Toe sardines. What have we done to our feet ?

Note that form follows function. If you are observant, you will see the deformation of the 5 digit, just like in this case as the quadratus weakens and the long flexors dominate. The toe begins to spin laterally, and thus the plantar toe pad begins to deform medially, look closely, you can see that here in the video.

Does this look like your foot ? There are a few subtle issues here. 

In the foot, the toe that delineates abduction and adduction of the toes is the 2nd toe. The 2nd toe is considered the anatomic middle of the digits and forefoot. Any toe or movement that moves away from the 2nd toe is abduction and any movement towards the 2nd toe is adduction. This is obviously different than in the hand where the 3rd digit, the one you use during road rage, is the reference digit. Next time you are questioned, tell them you threw them your reference finger, not “the bird”, it is a more accurate descriptor.

In this foot, note how neatly and tightly packed the cute little toes are, all snuggled up to their brothers and sisters. Remember, form follows function. Obviously function has been low on these fellas, at least in abduction.  This often comes from snug toe box footwear and lack of abduction (toe spread) use.  But make no mistake, this is a weak foot.

Today we wish to really focus your attention to an old topic, just a revisit. We can see the 4th and 5th toes curl under from the probably weak lateral head of the quadratus plantae thus encouraging unopposed oblique pull of the long flexors of the digits (FDL). See this post here for an explanation of this phenomenon.  There is also obvious imbalance between the long and short flexors and extensors in these toes, the long flexors are expressing more tone, and that means the long extensors are deprived. 

Note that form follows function. If you are observant, you will see the deformation of the 5 digit, just like in this case as the quadratus weakens and the long flexors dominate. The toe begins to spin laterally, and thus the plantar toe pad begins to deform medially, look closely, you can see that here in the video. This spin can carry the toe nail so far laterally sometimes that the nail can begin to touch the ground during gait and cause painful nail lifting with even some losing the nail. 

There is plenty of life left in this foot, but you have to get to it quickly and get them in lower heeled shoes if tolerable and ones with a wider toe box.  The client needs to be retaught how to access the toe extensors and abductors. Lumbrical retraining, which is a recurrent topic here on our blog, should also be instituted. 

Shawn Allen, one of the gait guys

Pincher nails.  Who knew !?

Written by Dr. Shawn Allen

*note: there are two photos here in today’s blog post, look for the side scroll arrows and click on the small box in the upper left corner if you cannot see the photo

 We have seen this one for years in our clinics but we never got around to researching it and pondering the condition more deeply.  Here is our mantra for today, Form follows Function.

Studies seem to be undecided on the cause of this entity. Some suggest that pincer nails are caused by lack of upward mechanical forces on the toe pad where others remark that they can be observed amongst the healthy mechanical walkers. Hitomi’s study suggests that the affected toes fail to receive adequate physical stimulation from proper toe and forefoot loading. Please read on, this gets interesting.

According to Hitomi’s study, in both the barefoot and shod state,

“the pincer nail group had significantly lower pressure on the first toe than the control group. In both the barefoot and shod state, the peak pressure area was mostly the metatarsal head area in the pincer nail group, whereas it was mostly the first toe area in the control group. Binomial logistic regression analysis revealed that peak pressure area was a significant risk factor for pincer nail development.”

This seems to suggest that there is insufficient or aberrant use of downward pressure on the toes and into the toe pads. Hitomi speaks of the locale of the peak pressure, seemingly proposing from this study that it should not be under the metatarsal heads. This, in our experience and thinking, could suggest that more long flexor dominance is present. This long flexor activity seems to create some disfunction not only in the activity of the lumbrical muscles but also altered pressures in the metatarsal (MET) heads.  It certainly alters distal toe pressures which can alter skin and nail responses (see our blog post on subungal hematomas for more on this topic where we discuss principles of counter pressure and shear forces). We try to teach a “spread and reach with long flat toes” approach to our clients in correcting bad habits such as toe hammering and gripping (which are often a result of flawed biomechanics elsewhere).

The nail bed is very rich in vasculature (hence the cause of the dreaded hematoma, the black toenail) and nerve endings.  The nail bed is a derivative of the epidermis containing keratin which gives it its hard nature. The nail consists of the nail plate, the nail fold, the nail matrix, the sterile matrix and the hyponychium. There are many factors that go into the formation of a normal nail, including blood flow, nutrition, local neurogenic factors and not to forget, mechanical loading issues. Failure of any of these issues can lead to softening, brittle, thinning, diseased or malformed nails. The nail grows from a nail root in front of the cuticle and grows distally at a slow but (usually) steady rate.  It is interesting to note that the long extensor tendon (EDL) attachment is close to the proximal nail bed root area thus it brings forward thinking of possible imbalances between long and short flexors and extensor tendons/muscles and their patterns of imbalance in toe gripping and hammering that could cause a change in function which could drive a change in form.  We have all heard it, form follows function, why should this area be any different ?

