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Case Study 1: Knee Pain in a High School Distance Runner

Filed under: Uncategorized — Shon @ 6:45 am March 10, 2011

Background/Purpose:  This case was interesting, as  the physician diagnosis was one that I was a bit suspicious with initially.  The patient was a 16 year old cross country runner with anterior knee pain in the region of the tibial tuberosity, both on right and left sides.  The physician diagnosis was one of Osgood-Schlatter disease, a traction apophysitis or "pulling away" of the growth plate where the quadriceps tendon attaches to the tibia.

I was skeptical because of the athlete's age (at 16 he was on the "old" side of the diagnosis),  the fact that the athlete had not grown in height or weight significantly in the previous year (Osgood- Schlatter occurs near the time of a growth spurt) and the fact that the physician did not order x-rays, which would have solidified a definitive diagnosis.


History:  The athlete's history was a one month history of  bilateral knee pain with a sudden increase in training volume during pre-season cross country practice.   Pain was not only present in the tibial tubericle, but 1.5 inches below it.  Pain was rated 6-7/10 at worst.  Coming down stairs (eccentric quadriceps activity) made pain worse. 

Key Findings:  Most significantly, the tibial tuberosity was not prominent on observation , nor on palpation.  Equally important were his mobility and strength impairments. 

Mobility:  First, knee flexion was limited to 125 degrees bilaterally ( 145 degrees would have been expected).  Hip flexion passively was limited to 110 degrees, (135-140 degrees would be expected).  Ankle dorsiflexion was 10 degrees,; fine for walking, but less than the 15-20 degrees needed for running.  There was not significant IT band tightness noted (surprisingly). Hamstring tightness was mild.

Strength:  Hip flexion greater than 90 degrees tested at 33 lb. right, 29 lb. left  with hand held dynamometry.  Glute (max) activity in prone was preceded by hamstring activity with active hip extension.  Additionally, neutral lumbar positioning could not be held with straight or bent leg hip flexion on either side without increasing the lordosis . 

Treatment:  This athlete was seen for 10 visits over 3.5 weeks.    We focused on the following:

 1)  Increasing hip flexion mobility through joint mobilization followed by hurdle mobility drills in sagittal and transverse planes while maintaining "neutral" spine and resisting flexion/ extension/ rotation. 

2)  Increasing ankle mobility, again with joint mobilization followed by wall-ankle mobilization drills  

 3) Static psoas strengthening, first with no weight, then  progressing to 4 lb., 15-30 seconds/set, up to 10 sets/ side.

4)  Glute sets, prone, 30 seconds/ x 10, progressing to prone hip extension with glute setting.

Treatment occurred after cross country practice, as the athlete was in season.

Outcomes:  Over the first 5 treatments, the athlete's pain decreased from 6-7/10 to  2-3/10 with training as well as with stairs.  Pain now was only prominent with down hill running. 

The next 5 treatments weaned the athlete from manual therapy/joint mobilization as hip and ankle mobility improved significantly.  Emphasis was on increasing abdominal, hip flexor and gluteal strength, while monitoring tolerance for cross country training, which continued to improve. 

On final re-assessment at 3.5 weeks, pain decreased to<1/10 with full training levels, including downhill running.  Active hip flexion in supine increased to >135 degrees bilaterally with a neutral spine.  Ankle dorsiflexion increased to 20 degrees bilaterally.  Psoas strength increased to40 lbs. bilaterally, while hip extension occurred with synchronous gluteal and hamstring firing.  The athlete continued independently with psoas/ gluteal strengthening, hurdle   as well as ankle self mobilization.  His season culminated with a state championship appearance with no residual knee pain.

Discussion and Rationalle

Based on my evaluation findings, I felt that the athlete's tibial tuberosity pain was multifactorial.  First, psoas weakness may have placed the onus of hip flexion on the tensor fascia lata and rectus femoris, which act below 90 degrees.  This may also have led to loss of active/ passive hip flexion seen initally.  Additionally, loss of ankle dorsiflexion probably led to early heel lift, which placed additional stress on the quadriceps earlier in the running gait cycle.  This may have also led to loss of hip extension in the late part of  single leg stance, hence the decreased gluteal activity noted in the initial evaluation.

Treatment rationale was to 1) restore appropriate mobility first, then 2) activate/ strengthen weak proximal hip musculature.  This occurred gradually and progressively over the 3.5 weeks the athlete was seen.  Training continued during this time, as discussed with his physician and parents.  Symptoms, while painful, were not debilitating, and lessened progressively over the course of treatment.  Training also allowed a "functional barometer" to assess our clinical progress.

Based on the athlete's successful outcome, I feel the rationale for his care was appropriate and effective.  Moving forward, perhaps changes in his training, including appropriate weight training as well as more dynamic sprint drills may prove beneficial to engage the torso and lower extremities to a greater extent vs. traditional distance training.  Obviously, continuing home exercise routine at least 2-3 times weekly is paramount as well in order to minimize risk of re-occurrence.