Knee hyperextension? Or does this photo suggest something more ?

You walk into the exam room and see a patient standing there just like this, What thoughts immediately flood your head ?
For me, I quickly start to juggle some things like, this:

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- anterior-meniscofemoral impingement ? Are his first words going to be knee pain ?
- tibial tuberosity/osgood type traction issue due to quad dominance? Are his first words going to be knee pain?
-loss of ankle rocker? Are his first words shin pain or plantar foot pain?
- tibialis posterior tendinitis ? Is he going to point to the medial ankle gutter or lower medial shin as his pain area?
-likely anterior pelvis tilt (hence weak lower abdominals), weak glutes, low back pain ?
-hamstring tightness, cramps, pain, posterior knee pain?

Just rambling real fast this morning after seeing this picture on an old hard drive.
Train your brain to think fast, think of possibilities top to bottom, don't wait for your patient to tell you where their problem is.
I play this game when i ask all my patients to walk to the back of the office to my exam room. I am watching, thinking, mental gymnastics.
Our jobs are to solve puzzles, put meaningful pieces together, to solve problems.
I use the analogy of building a puzzle. You open the box, search out the straight peripheral edges, then clump together colors, patterns. Your history and examination and gait observation should be about a process of putting together the most likely clinical picture and puzzle. And then you start to execute. Sometimes you have to walk things back, but you have to start somewhere.
But, if you wait until you get into the room, wait for the patient to say, "anterior knee pain" to start your thinking, it is easy to get tunnel vision and forget all of the other possible pieces of the puzzle that might be playing into that anterior knee pain.
REmember this, how your client moves , poorly or well, is not the problem, it is just how they are moving with the pieces and patterns available to them or how they are avoiding patterns that are painful. How they move is not the problem, it is their strategy. It is our job to find out why they are moving that way, and if it is relevant to their complaint.
Start big, funnel to small.

Shawn Allen, the other gait guy
#gait, #gaitanalysis, #gaitproblems, #clinicalthinking, #buildingpuzzles

The knee follows the arch/ankle.

*in the video, watch the left knee
Hopefully this video and post will make you think deeper about patellofemoral tracking, runners knee, meniscal issues and anterior knee pain syndromes as a whole.

This is subtle, but in this case, this is relevant to the LEFT knee complaints of this client.
When the foot complex is a little weak, the arch can collapse more than it should, rendering too much pronation, this means the talus will adduct, plantarflex and medially rotate more than it should. Since the tibia sits on top of this talus it must follow. This will allow more internal tibia spin (medial rotation) and this will drag the knee medially (it appears in the video to be a valgus load but it is more internal/medial rotation than valgus).
So, what the foot-ankle complex does, the knee follows. Conversely, when the knee moves medially or valgus because of a hip weakness (poor external rotation control) the foot will move medially.
So, are you going to "fix" this with an orthotic ? A stability shoe? Or are you going to actually help the client gain better control ?
You can see that our "raise the toes, to raise the arch" helps the client find the more appropriate arch posture with the help of more anterior compartment engagement and windlass effect at the 1st MPT-hallux joint. This is where our reteaching of the component parts via "motor chunking" via the Shuffle Walk (see our youtube channel) can help them control the rate and amount of arch "collapse" and thus control the rate of medial knee spin.
i say it on our podcast all the time, the knee is a simple sagittal hinge joint between 2 multiaxial joints. It is often a follower, not a leader.
Or you can bandaid this client with an expensive orthotic and never fix their problem. This keeps them coming back over and over for symptom management. It is a good business model (insert sarcasm), but helping this client learn and remedy their deficiency is a better one. Happy people talk to their friends, even strangers.

Shawn Allen, the other gait guy

#gait, #gaitproblems, #gaitanalysis, #ovepronation, #archcollapse, #valgusknee, #tibialspin, #internalhiprotation, #thegaitguys, #kneepain, #runnersknee, #patellapain, #anteriorkneepain

What do the hip flexors have to do with the knee extensors ?


"It is not about your test, it is what your client displays in your test that matters. They will try to find a way. The load has to go somewhere, and they will find a place to put it, they always do. Finding out how your client cheats, compensates, recruits and fails is the value of the assessment."

This is just a small example of how I approach a client through small assessment window.
As best as I am able, knowing the absolute limitations of a supine examinations translation to vertical loading, I will approach a client's ability to stabilize in all 3 planes of movement. Today, i will micro-dissect a thought process.

The straight leg resistance test (SLR):
just a few incomplete thoughts on a SAGITTAL perspective (so as to avoid writing a book).
I will do it looking at **pelvis posture (anterior, posterior, oblique), lumbar spine posture (incr/decr lordosis), if they can keep their knee locked in a position, does the pelvis rotate, do they want to deviate into internal or external rotation at the hip, do they plantar or dorsiflex their ankle or toes. Lots to see here in how a client will recruit, and this is just a small snapshot of things they might do. Yes, head position, arm position were left out , again, to avoid a longer post today.
I will add consistent (as best as possible) resistance in the SLR test , with full locked knee, at hip 30, 45 and then full straight leg SLR (at the client's hamstring tension limit), then again at 45 degree knee lock with partial hip flexion, 90 degree hip and knee. I am changing loading vectors frequently to see if their is a directional loading failure. I am looking for their ability to provide ample resistance, and how they might cheat (see above).
But here is how my mind works through the test on the most basic level, which will give me insight on the above cheats** the client may employ.
* In the MOST SIMPLEST thought of the assessment, can they EFFECTIVELY stabilize the pelvis to the lumbar spine, can they stabilize the femur into the pelvis, can they stabilize the tibia onto the femur? It is how they choose to engage the system that matters, and that might be partly why their "Screen" shows up shoddy and may be a window into their pain.
The question is, if they fail, where are they failing and what tissues are overburdened or over protecting ? Where is the load, and where NOT is the load, going ?

"It is not about your test, it is what your client displays in your test that matters. They will try to find a way. The load has to go somewhere, and they will find a place to put it, they always do. Finding out how your client cheats, compensates, recruits and fails is the value of the assessment. This is how you need to be thinking when you perform many of the mostly useless orthopedic tests in the textbooks.

