

Grade 2

Minimal pain is present towards the end of a training run; performance is not affected. Appropriate treatment may be necessary to prevent a grade 3 injury.

Grade 3

Pain is present at an earlier onset of training, and interferes with the speed and duration of a training session. Treatment and training modification are necessary to prevent a grade 3 injury from progressing to a grade 4 injury.

Grade 4

Pain restricts training and is also noticeable during activities of daily living; the athlete can no longer continue sport-specific training. Low-impact training, such as swimming, running in a pool, and biking, can be implemented for cardiovascular fitness and aggressive muscu- loskeletal therapy can reduce the severity of the injury. The goal of therapy is to reduce inflammation and restore strength and flexibility of the hip and thigh musculature, allowing for the athlete to return to pain-free sport-specific training.

Grade 5

Pain interferes with training as well as activities of daily living. Aggressive therapy is required and surgery may be necessary. (Source: 7,43)

IBFS12

Appropriate treatment of a grade 1 or grade 2 ITBFS injury would consist of:

  • Manual adjustments to the ankle and foot, as well as medial glide mobilization of the patella to free up joint motion and improve tracking of the patella (45).
  • Deep tissue procedures, such as the Graston Technique (manual therapy that utilizes specially designed devices) and Active Release Technique (a patented manual therapy technique), to break up scar tissue and restore soft tissue motion (59). There is considerable clinical evidence to support the effectiveness of deep tissue procedures in treatment of strain/sprain injuries (60,61). A home exercise program for myofascial release therapy can be taught on a foam roller (Figure 12).
  • Ultrasound and electric muscle stimulation combination therapy to restore normal muscle tone, help in the healing process, and reduce pain (50,62). Iontophoresis with dexamethasone is also a useful modality to decrease inflammation (63).
  • Inflammation reduction by taking nonsteroidal anti-inflammatory medications per prescription, and applying a cold pack to the lateral aspect of the knee 20 minutes on/one hour off, repeated throughout the day.
  • Implementation of a strength training program for the gluteus medius, GM, and quadricep musculature. Exercises should include squats, standing hip abduction, and supine floor bridges with alternating leg lifts (Figures 13 A-C). Strengthening the gluteus musculature has been shown to be instrumental in returning athletes to pain-free running (10,51). Strengthening exercises should be progressed with no or little discomfort (64). When pain free training resumes, it is my opinion that a leg workout can be included once a week, with at least 48 hours rest before or after a long run.
  • Stretching routine. I have found that a 15-20 minute flexibility routine with a resistance band helps in decreasing delayed onset muscle soreness, as well as improving flexibility through hysteresis/creep. The flexibility routine should include stretching of the hamstrings, quadriceps, adductors, ITT, and external rotators of the thigh (65,66,67). Longer stretching (30-60 seconds), with short intermittent contractions of the antagonist, has been shown to be one of the best mobilization techniques for a painful muscle/tendon (11).
  • A recommendation to change running shoes every 300-500 miles of use, at which point the shoe loses 50% of its shock absorption capability (8,14).
  • A recommendation to use appropriate arch supports as necessary. A runner with pes planus will usually overpronate, leading to increased internal rotation of the tibia, a risk factor for ITBFS. A good sneaker with a firm heel counter and an inside arch support will help correct overpronation. If necessary a semirigid orthosis with a medial arch support no higher then 5/8 inch can be utilized to further control pronation. A runner with pes cavus has limited pronation and poor shock-absorbing capabilities. The high-arch runner should get a sneaker with good cushioning; if necessary a semirigid orthosis or cushioned liner can be added (1,8).
  • Recommendation for appropriate training limits. For marathon runners, initially a training base of four miles at 65%-75% maximum heart rate needs to be established. Later, a progressive training schedule should be followed that allows for adaptation of the supporting structures of the knee to withstand future increased stress loads. Long training runs, usually done on the weekend, should be limited to a pace that requires 65-75% maximum heart rate to improve aerobic capacity. During the week, a shorter 4-8 mile interval run at 85-90% maximum heart rate is recommended to improve anaerobic capacity. Hill training should be added gradually because of the increased load placed on the knee joint. The average marathon training schedule consists of 3 shorter runs during the week, and 1 longer run on the weekend. Total mileage should not be increased by more then 10% per week (33,46,50).

IBFS13

Early therapy and intervention (as above) are important to prevent a grade 3 ITBFS injury from progressing to a grade 4 or 5 injury. In the early stages of a grade 3 injury, one week of activity modification from the offending training regimen is recommended, as well as treatment procedures similar to those used to treat a grade 1 or 2 injury. Modified activity with swimming, running in the pool, bicycling, or an elliptical machine would be useful in maintaining aerobic fitness and allow for proper healing. Treating a more advanced grade 3 or grade 4 ITBFS injury would involve a longer bout of modified activity and rest from an offending activity, and a slower progression of weight training and stretching (68,69,70).

Chronic ITBFS may not always resolve with conservative therapy. In recalcitrant ITBFS, other treatment methods may need to be considered, such as steroid injection therapy and surgical procedures. Steroid injections, used judiciously, have been shown to reduce symptoms and inflammation (1,11,12,13). Steroid injection therapy should be followed by a properly progressed strength, flexibility and car- diovascular program to restore function before training resumes. Surgery should only be considered if all other means of therapy fail and the athlete is not willing to give up his sports activity (23). One type of surgery involves lengthening of the ITT at the level where the friction accumulates and typically involves two small incisions. The first incision is in the posterior fibers of the ITT that lie over the LFE when the leg is flexed to 30 degrees. The second incision is placed in the anterior fibers of the ITT proximal to the first incision, and is a “Y” shape to allow for maximal lengthening (1,9). In a study by Holmes et al., open release-excision, a surgical procedure involving removal of an ellipse of tissue that abrades the LFE, was found to be a safe and effective surgical procedure (71).

Conclusion

ITBFS is a common non-traumatic overuse injury that is particularly common in long distance runners. Certain biomechanical malalignments, such as rearfoot varus; forefoot varus; genu varum; pes cavus; a prominent LFE; weak GM, gluteus medius and Quadriceps musculature; and tight TFL, ITT, and lateral retinaculum predispose runners to ITBFS. The risk of ITBFS can be reduced if athletes follow a properly progressed training program that allows for adaptation of the structures supporting the pelvis, thigh and knee. To prevent injury, these athletes should incorporate proper footwear, semirigid orthosis as necessary, a lower body flexibility and strength training routine, and cross training into their workouts.

ITBFS can usually be treated successfully with a conservative rehabilitation program that includes modified training and a flexibility and strength home exercise program. When the athlete can run 3-4 miles pain-free on a treadmill, he can progress his training program carefully to prevent re-injury. Sometimes ITBFS is resistant to conservative therapy and a cortisone injection or surgery may need to be considered as alternative treatment options. Surgery, when necessary, may involve lengthening the ITT and removing a section of the posterior aspect of the ITT that is impinging on the LFE.

