Some stuff you need to know about running spikes.

I see many track runners in my office, from middle school all the way into the USA Masters Division.  A few years ago one of the top USA Masters Milers came to see me on Friday before heading off to a national meet. He showed me some of his spikes (see pics above) and complained the there was something off on the spikes on the left, the Nike Mambas.  The shoe to the right is the Nike Zoom Miler.

You need to understand a bit of the physics of running turns to understand what is missing for this runner in this pair of spikes.  Things do change if you are running on a sloped track, but those are only found indoors and are not all that common to run on for most folks so we will stick with the thinking on flat tracks.

What you should be able to easily detect is that the Nike Mamba’s are missing the lateral 5th metatarsal forefoot spike on the cleat plate.  And you need to then realize that this is the right shoe, so it is the outside foot/leg on the track. It is the foot that will be pushing off harder from the outside on the turns to keep the centripetal forces of running a curve from allowing the runner to fall off the curve into the outer lanes. This right foot will always be pushing from outside to inside to maintain the body’s progression in the desired lane, when running the curves.

Think about it for a minute. In order to run in a circle, or a curve in this situation, the outside foot always has the tendancy to be more inverted to keep foot contact on the ground. This is where a Forefoot varus MIGHT come in handy ! This means the foot will be tipped to the outside a little, because of the curve and because the body will be leaning into the center of the track on the curves. Thus the foot and shoe will be relying on more lateral foot pressures to drive the body mass back into the lane since centripetal forces will always be driving you laterally out of the lane.  Thus, the lateral spikes on the right foot must be accommodating.  In the case of the Mamba shoe. there is only a sheet of black hard plastic over the midshaft-head of the 5th Metatarsal on the lateral foot. It is no wonder the runner was feeling like he was slipping on the turns (the front of the midfoot was not anchored to the ground, only the forefoot due to the spikes in that location). You can see clear evidence of the lateral slipping in the picture. Can you see the orange/brown patch where he was slipping ? A spike there in that area would have been wonderful.  Slipping is a power leak and a risk for injury.  If the foot is trying to gain purchase into/onto the track with the foot inverted there needs to be traction at that lateral foot, what is referred to as the Lateral Column.  You can see why the Nike Zoom Miler was a better choice, there is a nice spike placement under the lateral foot for just this measure, and there is no evidence of slippage wear.  He told me that the Mamba was a steeplechase designed shoe but we still both felt that the issue remained relevant even in that event. The Nike website however states that “the Nike Zoom Mamba Men’s Track and Field Shoe is perfect for the 800-5000m track athlete” so we think they have missed an issue here in our opinion.

I could make a better case for the Mambas if  they were for a 100m straight run but I would still like a 5th metatarsal /lateral spike where there isn’t one.  I will occasionally file spikes to get the perfect feel for the athlete.  It is usually the 5th metatarsal and 1st metatarsal spikes I mess with, merely to help hone the athletes feel on the track. The problem is that each track has a different feel so it is less of an occurrence in recent years.

It is good to know your shoes, it is good to know your physics. It is great to know them both and melt them together to solve problems.  Not all spikes are created equal, not all tracks are the same, not all events are the same and certainly not all feet and the athlete’s who own them are the same.  And on the topic of Forefoot Foot types, both the forefoot varus and forefoot valgus foot might have a problem with the Mamba’s depending on their strength, skill and strategies for ground purchase.  Hopefully your shoe store and your track and cross country coaches know these issues. You might want to bring this blog post to their attention however, just in case.

Dr. Shawn Allen

Tom Purvis hits some strong points in this video about squatting, hip hinges, ankle dorsiflexion, and movement as a whole.  * Keep in mind, this is all sagittal plane stuff….. it gets far more complicated when there are lateral (frontal) plane or rotational (axial) considerations ….. these are the “knees out” dialogues and debates you have read over and over on the web in the last year.

Dr. Shawn Allen

addendum:

Food for thought after posting today’s Tom Purvis squat video.