This is key,
a SLR screen will not show you any of this, it will just show you their range of motion, nothing more, not how they did it, what parts worked harder than other parts, and which parts are weak, injured or inhibited, for example. It is not what a client does, it is how they go about it that has the most value to you in helping them.

Today's article below is what spurred my rant today. It gives light that most already know, that everything is connected. And perhaps we can translate it into deeper thoughts for our clients, namely, what part is not doing its job, and where are they not connecting the parts, and where are they putting the loads ?

From the Ema study:
"Our findings indicate that hip flexion training results in substantial neuromuscular adaptations during knee extensions similar to those induced by knee extension training."-Ema et al.

We need a stable and strong core-spine-pelvis connection to display powerful knee extension, and, we need a stable and strong femur-pelvis connection as well. So, where is your client doing more or less of the work, and is it related to their hip, low back or knee pain? Or are they tossing it into the ankle perhaps? This is the beauty of the game we all play every day, if we are actually paying attention.

Now, remember my discussion last week about "adding strength to dysfunction" ? Where is your client going to put the load?, the answer, where they can/able. And that doesn't exactly mean where they should be putting it. Mindless prescription of corrective exercises is a real problem in my opinion.

Shawn Allen, the other gait guy.

#gait, #gaitproblems, #gaitanalysis, #correctiveexercises, #running, #hipflexors, #kneeextension, #SLR, #corestrength, #thegaitguys

Scand J Med Sci Sports. 2018 Mar;28(3):947-960. doi: 10.1111/sms.13008. Epub 2017 Nov 22.
Neuromuscular adaptations induced by adjacent joint training.
Ema R1,2, Saito I3, Akagi R1,3.

Where the knee hinges matters.

It is easy to see the big things, but, we sometimes forget that the small things matter.
Sometimes it take an obvious glaring asymmetry to make us appreciate that the small asymmetries can make the same or similar impact over a long period of time. Rivers can carve out canyons over time.

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Here we see the gross difference that polio can make in leg size and in leg length. We must remember that changing a leg length also changes the symmetrical relationship of where the 2 knees hinge. A foot that pronates more than the other leg can lower the knee hinge point just a little because the talus drops further from its vertical height. We know very well that it for certain alters the hinge direction, posturing it more medially, but we cannot forget that a cranky knee on a side where the foot is flatter or pronates more excessively than the other is not to be ignored.
In this photo, we have dotted the knee at the same point on the patella. It is clear the knees will not hinge at the same time, thus stride and step lengths will change, and step width will be impacted. The pelvis will also spin more to one side on a pelvis that is lower on one side. This will impact lumbar spine sagittal happiness and stability/mobility. Hip and pelvis drift are real things in this case, and need your attention. *Just like a client that has a painful foot, a more pronated foot, more tibial torsion on one side etc. these things matter, and they often matter years down the road when many thousands of miles have been clocked into the subtle asymmetry. Sometimes these little things matter in our athletes too, who put the pedal to the floor asking the body for more.

Come hear our lecture tonight on www.onlineCE.com. You have to sign up early to get in. We won't disappoint. See you then. 7pm central time.

So you say your client needs more ankle rocker? Faking out ankle dorsiflexion and ankle rocker.

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I was reminded again yesterday, after yet another foot pain client came in to see me, that many do not understand the absolute and deeper ramifications of putting an orthotic into a shoe (and onto a foot) and what effects of doing so can have on changing a necessary adaptation.

This client had medial heel pain, not plantar heel pain, not the posterior calcaneal area, the medial edge (see photo). The edge where the inside/medial edge of the calcaneus/heel meets the ground. This client could reproduce the pain on palpation and could reproduce it if they stood up, and everted the heel just a tiny bit.

This client had a healthy appearing foot and arch. But, as often is the case, appearances are deceiving. 

Here was the major problem:

- client had loss of terminal ankle dorsiflexion from prior fracture immobilization

 

- top end calf weakness * (see later)

- client had clear fatiguability of the anterior shin compartment muscles, and mild toe extensor weakness

- the client had high arched supportive orthotics

So, what is happening here, and often happens with the above limitations, the client does not have the muscular ability to maintain the arch sufficiently from the big players, as noted. In other words, the ankle has lost mobility and the foot has lost stability, a common pattern. To make up for a loss of ankle dorsiflexion we often collapse the arch a sufficient amount to pitch the talus medially and forward to help the tibia progress forward the requisite amount needed for forward locomotion across the foot-ankle complex. This is a normal compensation, and in time there may be a pathologic cost. This medial approach of the talus and arch collapse, requires calcaneal eversion. This eversion means more medial calcaneal loading into the shoe, orthotic or ground, including medial soft tissue (mostly fat pad) loading between the ground and the everting calcaneus.  

This is a normal compensatory strategy to move forward over a restricted ankle dorsiflexion range. However, the doctor this client saw previously (for plantar fascitis), felt that this motion was a problem they needed to block with an orthotic. One that resisted the heel eversion and more than normal arch collapse/pronation cycle. This remedy resolved the plantar fascial pain. But, the medial heel pain began shortly thereafter. 

So, here we have a client that is compensating, and finding a way (though there are biomechanical costs to this way), to get past a limitation, loss of ankle rocker in this case. But, the doctor put an orthotic in the shoe that stopped this "way".  Now the client has to evert the heel even harder, because of the presence of the orthotic preventing it) and it is causing a "bite" or friction plus compression of the medial soft tissues. 

So, this client now still cannot compensate well, in the manner they have attempted to do so, because of the orthotic. So, where are the loads going to go now ? Yes, some are being rammed into the medial aspect of the orthotic, but some are likely going to so elsewhere. Remember, the client is trying to progress their mass over and past the limited ankle rocker, and more pronation was their strategy. But, the orthotic is preventing that.  So, the loads are very likely going to move up the chain (because the orthotic is muting loads down into the foot). 

______

Me:     "Oh, wait, "Mr. Jones", didn't you say you were just recently beginning to have some posterior knee pain ?  Let me tell you why you are hyperextending your knee a little more than normal and taxing out your gastrocneumius.* One way you can progress forward, if you cannot do it through ankle rocker, is to extend your knee a little by contracting your quadriceps a small amount at midstance.  Lets discuss why the orthotic is not helping you, not solving your problem, and creating some new issues for you. Then lets get down to fixing the root problem."