References

  1. Anderson GS. Iliotibial Band Friction Syndrome. The Australian Journal of Science and Medicine in Sport 1991; 81-83.
  2. Newell SG, Bramwell ST. Overuse Injuries to the Knee in Runners. The Physician and Sportsmedicine 1984; 12(3):80-92.
  3. Wen DY, Puffer JC, Schmalzried TP. Injuries in Runners: A Prospective Study of Alignment. Clinical Journal of Sports Medicine 1998; 8:187-194.
  4. Taunton JE, Ryan MB, Clement DB, McKenzie DC, Lloyd-Smith DC, Zumbo BD. A retrospective case-contol analysis of 2002 running injuries. British Journal of Sports Medicine 2002; 36:95-101.
  5. Kaufman KR, Brodine SK, Shaffer RA, Johnson CW, Cullison TR. The Effect of Foot Structure and Range of Motion on Musculoskeletal Overuse Injuries. American Journal of Sports Medicine 1999; 27(5):585-593.
  6. Brill PA, Macera CA. The Influence of Running Patterns on Running Injuries. Sports medicine 1995; 20(6):365-368.
  7. Schwellnus MP, Theunissen L, Noakes TD, Reinach SG. Anti-inflammatory and combined anti-inflammatory/ analgesic medication in the early management of iliotibial band friction syndrome. S Afr Med J 1991; 79:602-606.
  8. Barber FA, Sutker AN. Iliotibial Band Syndrome. Sports Medicine 1992; 14(2):144-148.
  9. Orchard JW, Fricker PA, Abud AT, Mason BR. Biomechanics of Iliotibial Band Friction Syndrome in Runners. American Journal of Sports Medicine 1996; 24(3):375-379.
  10. Fredericson M, Cookingham CL, Chaudhari AM, Dowdell BC, Oestreicher N, Sahrmann S. Hip Abductor Weakness in Distance Runners with Iliotibial Band Syndrome. Clinical Journal of Sport Medicine 2000; 10:169-175.
  11. Dahan R. Rehabilitation of Muscle- Tendon Injuries to the Hip, Pelvis, and Groin Areas. Sports Medicine and Arthroscopy Review 1997; 5:326-333.
  12. McNicol K. Iliotibial Tract Friction Syndrome in Athletes. Canadian Journal of Applied Sport Sciences 1981; 6(2): 76-80.
  13. Gunter P, Schwellnus MP. Local corticosteroid injection in iliotibial band friction syndrome in runners: a randomized controlled trial. British Journal of Sports Medicine 2004; 38:269-272.
  14. Messier SP, Edwards DG, Martin DF, Lowery RB, Cannon DW, James MK, Curl WW, Read HM Jr., Hunter DM. Etiology of iliotibial band friction syndrome in distance runners. Medicine and Science in Sports and Exercise 1995; 27(7):951-960.
  15. Noble C. Iliotibial band friction syndrome in runners. American Journal of Sports Medicine 1980; 8(4):232-234.
  16. Kwak SD, Ahmad CS, Gardner TR, Grelsamer RP, Henry JH, Blankevoort L, Ateshian GA, Mow VC. Hamstrings and Iliotibial Band Forces Affect Knee Kinematics and Contact Pattern. Journal of Orthopaedic Research 2000; 18:101-108.
  17. Kirk KL, Kuklo T, Klemme W. Iliotibial Band Friction Syndrome. Orthopedics?(orthobluejournal.co m) 2000; 23(11) 1209-1215.
  18. Noble AH, Hajek MR, Porter M. Diagnosis and Treatment of Iliotibial Band Tightness in Runners. The Physician and Sportsmedicine 1982; 10(4):67-74.
  19. Orvava S. Iliotibial Tract Friction Syndrome in Athletes – An Uncommon Exertion Syndrome on the Lateral Side of the Knee. British Journal of Sports Medicine 1978; 12(2):69-73.
  20. Birnbaum K, Siebert CH, Pandorf T, Schopphoff E, Prescher A, Niethard FU. Anatomical and biomechanical investigations of the iliotibial tract. Surg Radiol Anat 2004; 26:433-446.
  21. Renne JW. The Iliotibial Band Friction Syndrome. The Journal of Bone and Joint Surgery 1975; 57A(8):1110-1111.
  22. Provencher MT, Hofmeister EP, Muldoon MP. The Surgical Treatment of External Coxa Saltans (the Snapping Hip) by Z-plasty of the Iliotibial Band. American Journal of Sports Medicine 2004; 32(2):470-476.
  23. Martens M, Librecht P, Burssens A. Surgical Treatment of the iliotibial band friction syndrome. American Journal of Sports Medicine 1989; 17(5):651-654.
  24. Sutker AN, Barber A, Jackson DW, Pagliano JW.Iliotibial Band Syndrome in Distance Runners. Sports medicine 1985; 2:447-451.
  25. Anderson K, Strickland SM, Warren R. Hip and Groin Injuries in Athletes. American Journal of Sports Medicine 2001; 29(4):521-533.
  26. Terry GC, LaPrade RF. The Biceps Femoris Muscle Complex at the Knee: Its Anatomy and Injury Patterns Associated with Acute Anterolateral-Anteromedial Rotary Instability. American Journal of Sports Medicine 1996; 24(1):2-8.
  27. Staubli HU, Rauschning W. Popliteus Tendon and Lateral Meniscus: Gross and Multiplanar Cryosectional Anatomy of the Knee. American Journal of Knee Surgery 1991; 4(3):110-121.
  28. Brignall CG, Brown RM, Stainsby GD. Fibrosis of the Gluteus Maximus as a Cause of Snapping Hip. The Journal of Bone and Joint Surgery 1993; 75A(6):909-910.
  29. Doucette SA. The effect of exercise on patellar tracking in lateral patellar compression syndrome. American Journal of Sports Medicine 1992; 20(4):434-440.
  30. White RA, Hughes MS, Burd, T, Hamann J, Allen WC. A New Operative Approach in the Correction of External Coxa Saltans. American Journal of Sports Medicine 2004; 32(6):1504-1508.
  31. Gruen GS, Scioscia TN, Lowenstein JE. The Surgical Treatment of Internal Snapping Hip. American Journal of Sports Medicine 2002; 30(4):607-613.
  32. Terry GC, Hughston JC, Norwood LA. The anatomy of the iliopatellar band and iliotibial tract. American Journal of Sports Medicine 1986; 14(1):39-45.
  33. Norkin CC, Levangie PK. Joint structure and function: a comprehensive analysis, 2nd ed. Philadelphia: F.A. Davis, 1992:448-458.
  34. Donatelli RA. The biomechanics of the foot and ankle, 2nd ed. Philadelphia: F.A. Davis, 1996.
  35. Michaud TC. Foot orthosis and other forms of conservative foot care. Newton MA: Thomas C. Michaud, 1997.
  36. Swanson SC, Caldwell GE. An integrated biomechanical analysis of high speed incline and level treadmill running. Medicine & Science in Sports & Exercise 2000; 32(6):1146-1155.
  37. Scott SH, Winter DA. Internal forces at chronic running injury sites. Med Sci Sports Exerc 1990;22(3):357-369.
  38. Schepsis AA, Jones H, Haas AL. Achilles tendon disorders in athletes. Am J Sports Med 2002;30(2):287-305.
  39. Sanders TG, Miller MD. A Systematic Approach to Magnetic Resonance Imaging Interpretation of Sports Medicine Injuries of the Knee. American Journal of Sports Medicine 2005; 33(1):131-148.
  40. Muhle C, Ahn JM, Yeh LR, Bergman GA, Boutin RD, Schweitzer M, Jacobson JA, Haghighi P, Trudell DJ, Resnick D. Iliotibial Band Friction Syndrome: MR Imaging Findings in 16 Patients and MR Arthrographic Study of Six Cadaveric Knees. Radiology 1999; 212:103-110.
  41. Nemeth WC, Sanders BL. The Lateral Synovial Recess of the Knee: Anatomy and Role in Chronic Iliotibial Band Friction Syndrome. Arthroscopy: The Journal of Arthroscopic and Related Surgery 1996; 12(5):574-580.
  42. Kendall FP, McCreary EK, Provance PG. Muscles:Testing and Function, 4th edition. Baltimore: William & Wilkins, 1993.
  43. Sundqvist H, Forsskahl B, Kvist M. A promising novel therapy for Achilles Peritendinitis: double-blind comparison of glycosaminoglycans polysulfate And high-dose indomethacine. Int J Sports Med 1987;(8):298-303
  44. Smart GW, Taunton JE, Clement DB. Achilles tendon disorders in runners – a review. Med Sci Sports Exerc 1980;12(4):231-243.
  45. Menetrey J, Fritschy D. Subtalar subluxation in balet dancers. Am J Sports Med 1999;27(2):143-149.
  46. Smurawa TM. The Endurance Triathlete, Racing and Recovery.
  47. Scott WN. The Knee. Mosby, St. Louis. MO 1994.
  48. Martin DE, Coe PN. Better Training for Distance Runners. Illinois: Human Kinetics, 1997.
  49. LaPrade RF, Meunch C, Wentorf F, Lewis JL. The Effect of Injury to the Posterolateral Structures of the Knee on Force in a Posterior Cruciate Ligament Graft. American Journal of Sports Medicine 2002; 30(2):233-238.
  50. Reid DC. Sports Injury Assessment and Rehabilitation. New York: Churchill Livingston Inc., 1992.
  51. Doucetter SA, Child DD. The Effect of Open and Closed Chain Exercise and Knee Joint Position on Patellar Tracking in Lateral Patellar Compression Syndrome. JOSPT 1996; 23(2):104-110.
  52. Hyde TE, Gengenbach MS. Conservative Management of Sports Injuries. Baltimore, Maryland: Williams & Wilkins, 1997.
  53. LaPrade RF, Konowalchuk BK. Popliteomeniscal Fascicle Tears Causing Symptomatic Lateral Compartment Knee Pain: Diagnosis by the Figure-4 Test and Treatment by Open Repair. American Journal of Sports Medicine 2005. AJSM PreView published on July 6, 2005 as doi:10.1177/0363546504274144.
  54. LaPrade RF, Bollom TS, Wentorf FA, Wills NJ, Meister K. Mechanical Properties of the Posterolateral Structures of the Knee. American Journal of Sports Medicine 2005. AJSM PreView published on July 7, 2005 as doi:10.1177/0363546504274143.
  55. Jones CDS, Keene GCR, Christie AD. The Popliteus as a Retractor of the Lateral Meniscus of the Knee. Arthroscopy: The Journal of Arthroscopic and Related Surgery 1995; 11(3):270-274.
  56. LaPrade RF, Hamilton CD. The Fibular Collateral Ligament-Biceps Femoris Bursa: An Anatomic Study. American Journal of Sports Medicine 1997; 25(4):439-443.
  57. Biedert RM, Stauffer E, Friederich NF. Occurrence of free nerve endings in the soft tissue of the knee joint. American Journal of Sports Medicine 1992; 20(4):430-433.
  58. Bach BR, Minihane K. Subluxating Biceps Femoris Tendon: An Unusual Case of Lateral Knee Pain in a Soccer Athlete. American Journal of Sports Medicine 2001; 29(1):93-95.
  59. Kvist M, Jarvinen M. Clinical Histochemical and Biomechanical Features in Repair of Muscle and Tendon Injuries. International Journal of Sports Medicine. 1982; (3): 12-14.
  60. Walker JM. Deep Transverse Frictions in Ligament Healing. The Journal of Orthopaedic and Sports Physical Therapy 1984; 6(2):89-94.
  61. Brosseau L, Casimiro, Milne S, Robinson VA, Shea BJ, Tugwell P, Wells G. Deep transverse friction massage for treating tendinitis. The Cochrane Collaboration 2005; Volume (2).
  62. Gum SL, Reddy GK, Stehno-Bittel L, Enwemeka CS. Combined ultrasound, electric muscle stimulation, and laser promote collagen synthesis with moderate changes in tendon biomechanics. Am J Phys Med Rehabil 1997;76(4):288-296.
  63. Pellecchia GL, Hamel H, Behnke P. Treatment of Infrapatellar Tendinitis: A Combination of Modalities and Transverse Friction Massage Versus Iontophoresis. Journal of Sport Rehabilitation 1994; 3:135-145.
  64. Cohen ZA, Roglic H, Grelsamer R, Henry JH, Levine WN, Mow VC, Ateshian GA. Patellofemoral Stresses during Open and Closed Kinetic Chain Exercises. American Journal of Sports Medicine 2001; 29(4):480-487.
  65. Morelli V, Smith V. Groin Injuries in Athletes. American Family Physician 2001; 64(8):1405-1414.
  66. Heidt RS Jr., Sweeterman LM, Carlonas RL, Traub JA, Tekulve FX. Avoidance of Soccer Injuries with Preseason Conditioning. American Journal of Sports Medicine 2000; 28(5):659-662.
  67. Mirzabeigi E, Jordan C, Gronley JK, Rockowitz NL, Perry J. Isolation of the Vastus Medialis Oblique During Exercise. American Journal of Sports Medicine 1999; 27(1):50-53.
  68. James SL, Bates BT, Osternig LR. Injuries to runners. Am J Sports Med 1978;6(2): 40-50.
  69. Clement DB, Taunton JE, Smart GW. Achilles tendonitis and peritendinitis: etiology and treatment. AM J Sports Med 1984;12(3):179-184.
  70. Leadbetter WB. Cell matrix response in tendon injury. Clin Sports Med 1992;11(3): 533-579.
  71. Holmes JC, Pruitt AL, Whalen NJ. Iliotibial band syndrome in cyclists. American Journal of Sports Medicine 1993; 21(3):419-424.

©2006 Dubin Chiropractic

Special thanks to Audrey Mahoney for creating the illustrations.

Achilles Tendinopathies in Runners: Causes, Treatment, and Prevention

Download as pdf

achilles1The Achilles tendon, which runs from the top of the heel to the back of the calf, is a strong, non-elastic, fibrous tissue that attaches the gastrocnemius muscle (Figure 1A) and the soleus muscle (Figure 1B) to the calcaneus (heel bone) (1). Another name for the muscle group sharing the Achilles tendon is the “triceps surae.” The Achilles tendon can effectively absorb ground reactive forces associated with running that can approach 6-8 times body weight with an average of 800 foot strikes per mile (2, 23). Injury to the Achilles tendon or its surrounding sheath, the paratendon, can be the result of overuse, improper training, gait abnormalities, age related degenerative changes, or improper footwear (1-7). Recreational runners who prematurely increase the intensity, duration, and/or frequency of their training sessions are prone to developing Achilles tendon injuries because the Achilles tendon does not have the time to adapt to the increased demand. Improper training may lead to microtears and degenerative changes to the Achilles tendon or the surrounding paratendon, weakening the tendon and predisposing it to further injury. Achilles tendon injuries usually occur gradually, increasing in severity without proper treatment and rehabilitation. Symptoms of Achilles tendon injuries can include one or more of the following:

  • diffuse or localized swelling and tenderness around the tendon
  • pain with the first few steps after getting out of bed in the morning
  • exacerbation of the injury upon walking uphill.

Conservative therapy can aid in the normal reparative processes of Achilles tendon healing, thereby allowing athletes to return to their sport more quickly (4, 8).

There are three classifications of Achilles tendon injuries: tendinosis, tendonitis, and paratenonitis. Achilles tendinosis is a non-inflammatory asymptomatic condition that may lead to abnormal thickening of the tendon or other structural degenerative changes. These degenerative changes compromise the strength and function of the Achilles tendon, predisposing it to further injury. Achilles tendonitis and paratenonitis are painful inflammatory conditions of the Achilles tendon and surrounding paratendon respectively (1, 9, 10, 11).

To develop effective treatments for these injuries, it is necessary to understand the biomechanics of the ankle joint, the function of the triceps surae during a normal running gait, and the conditions that predispose the Achilles tendon to injury.

