Flexible hammer toes

IF you've been with us all along you know this one by heart. All you have to do is test it to confirm (never assume, ever !). 
And remember, sometimes people present with their problem, and sometimes they present with a layered compensation to strategize and cope with the underlying problem. It is your job to determine that.
You must recognize here:
flexible hammer toe early development. It is a compensation for weakness somewhere in the chain. It is a gripping strategy to make up for something somewhere. It is not normal, it is a clue.

1- over activity of the short extensors & and long flexors
2- under activity of the long extensors & and short flexors
3- thusly, distal displacement of the Metatarsal fat pad complex
4- and lotsa other things (but we will not detract from the major cursory observation point here today)

Loading this forefoot is troubled, in many ways...... so many that we will not go it here. We have written about these things in long form so many times, just head over to the blog and search. This client did not have any foot or ankle issues, they had impaired hip rotation and extension and were complaining of low back pain. They have obviously been coping through the entire chain for awhile. Be Sherlock Holmes in your practice today, look for the clues.

-Dr. Allen

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/

So you think you are an iliotibial band syndrome guru ?  This study has some interesting provoking thoughts about the mechanics we have all previously assumed. It is good to challenge established teachings, for it is only through interrogating old ways that we may see the true light of things.

The iliotibial band (ITB) syndrome is a common overuse injury that is commonly misunderstood. It has been regarded as a friction syndrome where the ITB rubs against he lateral femoral epicondyle because of its previously assumed variable function, below 30 degrees knee extension it has been though to act as an extensor of the knee, and above 30 degrees (ie more knee flexion) it has been thought to act as flexor.  It is thought to be a culprit (with the biceps femoris) of the shift phenomenon in the “pivot shift test” for posterolateral rotatory instability of the knee (PLRI).  Here is an interesting perspective from a 2006 journal article.

“In all cadavers, the ITB was anchored to the distal femur by fibrous strands, associated with a layer of richly innervated and vascularized fat. In no cadaver, volunteer or patient was a bursa seen. The MR scans showed that the ITB was compressed against the epicondyle at 30° of knee flexion as a consequence of tibial internal rotation, but moved laterally in extension. MR signal changes in the patients with ITB syndrome were present in the region occupied by fat, deep to the ITB. The ITB is prevented from rolling over the epicondyle by its femoral anchorage and because it is a part of the fascia lata. We suggest that it creates the illusion of movement, because of changing tension in its anterior and posterior fibres during knee flexion. Thus, on anatomical grounds, ITB overuse injuries may be more likely to be associated with fat compression beneath the tract, rather than with repetitive friction as the knee flexes and extends.”

We found this article interesting because it challenges many thoughts about its actual movement, (“it creates an illusion of movement”) because of changing of tension in the anterior and posterior fibres. As this article suggests, it is unlikely that there is any forward and backward motion of the band over the epicondyle during flexion and extension, rather the illusion of movement is from a gradual shifting of load to and from the anterior and posterior fiber bundles during flexion/extension. It is also an interesting article to us because it suggests and challenges that the clinical phenomenon is associated with fat compression rather than friction over the epicondyle.  The authors go into discussion of how the fat beneath the distal ITBand at the knee level is well vascularized and that Pacinian corpuscles can be present in adipose tissue supporting the view that fat compression may have a proprioceptive role and a roll in pain production when the corpuscles undergo hypertrophy in such a clinical setting.

Just remember what we have been saying all along when treating what you think are lateral chain problems, the ITBand receives most of the tendon of the gluteus maximus so do not forget to examine the hip and pelvis function, but so not forget the critical contribution that impaired foot and ankle function can have proximally at the knee.

This study has some interesting provoking thoughts about the mechanics we have all previously assumed. It is good to challenge established teachings, for it is only through interrogating old ways that we may see the true light of things.

If you are looking for more of our thoughts on this topic, we discussed a clinical case in our last podcast (link here). 