Some things to think about.  Orthotics are not bad, but the user has to know when they are a device to help a client progress through a problem, and when they are inappropriate. Not all increased pronation is bad, particularly when it helps a client get through a problem. But, fix the root problem, and then help them regain proper amounts of pronation.

Oh, and one more thing, all you "drive more ankle rocker and dorsiflexion" people out there. Are you driving more ankle dorsiflexion, or are you merely pressing the talus into more medial posturing, plantarflexion and adduction? These are the talar motions in pronation. And when you pronate, you get more ankle rocker, faked out ankle rocker. So, are you truly helping your client get more ankle rocker and dorsiflexion ? Is this increased pronation what they are doing during their squats, to "apparently" get enough ankle rocker/dorsiflexion?  Be careful all those new found ankle rocker mobility drills are not just making your client pronate more than normal. We know it happens, we see all the time. Loss of ankle mobility and loss of foot stability are often a paired phenomenon, they are trying to talk to you and tell you to treat the root cause.

-Dr. Allen, one of the gait guys

Unless you have ownership....

Compliance is often the issue ...especially in younger folks

Just say no to the exercise video. You need:

  • understanding on the patients part of the pathology and the importance of the rehab
  • buy in on the patients part
  • a way to monitor progress with objective outcomes

a nice review article in LER, full text here

additionally, this was covered in a great PODcast by David Pope here: http://physioedge.com.au/physio-edge-039-patellofemoral-pain-adolescents-dr-michael-rathleff/

Forefoot varus and patellofemoral cartilage damage.

So you just give everyone a FOOT TRIPOD and ANKLE ROCKER exercise and think the world will all be sunshine and rainbows huh ? Beware all you movement wizards, there is far more to it !

"Knowing enough to think you're doing it right, but not enough to know you're doing it wrong." - Neil deGrasse Tyson

So your client has knee pain huh ? Look far and wide, this is a global game amigos.
"Of the 51% of limbs with forefoot varus, 91.3% had medial and 78.3% had lateral PFJ cartilage damage. . . . . this study suggest a relationship between forefoot varus and medial PFJ cartilage damage in older adults"- Lufler et al. (study link below)

*If you do not know your client has a rigid forefoot varus, and they have hip or low back pain and cannot keep their glutes activated and participating in movements, how long are you going to fail your client ? The forefoot varus may need addressed because of the excessive, abrupt degree of internal spin on the limb.

If you are truly going to treat people, people who move (yes, that means everyone !), you have to know feet and gait, BOTH. Your knowledge must go far past rudimentary knowledge of:
- high / low arch
- flat feet
- prontation and supination
- orthotics and footbeds

You will have to know your foot types, you will have to understand shoe anatomy, foot anatomy, flexible semi-flexible and rigid foot types, compensated and uncompensated foot types, and of course know how each of these responds under various loading responses. Forefoot varus will load differently in cutting sports than in sagittal locomotion such as walking and running (both of which are different even in themselves despite both being sagittal). A foot that looks like it has a flat collapsed arch has far more to it than that, and thus remedy and intervention MUST go far beyond rudimentary interventions like a "stability shoe" or orthotic. Are you practicing, coaching, training and being part of your client's solution, or are you part of the problem ? If you want to get better at this stuff, we cover it all in our several hour (very difficult for some) National Shoe Fit program (the link is on our website if you wish to become a foot/gait/shoe jediwww.thegaitguys.com). Do not be mistaken, this is far more than "shoe Fit". To know how to properly shoe fit someone, you have to know the foot types and how they compensate, load, and respond. Without this knowledge, you are just another bump in the "road of problems" without ample solutions.

- Dr. Shawn Allen, one of the gait guys

The Association of Forefoot Varus Deformity with Patellofemoral Cartilage Damage in Older Adult Cadavers. Lufler, Stefanik, Niu, Sawyer, Hoagland, Gross http://onlinelibrary.wiley.com/doi/10.1002/ar.23524/full

images courtesy of aaronswansonpt.com and studyblue.com

Can you spot the problem?

Take a look at the pictures before proceeding, knowing that this gal presented with L sided outside knee pain and see if you can tell what may be wrong. She does wear orthotics. 

Take a good look at the lateral flare on each of these shoes. Yes, it is a Brooks Pure series with a 4mm drop. Yes the shoe has a medial (sl larger) and lateral flare, posteriorly and anteriorly.

Do you see the discoloration and increased wear on the lateral heel counter on the left compared to the left? There is also increased wear of the lugs on the outside of this left shoe. The forefoot is also worn into slight varus, but this difficult to see. The shoe, especially in combination with her orthotic, is keeping her in varus (ie inverted) for too long, taking her knee outside the saggital plane and contributing to her knee pain. 

ROTATE YOUR SHOES!

Knee pain and hyperpigmentation.

Seen this?   Take a look at these legs. Have you seen anything similar in a client, patient or perhaps yourself? This gent came in with knee pain  and we were looking at his feet. It turns out that this was a reaction to an antibiotic he had taken 3 years ago!  Hyperpigmentation can be caused by bacterial infections, congenital problems, lime Cafe au Lait spots, endocrine disorders, like Addison’s disease and hyperthyroidism, hemochromatosis as well phototoxic reactions from the use of systemic or topical antibiotics (1, 2) or from contact with certain plants or foods in conjunction with sun exposure (3).     Often initially, patients develop an reddened skin response caused by an allergic reaction. The inflammatory response often includes lymphocytes, eosinophils, and edema, which can result in a “blister like” reaction on sun-exposed skin. Over time, hyperkeratosis and melanocytic hyperplasia (increased numbers of the cells that give your skin pigmentation) develop, causing hyperpigmentation (1).    Some medications result directly in hyperpigmentation, without sun exposure, in a diffuse pattern, like on the gent we see here (4-9). The tables included in reference 2 can provide additional clues  Keep your eyes open! Who knows what the medications may have done to thwart your efforts in the healing response!    Gould JW, Mercurio MG, Elmets CA. Cutaneous photosensitivity diseases induced by exogenous agents.  J Am Acad Dermatol . 1995;33:551–73. 
  http://www.aafp.org/afp/2003/1115/p1955.html  
 Friedlander SF. Contact dermatitis.  Pediatr Rev . 1998;19:166–71 
 Crowson AN, Magro CM. Recent advances in the pathology of cutaneous drug eruptions. Dermatol Clin . 1999;17:537–60.,viii 
 Pepine M, Flowers FP, Ramos-Caro FA. Extensive cutaneous hyperpigmentation caused by minocycline.  J Am Acad Dermatol . 1993;28(2 pt 2):292–5. 
 Kelly AP. Aesthetic considerations in patients of color.  Dermatol Clin . 1997;15:687–93. 
 Goroll AH, Mulley AG Jr, eds. Primary care medicine: office evaluation and management of the adult patient. 4th ed. Philadelphia: Lippincott Williams & Wilkins, 2000 
 Skin diseases of general importance—part II. In: Cecil RL, Goldman L, Bennett JC. Cecil Textbook of medicine. 21st ed. Philadelphia: Saunders, 2000: 2288–98 
 Friedlander SF. Contact dermatitis.  Pediatr Rev . 1998;19:166–71.