BIOMECHANICS OF THE ANKLE JOINT AND ACHILLES TENDON WITH RUNNING

A runner’s gait can be separated into two phases: the stance phase and the swing phase. During the stance phase, the foot contacts and adapts to the ground surface; during the swing phase, the leg accelerates forward and prepares for ground contact. The stance phase with walking consists of the following sub-phases: initial contact, loading response, midstance, and terminal stance (Figures 2). During initial contact, the heel contacts the ground surface. The loading response occurs immediately after initial contact, ending when the contralateral foot lifts off of the ground surface. During the loading response, the foot and ankle adapt to the terrain and absorb ground reactive forces. Double limb support occurs during initial contact and the loading response, when both feet are in contact with the ground surface. The midstance phase starts when the contralateral foot lifts off of the ground surface; the contralateral leg is now the swing leg. The midstance phase ends as the forward momentum of the swing leg and the tension on the triceps surae of the stance leg cause the heel to lift off of the ground surface. The terminal stance phase begins when the heel lifts off of the ground and ends when the swing leg contacts the ground. The running stance phase differs from the walking stance phase in that the stride is elongated, the cadence is increased, and double limb support is eliminated (Figures 3) (6, 12, 13).

achilles2

achilles3

achilles4_5There are two types of active muscle contractions: eccentric and concentric. An eccentric contraction involves lengthening of a muscle as it attempts to decelerate a particular movement, while a concentric contraction involves shortening of a muscle as it generates force to produce movement across a joint. Most overuse soft tissue injuries are caused by repetitive eccentric forces that exceed the tensile strength of the tissue that is attempting to decelerate a particular movement. The Achilles tendon is the strongest tendon in the body; normally it does not incur injury when absorbing the eccentric forces exerted on it during running or jumping (1). However certain gait abnormalities, tightness of the calf musculature, improper training, and age-related changes can predispose the Achilles tendon to repetitive microtrauma and injury.

The ankle joint is actually two joints: the talocrural joint and the subtalar joint. The talocrural joint is the articulation between the leg bones (tibia and fibula) and the talus (an ankle bone) (Figure 4). Two types of movements primarily occur at the talocrural joint: plantarflexion and dorsiflexion. Plantarflexion of the talocrural joint involves the toes pointing downwards as the heel lifts off of the ground (Figure 5). Plantarflexion of the ankle joint occurs when conducting a calf raise as the triceps surae contracts concentrically. Dorsiflexion of the ankle joint involves approximation of the leg towards the foot and occurs throughout the midstance phase of gait (Figure 6).

achilles6During the midstance phase of gait, the triceps surae contracts eccentrically, exerting force through the Achilles tendon to decelerate forward movement of the stance leg over the foot (2, 4, 14). Dorsiflexion of the ankle joint is dependent on flexibility of the triceps surae. A tight tricep surae limits dorsiflexion of the ankle joint, placing excessive eccentric strain on the Achilles tendon throughout midstance, predisposing it and the surrounding paratendon to injury.

The subtalar joint of the ankle consists of the articulation between the talus and the underlying calcaneus (Figure 7). Two primary movements occur at the subtalar joint: inversion and eversion. Subtalar joint inversion involves the calcaneus turning inward (Figure 8). The ankle joint is stabilized in subtalar inversion as the ligaments and surrounding structures on the outside of the ankle become taut. Inversion of the calcaneus occurs during the initial contact phase to prepare for ground contact, and later in the terminal stance phase to provide a rigid platform for toe-off. Subtalar joint eversion involves the calcaneus turning outward (Figure 9). Eversion of the calcaneus occurs during the loading response and continues into the beginning of midstance. From loading response to midstance the foot and ankle change from a rigid lever into a mobile shock absorber and adapt to the terrain.

achilles7achilles8_9

Initially, when the foot strikes the ground, it is in supination; the talocrural joint is neutral and plantarflexing, the subtalar joint is inverted, and the forefoot is adducted – toes are directed towards the midline (Figure 10). The supinated position maintains stability of the ankle joint during initial contact with the ground. After initial contact the ankle pronates, the talocrural joint dorsiflexes, the subtalar joint everts, and the forefoot abducts – toes are pointed away from the midline (Figure 11). The ankle pronates during the loading response and into the beginning of midstance, allowing the ankle and foot to absorb compressive forces and become a mobile adaptor to the ground. During pronation the triceps surae contracts eccentrically to decelerate eversion and dorsiflexion at the ankle joint. The ankle re-supinates during midstance to create a rigid lever for effective toe-off.

achilles10During initial contact the calcaneus is normally in 2-3 degrees of inversion. However, certain structural abnormalities can change normal inversion. One such structural abnormality, rearfoot varus, involves excessive inversion of the calcaneus during initial surface contact. To compensate for rearfoot varus, the subtalar joint pronates excessively and at a faster speed than normal to allow for the medial aspect of the calcaneus to contact and adapt to the terrain. The excessive pronation of the subtalar joint, which occurs at an increased velocity from initial contact to midstance, places an increased eccentric load on the Achilles tendon, predisposing the tendon to injury.

achilles11Forefoot varum is another structural abnormality that predisposes the Achilles tendon to injury. In this condition the forefoot has an increased inversion tilt as compared to the rearfoot. Forefoot varum leads to prolonged pronation through midstance and into terminal stance to allow for the inside of the forefoot to contact the ground surface. During the beginning of midstance and into terminal stance of a normal running gait, the subtalar joint re-supinates to change the foot into an effective rigid lever for toe-off. However, a runner’s gait with forefoot varum may exhibit prolonged pronation throughout midstance causing the subtalar joint to rapidly re-supinate and create a rigid lever for toe-off. Prolonged pronation into midstance followed by an attempt of the subtalar joint to re-supinate causes a bowstring effect on the Achilles tendon (Figure 12). The bowstring effect places an increased eccentric load on the medial side of the Achilles tendon, predisposing it to injury (5, 15, 23, 24).

achilles12The subtalar joint in a runner with a flat inside arch (pes planus) tends to overpronate, causing an increased eccentric strain on the Achilles tendon. The subtalar joint in a runner with a rigid high inside arch (pes cavus) has limited pronation. Limited pronation decreases the ability of the foot and ankle to absorb ground forces, leading to transmission of excessive forces through the Achilles tendon and other adjacent structures.

Runners in their 30s and 40s have an increased risk of developing Achilles tendon injury because the collagen (supportive subunits of muscles, tendons, and ligaments) of the triceps surae degrades with age (16). Without adequate time to rest and heal between bouts of exercise the tricep surae of these athletes are predisposed to injury. To prevent injury older athletes should train on softer surfaces and cross-train with exercises such as cycling, swimming, cross country skiing, rollerblading, and use of a quality elliptical machine.

Factors predisposing an athlete to developing Achilles tendon injuries include tight gastrocnemius and soleus musculature, overpronation and increased velocity of pronation from initial contact through the beginning of midstance, prolonged pronation during midstance, age-related degenerative processes of the Achilles tendon, and training programs that do not allow for adaptation of the Achilles tendon. Initial training programs that incorporate too many uphills or downhills, high intensity interval training, and excessive mileage, lead to injury because the Achilles tendon is not allowed to adapt.

GRADES OF TENDON INJURIES AND PHASES OF TISSUE REPAIR AND TREATMENT

There are five grades of tendon injuries:

Grade 1 – Pain does not occur during normal activity, but generalized pain is felt in the Achilles tendon about 1 to 3 hours after sport-specific training has ended. Tenderness in the Achilles tendon usually resolves within 24 hours without intervention.

Grade 2 – Minimal pain is present in the Achilles tendon towards the end of the sport-specific training session, but performance is not affected. Appropriate treatment may be necessary to prevent a Grade 3 injury.

Grade 3 – Pain is present in the Achilles tendon at the onset of training, and interferes with the speed and duration of a training session. Treatment and training modification are necessary to prevent a grade 3 injury from progressing to a grade 4 injury.

Grade 4 – Pain in the Achilles tendon restricts training and is also noticeable during activities of daily living; the athlete can no longer continue sport-specific training. Low impact training, such as swimming and biking, can be implemented for cardiovascular fitness and aggressive musculoskeletal therapy can decrease the severity of the injury. The goal of therapy is to restore structural integrity of the tissues allowing for the athlete to return to pain-free sport-specific training.

Grade 5 – Pain in the Achilles tendon interferes with training as well as activities of daily living. The Achilles tendon becomes deformed and there is a loss of function of the triceps surae (5). Aggressive therapy is required and surgery may be necessary.

Conservative therapy is usually successful for treatment of Achilles tendon injury. A thorough history and examination will help find the cause of the Achilles tendon injury. Was the injury caused by improper training techniques, age related degenerative changes, a tight tricep surae or biomechanical dysfunction of the rear or forefoot? Initial goals of therapy are to reduce swelling and inflammation of the tendon and paratendon to alleviate acute tendon injury or chronic flare-ups so the patient can perform activities of daily living with less pain. Pain-free modified training can then be implemented to improve strength and flexibility of the triceps surae, as well as cardiovascular fitness. The end goal is to return the athlete to pain free running. However, even if the pain dissipates, the athlete should be made aware that it takes time for the Achilles tendon to regain full strength and function. With fewer blood vessels then muscles, tendons have a limited oxygen and nutrient supply. Faced with this shortage, tendons take a longer time to heal than muscles.

There are three phases of tissue repair: the reactive phase, the regenerative phase, and the remodeling phase. The reactive phase is the initial inflammatory response to microtrauma. Vasodilation of the blood vessels surrounding the injured tendon or muscle occurs, causing swelling, pain, and loss of function. To limit the immobilizing effects of the reactive phase, RICE (rest, ice, compression, and elevation) should be applied to the injured region. During the regenerative phase dead cells are cleared out, tiny blood vessels are restructured to help supply oxygen to the damaged tissue, and collagen is laid down for repair. The reparative collagen is initially weak, but with time its strength improves. After 7-14 days, damaged muscle regains approximately 50% of its strength; tendons may take a longer time to regain their strength. During the remodeling phase, the reparative collagen matures. After completing a proper medical treatment program and complying with a home strength-training and flexibility routine, the athlete may regain 100% strength. The remodeling phase can take up to six months for muscle repair and even longer for tendon repair, depending on the severity of the injury (11, 17, 18).

Appropriate treatment of a grade 1 or a grade 2 Achilles tendon injury consists of:

1. Manual adjustments to the ankle and foot to free up joint motion (25).

2. Deep tissue procedures, such as Graston Technique and Active Release Technique, to break up scar tissue in the affected tendon or paratenon and restore soft tissue motion and glide (19).

3. Ultrasound and electric muscle stimulation are useful modalities to restore normal muscle tone, help in the healing process, and decrease pain (17, 20).

achilles134. Inflammation reduction by icing the Achilles tendon for 20 minutes on, 1 hour off, repeating throughout the day, and use of NSAIDs (non-steroidal anti-inflammatory drugs) per primary doctor recommendation. Iontophoresis with dexamethasone is also a useful modality to decrease inflammation.

5. A strength training program for the gastrocnemius and soleus musculature, including standing and seated calf raises (Figure 13A and 13B). Studies have indicated that emphasizing eccentric strength training of the triceps surae has been beneficial in treatment and prevention of future Achilles tendon injuries (26, 27). Dorsiflexion strengthening exercises should also be implemented to increase the strength of the tibialis anterior and extensor musculature (Figure 14). Strengthening exercises should progress appropriately with no or little discomfort.