Shawn and Ivo, 

the gait guys

Fairclough J, Hayashi K, Toumi H, et al. The functional anatomy of the iliotibial band during flexion and extension of the knee: implications for understanding iliotibial band syndrome. Journal of Anatomy 2006;208(3):309-316. doi:10.1111/j.1469-7580.2006.00531.x

Part 2: “Standing on Glass” Static Foot/Pedograph Assessment

* note (see warning at bottom): This is a static assessment dialogue. One cannot, and must not, make clinical decisions from a static assessment. The right and left sides are indicated by the R and L circled in pink. There are 4 photos here today.

Blue lines: Last time we evaluated possible ideas on the ORANGE lines here, it would be to your advantage to start there. 

We can see a few noteworthy things here in these photos. We have contrast-adjusted the photo so the pressure areas (BLUE) are more clearly noted. There appears to be more forefoot pressure on the right foot (the right foot is on the readers left), and more rearfoot pressure on the left (not only compare the whiteness factor but look at the displacement of the calcaneal fat pad (pink brackets). There is also noticeably more lateral forefoot pressure on the left. There is also more 3-5 hammering/flexion dominance pressure on the left.  The metatarsal fat pad positioning (LIME DOTS represent the distal boundary) is intimately tied in with the proper lumbrical muscle function  (link) and migrates forward toward the toes when the flexors/extensors and lumbricals are imbalanced. We can see this fat pad shift here (LIME DOTS). The 3-5 toes are clearly hammering via flexor dominance (LIME ARROWS), this is easily noted by visual absence of the toe shafts, we only see the toe pads. Now if you remember your anatomy, the long flexors of the toes (FDL) come across the foot at an angle (see photo). It is a major function of the lateral head of the Quadratus plantae (LQP) to reorient the pull of those lesser toe flexors to pull more towards the heel rather than on an angle. One can see that in the pressure photos that this muscle may be suspicious of weakness because the toes are crammed together and moving towards the big toe because of the change in FDL pull vector (YELLOW LINES). They are especially crowding out the 2nd toe as one can see, but this can also be from weakness in the big toe, a topic for another time. One can easily see that these component weaknesses have allowed the metatarsal fat pad to migrate forward. All of this, plus the lateral shift weight bearing has widened the forefoot on the left, go ahead, measure it. So, is this person merely weight bearing laterally because they are supinating ? Well, if you read yesterday’s blog post we postulated thoughts on this foot possibly being the pronated one because of its increased heel-toe and heel-ball length. So which is it ? A pronated yet lateral weight bearing foot  or a normal foot with more lateral weight bearing because of the local foot weaknesses we just discussed ? Or is it something else ? Is the problem higher up, meaning, are they left lateral weight bearing shift because of a left drifted pelvis from weak glute medius/abdominal obliques ?  Only a competent clinical examination will enlighten us.

Is the compensation top-down or bottom up, or both in a feedback cycle trying to find sufficient stability and mobility ? These are all viable possibilities and you must have these things flowing freely through your head during the clinical examination as you rule in/rule out your hands-on findings.  Remember, just going by a screen to drive prescription exercises from what you see on the movement screen is not going to necessarily fix the problem, it could in fact lead one to drive a deeper compensation pattern. 

Remember this critical fact.  After an injury or a long standing problem, muscles and motor patterns jobs are to stabilize and manage loads (stability and mobility) for adequate and necessary movement. Injuries leave a mark on the system as a whole because adaptation was necessary during the initial healing phase. This usually spills over during the early movement re-introduction phase, particularly if movement is reintroduced too early or too aggressively.  Plasticity is the culprit. Just because the injury has come and gone does not mean that new patterns of skill, endurance, strength (S.E.S -our favorite mnemonic), stability and mobility were not subsequently built onto the apparently trivial remnants of the injury.  There is nothing trivial if it is abnormal. The forces must, and will, play out somewhere in the body and this is often where pain or injury occurs but it is rarely where the underlying problem lives.

Come back tomorrow.  We will try to bring this whole thing together, but remember, it will just be a theory for without an exam one cannot prove which issues are true culprits and which are compensations. Remember, what you see is often the compensatory illusion, it is the person moving with the parts that are working and compensating not the parts that are on vacation.  See you tomorrow friends !