Seen this?

Take a look at these legs. Have you seen anything similar in a client, patient or perhaps yourself? This gent came in with knee pain  and we were looking at his feet. It turns out that this was a reaction to an antibiotic he had taken 3 years ago!

Hyperpigmentation can be caused by bacterial infections, congenital problems, lime Cafe au Lait spots, endocrine disorders, like Addison’s disease and hyperthyroidism, hemochromatosis as well phototoxic reactions from the use of systemic or topical antibiotics (1, 2) or from contact with certain plants or foods in conjunction with sun exposure (3).  

Often initially, patients develop an reddened skin response caused by an allergic reaction. The inflammatory response often includes lymphocytes, eosinophils, and edema, which can result in a “blister like” reaction on sun-exposed skin. Over time, hyperkeratosis and melanocytic hyperplasia (increased numbers of the cells that give your skin pigmentation) develop, causing hyperpigmentation (1).  

Some medications result directly in hyperpigmentation, without sun exposure, in a diffuse pattern, like on the gent we see here (4-9). The tables included in reference 2 can provide additional clues

Keep your eyes open! Who knows what the medications may have done to thwart your efforts in the healing response!

  1. Gould JW, Mercurio MG, Elmets CA. Cutaneous photosensitivity diseases induced by exogenous agents. J Am Acad Dermatol. 1995;33:551–73.
  2. http://www.aafp.org/afp/2003/1115/p1955.html
  3. Friedlander SF. Contact dermatitis. Pediatr Rev. 1998;19:166–71
  4. Crowson AN, Magro CM. Recent advances in the pathology of cutaneous drug eruptions.Dermatol Clin. 1999;17:537–60.,viii
  5. Pepine M, Flowers FP, Ramos-Caro FA. Extensive cutaneous hyperpigmentation caused by minocycline. J Am Acad Dermatol. 1993;28(2 pt 2):292–5.
  6. Kelly AP. Aesthetic considerations in patients of color. Dermatol Clin. 1997;15:687–93.
  7. Goroll AH, Mulley AG Jr, eds. Primary care medicine: office evaluation and management of the adult patient. 4th ed. Philadelphia: Lippincott Williams & Wilkins, 2000
  8. Skin diseases of general importance—part II. In: Cecil RL, Goldman L, Bennett JC. Cecil Textbook of medicine. 21st ed. Philadelphia: Saunders, 2000: 2288–98
  9. Friedlander SF. Contact dermatitis. Pediatr Rev. 1998;19:166–71.

Low back pain and quadriceps compensation. A study.

“Neuromuscular changes in the lower extremity occur while resisting knee and hip joint moments following isolated lumbar paraspinal exercise. Persons with a history of LBP seem to rely more heavily on quadriceps activity while jogging.“- Hart et al.

Recently I discussed a paper (link below) about how soleus  motoneuron pool excitability increased following lumbar paraspinal fatigue and how it may indicate a postural response to preserve lower extremity function.
Today I bring you an article of a similar sort.  This paper discusses the plausibility that a relationship exists between lumbar paraspinal muscle fatigue and quadriceps muscle activation and the subsequent changes in hip and knee function when running fatigue ensued. 


"Reduced external knee flexion, knee adduction, knee internal rotation and hip external rotation moments and increased external knee extension moments resulted from repetitive lumbar paraspinal fatiguing exercise. Persons with a self-reported history of LBP had larger knee flexion moments than controls during jogging. Neuromuscular changes in the lower extremity occur while resisting knee and hip joint moments following isolated lumbar paraspinal exercise. Persons with a history of LBP seem to rely more heavily on quadriceps activity while jogging.”- Hart et al.

Whether this or any study was perfectly performed or has validity does not matter in my discussion here today. What does matter pertaining to my dialogue here today is understanding and respecting the value of the clinical examination (and not depending on a gait analysis to determine your corrective exercise prescription and treatment). When an area fatigues and cannot stabilize itself adequately, compensation must occur to adapt. Protective postural control strategies must be attempted and deployed to stay safely upright during locomotion. The system must adapt or pain or injury may ensue, sometimes this may take months or years and the cause is not clear until clinical examination is performed. Your exam must include mobility and stability assessments, motor pattern evaluation, and certainly skill, coordination, ENDURANCE and strength assessments if you are to get a clear picture of what is driving your clients compensation and pain. 

So, if your client comes in with knee, hip or ankle pain and a history of low back pain, you might want to pull out these articles and bash them and other similar ones into your brain. Remember what I mentioned when i reviewed the soleus article ? I mentioned that the reduced ankle dorsiflexion range may be from a soleus muscle postural compensation reaction to low back pain. In today’s discussion, impairment of the hip ranges of motion or control of the knee (from quadriceps adaptive compensation) may also be related to low back pain, in this case, paraspinal fatigue.  

Sometimes the problem is from the bottom up, sometimes it is from the top down. It is what makes this game so challenging and mind numbing at times. If only it were as simple as, “you need to work on abdominal breathing”, or “you need to strengthen your core”.  If only it were that simple. 