6. Use of a step or slant board to stretch the triceps surae (Figure 15A and 15B). A stretching and strengthening routine for the lower extremities, using a resistive band, can be implemented to improve strength of the dorsiflexors and evertors and flexibility of the hamstring and calf musculature.

achilles147. A recommendation to replace running sneakers after 250-400 miles of use, at which point the shoe loses 40% of its shock absorption abilities.

8. The possible recommendation of appropriate arch supports. A runner with a flat inside arch, pes planus, will usually overpronate, placing an increased strain on the Achilles tendon. A good sneaker with a firm heal counter and an inside arch support will aid in correcting overpronation and help in preventing Achilles tendon injury. If the Achilles tendon injury does not resolve with sneaker adjustment, a semi-rigid orthotic with no more than 5/8” medial arch support is useful. A temporary 1/8” heel lift can also be added to the orthotic to limit dorsiflexion of the foot; this takes pressure off of the injured Achilles tendon. A runner with a high inside arch has limited pronation and poor shock absorption. The high arch runner should get a sneaker with good cushioning; if necessary a semi-rigid orthotic or cushioned liner can be added (3, 4, 8, 13, 28).

achilles159. A night splint that maintains the ankle and foot in slight dorsiflexion can help to alleviate morning stiffness in the Achilles tendon (23). For more advanced cases of Achilles tendon injury a walking splint can alleviate stress on the slowly healing tendon.

10. Recommendations for appropriate training limits. For marathon runners, an initial training base of four miles at 65%-75% maximum heart rate. A gradual progressive training schedule should follow. A proper warm-up, consisting of a slow jog, increases the blood supply to the muscles and tendons, making them more efficient in absorbing loads. Hill training should be added gradually to a training route because uphill running increases the eccentric load on the Achilles tendon.

Early therapy and intervention are important to prevent a grade 3 tendon injury from progressing to a grade 4 or a grade 5 tendon injury. In the early stages of a grade 3 tendon injury, one week of modified activity is recommended, along with treatments similar to those administered for grade 1 and grade 2 injuries. Modified activity with swimming, running in the pool, bicycling, or using a quality elliptical machine maintains aerobic fitness and allows the triceps surae to heal properly before the athlete resumes full training. Treatment of a more advanced grade 3 or grade 4 tendon injury involves a longer bout of modified activity, rest from the offending activity, and a slower progression of weight training and stretching (3, 4, 18).

Chronic Achilles tendon injuries may not always resolve with conservative therapy. Initially, microscopic tears in the Achilles tendon or paratendon repair naturally with Type III collagen. Type III collagen is immature, disorganized scar tissue that temporarily binds the damaged tendon fibers. Type III collagen is later replaced by Type I collagen, mature scar tissue that has a similar parallel arrangement of fibers as the normal tendon tissue. With time and a properly progressed rehabilitation program the Type I collagen scar regains the tensile strength of the normal tendon tissue. However, sometimes the type III collagen is not always replaced by type I collagen in the later stages of healing. The immature scar tissue remains a chronically inflamed and weakened structure that may be palpated as a tender nodule, usually located on the medial side of the Achilles tendon. The degenerative scar tissue may be resistant to conservative care, and attempting to train on the injured tendon may cause further injury. An athlete who wants to return to running without pain may need to consider surgery. Magnetic Resonance Imaging has been shown to be extremely sensitive to pathological changes in the Achilles tendon and may be a useful tool for the surgeon in discovering degenerative tissue that needs debridement. Surgery usually involves excision of the degenerative intratendinous lesion, followed by rehabilitation. In cases of chronic paratenonitis “brisement” – distension of the paratenon-tendon-interface may help to resolve paratenonitis (23, 29, 30, 31).

CONCLUSION

Athletes participating in sports involving repetitive jumping and running are predisposed to developing Achilles tendon injury. Achilles tendon injuries can be reduced by following a properly progressed training program that allows for adaptation of the Achilles tendon to adapt to increased eccentric loads. Certain biomechanical dysfunction, such as, rearfoot varus, forefoot varus, pes cavus, tight and weak triceps surae, and age-related degenerative changes, also predispose an athlete to Achilles tendon injury. To prevent injury athletes with these dysfunctions should incorporate proper sneaker wear – if necessary semi-rigid orthotics – as well as lower body flexibility, strength and cross training. Achilles tendon injuries can usually be treated successfully with a conservative rehabilitation program that includes modified training and incorporates eccentric strength training of the triceps surae. The athlete must be made aware that it takes time for the Achilles tendon to heal even with rehabilitation. After the Achilles tendon regains function and becomes pain free, the athlete should implement an appropriate training program to prevent re-injury. Sometimes Achilles tendon injuries are resistant to conservative therapy. In such cases surgery and proper rehabilitation may be necessary to remove the degenerative tissue from the tendon or paratendon to allow for proper healing and restoration of strength and function.

REFERENCES

1. Scioli MW. Achilles Tendinitis. Orthopedic Clinics of North America. 1994; 25(1): 177-182.

2. Scott SH, Winter DA. Internal forces at chronic running injury sites. Medicine and Science in Sports and Exercise. 1990; 22(3): 357-369.

3 James SL, Bates BT, Osternig LR. Injuries to runners. The American Journal of Sports Medicine. 1978; 6(2): 40-50.

4. Clement DB, Taunton JE, Smart GW. Achilles tendonitis and peritendinitis: Etiology and treatment. The American Journal of Sports Medicine. 1984; 12(3): 179-184.

5. Sundqvist H, Forsskahl B, Kvist M. A promising novel therapy for Achilles peritendinitis. International Journal of Sports Medicine. 1987; (8): 298-303.

6. Donatelli RA. The Biomechanics of the Foot and Ankle. F.A. Davis Company. 1996; (2nd edition).

7. Backman C, Friden J, Widmark A. Blood flow in chronic Achilles tendinosis. Acta Orthop Scand. 1991; 62(4): 386-387.

8. Schepsis AA, Leach RE. Surgical management of Achilles tendonitis. The American Journal of Sports Medicine. 1987; 15(4): 308-315.

9. Kalebo P, Allenmark C, Peterson L, Sward L. Diagnostic value of ultrasonography in partial ruptures of the Achilles tendon. The American Journal of Sports Medicine. 1992; 20(4): 378-381.

10. Martti KH, Lehto MU, Laszlo J, Markku J, Helmer KT. An immunohistologic study of fibrinectin and fibrinogen. The American Journal of Sports Medicine. 1988; 16(6): 616-623.

11. Banks AS, Downey MS, Martin DE, Miller SJ. Foot and Ankle Surgery. Lipincott Williams and Wilkins. 2002; 2 (3rd edition).

12. Norkin CC, Levangie PK. Joint Structure and Function: A Comprehensive Analysis. 1992; 2nd edition: 448-458.

13. Michaud TC. Foot Orthosis and Other Forms of Conservative Foot Care. 1997.

14. Rodgers MM. Dynamic Biomechanics of the Normal Foot and Ankle During Walking and Running. Physical Therapy. 1988; 12(68): 1822-1829.

15. Smart GW, Tanton JE, Clement DB. Achilles Tendon Disorders in Runners. Medicine and Science in Sports and Exercise. 1980; 4: 231-243.

16. Strocchi R, Depasquale V, Guizzardi S, et al. Human Achilles tendon: morphological and morphometric variations as a function of age. Foot Ankle. 1991; 12: 100-104.

17. Reid D. Sports Injury Assessment and Rehabilitation. Churchill Livingston International. 1992.

18. Leadbetter WB. Cell Matrix Response in Tendon Injury. Clinics in Sports Medicine. 1992; 11(3): 533-579.

19. Kvist M, Jarvinen M. Clinical Histochemical and Biomechanical Features in Repair of Muscle and Tendon Injuries. International Journal of Sports Medicine. 1982; (3): 12-14.

20. Gum SL, Reddy GK, Stehno-Bittel L, et al. Combined ultrasound, electric stimulation, and laser promote collagen synthesis with moderate changes in tendon biomechanics. American Journal of Physical Medicine and Rehabilitation. 1997; 76: 288-296.

21. Hamill J, Bates BT, Holt KG. Timing of lower extremity joint actions during treadmill running. Medicine and Science in Sports and Exercise. 1991; 807-813.

22. Astrom M, Westlin N. Blood Flow in Chronic Achilles Tendinopathy. Clinical Orthopaedics. 1994; (308): 166-172.

23. Schepsis AA, Jones H, Haas LA. Achilles Tendon Disorders in Athletes. The American Journal of Sports Medicine. 2002; 30(2): 287-305.

24. Tiberno D. Pathomechanics of Structural Foot Deformities. Physical Therapy. 1988; 68(12): 1840-1849.

25. Menetrey J, Fritschy D. Subtalar Subluxation in Ballet Dancers. The American Journal of Sports Medicine. 1999; 27(2): 143-149.

26. Shalabi A, Wilberg MK, Svennson L, Aspelin P, Movin T. Eccentric Training of the Gastrocnemius- Soleus Complex in Chronic Achilles Tendinopathy Results in Decreased Tendon Volume and Intratendinous Signal as Evaluated by MRI. The American Journal of Sports Medicine. 2004; 32(5): 1286-1296.

27. Fahlstrom M, Lorentzon R, Alfredson H. Painful Conditions in the Achilles Tendon Region in Elite Badminton Players. The American Journal of Sports Medicine. 2002; 20 (1): 51-54.

28. Gross ML, Davlin L, Evanski PM. Effectiveness of Orthotic Shoe Inserts in the Long-Distance Runner. 1991; 19: 409-412.

29. Maffulli N, Ewen SB.W., Waterston SW, Reaper J, Barrass V. Tenocytes from Ruptured and Tendinopathic Achilles Tendons Produce Greater Quantities of Type III Collagen than Tenocytes from Normal Achilles Tendons. The American Journal of Sports Medicine. 2000; 28(4): 499-505.

30. Paavola M, Kannus P, Paakkala T, Pasanen M, Jarvinen M. Long Term Prognosis of Patients with Achilles Tendinopathy. The American Journal of Sports Medicine. 2000; 28(5): 634-642.

31. Maffulli N, Testa V, Capasso G, Sullo A. Calcific Insertional Achilles Tendinopathy. The American Journal of Sports Medicine. 2004; 32(1): 174-182.

Special thanks to Audrey Mahoney for creating the illustrations.

Anterior Cruciate Ligament Injury: Pre- and Post-operative Rehabilitation

Download as pdf

acl_1The anterior cruciate ligament (ACL) is a tough fibrous structure that attaches the tibia (lower leg bone) to the femur (thigh bone) (Figure 1). This ligament helps to stabilize the knee by preventing excessive forward movement of the tibia on the femur. ACL injuries commonly occur in athletes participating in sports such as football, basketball, soccer, and volleyball, where movements such as cutting, pivoting, single leg landing and rapid decelerations are routinely performed. Tearing of the ACL is most commonly caused by landing awkwardly or cutting on a fully extended or slightly flexed leg with the foot turned outward (Figure 2).