Hitomi also mentioned something interesting in his study, the observation that bed ridden clients seem to have a predilection to pincer toes.  This at least seems to fit the aberrant loading patterns, in this case an absence of. The study also started some interesting thinking in us when it mentioned a hypothesis,

“that human nails are constitutively equipped with an automatic shrinkage function that allows them to adapt to daily upward mechanical forces.”

This was a fascinating hypothesis to us. It seems to make sense. If constant downward pressure on the toe pads were present, the toe nails would always be undergoing a flattening and spreading response so it could make sense that the nails have a built in curve and shrinkage function offsetting and adapting to the constant distorting pressures (the flattening and spreading forces).  Hence, some possible clarity in Hitomi’s hypothesis that pincer nails are caused by lack of (and in our thinking, distorted) upward mechanical forces on the toe pad.  And, when those distorting pressures are placed elsewhere (ie. the MET heads or tips of the toes as in our subungal hematoma hypothesis) or faulting gripping or hammering loading the automatic shrinkage function is left to dominate.

We think Hitomi’s hypothesis is correct. Here is why (this is paraphrased from our blog post on subungal hematomas and our revolutionary thinking on why they occur and it seems to fit well with pincer nail formation as well).

…  when the skin is pulled at a differential rate over the distal phalange (from gripping of the toes rather than downward pressing through the toe pad) there will be a net lifting response of the nail from its bed as the skin is drawn forward of the backward drawn phalange  (there is a NET movement of skin forward thus lifting the nail from its bedding).  For an at-home example of this, put your hand AND fingers flat on a table top. Now activate JUST your distal long finger flexors so that only the tip of the fingers are in contact with the table top (there will be a small lifting of the fingers). There should be minimal flexion of the distal fingers at this point. Note the spreading and flattening of the nail.  Now, without letting the finger tip-skin contact point move at all from the table, go ahead and increase your long flexor tone/pull fairly aggressively. You are in essence trying to pull the finger backward into flexion while leaving the skin pad in the same place on the table. Feel the pressure building under the distal tip of the finger nail as the skin is RELATIVELY drawn forward.]   This is fat pad and skin being drawn forward (relative to the phalange bone being drawn backward) into the apex of the nail. Could this be magnifying the curvature of the nail and not offsetting the “automatic curving and shrinkage” function of the nail ? We think it is quite possible.

So, there you have it. We will dive deeper on this topic another time, but after reading Hitomi’s study our brain’s started buzzing because we had discussed this process similarly a few years back in our Subungal Hematoma blog post.

And, if you are thinking about chronic repeated ingrown toe nails with this clinical entity, your thoughts are clearly on a logical path.  There is a correlation it seems.

And, as for the horrific metal bar correction you see in the other photo above, this too is new to our eyes.  It seems rather medieval, something one might see in the gallows of yesteryear.  And if that doesn’t curl your hair and make you nauseated, try looking at what this one guy did, a DIY remedy (caution, not for the feint of heart). https://www.mja.com.au/journal/2005/182/4/diy-pincer-nail-repair-brace-yourself

ShawnAllen, one of the gait guys

References:

Foot loading is different in people with and without pincer nails: a case control study  Hitomi Sano1*, Kaori Shionoya2 and Rei Ogawa1  Journal of Foot and Ankle Research 2015, 8:43

Ahh yes, the lumbricals. 

One of our favorite muscles. And here it is in a recent paper! This one is for all you fellow foot geeks : )

Perhaps the FDL (which fires slightly earlier than the FHL) and FHL (which fires slightly later and longer) at loading response, slowing pronation and setting the stage for lumbrical function from midstance to terminal stance/preswing (flexion at the metatarsal phalangeal joint (it would have to be eccentric, if you think about this from a closed chain perspective) and extension (actually compression) of the proximal interphalangeal joints.

“The first lumbrical arose as two muscle bellies from both the tendon of the FDL and the tendinous slip of the FHL in 83.3 %, and as one muscle belly from the tendon of the FDL or the tendinous slip of the FHL in 16.7 %. These two muscle bellies subsequently merged to form the muscle belly of the first lumbrical. The second lumbrical arose from the tendinous slips of the FHL for the second and third toes as well as the tendon of the FDL in all specimens. The third lumbrical arose from the tendinous slips of the FHL for the third and fourth toes in 69.7 %, and the fourth lumbrical arose from the tendinous slip of the FHL for the fourth toe in 18.2 %. Some deep muscle fibers of the fourth lumbrical arose from the tendinous slip of the FHL for the second toe in 4.5 %, for the third toe in 28.8 %, and for the fourth toe in 15.2 %.”

Hur MS1, Kim JH, Gil YC, Kim HJ, Lee KS. New insights into the origin of the lumbrical muscles of the foot: tendinous slip of the flexor hallucis longus muscle. Surg Radiol Anat. 2015 May 12. [Epub ahead of print]

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 ?

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