Lateral knee pain

Chris is a half-marathon runner for Stotan Racing, a Nike sponsored running team in Central New York.

Chris arrived at my office complaining of L lateral knee pain.  Based on the initial palpation I performed, I thought it might be ITB Friction Syndrome, but the first thing I did was test for hyper-mobility/instability.

Anterior/Posterior Drawer Tests were negative, as was the Lachman’s.  The Valgus Stress (MCL Sprain Test) was also negative.  I then proceeded with the Varus stress test (LCL Sprain Test) to determine if there was any damage to the fibular collateral ligament (also known as the lateral collateral ligament, or LCL).  The LCL Sprain Test was negative.

Next, I tested Apley’s Compression for any meniscus problem.  L Lateral and medial meniscii were both negative…  Apley’s Decompression with lateral medial/tibial rotation was also negative.

Next, I tried the ITB friction test, and this was a positive (4/10) on the pain scale.

AROM testing revealed both knee flexion and extension to be WNL, 135˚ and 0˚, respectively.  Slightly abnormal external tibial rotation was observed at 10-15˚.

Since I wasn’t picking up much in terms of ‘causality’, I decided to run through the hip ROM tests.

AROM L hip flexion was somewhat restricted at approx. 75˚, with PROM exhibiting a soft end-feel, and RROM performed with no pain.

AROM L hip extension was WNL at 35-40˚, with a soft PROM end-feel.  RROM did however, create some lateral knee pain.

AROM, PROM, and RROM for L internal hip rotation were all WNL.

AROM L hip external rotation was restricted to 45˚.  PROM was soft, and no pain was observed with RROM.

Hip abduction and adduction were WNL for all tests.

The limited external rotation made me think ‘short/tight, TFL/Gmax’, which fed into the possibility of ITB Friction Syndrome.  The restricted hip flexion and abnormal external tibial rotation left me thinking ‘short/tight biceps femoris (lateral hamstring)’, not so much ITB Friction Syndrome, but maybe some lateral patellar tracking leading to Chondromalacia.  (I immediately performed the patella femoral compression test, but discovered neither grating nor pain).

To begin treatment, I first performed the ITB Friction Syndrome protocol for Knee and Thigh Conditions.  This included Gmax compression broadening and TFL myofascial release, the Gmax lateral fiber stretch and TFL stretch. I then performed ITB mobilization.

I ended the session by instructing Chris in the ‘home’ stretching techniques for the TFL/Vastus Lateralis, Gmax, and Biceps Femoris.  I also instructed him in strengthening exercises for the lateral hip rotators, VMO, and medial hamstrings.

I asked him to text me about his progress, or lack thereof, over the next few days.  Chris did so, but he was not experiencing any improvement of his L lateral knee pain.  Unfortunately, I was unable to resolve the problem, based on Chris’ description of his pain and my assessment/treatment choices.  I rescheduled him immediately, but felt that I was missing something.

I had tried to follow the logic of Occam’s Razor, and look for the simplest or most obvious answer to the problem, first.  This being ITB Friction Syndrome or Lateral Patellar Tracking, but neither appeared to be the correct solution.  I had to dig deeper.  So, before Chris next session I reviewed movement system impairment syndromes of the knee and the foot /ankle, especially during running.

Review of the knee was great stuff, but didn’t clarify much regarding Chris’ L lateral knee pain.  I was starting to think that Chris’ problem might not be lateral knee, but something else (close by) that could be mistaken for lateral knee pain.

I found some ideas that made sense in ‘Movement Impairment Syndromes of the Foot and Ankle’, (Sahrmann, Elsevier, 2011).  I also reviewed the Knee/Thigh material and Lower Leg, Ankle, and Foot Conditions in Clinical Massage Therapy (Waslaski, 2012), to see if there was something I was missing, but I couldn’t get anything to add up, so I moved on to reviewing the respective DVDs.

The DVD for Complicated Knee Conditions had a section that addressed a fixated fibular head, so I reviewed that material and decided to test Chris’ L proximal fibular head to determine whether or not it was stuck.  I also reviewed ‘Movement Impairment Syndromes of the Foot and Ankle’, (Sahrmann, Elsevier, 2011).  Sahrmann did not address a fixated fibular head, but did go into depth concerning what she termed ‘Proximal Tibiofibular Glide Syndrome’ (PTGS).