Skiers usually injure the ACL when they catch the inside edge of a ski on ice, causing them to lose control and fall backwards as they hyperflex the knee. The injured athlete may report hearing a “pop” and that it felt like the knee was being stretched apart. Examination of the knee may reveal extensive swelling around the knee joint, loss of full extension of the knee and an inability of the athlete to bear weight on the injured leg. Manual testing may reveal excessive forward movement of the tibia on the femur.

acl_2Once the athlete is diagnosed with an ACL injury, the first step is to decide whether to undergo surgery to reconstruct the torn ligament, or to rehabilitate the knee without surgery. ACL reconstructive surgery would be recommended for athletes who continue to suffer from repetitive bouts of the knee giving away, or for those athletes who want to return to a highly competitive sport level. Athletes deciding not to have reconstructive surgery may be able to return to an active lifestyle after completing a rehabilitation program; however, they must learn to modify their activities to accommodate for the compromised stability of the knee due to the lost check-rein function of the ACL.

Pre-operative rehabilitation is important for those athletes who choose to undergo surgical reconstruction. The main goals of the pre-operative rehabilitation protocol are to reduce swelling around the knee joint, and to restore full range of motion and functional strength to the injured limb. The pre-operative rehabilitation phase prepares the patient physically and mentally for both the surgery and the postoperative rehabilitation program.

Post-operative rehabilitation begins immediately after surgery. The most important goals in the first two weeks are to reduce swelling and restore full range of motion of the knee in extension and flexion. Once range of motion is restored and swelling is minimized, the progression of the post-operative program depends on the patient’s determination, level of swelling and pain, and the clinician’s knowledge of the normal biological progression of healing of the reconstructed ligament. Some athletes progress rapidly in the post-operative phase of rehabilitation and may begin sport-specific training at a low intensity level in two to three months. However, full functional rehabilitation of the reconstructed ACL may not occur until six to 12 months post-operatively. The therapist must be careful on the progression of the rehabilitation exercises and on the timetable for returning the athlete to their particular sport. An accelerated rehabilitation program under a controlled environment allows the athlete to return to sport sooner, without increasing the risk of complications.

Origin and Insertion Points of the Anterior Cruciate Ligament

The bottom of the femur consists of the medial and lateral femoral condyles, circular bony protuberances that are separated by an intercondylar notch. The top of the tibia consists of the medial and lateral tibial plateaus, flat slightly concave surfaces that articulate with the respective femoral condyles. The anterior cruciate ligament originates from the posterior outer aspect of the intercondylar notch and proceeds anteriorly, where it inserts onto the outside edge of the medial tibial plateau (see Figure 1).

acl_3

Graft Tissue Healing Post-Surgery

In athletes, a torn anterior cruciate ligament is typically removed and replaced by their own tissue that is similar in length and strength. The two most common self-tissue grafts are the bone-tendon-bone (specifically, tibial tuberosity bone – patella tendon – patella bone graft) (Figure 3A), and the hamstring tendon graft (specifically, the tendons of the inside hamstring muscle [semitendinosis], and adjacent groin muscle [gracillis]) (Figure 3B). The selected graft tissue would be surgically placed in the anatomical location of the previous ACL and then secured by interference screws.

Both types of grafts have advantages and disadvantages. The surgeon selects the appropriate type of surgery based on the patient’s sport and the movements most frequently used.

A study by Rodeo et al evaluated tendon-to-bone healing in a dog model and found that a firm attachment of tendon to bone occurred at 12 weeks post-surgery. At two weeks post surgery there was still no continuity between the graft tendon and the insertion point in the bone. At four weeks there was minimal continuity between tendon and bone. At eight weeks there was considerably improved continuity between tendon and bone. After 12 weeks the tendon graft was safely secured to the surrounding bone, at which point failure of the graft-insertion point was minimal.

Based on the results of the above study, from zero to four weeks post-surgery therapy should focus on decreasing inflammation and restoring full range of motion of the knee. Swimming, stationary cycling, isometric contraction exercises, and other low-force muscle integrating techniques can be implemented in the earlier stages of rehabilitation. If the patient experiences pain, swelling or decreased range of motion of the knee, the inflammation should be reduced, range of motion restored, and the intensity of the rehabilitation phase should be slowed down. During the 12-week healing period, exercise selection should be carefully monitored by a skilled therapist to reduce the risk of complications.

Rehabilitation of the Knee: Decrease Swelling and Restore Range of Motion

Rehabilitation after ACL reconstruction surgery should initially focus on decreasing inflammation and restoring normal range of motion. Every patient heals differently; the progression of the rehabilitation program should be customized to the athlete and progressed to their tolerance.

Initially decreasing inflammation around the knee joint using ice, compression, and elevation is feasible with a couple of icepacks, an ace bandage, and pillows to prop the leg up. Ice therapy should be maintained 20 minutes on and one hour off, multiple times per day. Ankle pumps (flexion and extention of the foot) with the leg elevated can be conducted five minutes per hour to further reduce swelling. A Cryo-Cuff, if available, is a more advanced method of decreasing inflammation. The Cryo-Cuff can be wrapped around the knee and filled with ice water. A cooler of ice water is attached by tubing to the CryoCuff and can be used to replace the old water in the cuff with ice cold water every hour. Anti-inflammatory medication is also useful in reducing swelling around the knee joint.

The next couple of steps of the post-operative phase should be conducted to the patient’s tolerance.

The patient should use crutches following the first two days post-surgery, with minimal weight bearing. Additional weight may be applied to the injured leg, with crutches, as tolerated. By the end of the first week, the patient may ambulate without the support of crutches if a normal walking gait cycle with full weight bearing can be sustained with no noticeable instability. The patient should be able to ambulate without crutches six to seven days post-operatively.

Restoring full range of motion of the injured knee, particularly in extension, should be a priority in the first two weeks post-surgery. After the first week of post-operative rehabilitation, the patient should be able to fully extend the leg and flex the leg to 110 degrees. At this point, full extension is the most important goal; flexion of the knee improves steadily as swelling around the knee joint decreases. If full extension of the knee is not restored within two weeks post-surgery, scar tissue may develop in the joint, preventing the restoration of full knee extension.

The continuous passive motion machine (CPM), an electrical motor-driven device, may be used in the hospital immediately following recovery from surgery. This machine has shown promise in helping to restore normal motion and flexibility of the injured leg. The CPM supports the leg while moving it from full extension to a progressively set degree of flexion. There is a ten-second pause at the end of each movement, during which time the patient will isometrically contract the quadriceps (front thigh muscles).

acl_4

After the patient is released from the hospital, a specific series of exercises (provided by a trained therapist) should be done as often as possible to restore full range of motion of the knee in extension. Passive extensions (Figure 4A) and weighted extensions and prone leg hangs (Figure 4B) are useful exercises for restoring extension of the knee. During passive extensions, the patient can lie on the back with the heel propped up on pillows. Once the leg is relaxed in extension, the patient can periodically contract the quadricep musculature to push the knee further into extension. The patient then holds the quadracep contraction for five seconds, then returns to relaxed extension. This exercise should be done for 15 minutes and repeated every waking hour. If extension is not achieved this way, the patient may progress to weighted extension exercises by placing a five to ten pound weight just above the knee and following a similar procedure as passive extensions. The patient should be instructed to perform this exercise for ten minutes, taking the weight off for one minute and repeating multiple times during the day. Prone leg hangs (Figure 4B) can also aid in restoring extension of the knee. Have the patient lie on the stomach with the knee just past the edge of the table or bench with the knee in full extension; use a weight if struggling with full extension. The patient should perform this exercise for ten minutes, by gently flexing and extending the knee and repeating multiple times per day.

Towel stretch extension exercises (Figure 4C) can be incorporated if the above exercises are not restoring extension appropriately. The patient sits on a bench, places a towel around the foot of the injured leg, and applies tension to the towel to dorsiflex the foot, pulling the toes backward. The patient then raises the heel off of the ground to bring the knee into extension while placing the other hand on the thigh to stabilize the leg.

The patient would lie down on the back with the ankle raised and secured into a heel rest; a pad would be placed above and below the knee joint. These pads are secured by ropes passing through a ratchet system that would be tightened to force the knee into full extension (Figure 4D).

A normal gait cycle depends on a person’s ability to lock the knee in full extension while weight bearing. The following resistive tubing exercise can aid in accomplishing this goal. Resistive tubing can be secured above the standing patient’s knee cap and anchored to a bench behind the patient; the resistive force of the tubing will promote full extension while standing.

acl_5

Heel slides, supine leg hangs, and prone flexion exercises with the Flexband® (Figures 5A, 5B, and 5C) can be used to restore flexion of the injured knee. Heel slides are conducted with the patient lying on the back, sliding the heel towards the buttocks until tension is felt; the position is then held for one to two minutes. Then the heel slides down into full extension. This exercise should be repeated ten times, once every waking hour. See Figure 5A.

Supine leg hangs are conducted with the patient lying on the back, grasping the hands behind the thigh and lifting the thigh towards the chest with the leg flexed. The patient then allows the leg to drop down into flexion, holding this position for two minutes. The knee is then returned to a relaxed extended position and repeated multiple times throughout the day. See Figure 5B.

Prone (on the stomach) flexion exercises can be conducted with the Flexband®. Starting out on the back, the patient creates a toe-loop with the Flexband® around the injured knee’s foot and then turns onto the stomach. The band is then swung over the head, slowly increasing the band’s tension, hand over hand, while the ankle is aligned to the buttocks. The stretch should be held for three to four minutes, repeated several times throughout the day. See Figure 5C.

Rehabilitation of the Knee: Restoring Static Restraints, Dynamic Restraints, Proprioception and Sport-Specific Skills

The static restraints of the knee are the ligaments and bony architecture that limit movement. Surgical reconstruction of the ACL restores the check-rein function of the ligament by preventing excessive forward movement of the tibia on the femur.

The dynamic restraints of the knee are the muscles and tendons that surround the knee. These muscles and tendons maintain joint position and react to changing loads and forces. Post-surgery rehabilitation depends on restoring the function of these dynamic restraints, with the main focus on restoring flexibility and strength to the hamstring and quadriceps musculature. During the initial phases of rehabilitation, isometric strength training exercises are implemented, where the muscle neither shortens nor elongates, but force is generated. A straight leg raise is an example of an isometric strength training exercise for the quadriceps musculature. Later in the post-operative rehabilitation phase, exercises will be conducted to develop eccentric strength (whereby the muscle elongates to decelerate a particular movement) and concentric strength (whereby the muscle shortens to promote a particular movement). An example of an eccentric exercise would be step-downs off of a two-inch box with the good leg. During a step-down the quadriceps of the injured leg will eccentrically fire to decelerate and control leg flexion; simultaneously the gluteus musculature of the injured leg would fire to stabilize the pelvis so the body doesn’t tilt to the side of the uninjured leg that is stepping down. An example of a concentric strengthening exercise would be forward stepups, whereby the quadriceps would concentrically contract to force the leg to extend. Rehabilitation of the dynamic restraints will aid in taking stress off of the repaired ACL, preventing re-injury.

Proprioception is best defined as reception of sensory input from mechanoreceptors (specialized cells located in the skin, muscles, tendons, ligaments, and joints), the visual field, and the vestibular system. This sensory input is processed at the spinal cord, then at the mid-brain or the more complex cerebral region. Then a reflex or motor response is generated and then regulated until the desired movement is attained. There are three main types of reflexes, the fastest being the involuntary knee jerk reflex that involves no brain processing or thought. The second fastest reflex involves thought processing through the midbrain, and the slowest reflex involves more involved thought processing in the cerebrum. Repetitive balance and movement drills can transfer reflexes that initially involve complex sensory processing in the cerebrum to the mid-brain, leading to faster more precise movement patterns. Proprioception training involves retraining and fine tuning reflexes and movement patterns through balance drills, agility drills, plyometric jumping drills, and sportspecific training. Proprioception training will increase the state of readiness of the knee joint, decreasing the chance of re-injuring the ACL upon return to sport.