Dr. Shawn Allen, one of the gait guys


References:
J Electromyogr Kinesiol. 2011 Jun;21(3):466-70. doi: 10.1016/j.jelekin.2011.02.002. Epub 2011 Mar 8.
Effects of paraspinal fatigue on lower extremity motoneuron excitability in individuals with a history of low back pain. Bunn EA1, Grindstaff TL, Hart JM, Hertel J, Ingersoll CD.

J Electromyogr Kinesiol. 2009 Dec;19(6):e458-64. doi: 10.1016/j.jelekin.2008.09.003. Epub 2008 Dec 16. Jogging gait kinetics following fatiguing lumbar paraspinal exercise.
Hart JM1, Kerrigan DC, Fritz JM, Saliba EN, Gansneder B, Ingersoll CD

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Holy twisted tibias Batman! What is going here in this R sided knee pain patient?

In the 1st picture note this patient is in a neutral posture. Note how far externally rotated her right foot is compared to the left. Note that when you drop a plumbline down from the tibial tuberosity it does not pass-through or between the second and third metatarsals. Also note the incident left short leg
In the next picture both of the patients legs are fully externally rotated. Note the large disparity from right to left. Because of the limited extra rotation of the right hip this patient most likely has femoral retro torsion. This means that the angle of her femoral head is at a greater than 12° angle. We would normally expect approximately 40° of external Rotation. 4 to 6° is requisite for normal gait and supination.

In the next picture the patients knees are fully internally rotated you can see that she has an excessive amount of internal rotation on the right compare to left, confirming her femoral antetorsion.

When this patient puts her feet straight (last picture), her knees point to the inside causing the patello femoral dysfunction right greater than left. No wonder she has right-sided knee pain!

Because of the degree of external tibial torsion (14 to 21° considered normal), activity modification is imperative. A foot leveling orthotic with a modified UCB, also inverting the orthotic is helpful to bring her foot somewhat more to the midline (the orthotic pushes the knee further outside the sagittal plane and the patient internally rotate the need to compensate, thus giving a better alignment).

a note on tibial torsion. As the fetus matures, The tibia then rotates externally, and most newborns have an average of 0- 4° of internal tibial torsion. At birth, there should be little to no torsion of the tibia; the proximal and distal portions of the bone have little angular difference (see above: top). Postnatally, the tibia should twist outward (externally) a total of 15 degrees until adult values are reached between ages 8 and 10 years of 23° of external tibial torsion (range, 0° to 40°). more cool stuff on torsions here

Wow, cool stuff, eh?

What are we listening to this week?     The Physio edge podcast with David pope. This week they interview Kurt Lisle about anterior knee pain. Here is our synopsis:     One of the things they empahasized right off the bat was that patellofemoral pain not only refers about the knee but also below or most importantly posterior to the knee. The fat pad had a tendency to refer more locally where is other structures can refer to other areas.    Aggravating factors for patello femoral dysfunctional pain tends to be flexion or activities involving flexion as well as compression of the knee and rest is in alleviating factor.    The fat pad pain tends to be to either side of the patellar tendon and sometimes directly under it. This can be aggravated by standing, particularly with the knee and hyperextension, which compresses the fat pad.    Patellar tendon pain tends to remain at the inferior pole of the patella on the tendon whereas patellofemoral pain has a tendency to refer more.      Physical examination pearls:     Patellar tendonopathy alone generally does not have effusion present where as the patellofemoral or fat pad injury may.   Is there pain in passive hyperextension? This generally can mean fat pad injury or potential he ligamentous injury.   Visually you may palpate a thickened fat pad, particularly in females.   Pain with passive motions generally points away from patellar tendon.   Dialing in as to where and when they are having their pain is an important part of the functional evaluation.   Kurt likes to do a table top examination first to ensure functional integrity of the knee before jumping right to functional tasks. His concerns are (which are valid) is the knee up to the task you’re about to ask it to do? Good advice here. He emphasizes the need to be systematic and consistent in your examination, no matter how you examine them. Develop a routine that you follow each and every time. He recommends passively looking at the knee in extension and 90° flexion.    There is a discussion on functional movement about the hip and pelvis, knee, and foot and ankle. Emphasis is made, for example at the knee, as to “is the knee moving medially and laterally or are the femur and tibia rotating mediately or laterally” in which is precipitating the pain?    “Catching” of the patella is often due to patellofemoral pathology such as a subchondral defect, slap tear of the chondral surface, or abnormalities of the trochlea of the femur.    Advanced imaging strategies are also discussed with a brief overview of some of the things to look for.    Finally treatment strategies were discussed. It is emphasized that identifying the specific activity or change activities that’s causing any pain he’s made as well as activity modification. We were happy to hear that footwear and its role in knee as well as hepatology was discussed as well as looking at occupational contributions to the pain.    There was emphasis on exercise specificity particularly with respect to if the problem was unilateral not giving “blanket” exercises for both knees but rather concentrating on the symptomatic side.    A discussion on the use of EMG and activation patterns was also entertained with some good clinical pearls here. More marked rather than subtle changes and activation side to side seem to be more clinically significant. In other words, with respect training, can they achieve similar levels of activation on each side with a similar activity (for example isometric knee extension with the leg bent 60°).    The judicious use of tape from a functional testing standpoint was interesting. Emphasis was made that tape is not a cure and will merely a tool.     All in all and informative, concise podcast with some great clinical pearls and a nice review of the knee and patellofemoral pain.          link to PODcast:  http://physioedge.com.au/pe-029-acute-knee-injuries-with-kurt-lisle/

What are we listening to this week? 

The Physio edge podcast with David pope. This week they interview Kurt Lisle about anterior knee pain. Here is our synopsis:

One of the things they empahasized right off the bat was that patellofemoral pain not only refers about the knee but also below or most importantly posterior to the knee. The fat pad had a tendency to refer more locally where is other structures can refer to other areas.

Aggravating factors for patello femoral dysfunctional pain tends to be flexion or activities involving flexion as well as compression of the knee and rest is in alleviating factor.

The fat pad pain tends to be to either side of the patellar tendon and sometimes directly under it. This can be aggravated by standing, particularly with the knee and hyperextension, which compresses the fat pad.

Patellar tendon pain tends to remain at the inferior pole of the patella on the tendon whereas patellofemoral pain has a tendency to refer more.