The principal movement impairment (pain) associated with PTGS is posterior and or superior motion of the fibula on the tibia during active hamstring contraction (especially during running).  The principal positional impairment is the fibula located anteriorly, posteriorly, superiorly, or inferiorly to the normal position on the tibia after trauma, particularly an ankle sprain.  Pain in the posterolateral or lateral aspect of the tibiofibular joint is often associated with running, or general tibiofibular pain is associated with a history of lateral ankle sprains.  Hamstring length and talocrural dorsiflexion impairment (Insufficient Dorsiflexion Syndrome, IDS) are common with this diagnosis.  PTGS is either a positional fault generally occurring after ankle and foot trauma (ankle sprain) or movement impairment (pain) as a result of hamstring contraction pulling the fibula posteriorly.

From my previous work with Chris, I knew that there was some L hamstring tightness as well as L external tibial rotation.  The external tibial rotation was leading me toward thinking ‘a possible fixated fibular head’, but I also wanted to test for PTGS and insufficient talocrural dorsiflexion.

At the beginning of this session, I asked Chris about any previous ankle sprains, particularly left ankle sprains, and he reported that he had had several over the years.

Next, I assessed the four single-plane movements of the ankle joint:

AROM for plantar flexion was WNL (30-50˚).  PROM was soft/ligamentous.  RROM was negative.

AROM for dorsiflexion was restricted (<20˚).  PROM was bone-on-bone.  RROM was negative.

AROM for inversion was WNL, but all the way out to 50˚, maybe 50˚+.  PROM was soft/ligamentous.  RROM was negative.

AROM for eversion was restricted (<15˚).  PROM was bone-on-bone (normal).  RROM was negative.

I put Chris in the prone position and began treatment by releasing the plantar flexors—gastrocnemius, soleus, tibialis posterior, flexor digitorum longus, flexor hallicus longus, peroneus brevis, peroneus longus and plantaris—trying to restore normal muscle resting lengths. I then retested dorsiflexion ROMs.  There was no change in AROM and PROM was still bone-on-bone.  I concluded possible Insufficient Dorsiflexion Syndrome (fixated talus).

I then moved Chris into the supine position with his left hip and knee both flexed at 45˚. I grasped Chris’ fibular head between my thumb and first two fingers (being careful not to irritate the common fibular (peroneal) nerve.  I then tested the mobility of the fibular head by trying to create both anterior and posterior motion.  I was looking for either a fixation (hypomobility), or hypermobility in the form of excessive posterior glide.  There was no fixation, but significant posterior hypermobility.  As I pushed the fibular head posteriorly, Chris reported lateral knee discomfort similar to what he was experiencing when running.

I then tested Chris’ R fibular head in an identical manner, to compare sides.  There was neither a fixation, nor hypermobility, as compared to the left leg.

My conclusion was that Chris had a combination of a fixated L talus and short/tight L lateral hamstring.  Every time his hammy contracted, the fibular head was getting pulled posteriorly, irritating the common fibular nerve and causing lateral knee pain (at the proximal tibiofibular joint).  The fixated talus may have contributed to a fixated (hypomobile) distal fibular head, which in turn contributed to the hypermobile proximal fibular head.

Hamstring length and talocrural dorsiflexion impairment are common with this diagnosis.  Positions when the lateral hamstring is stretched or when the talocrural joint is at the end-range of motion can reproduce the symptoms.  Correction of a suspected positional impairment or stabilization of the proximal fibular head during the stretch (contracting biceps femoris) decreases symptoms.

The positional or movement impairments are difficult to see and palpate, but when correction of a suspected positional impairment or stabilization against a suspected motion decreases the symptoms, the diagnosis is supported.

I proceeded to:

  • Release the L biceps femoris (and teach Chris how to stretch the biceps femoris and strengthen the L medial hamstrings).
  • Release the L ankle inverters—extensor hallicus longus, flexor digitorum longus, flexor hallicus longus, tibialis anterior, and tibialis posterior—to restore normal muscle resting lengths, and return the L ankle everters—extensor digitorum longus, peroneus brevis, peroneus longus, and peroneus tertius—to normal muscle resting lengths, so they could be strengthened.
  • Teach Chris how to stretch the ankle inverters and strengthen the ankle everters.
  • Mobilize the L talus with ankle joint play (arthrokinetics).
  • K-tape the head of the L proximal fibula to resist posterior glide.

Chris ran with no pain immediately following the session (on a treadmill), and continues to train and race pain-free.

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