Full functional rehabilitation of the knee depends on restoring static stability, dynamic stability, and proprioception. The rehabilitation program should be individualized in regards to the patient’s coordination, desire, and specific sport.

Weeks 0-2

The goals of the first two weeks of post-operational rehabilitation are to reduce swelling, restore full range of motion in extension and flexion, ambulate without the use of crutches, and sit down and stand from a seated position. Straight leg raises, side raises/abduction exercises, and assisted leg extensions to full extension (with the help of the therapist or the opposite foot) are good exercises to initiate muscle firing of the quadriceps and gluteus musculature.

Muscles located in and above the back of the thigh, the hamstrings and gluteus structures, stabilize the pelvis during ambulation and squatting-type movements. Two exercises that are instrumental in returning coordinated strength to the leg are isometric co-contractions of the hamstring and quadriceps musculature, and the other is properly performed quarter squats and full chair squats. The co-contractions should initially be conducted at 30 degrees of flexion, progressing at ten-degree intervals up to 90 degrees. Squats should be conducted at the patient’s tolerable range of motion in a controlled manner. During the squat, the patient should focus on squeezing the hamstrings and gluteus musculature during the downward movement of the squat and keep a vertical shin angle; these two actions will prevent the patient from leaning forward and placing undue stress on the knee joint. As the patient squats down, the quadriceps musculature fires to decelerate flexion of the leg, while the hamstring and gluteus musculature fire to decelerate the pelvis from rotating forward. The hamstring musculature also aids the reconstructed ACL in its check-rein function on the tibia. These exercises are crucial in developing the coordinated muscular activity of the hamstring, gluteus and quadriceps musculature that is necessary for a normal walking gait during full weight-bearing on a flat surface, as well as walking up and down stairs and getting into a seated position.

Step-downs (Figure 6A) are another useful exercise that can be included in the second week of post-operational rehabilitation. For this exercise, the patient stands with both legs on a designated raised surface and then steps down to the ground with the non-injured leg. These exercises should be conducted in front of a mirror to ensure proper technique. Apprehension in flexing the injured leg or weakness in the gluteus musculature on the same side will cause the patient’s pelvis to drop down to the side of the leg that is stepping down. Correct technique of step-downs is necessary for the patient to maintain hip stabilization, prevent pelvis drop, and proper cocontraction of the hamstring and quadriceps musculature of the injured leg to achieve a controlled leg flexion as the other foot touches the ground surface. Step-downs should commence at two inches off the ground for 25 controlled repetitions. The step-down height can be increased to four, six, and eventually eight inches as the patient regains motor control of the hip stabilizers, gluteus and hamstring musculature, as well as the decelerator of leg flexion, the quadriceps musculature.

acl_6aAccording to Bill Knowles, director of iSPORT at the Vermont Orthopaedic Clinic in Rutland, Vermont, after ACL repair, the sutures are usually removed between ten days and two weeks post surgery. Once the wound is healed, pool therapy can begin. Bill Knowles recommends specialized pool routines for “total body training with an emphasis on hip and knee flexion and extension movements, as well as core strength exercises to include all of the muscles involved in stabilizing the torso from the hips to the shoulder.” The patient holds floatation bars while conducting various movements in the pool to improve the coordinated strength of the hip stabilizers, knee extensors and flexors, as well as the core strength musculature.

After 115 degrees of leg flexion is attained, stationary cycling can commence to increase range of motion of the knee joint, as well as provide light endurance exercise. Other exercises that be used to increase range of motion and muscle coordination are swimming and the elliptical machine.

All of the above exercises included in the second week of the post-operative rehabilitation phase should be conducted to the patient’s tolerance and in a controlled setting. If swelling occurs or if there is decreased range of motion in the knee joint, the progression of the rehabilitation phase should be slowed down, the range of motion restored, and the swelling reduced.

Weeks 3-5

acl_6bIn weeks 3-5, functional exercises can be added to the rehabilitation routine. The following exercises are recommended:

  1. Balance star drills on a flat surface – balance while reaching forward with the good leg or opposite arm.
  2. Bulgarian squats – with the good leg up on a bench/chair, perform the squat with the injured leg (Figure 6B).
  3. Pelvic bridge lying on the back, legs flexed to 90 degrees, lift the buttocks off of the floor while squeezing the glutes and the hamstrings.
  4. Balance drills on a disco-sit/curved seat cushion.
  5. Ball squats without weights, and later with weights held by the patient during the squat (Figure 6C).
  6. Single leg Romanian deadlifts – on a step box, bend forward from the trunk while holding a weighted ball with both hands in front, and balance on the deconditioned leg (Figure 6D).
  7. Leg Presses – single leg.
  8. Abduction, adduction, single leg extensions, calf raises.
  9. Ball tosses while balancing on a balance board.
  10. Lunges.
  11. Exercise ball hamsting curls.
  12. Towel stretches and standing extension stretches with resistive tubing.

Delayed onset muscle soreness is expected. If there is normal range of motion, no immediate swelling, and muscle pain dissipates in two to three days, the patient can continue to progress with the rehabilitation routine. acl_6c_d

Weeks 6-8

  1. Progress to heavier weights with the above exercises.
  2. Continue towel stretches and Flexband® stretches to maintain and increase range of motion of the knee in both flexion and extension.
  3. Proprioception drills, e.g. wobble board exercises balancing on two legs, balancing on one leg, ball tosses while balancing, done with the eyes closed for advanced drills.

Weeks 8-11

Romanian deadlifts.

Light sport-specific training, e.g. a basketball player shooting free throws or conducting passing drills.

Week 12

If the patient has full range of motion and strength of the musculature surrounding the knee, he or she may start a running program: Treadmill running for ten to 15 minutes, level surface running on cement for 2030 minutes, hill running, sprinting, figure 8’s, side sliding, start and stop shuttle runs, and 45-degree cutting. Jumping drills can teach the athlete how to land softly while sitting back and incorporating the hamstring and gluteus musculature. These agility drills can be progressed as tolerated.

4-6 Months

The patient can return to full light sport participation if assuming full range of motion, 90 percent strength of the hamstrings and quadriceps musculature (as compared to the healthy leg) and success in conducting all of the agility drills with no pain or swelling.

The therapist should explain to the patient that while it is okay to return to full light sport specific training, it can take up to three months of participation in their sport to regain the complex movement patterns of the particular sport. It may take up to seven months to a year for “ligamentization” of the grafted tissue, whereby the grafted tissue becomes almost identical, in its properties, to the original anterior cruciate ligament.

Post Surgical Treatment of the Anterior Cruciate Ligament at Dr. Dubin’s office

Treatment of the repaired ACL at this office would commence after the sutures are removed and the wound is healed, approximately two weeks post-surgery. Treatment would consist of:

  • Specific muscle work, including active release technique, to free up soft tissue motion of the surrounding knee musculature, helping to restore normal range of motion of the knee in flexion and extension;
  • Ultrasound and electric muscle stimulation combo therapy to break up scar tissue and restore normal muscle tone;
  • Patella mobilization techniques.

The above treatment protocols would aid in breaking up scar tissue and restoring proper joint and soft tissue range of motion.

Good communication and repeat follow-ups among the physician and therapists are crucial in creating and maintaining the optimum treatment protocol for pre- and postsurgery rehabilitation of the anterior cruciate ligament, allowing for a safer and quicker return of the athlete to their particular sport.

Acknowledgements

This paper was made possible with the help and expertise of Keith Callanan MPT, CSCS, of Elite Physical Therapy (781-297-0979) and Bill Knowles ATC, CSCS, Director of iSPORT (802-422-6191). I recommend their services to all patients who are suffering from anterior cruciate ligament injuries.

If you have any questions or want to set up an appointment with Dr. Dubin please call 617-471-2444.

References

1) Shelbourne DK, Rowdon GA: Anterior Cruciate Ligament Injury. The Complete Athlete, Sports Med 17(2) 132-140, 1994.

2) Rodeo SA, Arnoczky SP, Torzilli PA, Hidaka C, Warren R: Tendon-healing in a bone tunnel. J Bone Joint Surg 75A: 1795-1803, 1993.

3) O’Neill, Daniel F. , New Hampshire Knee Center, The 1st Week Post-Op 2003

4) Rinsberg MA, Mork M, Jenssen HK, Holm I: Design and Implementation of a Neuromuscular Training Program Following Anterior Cruciate Ligament Reconstruction. J of Othopaedic and Sports Physical Therapy 2001; 31 (11): 620-631.

5) Hewett TE, Paterno MV, Myer GD: Strategies for Enhancing Proprioception and Neuromuscular Control of the Knee. Clinical Orthopaedics and Related Research 2002; number 402: 76-94.

6) Bill Knowles ATC, CSCS, director of iSPORT at the Vermont Orthopaedic Clinic, Rutland, Vt.

7) Keith Callanan, MPT. Owner of Elite Sports. Inc. Stoughton, Ma.

8) Amiel D, Kleiner JB, Roux RD, Harwood FL, Akeson WH: The Phenomenon of “Ligamentization”: Anterior Cruciate Ligament Reconstuction with Autogenous Patellar Tendon. J of Orthopaedic Research 1986; (4): 162-172.

Additional references

Reid D: Sport Injury Assessment and Rehabilitation. 1992.

Norman, SW: The Knee. 1994.

Medial Epicondylitis / Pitcher’s Elbow

Download as pdf

Prolonged repetitive throwing motions such as those familiar to baseball pitchers are a risk for developing repetitive strain injuries to the muscles, ligaments, and tendons supporting the inside of the elbow. These injuries are also common in athletes participating in overhead activities like tennis, badminton, and javelin throwing. The main symptom of this so-called “pitcher’s elbow” is a gradual onset of pain on the inside of the elbow that may travel down the inside of the forearm. Such high-velocity throwing motions place a lot of strain on the structures on the inside of the elbow, leading to microtears and possibly to the development of a repetitive strain injury. Ongoing sport participation without proper treatment may lead to an increase in the severity of the elbow pain, elbow swelling, and eventually decreased performance, like a slower fastball or a compromised tennis serve. This injury is known as medial epicondylitis. Prolonged injury without treatment may lead to an inability to compete.

Understanding which muscles, tendons, and ligaments are contracting, being pre-stretched, or are stabilizing the elbow joint in each of the five phases will help in developing a proper treatment and prevention program for medial epicondylitis.

Evaluation of the Pitching Motion

An effective pitching delivery (or overhead serve) involves rotation of the hips and torso in coordination with movement of the shoulder, elbow, and wrist. Two very successful professional pitchers, Nolan Ryan and Roger Clemens, were able to pitch effectively and relatively injury-free during their careers due to their regimented strength and conditioning programs and proper pitching mechanics. On the other hand, many pitchers with great arm strength but poor biomechanics have seen a premature end to their careers due to shoulder and elbow injuries. This article will focus on the biomechanics of pitching and stress placed on the elbow joint, which may lead to the development of medial epicondylitis.