Physical examination pearls:

  • Patellar tendonopathy alone generally does not have effusion present where as the patellofemoral or fat pad injury may.
  • Is there pain in passive hyperextension? This generally can mean fat pad injury or potential he ligamentous injury.
  • Visually you may palpate a thickened fat pad, particularly in females.
  • Pain with passive motions generally points away from patellar tendon.
  • Dialing in as to where and when they are having their pain is an important part of the functional evaluation.

Kurt likes to do a table top examination first to ensure functional integrity of the knee before jumping right to functional tasks. His concerns are (which are valid) is the knee up to the task you’re about to ask it to do? Good advice here.
He emphasizes the need to be systematic and consistent in your examination, no matter how you examine them. Develop a routine that you follow each and every time. He recommends passively looking at the knee in extension and 90° flexion.

There is a discussion on functional movement about the hip and pelvis, knee, and foot and ankle. Emphasis is made, for example at the knee, as to “is the knee moving medially and laterally or are the femur and tibia rotating mediately or laterally” in which is precipitating the pain?

“Catching” of the patella is often due to patellofemoral pathology such as a subchondral defect, slap tear of the chondral surface, or abnormalities of the trochlea of the femur.

Advanced imaging strategies are also discussed with a brief overview of some of the things to look for.

Finally treatment strategies were discussed. It is emphasized that identifying the specific activity or change activities that’s causing any pain he’s made as well as activity modification. We were happy to hear that footwear and its role in knee as well as hepatology was discussed as well as looking at occupational contributions to the pain.

There was emphasis on exercise specificity particularly with respect to if the problem was unilateral not giving “blanket” exercises for both knees but rather concentrating on the symptomatic side.

A discussion on the use of EMG and activation patterns was also entertained with some good clinical pearls here. More marked rather than subtle changes and activation side to side seem to be more clinically significant. In other words, with respect training, can they achieve similar levels of activation on each side with a similar activity (for example isometric knee extension with the leg bent 60°).

The judicious use of tape from a functional testing standpoint was interesting. Emphasis was made that tape is not a cure and will merely a tool.

All in all and informative, concise podcast with some great clinical pearls and a nice review of the knee and patellofemoral pain.


link to PODcast: http://physioedge.com.au/pe-029-acute-knee-injuries-with-kurt-lisle/

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Medial knee pain in a skier.   Considering an orthotic?  You had better know what you are doing! 

Can you guess why this gal has pain in both knees? Especially when skinning up a hill and skiing down? 

 Take a close look at the photos above and notice the orientation of her knee with her foot. Now look at you tuberosity and drop a line straight downward.  This line should pass through or slightly lateral to the second metatarsal shaft. Can you see how it falls to the outside of this? Perhaps even between the third and fourth metatarsal?

This gal has bilateral internal tibial torsion.  When she wears a standard foot bed (creates a level surface for the right for the foot) or an orthotic without appropriate posting, it pushes her knee outside of the saggital plane. This creates abnormal patellofemoral tracking  and appears to be a major contributor to her pain. 

 You will notice that we placed a valgus post under the orthotic(  a post that is canted from lateral to medial) which pushes her knee to the midline as the first ray descends.  You can see her alignment is better with her boots on and the changes. 

 The bottom line? Know your torsions and versions.  Posting a patient like this incorrectly could result in a meniscal disaster!

How relaxed, or shall we say “sloppy” is your gait ?  Look at this picture, the blurred left swing leg tells you this client has been photographed during gait motion.   Now, visualize a line up from that right foot through the spine. You will see that it is clearly under the center/middle of the pelvis. But of course, it is easier to stand on one leg (as gait is merely transferring from one single leg stance to the other repeatedly) when your body mass is directly over the foot.  To do this the pelvis has to drift laterally over the stance leg side.  Sadly though, you should be able to have enough gluteal and abdominal cylinder strength to stack the foot and knee over the hip. This would mean that the pelvis plumb line should always fall between the feet, which is clearly not the case here.  This is sloppy weak lazy gait. It is likely an engrained habit in most people, but that does not make it right. It is pathology, in time something will likely have to give.   This is the cross over gait we have beaten to a pulp here at The Gait Guys over and over … . . and over.   This gait this gait, this single photo, means this client is engaging movement into the frontal plane too much, they have drifted to the right. We call it frontal plane drift. To prevent it, it means you have to have an extra bit more of lateral line strength in the gluteus medius and lateral abdominal sling to fend off pathology. You have to be able to find functional stability in the stacked posture, and this can take some training and time.  Make no mistake, this is a faulty movement pattern, even if there is not pain, this is not efficient motor patterning and something will have to give. Whether that is lateral foot pain from more supination strategizing, more tone in the ITB perhaps causing lateral knee or hip pain, a compensation in arms swing or thoracic spine rotation or head tilt  … … something has to give, something has to compensate.   So, how sloppy is your gait ?   Do you kick or scuff the inside of your opposite shoe ? Can you hear your pants rub together ? Just clues. You must test the patterns, make no assumptions, please.  Shawn Allen, one of the gait guys

How relaxed, or shall we say “sloppy” is your gait ?

Look at this picture, the blurred left swing leg tells you this client has been photographed during gait motion. 

Now, visualize a line up from that right foot through the spine. You will see that it is clearly under the center/middle of the pelvis. But of course, it is easier to stand on one leg (as gait is merely transferring from one single leg stance to the other repeatedly) when your body mass is directly over the foot.  To do this the pelvis has to drift laterally over the stance leg side.  Sadly though, you should be able to have enough gluteal and abdominal cylinder strength to stack the foot and knee over the hip. This would mean that the pelvis plumb line should always fall between the feet, which is clearly not the case here.  This is sloppy weak lazy gait. It is likely an engrained habit in most people, but that does not make it right. It is pathology, in time something will likely have to give. 

This is the cross over gait we have beaten to a pulp here at The Gait Guys over and over … . . and over.   This gait this gait, this single photo, means this client is engaging movement into the frontal plane too much, they have drifted to the right. We call it frontal plane drift. To prevent it, it means you have to have an extra bit more of lateral line strength in the gluteus medius and lateral abdominal sling to fend off pathology. You have to be able to find functional stability in the stacked posture, and this can take some training and time.  Make no mistake, this is a faulty movement pattern, even if there is not pain, this is not efficient motor patterning and something will have to give. Whether that is lateral foot pain from more supination strategizing, more tone in the ITB perhaps causing lateral knee or hip pain, a compensation in arms swing or thoracic spine rotation or head tilt  … … something has to give, something has to compensate. 