Shawn and ivo, the gait guys

* note: This is a static assessment dialogue. One cannot, and must not, make clinical decisions from a static assessment. As in all assessments, information is taken in, digested and then MUST be confirmed, denied and/or at the very least, folded into a functional and clinically relevant assessment of the client before the findings are accepted, dismissed and acted upon. As we always say, a gait analysis or static pedograph-type assessment (standing force plate) is never enough to make decisions on treatment to resolve problems and injuries. What is seen and represented on either are the client’s strategies around clinical problems or compensations.  Today’s photo and blog post are an exercise in critical clinical thinking to get the juices flowing and to get the observer thinking about the client’s presentation and to help open up the field to questions the observer should be entertaining.  The big questions should be, “why do i see this, what could be causing these observances ?”right foot supinated ? or more rear and lateral foot……avoiding pronation ?

Unilateral heightened toe extensor tone.

What do we have here ? Well, it is obvious. The left foot is showing increased short extensor tone (EDB: extensor digitorum brevis) and heightened long flexor tone (FDL: flexor digitorum longus). This is the classic pairing for hammer toe development.  We also know from this post (link) and from this post (link) that this presentation is closely related with lumbrical weakness and distal fat pad migration.

So, at an assessment took we like to play games. Mental games to be precise. When we see something like this we immediately begin the mental gyrations of “what could have caused this, and what could this in turn be causing”. Remember, what you see is often not the problem, rather your clients compensation around the problem.  In this case, what goes through your mind ?  Without deep thought, our knee jerk thoughts are:

• possible loss of ankle rocker dorsiflexion (the increased EDB tone can be recruited to help drive more ankle dorsiflexion indirectly)
• plantar intrinsic weakness ?
• flip flops or slip on shoes where the heel is riding up and down inside the shoe/sloppy fit ?  (initiating a gripping response from the FDL)
• weak tib anterior (recruiting EDB to help)
• weak peroneus tertius (recruiting EDB again)
• Ankle /foot instability (more FDL gripping will help gain ground purchase)
• lateral ankle instablity (same thing, more gripping)
• Weak gastrosoleus (since the FDL is a posterior compartment neighbor it can kick into high gear and help with posterior comparment function, we have a whole video case based around this issue, check this out ! )
• premature departure off of the good side leg, and thus an abrupt loading response onto this affected side can challenge the frontal plane of the body and thus require more grip response at the foot level.
• how about simple weakness of the lumbricals or FDB , the short flexors. The long flexors will have to make up for it and present like this.  
• the list goes on and on … .

These are just some quick cursory thoughts, and by NO means a complete exhaustive list.  Just some quick thoughts.

But what about hip function ?  if ankle rocker is blocked in terminal stance and the FDL fire like this what will that do to hip extension ? Well, heel rise will be premature because of the limitation and thus hip extension will be abbreviated. Thus glute function will be impaired to a degree.  This can become a viscous cycle, each feeding off of each other.

This diagnostic stuff is a tricky and difficult game. If you think you can diagnose or fix a problem from just changing what you see you are mistaken, unless you like driving compensation patterns and future injuries into your clients.   There must be a hands on examination and assessment with an intact educated brain attached to the process.

Just some mental gymnastics for you today.  

Shawn and Ivo

the gait guys

The case of the missing toes.

OK, a bit dramatic but as you can see in the plantar view above, all you can see is the toe pads, the rest of the digit shafts are hidden.  

This is a classic example of a foot imbalance. We have talked about this many times before but the attached video link here  ( http://youtu.be/IIyg7ejYNOg ) shows it very well.  Read on.

