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Case Study 2-Foot Tendonitis in a Collegiate Volleyball Player

Filed under: Uncategorized — Shon @ 11:45 am March 31, 2011

Background/ Purpose

I had seen this 19 year old female volleyball player as a referral from her college's athletic trainer who I had a good referral relationship with.  From what I have observed clinically over the past 20 or so years,  most cases of tendinitis/tendonosis ususally have a component of joint mobility impairment adjacent to the injured area, and this case was no exception.


 The athlete was a 5'11" setter on her volleyball team.  She initially noted dorsal foot pain after beginning preseason volleyball training shortly after returning to school from summer break, located over the extensor hallucis longus (EHL) and to a lesser extent in the tibialis anterior (TA) tendon insertion.

(The origin and insertion of the EHL in a "classic" origin/ insertion diagram)

(What it looks like "for real" in the clinic)

(Tibialis anterior origin and insertion)

The athlete was treated in her college's training room with modalities and stretching without significant relief for 8 weeks.  She eventually sought care from a sports orthopedist in her hometown who placed her in a soft cast for 2 weeks without relief.   An MRI was negative for pathology of the left foot.   After this, she was referred to me for evaluation.

Chief Complaint:  Her main problem was left anterior foot pain, located over the extensor hallucis longus tendon and occasionally over the tibialis anterior (TA) tendon after 30-45 minutes of aggressive volleyball training/ competition.  She rated her pain at 7-8/10 at worst, and was present 20-30% of the day when not training. 

Key Observations:

In standing, the athlete presented with mild pes planus (low arch height/ foot flattening).

There was an apparent everted calcaneus in full weight bearing, with bilateral genu valgum (knee hyper-extension), as well as internal rotation of the tibia and femur in static standing.

(My patient was not quite this bad, but it gives you an idea)

In subtalar neutral position, measured  non-weight bearing in prone lying, the thing that stood out to me most was a plantar flexed first ray.  The first ray is the junction of the first cuneiform bone and the first metatarsal; the motions of the first ray are primarily plantar flexion and dorsiflexion  (There was also notable rearfoot varus, but I didn't feel this was contributory to her impairments/complaints at this time).

(An example of a plantarflexed first ray viewed in subtalar neutral)

Her gait was unremarkable for deviations with level surface walking.  Running/ jumping/ hopping was not assessed at this phase of the evaluation, as I was able to elicit symptoms in other ways (see Strength for details).


First MTP ("big toe") extension was limited at 45 degrees actively/ 50 degrees passively on the left side, compared to 60 degrees active, 75 degrees passive on the right (60 degrees is generally accepted as "normal" for most people).  First ray passive mobility was limited to neutral on the left (First metatarsal head level with second metatarsal head; normally, the first metatarsal moves above the second).  Right sided passive first ray mobility was normal. 


Ankle  dorsiflexion and great toe extension strength was normal but mildly painful;  all remaining left lower quarter strength was normal.  Plantar flexion strength decreased through 5 repetitions of unilateral heel raising by 20% (we measure this by heel- floor clearance in centimeters),  while increasing pain in the EHL to 7/10. 


The EHL was tender, as was the tibialis anterior tendon on the left side. 

My Thought Process in Treatment:

This was the first and only case of EHL tendinopathy that I have treated.  My first thoughts were  how and why do you get an isolated tendinopathy in such an "odd" area?  Outlined below is the hypothesis I used to develop my treatment plan:

1)  The plantarflexed first ray wants to move beyond neutral, but can't.  This may not be problematic in a sedentary individual, but in a repetitive jumping athlete such as a volleyball player the first ray is continually stressed at end range.  I felt perhaps as a result of this, the extensor hallucis longus, and to a lesser extent the anterior tibialis may have been trying to actively dorsiflex the  immobile first ray.  As the over activity of these groups manifested, a tendinopathy gradually developed, leading to my athlete's chief complaint (dorsal EHL/TA pain with aggressive volleyball activity).   