There are 5 main pitching phases: the wind-up phase, stride/cocking phase, acceleration 1 phase, acceleration 2 phase, and follow-through phase (Figs. 1A-1H).

pitcher1

During the wind-up phase (Fig. 1A), the opposite knee of the pitching hand (the stride leg) is lifted to about waist level, the torso is extended slightly, and the hips are rotated towards the batter. The main purpose of the wind-up is to generate energy that will be transferred from the hips and torso to the arm during the later phases of throwing. Another purpose of the wind-up is to hide the style of pitch from the batter before it is delivered to the plate.

During the stride/cocking phase (Figs 1B-C), the pitching arm extends behind the head as the hand goes down, back, and up into the cocked position. Also during this phase the stride leg moves down and forward and the foot lands flatly on the ground. This pitching phase prepares the body to transfer the stored energy from the hips and torso to the shoulder and arm.

During the acceleration 1 phase (Fig. 1D), the body rotates towards home plate over the stride leg as the pitcher’s chest and shoulder come forward. The pitching arm is placed in extreme external rotation and there as an increased “valgus strain” placed on the structures supporting the inside of the elbow. Stabilization of the elbow joint during the acceleration 1 phase is dependent on the integrity of the muscles surrounding the elbow joint (Figs. 2A-B) and of the medial collateral ligaments, located on the inside of the elbow (Fig. 3). Injury to the medial collateral ligament will decrease performance and cause pain on the inside of the elbow. If this problem goes untreated, further tearing of the ligament may occur, possibly necessitating surgery to correct the problem.

pitcher2The power of the pitch is transferred from the torso and lower trunk to the shoulder, arm, and hand during acceleration 2 (Figs. 1E-F). During this phase, the trunk springs from extension (stretching out) to flexion (bending in) and rotates towards home plate over the planted stride leg. At the same time, the shoulder rotates internally and the arm and hand accelerate towards the plate until the baseball is released from the hand.

The follow-through phase (Figs. 1G-H) is the last phase of pitching and involves deceleration of the arm and hand after the baseball is released. The pitching arm, elbow, and hand should go down, over, and outside the lead leg while the other leg swings forward in line with the stride leg. The purpose of the follow-through is two-fold: arm deceleration (where the legs and back muscles aid the muscles, ligaments, and tendons of the shoulder, elbow, and arm); and preparation (placing the pitcher in a fielding position ready to field a ball hit in his direction).

pitcher3During the cocking and acceleration 1 phases, the wrist is slightly extended, stretching the flexor muscles of the forearm-the flexor digitorum superficialis, flexor carpi radialis, and flexor carpi ulnaris (Fig. 2A)-and an increased “valgus strain” is placed on the medial collateral ligament. From acceleration 1 to acceleration 2, the wrist goes from a slightly extended position to a flexed position, causing a forceful contraction of the forearm flexors. The tendons attached to these forearm flexors have a common insertion point on the medial epicondyle, an outgrowth of bone found on the inside and bottom of the humerus (arm bone). When these muscles are under-prepared and stretched in this way, tension develops in the tendons at the insertion point on the medial epicondyle. Overuse may cause microtears in these structures, causing pain at the medial epicondyle in the elbow.

Improper pitching technique, including failure to utilize the trunk and torso effectively during the pitching phases, will place an increased workload onto the muscles, tendons, and ligaments of the arm, forearm, and hand, leading to overuse injuries. If the athlete does not improve pitching technique and/or fails to treat the condition appropriately, further injury will ensue, leading to the development of medial epicondylitis.

The overhead tennis or badminton swing would be similar to the cocking and acceleration 2 phases of the pitching motion. These athletes would benefit from exercises similar to those recommended for baseball pitchers.

pitcher4

Treatment and Prevention of Medial Epicondylitis/ Pitcher’s Elbow

Repetitive strain injuries in the elbow region are directly related to the strength of the muscles as compared to the force acting on the muscles, and also to the number of repetitions performed. Strength training exercises consisting of reverse curls, pronation exercises, wrist flexors, wrist extensions, tricep extensions, and bicep curls (Figs. 4A-4F) will increase the strength of the muscles surrounding the elbow, allowing them to sustain more tension before injury. Such exercises also decrease the strain sustained by the medial collateral ligament during the pitching phases. Strength and flexibility training of the shoulder, abdominal, and leg muscles should also be included. Consult with a doctor before starting these exercises.

Off-season and pre-season conditioning should include pitching technique drills focusing on balance during the leg kick, proper stride technique, and coordinated hip rotation/trunk flexion combined with shoulder, arm and hand movements. A pitch count should be planned, limiting the number of pitches thrown until a base is established, and the velocity of the pitches should be increased at an appropriate rate during practice and pre-season games. After pitching, ice should be applied to the shoulder and elbow immediately, or as soon as possible, to decrease inflammation. After strenuous outings or workouts, an experienced sports therapist should be consulted to help relax the musculature surrounding the shoulder and elbow to assist in the prevention of injury.

Treatment of Pitcher’s Elbow at Dr. Dubin’s office would consist of:

  • Deep tissue procedures to the muscles surrounding the shoulder, arm, and forearm to free up soft tissue motion
  • Chiropractic adjustments of the wrist and elbow joints to free up joint motion
  • Ultrasound and electric muscle stimulation combotherapy applied to the structures on the inside of the elbow to restore normal muscle tone, decrease pain, and absorb scar tissue
  • Implementation of a personalized home strength program (Figs. 4A-4F), noting the importance of increasing strength and flexibility of the trunk musculature and the shoulder musculature
  • Ice therapy applied to the elbow, 20 minutes on and one hour off after competition
  • Recommendation to meet with a pro to improve pitching or swing technique.

Note: Consult with a doctor or certified strength conditioning specialist before starting these exercises.

Patellofemoral Syndrome/Pain on the Front of the Knee

Download as pdf

knee1Patellofemoral Syndrome (PFS), pain in the front of the knee, is one of the most common complaints of athletes and active people. PFS is typically caused by a repetitive strain injury or a single traumatic event. Repetitive strain injuries occur when micro-tears in the muscles, tendons and ligaments surrounding the knee joint occur faster then tissue repair, while a single event is often a fall or other athletic impact. PFS is usually characterized by a dull aching pain on the front, bottom, or top of the knee, sometimes accompanied by swelling of the knee joint. Failure to treat this injury appropriately may lead to increased pain symptoms, further damage to the structures stabilizing the knee joint, and eventually an inability of the injured knee to support body weight. This syndrome commonly occurs in athletes or the “weekend warrior” participating in sports such as basketball, football, soccer, triathlons, or track and field events. These sports involve repetitive running, jumping and sometimes kicking, placing a lot of tension on the structures supporting the knee joint.

An understanding of the anatomy and the biomechanics of the knee joint during flexion (bending) and extension (straightening) of the leg will make it easier to comprehend how to effectively treat and prevent Patellofemoral Syndrome.

Anatomy of the Knee Joint

knee2The patella, or kneecap, is a conical shaped bone lying between the femur (thigh) bone and the tibia (lower leg) bone (Fig.1). The undersurface of the patella glides over the trochlea, a groove located at the bottom and front of the femur bone. The quadricep muscle group, which plays a vital role in the stability of the knee, is located on the front of the thigh and consists of four muscles, the vastus lateralis, vastus intermedius, vastus medialis and the overlying rectus femoris (Fig. 2). The quadricep muscles share a common tendon, the quadricep tendon, which anchors these muscles onto the top of the patella. The patella ligament acts as a downward continuation of the quadricep tendon, originating from the bottom of the patella and inserting onto the tibial tuberosity, an outgrowth of bone on the front of the tibia.

The two retinacula, sheath-like structures located on the front of the knee, are also important in knee stabilization. The lateral retinaculum attaches to the vastus lateralis and iliotibial band superiorly and descends to attach to the lateral aspect of the patella ligament. The medial retinaculum attaches to the lower part of the vastus medialis and descends to attach to the inside area of the patella ligament (Fig.2).

Biomechanics of the Knee Joint

The patella acts as a pulley system by supporting the mechanical work of the quadricep musculature during leg extension and also during deceleration of leg flexion. Proper function of this pulley system depends on the ability of the patella to track properly during leg extension and flexion. Muscle tightness in the outer knee area and muscle weakness in the inner knee area may compromise this tracking, and are often a root cause of knee injury. The structures that are often tight include those on the outside of the knee, such as the lateral retinaculum, vastus lateralis and iliotibial band (Fig. 3) while structures that are often weak include those on the inside of the knee, such as the vastus medialis and adductor magnus. In this situation, the patella may track too far laterally (towards the outside of the knee). Excess lateral tracking of the patella will decrease the efficiency of this pulley system during leg flexion and leg extension, predisposing these tissues to injury. A stretching program with the Flexband© and strengthening program incorporating squats and ball squeezes (Fig. 4A & 4B) will aid in tracking the patella properly and decreasing the risk of injury.

knee3There are three main types of muscle contractions: concentric, eccentric, and isometric. Each of these contractions may contribute to PFS in different ways. During a concentric contraction, a muscle shortens to perform a particular motion. The patella, quadricep muscle, quadricep tendon, and patella ligament create the “extensor mechanism” of the knee. When the quadricep muscles concentrically contract, they pull on the quadricep tendon, causing tension on the patella and patella ligament, leading to extension of the leg (Figure 4C). An athlete’s ability to kick a soccer ball or football is dependent on the concentric strength of the quadricep muscles and also on the flexibility of the hamstring musculature. The hamstring muscle group acts to decelerate extension of the leg. Inadequate flexibility of the hamstring musculature will place an increased strain on the quadricep muscles during leg extension, predisposing the athlete to the development of PFS.

During an eccentric contraction, a muscle will slowly elongate to decelerate a particular motion. While doing a squat (Fig. 4A) or during heel strike and mid-stance of the running gait cycle, the quadricep muscles, tendon, and patella ligament slowly elongate to decelerate leg flexion. Excessive eccentric loads (e.g. doing a squat with weights that are too heavy, or landing from a high jump) or repetitive eccentric motions (e.g. landing from frequent jumping, as in basketball) may lead to injury of the above structures and to the development of PFS.

During an isometric contraction, the muscle generates force but neither elongates or shortens, so such movement will not lead to injury. For example, the quadricep muscles isometrically contract when conducting a straight leg raising exercise (Fig. 4D). Isometric exercises are useful in the initial stages of rehabilitation by restoring strength of the “extensor mechanism” without compromising the structure or integrity of the joint.

knee4

Checklist for the prevention of Patellofemoral Syndrome:

  • Conduct a lower body strength training program (see Fig. 4A-4E). In addition to these movements, the program should include strengthening of the calf musculature, tibialis anterior, and core abdominal musculature.
  • After exercise, stretch with the Flexband and ice both knees for 20 minutes.
  • Cross train, rather than repeating one activity over and over. Substitute biking, cycling, and swimming for running, for example.
  • Slowly increase the duration or intensity of the training program; use the 10% increase in mileage per week rule.
  • Change sneakers every 250-400 miles, run on softer surfaces, and avoid hill training before a base of training is established.

Treatment of Patellofemoral Syndrome at Dr. Dubin’s office would consist of:

  • Deep tissue procedures to the quadricep musculature and surrounding knee structures to free up soft tissue motion
  • Mobilization of the patella and adjustments of the ankle and foot to free up joint motion
  • Ultrasound and electric muscle stimulation combo-therapy to restore normal muscle tone, decrease pain, and absorb scar tissue
  • Implementation of a personalized home strengthening and flexibility program
  • Possible recommendation of a semi-rigid orthotic
  • Ice therapy (20 minutes on and 1 hour off)
  • Possible recommendation of prescribed or over-the-counter anti-inflammatory medications (taken with food)
  • Temporary use of an elastic sleeve with a lateral stabilizing pad for the knee.

