Walking Off the Pain

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January/February 2003

By Sherry Brourman, PT

Sherry Brourman, PT (Left), helps correct a client's gait.

Musculoskeletal pain affects gait in a discernable diagnostic pattern. As a reflexive response to pain, there is a strategic compensation, causing the normal posterior to anterior weight shift, which should occur from heel strike to push off, to be slowed or lost. This results in a posterior center of mass (COM) throughout the gait cycle.

In a mechanically effective gait, COM will shift forward early in mid-stance and bring the body’s center of pressure (COP) forward, to the first metatarsals. In a posterior COM type of gait, the body’s COM fails to move forward in a timely manner, and the result is a delay in the advancement of the COP onto the forefoot.¹ Nearly all gait deviations will lead to this posterior COM type of gait and, conversely, a posterior COM type of gait will lead to gait deviations resulting in musculoskeletal pain.

A posterior COM type of gait requires less muscular energy to maintain balance per step than a neutral COM type of gait requires. This abnormal posterior shift as an alternative gravity-defying system also ultimately attenuates joints. It relies on joint endpoints and on ligamentous support, rather than the co-contractive quality of muscle as it otherwise supports the same joints in a neutral COM type of gait. In a neutral COM type of gait, where muscle is the major component in defying gravity, joint dependency is reduced and joint impact is neutralized. Within this system, time spent in dynamic balance or single support time-per-step is increased. Joint vulnerability is also reduced on a long-term basis, as all of those same gravity-defying muscles are strengthened, approximately 2,500 times-per-foot, per day.² Since most people have had structural pain of some kind, or have modeled the gait of a parent with some deviation, most people do exhibit a posterior COM type of gait.

Although gait analysis has been used for many years and many purposes, it is not the standard diagnostic tool or modality that it could be for most types of structural pain. Normal gait and many abnormal gaits have been discussed,^3-5 yet gait has not been proposed as a cause of musculoskeletal problems, thus gait correction is not considered to be one of the ways of treating those problems. Structural pain has a mechanical cause, and this has been described and demonstrated by numerous physicians and therapists, including Cailliet, Cyriax, Dorman, Feldenkrais, Gray, and Janda.

Posterior COM type of gait becomes an asymmetric, imbalanced, and dysfunctional mechanical force on one or more weight-bearing joints that will ultimately cause damage. The asymmetry can be lateral, as in excessive pronation; can be anterior/posterior, as in hyperextended knees; and can be unilateral or bilateral. Any of these types of asymmetries will elicit a strategic postural compensation throughout the body that may go unnoticed for years. In a 10-year study,⁶ Weber found the majority of low back injuries are secondary to repetitive movements. In his book, Clinical Anatomy of the Spine,⁷ Bogduk states that “for each individual, there is a fatigue factor. A paper clip bent back and forth several times will weaken and finally break.” And so the onset of strain, pain, weakness, and structural damage occurs gradually. It is in this same gradual manner that asymmetric gait affects structures, and this is why gait works as an assessment and treatment modality. These asymmetries are visual and easily tested using manual muscle testing, muscle length testing, and simple plumb lines. As a modality, simple gait corrections, practiced daily and combined with specific corroborative exercises, will with time remodel gait patterns. By evaluating the elements of gait, specifically how they contribute to a posterior COM, cause of pain is established. These findings then transfer instantly to a treatment modality with lifelong implications.

CASE STUDY

A 47-year-old anesthesiologist with otherwise good health presented with severe right-sided low back pain, stiffness, and intermittent, radiating pain down the ipsilateral posterior thigh, occasionally as low as the ankle. He had a history of several similar episodes over the course of 5 years, each with an onset following rigorous tennis playing or hiking. His MRI was positive for a 4-mm, L4-5 disc herniation. The previous incidents had been relieved in a few weeks with the help of anti-inflammatories, exercise, and restricting athletic activity. This incident was more intense, it had worsened during the initial 3 weeks, and he was still not responding to his normal treatment regime.

POSTURE AND GAIT EVALUATION

Upon initial evaluation, the patient presented with acute lower back and right leg pain that was exacerbated by any transitional movement, particularly from sitting to standing. Lumbar spine range of movement was severely restricted with right lateral bending (-50%) worse than left (-20%), and spinal flexion (painful at 10 degrees) was more painful than spinal extension (painful at 30 degrees). In standing, he had a moderate left reflex shift, ankle pronation, hyper-extended knees, definite posterior COM with a concomitant high sternum, a protruding chin, a forward head, and a minimally kyphotic thoracic spine. His natural arm position was 20 degrees anterior in the sagittal plane. Walking caused severe pain, but only for the first few minutes that he stood after sitting. None of the visible asymmetries equalized, even as his pain lessened temporarily with a small amount of walking. Sitting for a few minutes would cause the pain cycle to repeat, and walking for more than 5 minutes would also elicit his pain cycle, necessitating another sit, and another cycle of pain. He had been to physical therapy in the past and was using an extension protocol.⁸ This would provide some short-term relief, but none that could last through even brief periods of sitting.

On day 1, his gait evaluation showed his COM remaining posterior throughout stance and swing phases, and this was validated with plumb lines. His base of support was so narrow that his heels nearly touched during mid-stance and he walked with a 40-degree foot turnout. He also walked with bilateral extreme lateral heel strike, ankle pronation during mid-stance, and knee hyperextension, and all were worse on the left. Swing phase was rushed, step length was shortened, and he was fully joint dependent during all of single support; his knees and hips were at their extension endpoints. He exhibited a left-sided reflex shift in standing that translated in gait into a right lateral hip collapse, with contralateral pelvic drop. Forward propulsion and the momentum for it were psoas and quadriceps dominated, which created a contralateral mechanical “pop-off” in lieu of any visible push off. He did not appear to engage any of the posterior musculature for push off.