There is shortness and increased resting tone in the short toe extensors (EDB, extensor digitorum brevis) and long toe flexors (FDL=flexor dig. longus) with insufficiency in the short flexors and long extensors. This pairing creates a hammer toe effect.  In the video, you can see that these toes are showing early hammering characteristics, but not yet rigid ones. The key word there is, “yet” so this is still a correctable phenomenon at this point.  You can also clearly see the distal migration of the metatarsal fat pad. The fat pad has migrated forward of the MET heads and is being pulled forward by the excess tension in the long toe flexors. As this imbalance in the toe flexors and extensors develops, the forefoot mechanics get impaired and the lumbricals (which anchor off off the FDL) become challenged. Their contributory biomechanics, amongst other things, help to keep the fat pad in place under the metatarsal heads. You can see in this video link above that by proximally migrating (towards the heel) just the fat pad back under the MET heads the resting mechanics of the toes changes, for the better.  

Remember the other functions of the lumbricals ?  their other major functions, namely: thinking from a distal to proximal orientation (a closed chain mode of thinking), they actually plantarflex the metatarsal on the fixed phalynx, assist in dorsiflexion of the ankle, and help to keep the toes from clawing from over recruitment of the flexor digitorum longus.

Here is another blog post we did on a similar presentation.http://thegaitguys.tumblr.com/post/14766494068/a-case-of-plantar-foot-pain-during-gait-this

Proper balance of the toe flexors and extensors, and their harmony with lumbricals and fat pad amongst other things will give healthy long flat toes that can help the proximal biomechanics of the foot.  If you have neuromas, metatarsalgia, hammer toes, claw toes, migrating toes, bunions or hallux valgus amongst many other things, this might be a good place to start.   

There are exercises that can help this presentation, but understanding “the why” is the first step.

Shawn and Ivo

The Gait Guys

A case of plantar foot pain during gait.

This client came to see us after a surgical proceedure to remove a dead (osteonecrosis) medial sesamoid under the 1st metatarsal head and a later surgery to fix a progressing hammer toe of the 2nd digit. What we really want you to see is the huge divot/depression under the 2-3 metatarsal heads. Also note the accumulation and relocation of the normal MET head fat pad now located distal to the MET heads.  It is as if the fat pad is trying to hitch a ride on the toes now ! This is a case of Metatarsalgia secondary to fat pad displacement (displaced from the divot area to the flexor crease) secondary to surgical sequelae. 

What is additionally cool in this case is the fact that this client has an almost complete webbing of the 2-3 toes so many of the normal independent muscular functions are no longer independent. After the surgeries this person presents with tremendous loss of flexor and extensor function of the 2-3 toes.  Lumbrical testing was most obviously impaired, completely absent in fact, in these 2-3 toes. On the ground the patient was also unable to achieve any flexion-press of the toes into the ground, he was able to flexion/hammer curl which will obviously put them at risk for hammer toes in the future.  But what is important here is that without the ability to PRESS the toes into the ground particularly while in stance phase the lumbricals will not help to hold the fat pad in its normal location under the MET heads. Nor will they be able to to perform their other major functions, namely: thinking from a distal to proximal orientation (a closed chain mode of thinking), they actually plantarflex the metatarsal on the fixed phalynx, assist in dorsiflexion of the ankle, and help to keep the toes from clawing from over recruitment of the flexor digitorum longus.

This client’s MET head pain is obviously caused by lack of cushioning of the head since the fat pad is displaced. There are plenty of other biomechanical abberancies now, the Windlass mechanism will never be the same becuase it is without one of the sesamoids, the hallux short flexor (FHB) is impaired on the medial head without the sesamoid so hallux flexion will become a problem.  Do we really want to see such compromise of the medial tripod ? Heck no, we need sesamoid implants ! There is a novel idea ! When a sesamoid is taken out we need to replace it ! Think about it !

There is so much more to this case, but we will stop here. It’s Christmas after all ! This poor lady was told to wish from Santa for a medial sesamoid implant under the tree and a sudden spontaneous activation of the lumbricals to retract the fat pad back under the MET head so as to reduce her pain.  Hey, wishing can’t hurt !