So, how sloppy is your gait ? 

Do you kick or scuff the inside of your opposite shoe ? Can you hear your pants rub together ? Just clues. You must test the patterns, make no assumptions, please.

Shawn Allen, one of the gait guys

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What were they thinking? Oh, they weren’t thinking…

Here is a simple case of knowing your anatomy. 

make sure to use the toggle bar to the right and left of the picture to see all the pictures : )

This woman came in with right sided lateral knee pain with hiking and skiing; worse with fatigue, better with rest. The pain was localized at the lateral joint line and at the tibial fibular joint. 

She had been previously been diagnosed with tibial fibular hypermobility and subsequently had an arthrodesis (fusion) performed at that joint for knee pain. The surgery helped for a short time and a newer, slightly different pain developed. 

Yes, she has a moderate genu valgus, R > L. Yes, she has a left, anatomically short (tibial) Left leg. Yes, she has has NO MOBILITY at the tib/fib articulation and the focus of pain is just above at the joint line and at the lateral aspect of the patello femoral joint. 

The tibial fibular joint is a syndesmosis (not a true synovial or diarthrodial joint) that is supposed to have a a superio/inferior gliding motion (see diagram) with ankle dorsiflexion, due to the wedge shape of the talar dome and talo crural articulation. It also is supposed to have an anterior/posterior gliding movement at the superior aspect of the joint and a reciprocal movement in the opposite direction at the ankle (see diagram).

Whenever we take away movement in one area, it needs to occur somewhere else; in this case, at the femoral tibial joint and patello femoral joints.

Does it make sense that her left sided leg would cause hypermobility on the right side with a supinatory moment of the foot on the left to attempt to lengthen the leg and a pronatory movement of the foot on the right, in addition to valgus angulation of the joint on the right to attempt to “shorten” that extremity? Would this increased valgus angluation of the knee, in turn, cause abnormal, lateral, tracking of the patella? Wouldn’t the increased pronatory moment cause a more supple foot on that side with increased requirements for “push off” on that side with increased calf recruitment? Do you think that may impair proprioception on that side?

What if you put a sole lift in the left shoe (like we did) to help to alleviate some of the discrepancy and gave her some anterior compartment exercises (toes up walking, lift/spread/reach exercises, heel walking, simple balance on 1 leg exercises? Her world becomes a much better place to live in and she can return to the activities she loves to do with her 65 year old friends, like hiking 14′ers, skiing and mountain biking,

What we do to one joint affects all the others. You cannot make one change without expecting others. Be on the lookout and know your anatomy! This case was relatively straight forward. Many are not. Do a thorough exam and expect the unexpected. 

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Now THERE”S some internal tibial torsion!

So, this gent came in to see us with L sided knee pain after it collapsed with an audible “pop” during a baseball game. He has +1/+2 laxity in his ACL on that side. He has subpatellar and joint line pain on full flexion, which is limited slightly to 130 (compared to 145 right)

 We know he has internal torsion because a line drawn from the tibial tuberosity dropped inferiorly does not pass through or near the plane of the 2nd metatarsal (more on tibial torsions here)

What would you do? Here’s what we did:

  • acupuncture to reduce swelling
  • took him out of his motion control shoes (which pitch him further outside the saggital plane)
  • gave him propriosensory exercises (1 leg balance: eyes open/ eyes closed; 1 legged mini squats, BOSU ball standing: eyes open/eyes closed)
  • potty squats in a pain free range
  • ice prn
  • asked him to avoid full flexion

Is it any wonder he injured his knee? Imagine placing the FOOT in the saggital plane, which places the knee FAR outside it; now load the joint an twist, OUCH!

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L sided medial knee pain in a TKR patient

So, why does this gals L knee hurt, posterior and medial on the left?

  • L total knee replacement 6 years ago; she thinks they used too large a size, we would have to agree.
  • occassional peripatellar discomfort
  • current pain descending hills and stairs, posterior and medial on the left

Physical findings

  • tenderness at posterior, medial aspect of knee at the top of the tibial plateau
  • positive anterior and posterior drawer +2
  • McMurrays for clicking with valgus and varus stresses
  • negative valgus/varus stress
  • all muscles test strong except for one, which one is it?

Read on…

Here is our theory:

This particular muscle fires at heel strike and again from loading response until toe off (you can look at the diagram above if needed). It also acts as an acessory posterior cruciate ligament (PCL).

Think about the forces on the knee while descending hills or stairs. The momentum will carry the femur forward (or anteriorly). There needs to be something to reststrain this; enter the PCL.

Because of the laxity (and instability), the poplitues needs to fire to take up the slack. Palpation confirmed it being tender throughout its course, with most at the tibial attachment. The attachment is largest here, so that makes sense. The muscle also tested weak.

We gave her popliteus and 1 leg balancing exercises in addition to doing acupuncture (origin/insertion work) as pictured. 5 days later she was 60% improved. She may need to return to her ortho, depending on her response to additional care.

Think about the popliteus the next time someone has posterior medial knee pain, especially when descending.

Patello femoral pain? Thinking weak VMO? Think again…   “Atrophy of all portions of the quadriceps muscles is present in the affected limb of people with unilateral PFP. There wasn’t any atrophy of the quadriceps in individuals with PFP compared to those without pathology. Selective atrophy of the VMO relative to the vastus lateralis wasn’t identified in persons with PFP.”    http://www.physiospot.com/research/atrophy-of-the-quadriceps-is-not-isolated-to-the-vastus-medialis-oblique-in-individuals-with-patellofemoral-pain/

Patello femoral pain? Thinking weak VMO? Think again…

“Atrophy of all portions of the quadriceps muscles is present in the affected limb of people with unilateral PFP. There wasn’t any atrophy of the quadriceps in individuals with PFP compared to those without pathology. Selective atrophy of the VMO relative to the vastus lateralis wasn’t identified in persons with PFP.”

http://www.physiospot.com/research/atrophy-of-the-quadriceps-is-not-isolated-to-the-vastus-medialis-oblique-in-individuals-with-patellofemoral-pain/

Podcast 72: Neuroplasticity, EVA Shoe Foam, and Shoe Trends

Maximalist shoes and the death of Minimalism ? Could this be true ?