2)  Limited great toe extension placed additional demand on the EHL.  Limited great toe passive extension may have placed additional stress on the EHL as it worked to  extend the great toe actively before coming up against a passive motion restriction, resulting in more aberrant stress to the EHL.  This may also explain why the EHL hurt worse than the TA, as the TA inserrts more  proximally on  the first ray at the  medial cuneiform and first metatarsal.   

3)  Limited and painful plantar flexion strength was due to both decreased first ray mobility and decreased passive toe extension.  Plantar flexion in closed kinetic chain can be limited not only by Achilles tendon and/or gastroc/soleus pathology, but by limited ankle/ midfoot mobility and/or toe mobility; I believe this was the case here for reasons as outlined above.  (As a side note, decreased peroneal function can impact foot stability, but that is a post for another day). 


After the initial evaluation, I treated the athlete for 4 visits.  The second treatment after the evaluation (I wish I could say her first treatment was great, but in fact, it was pretty generic, as I had to digest my findings between the first and second visit in order to come up with a decent plan) included about 30 minutes of mobilization to normalize first ray dorsiflexion as well as great toe extension.   I also utilized a first ray taping technique I learned from Jenny McConnell, a well known Australian physical therapist after manual work was done.  We tested symptoms with a unilateral heel raise of ~ 5 repetitions; she felt no pain in either the EHL or TA.

She returned 6 days later with a 50% overall decrease in frequency and intensity of symptoms.  We continued with treatment as the second visit, but fashioned a "device" to stretch the first ray into dorsiflexion passively (actually a 1 inch stack of tongue depressors, cut to fit her first ray).  We utilized 5-10 sets of 30 seconds on/30 seconds off for closed chain stretching, done 1 time daily ( she was a busy student; more than 1 time daily would have been risking non-compliance).

Our next treatment, 3 days later, she was able to unilaterally heel raise 12 cm. heel-floor clearance for1-5 repetitions with 0/10 pain pre -treatment.  She also had no complaint of pain at all since the previous treatment.   There was also no pain elicited with EHL/TA resisted motions, and no significant point tenderness to palpation in these tendons.  We progressed both manual work, stretching and added a plantar flexion static strengthening progression.

Her last treatment consisted of home program review, as well as mobilization and taping.  Subjectively, she had mild pain during and after a pick-up basketball game, which dissipated a short time afterward without incident.  She returned to volleyball activity without incident.  In terms of long term follow up, I had treated her college roommate (whom she referred to us several months later) two times over the next 2 years; she stated my athlete continued to perform well with no dorsal foot pain.

Discussion: What I Would Do Differently Today:

This case dates back to the fall of 2004 .  In practice, I follow the 70/30 rule; that is 70% of how I practice is unchanged, while 30% changes based on research/ evidence, and my own outcomes across multiple patients.   If I saw this young lady today, here are some other things I would consider:

1)  More extensive soft tissue examination and (possible) treatment of the affected sites.  My bias at the time of this case was from a joint mobilization perspective.  Given the great outcome my athlete had, it is questionable that soft tissue work would have been necessary, but investigation into the pro/con of soft tissue specific therapy is something I take into account more readily now. 

2)  Look further up the kinetic chain.  With my athlete's genu recruvatum as well as her associated femoral/tibial internal rotation, I should have checked for associated IT band tightness, as well as psoas strength vs. tensor fasciae latae dominance, as well as gluteus medius / maximus function.  "Straight" tests of lower quarter strength were noted to be normal in the initial evaluation, but at the time I wasn't looking at single leg function as much then as I am now.  Addressing impairments along the kinetic chain is relatively simple and can limit other potential problematic issues down the road, particualrly in a competitive athlete.

3)  Observe the patient in actual practice, or at least talk to her coach .  I know this can be a logistical issue in terms of actual observation (it is tough for me to get out of the clinic on time most days, let alone to get to a  collegiate volleyball practice)  but at least speaking with someone who observes her function daily (i.e. her coach) can give better insight than "mocking up" a volleyball spike, block or jump serve in the enviromental constraints of a physical  therapy clinic.  Multiple factors may not allow true performance to be observed in the confines of a clinic, and real dysfunction may not be recognised as well as it can be where an athlete is most comfortable and natural.

As always, I look forward to any insight from readers who may have had either similar experiences personally or professionally.

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.