Merry Christmas and Happy Holidays to you all gang, whatever your faith we wish you well,

from Shawn and Ivo…… The Gait Guys

(PS: we included below more from the body of the article we wrote long ago called “The Lost Lumbricals”.  So for those of you who wish to geek out more on Christmas, read on …

______________

EXCERPTS FROM “THE LOST LUMBRICALS”

The lumbricals of the foot attach proximally to the sides of adjacent  tendons of the flexor digitorum longus (with the exception of the 1st, which only attaches to the medial side) and attach distally to the medial aspect of the head of the proximal phalynx and continue on to the extensor hoods in toes 2 through 5. Their typical function is described as flexion of the proximal phalynx and extension of the proximal and distal interphalangeal joints. They have the unique ability to compress the metatarsal-phalangeal and interphalangeal joints. These are “open chain” functions as described, unless you are in the habit of waving to people with your toes, they often are used quite differently in the gait cycle with the foot affixed to the ground.

The lumbricals are most active from midstance to preswing. That means they act predominantly in the closed chain. The lumbricals, along with the other intrinsic muscles of the foot, play a role in maintaining the medial longitudinal arch of the foot.  Along with the interossei, they play a role in stabilization of the forefoot during stance phase and rearfoot during preswing. One author has proposed that overpronation is due to a lack of neuromuscular control of the intrinsic foot muscles to stabilize the tarsal and metatarsal bones and therefore modulate the speed of pronation.

Thinking from a distal to proximal orientation (a closed chain mode of thinking), they actually plantarflex the metatarsal on the fixed phalynx, assist in dorsiflexion of the ankle, and help to keep the toes from clawing from over recruitment of the flexor digitorum longus.

Clawing toes during gait, which are considered abnormal, are defined as extension of the metatarsophalangeal articulation, and flexion of the proximal and distal interphalangeal joints result from a foot attempting to stabilize itself during the terminal stance and preswing phases of gait.  This is an attempt to help propel the body forward, often accompanied by overactivity of the flexor digitorum longus, tibialis posterior, flexor pollicus longus, and gastroc soleus groups. Overactivity of these groups causes reciprocal inhibition of the long toe extensors and ankle dorsiflexors (tibialis anterior for example), causing the toes to buckle further and a loss of ankle dorsiflexion; in short, diminished ankle rocker.

Now think about the changes in the gait cycle in the above scenario. There will be a resultant shortened step length, diminished ankle rocker, increased forefoot rocker and premature heel rise. This will necessitate an increased extension at the metatarsophalangeal joints, shifting the tendon of the lumbricals upward and behind the transverse metatarsal joint axis, causing even more extension now at this joint. Chronically over time, this causes displacement of the fat pads anteriorly from under the metatarsal heads and is one of the main reasons metatarsal head pain (metatarsalgia). In the past have you made the apparent simple diagnoses of metatarsalgia, shin splints, stress fractures or Morton’s neuroma without knowing a more plausible cause ?  Do you now feel you have better answers to these clinical phenomena ?

Now think about changes up the kinetic chain and the potential musculoskeletal implications of muscle inhibition, overfacilitation and joint dysfunction, often with neurological sequelae. With lumbrical dysfunction (weakness) and the resultant lack of ankle dorsiflexion, you have less hip extension.  So, you borrow some from the lumbar spine, with increased compressive forces there and an increase in the lordosis, which causes an increase in the thoracic kyphosis and cervical lordosis. We still need to get this leg up and forward to continue our progression ahead, so now we fire our hip flexors instead of the abdominal obliques. And because there needs to be cooperation of the abdominals and hamstrings to maintain pelvis neutrality, this further fuels inhibition of the gluteals thus further compounding the loss of hip extension. Now how about a little increased shoulder flexion on the contralateral side to assist getting that leg forward? Don’t forget that we have altered the thoracic kyphosis and thus changed scapulo humeral mechanics. Now neck/shoulder pain all from bad feet?  Maybe. These muscles developed and exist for a good reason, do your best not to dismiss them and their function the next time you see a tortured foot.

When patients have continued dysfunction, consider the base and where it all begins. Consider function in the context of where it occurs. Proper evaluation of the feet and gait can provide valuable clues as to the etiology or manifestation of continued problems. Important? You decide.