For more information on Patellofemoral Syndrome, or to schedule an appointment with Dr. Dubin, call 617-471-2444.

Note: Consult with a doctor before conducting the above exercise routines.

Hamstring Injury

Download as pdf

hammy1

One of the most common sport-related injuries is a hamstring pull or strain. The hamstring, a group of four muscles in the back of the thigh, can be felt stretched as you bend forward to touch your toes. Three of the four hamstring muscles, the semitendinosis, semimembranosis, and the long head of the bicep femoris, cross both the hip and knee joint and are the true hamstring muscles. At the top, these muscles have a common attachment to the ischial tuberosity (a bone at the bottom of the pelvis), and at the bottom, the tendons of these muscles then attach to the tibia and fibula (bones below the knee) (Figure 1). The other hamstring muscle, the short head of the bicep femoris, only crosses the knee joint.

There are two main types of hamstring injuries, and each affects a different part of the hamstring musculature. The first hamstring injury is most common in younger athletes and is caused by a sudden motion, such as an explosive sprint, a jump, or a kick. In this type of injury, the strain occurs at the muscular portion of the hamstring, resulting in pain in the middle of the back of the thigh. Swelling and later bruising may be present in the back of the thigh, and the athlete may limp or utilize crutches to take weight off of the injured leg.

Training errors in activities such as cycling and running usually causes the second type of hamstring injury. In this case, the hamstring strain occurs at the tendinous insertion on the ischial tuberosity of the pelvis. Tri-athletes, duathletes, and marathon runners are common sufferers of this injury, and will complain of pain in the lower buttock region that increases in severity as the foot of the injured leg strikes the ground.

By understanding the biomechanics of running and some concepts of cycling, it becomes easier to understand why hamstring injuries occur and how to prevent them. With both types of hamstring strains, chiropractic treatment and re-injury prevention exercises are effective management techniques.

Biomechanics of Running

There are two phases of running: the stance phase and the swing phase. The stance phase consists of foot-strike, mid-stance, and toe-off (Figure 2); and the swing phase consists of follow through, hip flexion and leg descent (Figure 3). During an eccentric contraction, muscle fibers will slowly elongate to slow down a particular motion, while a concentric contraction involves shortening of the muscle fibers to lift an object or move a limb in a particular direction. During leg descent and foot-strike, the pelvis flexes forward and the leg extends, the hamstring muscles are eccentrically contracting to slow down both of these particular movements (Figure 4). When the eccentric load exceeds the strength of the muscle fibers, tearing of the hamstring fibers occurs, resulting in a strain injury.

hammy2

hammy3

hammy4Flexibility and strength training of the hamstring musculature and the nearby muscles surrounding the pelvis and thigh will reduce the risk of injury. Strengthening the abdominal and gluteus maximus musculature is important in the prevention of a hamstring strain because these muscles aid the hamstrings in decelerating flexion of the pelvis during heel strike. Flexibility of the hip flexors and low back musculature is also important in the prevention of a hamstring strain injury. Tight hip flexors and low back musculature causes excessive flexion of the pelvis during foot-strike placing an increased strain on the hamstrings. Tightness in these muscles also inhibits strengthening of the gluteus maximus and abdominal musculature.

Strength training and Flexibility Training

See the following diagrams for examples of exercises to help strengthen and increase flexibility of the hamstring and surrounding muscles.

  1. Core training- chops, abdominal crunches, Russian twist (Figures 5, 6, 7)
  2. Straight leg deadlifts and squats- eccentrically strengthen the hamstring musculature
    (Figures 8,9)
  3. Flexibility training with the flexband

Talk to a doctor or certified strength conditioning specialist before attempting this or any new exercise program.

hammyexercises

Training Protocols for Running

The initial training phase should consist of establishing a good aerobic base, a comfortable slow pace where oxygen is plentiful, allowing the body to convert stored fats and glucose for energy. A heart rate monitor can be a useful tool in training at the appropriate pace. Aerobic conditioning should be conducted at approximately 70-80% of maximum heart rate (MHR), expressed in number of beats per minute. To determine your MHR, subtract your age from 220, or by looking at your heart rate monitor after a fast all-out run up a hill. After establishing a good aerobic base, pace can be increased to 85-90% maximum heart rate, a point called anaerobic threshold training. The anaerobic threshold is the point immediately before oxygen debt occurs, and will eventually become the race pace. With proper training, the anaerobic threshold will increase — allowing the athlete to run at a faster pace before reaching oxygen debt.

Competitive and elite athletes will conduct short distance interval anaerobic training runs at 95% maximum heart rate to increase their body’s ability to deal with muscle fatigue. At this fast pace, oxygen debt ensues and energy is now produced by the breakdown of glucose to lactate, with the byproduct of hydrogen ions. In order for muscle contraction to occur, calcium needs to bind to a particular protein in the muscle fibers. Hydrogen ions compete with calcium for these binding spots, eventually inhibiting muscle contraction. The body can only function for approximately two to three minutes at this faster pace, however maintaining this pace may mean the difference between an elite runner finishing first or third at the end of a race.

Progressing training runs appropriately will reduce the risk of developing a hamstring injury by preparing these muscles for an elongated stride, as well as allowing the body to function at faster speeds before muscle fatigue and eventual muscle failure may occur.

Biomechanics of Biking

Bike racers assume a racing position that is the most aerodynamic (least wind resistant) and that is conducive to the greatest strength through pedal stroke. A racing position that satisfies these two conditions allows racers to maximize their speed. Unfortunately, this racing position places an increased eccentric strain on the hamstring and erector spinae musculature, increasing the risk of a hamstring injury. Proper flexibility and strength training, as well as bicycle conditioning and correct bike fitting, are important in attaining this strategic position while decreasing risk of injury. For more information on proper bike fitting, provided by FitWerx, click here.

Case History

Leiha came to Dr. Dubin’s office with complaints of pain in the lower left buttock region. She stated that after running the Boston Marathon she had no pain. However, soon after the marathon she started to run with a friend to train for a 5k race; that’s when she began to experience pain. It is important to note that she had run the Boston Marathon at a slow pace and with a short stride, but trained for the 5k race at a faster pace and a longer stride. Leiha had not included squats or straight leg deadlifts in her strength training routine. The pain increased to where she could no longer train.

Examination revealed extreme tenderness in the left buttock region, where the hamstrings attach to the pelvis. Tightness was evident in the left hamstrings and iliotibial band. Dr. Dubin explained to Leiha that due to her sudden increase in pace of training, her hamstring musculature was not prepared for the eccentric load placed on them. This led to her injury.

With proper treatment (see below), Leiha’s condition was resolved after 5 visits. To prevent re-injury, she was instructed on a proper strength and flexibility routine and was instructed on a strategic plan to slowly progress the pace of her training runs.

Treatment at this office

  • Deep tissue procedures (Active Release Technique) to free up soft tissue motion of the hamstrings and surrounding musculature
  • Adjustments to free up joint motion of the lumbar spine
  • Ultrasound and electric muscle stimulation combo-therapy applied to the proximal hamstring tendons to break up scar tissue, restore normal muscle tone, and decrease pain.
  • Implementation of a proper strength and flexibility program
  • Advice on how to progress training runs more appropriately

For more information, or to set up an appointment with Dr. Dubin, please call 617-471-2444.

Low Back Pain

Download as pdf

lowback2Most people suffer from low back pain at some time in their lives. Common cases of low back pain include people who work in a prolonged flexed posture while sitting at a computer, or the “weekend warriors” who attempt to participate in activities such as golf, biking, and basketball without a proper training program.

Understanding the biomechanics of the lumbar spine and pelvis while bending forward and returning to the neutral position will illustrate why the loss of strength and flexibility in particular muscles predispose individuals to the development of low back pain.

Movement 1: Anterior Flexion of the Lower Back

The low back consists of five functional units. A functional unit (Fig. 1) consists of two vertebra, an adjoining disc, facet joints, and the surrounding musculature, ligaments and fascia.

Ligaments attach bone to bone, and fascia is a sheath of fibrous tissue that encloses muscles and muscle groups. There is approximately 9 degrees of flexion at each functional unit, allowing up to 45 degrees of forward flexion (Fig. 2A & 2B).

lowback1

At 45 degrees, the fascia, muscles, and ligaments of the low back are taut and no more flexion is allowed without forward rotation of the pelvis. An endpoint of motion in forward flexion of the low back is the point at which a person bends forward and can go no further pain. If the ligaments, fascia, muscles of the low back are not flexible, this endpoint of motion will be decreased and will result in a strain/ injury of the low back when attempting to bend forward to 45 degrees. In order to bend forward past 45 degrees, the pelvis has to rotate forward (Fig. 3).

lowback3lowback4

The anterior motion of the pelvis is dependent on the flexibility of the hamstrings and the gluteus maximus musculature. If the hamstrings and gluteus maximus musculature are not flexible, the pelvis will be limited in anterior flexion (Fig. 4). When this limited endpoint of forward flexion is exceeded, one will usually suffer from an acute onset of low back pain.

Movement 2: Return to Neutral Position from Flexion of the Low Back

When returning from a flexed low back posture, the gluteus maximus muscle (Fig. 5) will contract, derotating the pelvis from its anteriorly rotated. At the same time, the abdominal musculature contracts, tightening the fascia surrounding the low musculature, adding more stability to the lumbar spine.

Movement 1 and Movement 2 illustrate why flexibility of the lower back and hamstring musculature and proper strength training of the gluteus maximus and abdominal musculature are important in the prevention of low back pain. Having flexibility of the hip and external rotators of the hip, as well as strength in the quadracep can also aid in the prevention of low back pain.

Case Study

Bob came to Dr. Dubin’s office for care with complaints of low back pain. He stated that he worked as a stockbroker and sat looking at a computer screen all day. His low back pain came on gradually and became more severe with time. He did not belong to a gym, nor did he do a strength and flexibility training program at home.

Dr. Dubin conducted a thorough exam on Bob’s lower back to diagnose his condition. The treatment techniques utilized by Dr. Dubin at his office included: specific deep tissue procedures (active release technique) applied to the muscles in the low back to free up soft tissue motion; adjustments to free up joint motion; and combotherapy to help to relax the muscles, restore normal muscle tone, and break up scar tissue. Dr. Dubin tailored a home flexibility program for Bob involving the FlexBand® and a proper strength training program. Bob was also instructed on how to ergonomically correct his workstation to help alleviate the repetitive strain on his low back. Bob now does stretching exercises with the FlexBand® for 15 minutes a day (see below) and a regular (1-2 times a week) strengthening program for his low back. Bob’s low back pain has resolved, and his ongoing workout routine will continue to help in the prevention of future low back episodes.

How to Relieve Low Back Pain

Repeated, prolonged stress to the back and shoulders can lead to a multitude of injuries down the road. Most jobs require a prolonged (sitting or standing) slumped forward position, which results in a postural overstretch and eventual low back pain. Decrease and prevent lower back pain by doing a 15 to 20 minute daily stretching routine using a FlexBand®. These exercises will help prevent your low back pain.

Stretching Techniques