*Show sponsor: www.newbalancechicago.com

Lems Shoes.  www.lemsshoes.comMention GAIT15 at check out for a 15% discount through August 31st, 2014.

A. Link to our server: 

http://traffic.libsyn.com/thegaitguys/pod_73f.mp3

Direct Download: 

http://thegaitguys.libsyn.com/podcast-72

B. iTunes link:

https://itunes.apple.com/us/podcast/the-gait-guys-podcast/id559864138

C. Gait Guys online /download store (National Shoe Fit Certification and more !) :

http://store.payloadz.com/results/results.aspx?m=80204

D. other web based Gait Guys lectures:

www.onlinece.com   type in Dr. Waerlop or Dr. Allen,  ”Biomechanics”

______________

Today’s Show notes:

1. Neuroplasticity: Your Brain’s Amazing Ability to Form New Habits
new link (does not have the old photo ivo mentioned that he loved)
 
2. Last week we pounded the sand on EVA foam and maximalist shoes. There was alot of attention, emails and good social media discussion on the topic.  
LETS REVIEW IT
file:///Users/admin/Downloads/p142_Heel_shoe_interactions_and_EVA_foam_f_web_150dpi.pdf
 
3. Then there just last week there was an article in LER on “the death of minimalist shoes” ? 
READ THIS: 
The rise and fall of minimalist footwear | Lower Extremity Review Magazine
http://lermagazine.com/cover_story/the-rise-and-fall-of-minimalist-footwear
 

4.  Physical Therapy as Effective as Surgery for Meniscal Tear

Kathleen Louden

March 20, 2013
Torn Meniscus? Thinking about surgery? Think again…

5. Cast study: the broken foot tripod
The turned out foot. How far ahead (and how fast) can you think ?  
 There are many causes of the turned out foot. The above slide is just one of many logical and possible chain of events.   
 There are also reasons above the neck that cannot be ignored in creating the externally rotated foot (and in resolving it). Things are not always biomechanical in origin so remember this when you are continually doing activation and rehab interventions to get more glute or drive more internal limb spin and your results are met with a non-response.   
 Most of us like a biomechanical line of thinking when it comes to apparent biomechanical aberrancies from the norm.  However, more often than you probably think (go back and listen to podcast 58 on Cortical Brain Mapping of injuries), several more purely neurologic reasons are plausible.  For example, changes in input/output in unilateral activity within the pontomedullary reticular formation (PMRF) of the brain can lead to inhibition of the posterior chain muscles below the T6 spinal level (And anterior muscles above T6. And what is awesome is that there are ways to test this kinda stuff on a physical exam !  However, this blog post is not the place to teach these neurologic examination procedures.  But, if this sounds like Janda’s Upper and Lower Crossed Syndromes you are thinking soundly. Just remember though, if you are fixing what you see, you may not be fixing the problem, fix the cause that drove what you are seeing.  If you know your functional neurology you will know where these things come from, they are a cortical phenomenon).   
 Of the posterior compartment muscles below T6, the gluteus maximus is probably the largest of this group and when it is inhibited there is loss of control of its ability to stabilize single leg stance.  One strategy around a stability challenge would be to turn the foot/leg into the frontal plane (toe out) via external limb rotation.  Now we can use the remaining muscles in both the sagittal and frontal planes ! We are always more stable when we can engage two or more cardinal planes at the same time. 
 There are  many more reasons for the externally rotated limb/foot, for example vestibular dysfunction, cerebellar dysfunction, core dysfunction, impaired normal arm swing and the list goes on. We have talked about many of these reasons on many of our blog posts and podcasts. 
 Mental gymnastics when it comes to the brain are important, Keep your gait and human movement game sharp, work through scenarios in your head regularly because it is what is necessary when you are working up a client.   
 Shawn and Ivo 
 the gait guys

The turned out foot. How far ahead (and how fast) can you think ? 

There are many causes of the turned out foot. The above slide is just one of many logical and possible chain of events.  

There are also reasons above the neck that cannot be ignored in creating the externally rotated foot (and in resolving it). Things are not always biomechanical in origin so remember this when you are continually doing activation and rehab interventions to get more glute or drive more internal limb spin and your results are met with a non-response.  

Most of us like a biomechanical line of thinking when it comes to apparent biomechanical aberrancies from the norm.  However, more often than you probably think (go back and listen to podcast 58 on Cortical Brain Mapping of injuries), several more purely neurologic reasons are plausible.  For example, changes in input/output in unilateral activity within the pontomedullary reticular formation (PMRF) of the brain can lead to inhibition of the posterior chain muscles below the T6 spinal level (And anterior muscles above T6. And what is awesome is that there are ways to test this kinda stuff on a physical exam !  However, this blog post is not the place to teach these neurologic examination procedures.  But, if this sounds like Janda’s Upper and Lower Crossed Syndromes you are thinking soundly. Just remember though, if you are fixing what you see, you may not be fixing the problem, fix the cause that drove what you are seeing.  If you know your functional neurology you will know where these things come from, they are a cortical phenomenon).  

Of the posterior compartment muscles below T6, the gluteus maximus is probably the largest of this group and when it is inhibited there is loss of control of its ability to stabilize single leg stance.  One strategy around a stability challenge would be to turn the foot/leg into the frontal plane (toe out) via external limb rotation.  Now we can use the remaining muscles in both the sagittal and frontal planes ! We are always more stable when we can engage two or more cardinal planes at the same time.

There are  many more reasons for the externally rotated limb/foot, for example vestibular dysfunction, cerebellar dysfunction, core dysfunction, impaired normal arm swing and the list goes on. We have talked about many of these reasons on many of our blog posts and podcasts.

Mental gymnastics when it comes to the brain are important, Keep your gait and human movement game sharp, work through scenarios in your head regularly because it is what is necessary when you are working up a client.  

Shawn and Ivo

the gait guys