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

Hamstring Reverse Engineering:

The biceps femoris is an internal rotator of the thigh? You heard correctly. Think of how the lower extremity works in closed chain, not open. Check out this quick video with Dr Ivo on “reverse engineering”

What creates muscle tone, anyway?

Not for the timid, here is an excellent , free, full text article on spasticity. More importantly, it is an excellent review on what creates muscle tone and how it is maintained, starting and the spindle and moving centrally.  Think about this the next time you have a patient with mm spasm and you can se things in a whole new light

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3009478/

Irregular Arm Swing Could Be Early Sign Of Pending neurological disease.

Written by Dr. Shawn Allen

We’ve been saying this for quite some time now, the small subtle gait changes are often the first sign of things to come.

The attached article suggests that scientific measurement investigating irregular arm swing during gait could help diagnose the Parkinson’s disease earlier, giving greater opportunity to slow brain cell damage and disease progression.

In the study below Huang suggests that although we all know that classically the Parkinsonian disease is met with tremors, slow movements, stooped posture, rigid muscles, bradykinesia, speech changes etc, “by the time we diagnose the disease, about 50 to 80 percent of the critical cells called dopamine neurons are already dead,”

Previously, here at The Gait Guys, we have gone deep into discussions of arm swing and the phasic and anti-phasic natures of limb action in gait and how the four limbs interact neurologically, both centrally and peripherally. You can click here for just a sampling of our “arm swing” writings,   

In the study, because arm swing changes are one of the first gait parameters to diminish and decline, and because the decline is typically asymmetrical due to the fact that the disease is an asymmetrical one, the authors compared arm swing magnitude and asymmetry in patients with and without Parkinson’s as parameters to begin the assessments.  Most research to date has commented on the early loss of arm pendular swing but as they said here, “ but nobody had looked using a scientifically measured approach to see if the loss was asymmetrical or when this asymmetry first showed up,“ explained Huang.

What they discovered was that compared to the control group, “the Parkinson’s group showed significantly greater asymmetry in their arm swing (one arm swung significantly less than the other while walking),” and when the subjects walked faster, the arm swing increased but the amount of asymmetry remained unchanged.

On a slightly different tangent of thinking, an aside from the Parkinson’s disease disucussion, how truly sensitive is this limb swing thing you might ask ? Here, read this from this piece (How injury and pain reorganize the brain) we wrote a few years ago.

“Getting a cast or splint causes the brain to rapidly shift its resources to make righties function better as lefties, researchers found.
Right-handed individuals whose dominant arm had to be immobilized after an injury showed a drop in (brain) cortical thickness in the area that controls primary motor and sensory areas for the hand, Nicolas Langer, MSc, of the University of Zurich in Switzerland, and colleagues reported.
Over the same two-week period, white and gray matter increased in the areas that controlled the uninjured left hand, suggesting “skill transfer from the right to the left hand,” the group reported in the Jan. 17 issue of Neurology.
The findings highlight the plasticity of the brain in rapidly adapting to changing demands, but also hold implications for clinical practice, they noted.”

This article highlights the rapid changes in motor programs that occur. It does not take long for the body to begin to develop not only functional adaptations but neurologic changes at the brain level within days and certainly less than 2 weeks.

If you know your literature on this topic of arm swing symmetry, you know it is an arguable point.  According to the Lathrop-Lambach study (see link in the article just mentioned above), they mentioned that they feel a 10% baseline asymmetry is the norm.  This symmetry issue is an arguable point that no one is likely to ever win.  We tend to feel, as many others do, that asymmetry can be a major component and predictor to injury, and in today’s topic of discussion a possible determinant of higher level gait disease. 

Still think you should retrain arm swing ? Dive into our blog archives here on arm swing, you will find out that perhaps it is not your best first choice. Discover from our old writings who tends to dictate how much arm swing occurs. 

Shawn Allen, one of the gait guys

References:

http://www.medicalnewstoday.com/articles/173680.php

“Arm swing magnitude and asymmetry during gait in the early stages of Parkinson’s disease.”
Michael D Lewek, Roxanne Poole, Julia Johnson, Omar Halawa, Xuemei Huang
Gait & Posture, 2009, In Press, Corrected Proof, Available online 27 November 2009  DOI:10.1016/j.gaitpost.2009.10.013

Does gait (re)training alter peoples biomechanics? 

You bet it does! Should we be retraining peoples gait? We like to think, yes. What do you think?

“Overall, this systematic review shows that many biomechanical parameters can be altered by running modification training programmes. These interventions result in short term small to large effects on kinetic, kinematic and spatiotemporal outcomes during running. In general, runners tend to employ a distal strategy of gait modification unless given specific cues. The most effective strategy for reducing high-risk factors for running-related injury-such as impact loading-was through real-time feedback of kinetics and/or kinematics.’

Br J Sports Med. 2015 Jun 23. pii: bjsports-2014-094393. doi: 10.1136/bjsports-2014-094393. [Epub ahead of print]
Gait modifications to change lower extremity gait biomechanics in runners: a systematic review.
Napier C1, Cochrane CK1, Taunton JE2, Hunt MA1.

Development of the arch: Functional implications | Lower Extremity Review Magazine

A nice, referenced piece from one of our fav’s, Dr Michaud.

“Although early research suggested a limited connection between arch height and lower extremity function, more recent research confirms that arch height does indeed affect function. Information obtained from measurements that accurately identify the height of the medial longitudinal arch may lead to more effective treatment protocols. By identifying specific injuries associated with low and high arches, it may also be possible to prevent these injuries.”

Development of the arch: Functional implications | Lower Extremity Review Magazine