When the Short Toe Extensors Try to Rule the World !

A case of a runner with forefoot pain.

This is a runner of ours, one of the fastest young men in the state of illinois, top 10 in the country in mid-distance, top 20 in the USA in cross country.

He came in with left forefoot plantar pain.  He explained (in a matter of words) that he was having pain at full forefoot loading at heel rise /push off.

We watched him walk, saw this visual problem present itself in dynamic motion (yup, no stop frame video on this one, not when you see it about 10 times a month !) and noted a subtle left lateral hip/pelvis shift past what would be considered normal for frontal plane mechanics.

On the table this is a photo of his feet.  What do you see ?

We see a suspected (which you will try to confirm on examination) increase in short extensor (EDB, extensor digitorum brevis) muscle tone.  Increased long extensor (EDL, extensor dig. longus muscle) tone would have represented itself with the distal toes also extended but here we see a relative dominance of the long flexors (FDL, Flexor dig. longus) with the heightened short flexor increase.

We also see more confirmation of heightened long flexor tone (FDL) by the degree of heavy callus formation on the very tip of the 2nd toe (it was on all 4 lateral toes but the photo is not clear enough to demonstrate).  You can also see supporting evidence of heightened long flexor dominance by the subungual hematoma (bleeding under the 2nd toe nail). (How does this correlate ? Well, in most runners with excessive long flexor tone/use not only do they flex and claw so much in the shoes that the callus is on the tip of the toes but the nail also begins to lift as the  nail is caught on the sock liner of the shoe as the toe flexes, slowly, mile by mile pulling the toe nail from the nail bed thus bleeding underneath it).  Yes, it is NOT from the toes hitting the front end of the shoe !

Our examination confirmed weakness of all lumbrical muscles and of the flexor digitorum brevis and lateral quadratus plantae.  The patient could feel the strength/engagement difference as compared to testing on the right foot of the same muscle groups (we always compare side to side, for us and for the patient’s awareness).  The extensor digitorum brevis muscle mass on the lateral dorsum of the foot was tender as were the tendons along their course.  There was also weakness higher up in the kinetic chain at the lower division of the transversus abdominus and internal abdominal oblique, and frontal plane hip stabilizers (gluteus medius; anterior-middle-and posterior divisions).The 2nd and 3rd metatarsal heads were remarkably tender to palpation and it was obvious that the metatarsal fat pads had migrated distally from the lumbrical muscle weakness.

Sometimes a grasp response by the long flexors can represent a propioceptive /balance deficit during single leg stance phase so be sure to test those centers as well (cerebellar, vision, joint position sense, inner ear-vestibular apparatus). 

So, what is the take away for the non-medical person, the runner next door if you will ?  Lets just say, symmetry wins and when asymmetry is apparent, bring it up to the people that do your body work.  Hopefully, what you and they see will be assessed in a clinical light, and as a team you can get to the bottom of what is not working…….and in this case…..what was causing not only the plantar foot pain, but the left lateral hip sway outside the frontal plane.

———we are, The Gait Guys……Shawn and Ivo

The Gait Guys: Some strategies in Controlling the Foot Arches and Big Toe

As promised. We fixed the volume.  Less hiss next time. Enjoy

Dr. Shawn Allen of The Gait Guys speaks about proper stabilization of the medial foot and arch. Muscle specifically discussed are a team: FHB (flexor hallucis brevis), AbDuctor hallucis, and tibialis posterior. He discusses the functional anatomy, normal and pathologic movement patterns of the arch and first ray complex and big toe (hallux). His foot’s ability to show the optimal patterns for the arch and hallux are excellent examples. Follow up videos and DVDs will show more details you need to know, and some of the exercises he and Dr. Ivo Waerlop use to restore a foot that has lost these abilities. The DVDs are in the works. Take their lectures and CME on www.onlineCE.com. Visit them at www.thegaitguys.com and on their facebook PAGE & Twitter of the same name for daily feeds of unique things.