His hip, lower back, and abdominal musculature were all placed in positional insufficiency, and this was validated visually and through manual muscle testing. He also did not appear to engage abdominals for any part of the gait cycle. His arm swing was posteriorly dominated and weighted with extremely internally rotated shoulders. There was no trunk rotation and a forward head was also demonstrated with plumb lines. On testing standing hip flexion, the right sacroiliac joint was hypomobile. There was no observable reciprocal movement between his sacrum and lumbar spine. His gait showed no vertical displacement or spring,⁹ and instead there was a spatially level pattern. There was an extremely heavy heel strike, louder on the left side.

GAIT CORRECTIONS

His gait corrections were as follows:

Feet: widen base of support, neutralize heel strike by slightly internally rotating hips, and reduce foot turnout to 15 degrees.
Knees: slightly flex knees during heel strike to contribute to the spring or vertical displacement.
Hips: widen the left step using the right hip adductors at push off to eliminate the pelvic drop, putting the gluteus maximus in position for the necessary increase in hip extension in late stance. Increase the power of push off by using, in addition to hip adductors for width, gastroc/soleus and hamstrings for stride length.
Trunk: lift vertically upward and tilt slightly forward, from where trunk rotation was elicited and armswing could be activated to contribute to an overall fluid diagonal movement pattern with a neutral COM.

These gait corrections were prescribed over the course of 3 weeks. With the exception of the trunk correction to lift up and forward, they were all given from the feet up or distal to proximal. For each gait correction used, an exercise was chosen to reinforce that correction. For example, to widen base of support, hip abduction and adduction strengthening exercises were chosen. To decrease foot turnout, hip internal rotator strengthening as well as piriformis stretching exercises were used, which also helped to reduce the extreme lateral heel strikes.

To functionalize these, weight-bearing diagonalized exercises¹⁰ were also used at this point. Throughout the course of treatment, the patient was to include in his home program an extension protocol in combination with his corrective walking protocol, resulting in a much more effective overall treatment.

By the end of the first week, the corrections and exercises for trunk, feet and knees were in place. The patient was able to sit without pain for 10 minutes; come to stand with minimal discomfort; and find, feel, and use abdominals for all position transitions as well as for gait.¹¹ He was able to walk for 15 minutes without pain and his overall pain was reduced by 50%. The patient was sent home with these exercises and asked to practice his gait corrections four times per day for 5 minutes each time.

During week two, hip corrections and exercises were added. He was able to sit for up to 30 minutes without pain, position transitions became minimally uncomfortable, and he could walk for 30 minutes comfortably. The patient was asked to continue the 5-minute gait practice sessions and home exercises.

During the third week, trunk rotation and armswing corrections and exercises were added. His pain continued to reduce, the reflex shift was barely discernable, and the patient was sent home with gait practices and exercises. He was then seen once per month for 6 months, and he continued to improve throughout that time. The patient returned to full athletic activities with no repercussions.

Although this patient had treated his symptoms prior to his corrective gait work, the source of the pain—his primary movement pattern or gait—had been overlooked. By creating symmetry in that area, the treatments became more effective, and his gait became constructive instead of destructive to his healing. In order to prescribe appropriate corrective gait therapy, it is important to evaluate how the elements of gait for each patient are contributing to a posterior COM type of gait, and to be able to ascertain how those elements have eliminated the need for true dynamic balance in each step. Only with this balance, or an appropriate amount of time in single support, can each step present with an opportunistic period during which all of the gravity-defying spine-stabilizing muscles and systems get to perform to their potential and effectively eliminate the majority of structural vulnerability.

Sherry Brourman has been a physical therapist for 30 years. Her focus on gait stems from her own severe low back and leg pain, which she healed entirely by correcting her gait. She is the author of Walk Yourself Well (Hyperion, 1998), has a private practice, and teaches yoga in Los Angeles.

REFERENCES

Laslovich S, Brourman S, Wiebe J. The Effect of Volitional Alterations in Gait Mechanics on the Temporal Displacement of Center of Pressure. 2001. Unpublished Pilot Study.
Dananburg H. Gait style as an etiology to chronic postural pain. Part I: Functional hallicus limitus. J Podiatr Med. 1993;83:433-441.
Solderberg GL. Kinesiology: Application to Pathological Motion. Baltimore: Williams and Wilkins; 1986.
Kendall FP, McCreary EK, Provance PG. Muscle Testing and Function. 4th ed. Baltimore: Williams and Wilkins; 1993.
Hausdorf JM, Peng CK, Laden Z, et al. Is walking a random walk? Evidence for long range correlations in stride interval in human gait. The American Physiological Society. 1995:349-358.
Amundsen T, Weber H, Lilleas F, et al. Lumbar spinal stenosis. Spine. 1995; 20:1178-1186.
Bogduk N. Clinical Anatomy of the Lumbar Spine and Sacrum. 3rd ed. Melbourne: Churchill Livingstone; 1997.
McKenzie RA. The Mechanical Lumbar Spine. 5th ed. Walkanae, New Zealand: Spinal Publications; 1981.
Gard SA, Childress DS. What Determines Vertical Motion of the Human Body During Normal Gait. Chicago: Northwestern University Rehabilitation Engineering Research Program; 1999.
Gray GW. Lower Extremity Functional Profile. Adrian, Mich: Wynn Marketing; 1995.
Lee D. The Pelvic Girdle. 2nd ed. Edinburgh, Scotland: Churchill Livingstone; 1999.