Could this study below translate into the statement/question: 

“attempting to achieve sufficient dorsiflexion through the combined ‘foot pronation-ankle dorsiflexion’ mechanism, as opposed to just dorsiflexion from the ankle mortise joint alone, may change the dynamics of the entire limb…. in this case, hip flexion range observation. Is this because when dorsiflexion is cheated via foot pronation, instead of just ankle dorsiflexion, there is more internal tibia/femoral spin than would normally occur from just sagittal ankle hinging which can in turn impair terminal hip flexion range via impingement type action ? I think so. It would be cool to see what would have happened in the study had the pronating clients been shown my foot tripod restoration exercise (it’s on youtube).   -Dr. Allen

here is some new research on this point, for what it is worth.  It keeps the mind thinking though.

J Phys Ther Sci.  2015 Jan;27(1):285-7. doi: 10.1589/jpts.27.285. Epub 2015 Jan 9.The kinematics of the lower leg in the sagittal plane during downward squatting in persons with pronated feet.  Lee,Koh da,  Kim 

Abstract

[Purpose] This study aimed to examine changes in lower extremity kinematics in the sagittal plane during downward squatting by subjects with pronated feet. [Subjects and Methods] This study selected 10 subjects each with normal and pronated feet using a navicular drop test. The subjects performed downward squatting, in which the knee joints flex 90° in a standing position. We recorded the angles of the hip, knee, and ankle joint in the sagittal plane through motion analysis. For the analysis, the squatting phase was divided into phase 1 (initial squat), phase 2 (middle squat), and phase 3 (terminal squat) according to the timing of downward squatting. [Results] In the pronated foot group comparison with the normal group, thehip joint flexion angle decreased significantly in phases 2 and 3. The dorsiflexion angle of the ankle joint increased significantly in phase 3. The flexion angle of the knee joint did not differ between groups in any of the phases. [Conclusion] The pronated foot group utilized a different squat movement strategy from that of the normal foot group in the sagittal plane.

Rewiring.

The peripheral and central nervous systems are functionally
integrated regarding the consequences of a nerve injury: a
peripheral nerve lesion always results in profound and long lasting
central modifications and reorganization. (Kaas, 1991)
Does there need to be a lesion though ? A functional lesion will force changes just like an ablative lesion. Altered gait that persists from a sprained ankle or a painful knee will force central modifications and reorganization. This is why resolution of pain and aberrant function is critical. If you rehab to 80% you leave 20% on the table and that gets rewired into the system as the new norm. Remember, the entire system is watching, learning, adapting and rewiring all the time. This is why you must have a team in place to resolve all, if possible, of your client’s deficits. If you leave 20% of a problem on the table, and add endurance and strength to the “80%resolved:20%remaining”, you reorganize the central nervous system with that as the assumed norm moving forward. From this point forward, this is the architecture that all new patterns and forms are built from.  This sets up for long term rewiring of all of the connected parts, from motor, sensory, visual, gait, proprioceptive, vestibular and the list goes on and on. If you have ever wondered how a client can have so many areas of pain and dysfunction you might want to go back into their history and ask them if there was a single injury or event that occurred after which all their new problems started to stack up. 

If you are a gait analysis junkie, remember this principle above. All of the things you see in a person’s gait are not unconnected in many cases.  Much of what you see is a compensation around their problems, not the actual problem. 

Remember this principle: the peripheral nervous system attempts to repair by regrowth, the central nervous system attempts to repair by re-routing and reorganizing.

Dr. Shawn Allen

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Our neurology mentor, Dr. Carrick discusses the vestibular system and what can go wrong with it and what happens to our locomotion system when it doesn’t function properly.  

Know this gait, memorize it.  It is NOT a Parkinsonian gait. 

Here is what you need to know about the gait presentation in Normopressure hydrocephalus (NPH):

The gait changes are often subtle and progress as NPH progresses because of the changes in the brains ventricular tissues eventually compromising the sensory-motor tracts.
Early gait changes, MILD, may show a cautious gait. Steps length and stride length may be slowed and shortened. The gait may begin to show signs of being deliberate and calculated, less fluid and free. The appearance of unsteadiness or balance challenges may prevail. Once simple environmental obstacles may now present as challenges, things like curbs, stairs, weaving between tables in restaurants or wide open spaces where there is nothing to grasp onto for stability. Weakness and tiredness of the legs may also be part of the complaint, although examination discloses no paresis or ataxia. (Ropper)  A walking aid such as a cane may add comfort but often appears to be rarely used.

As the gait changes progress into the more MODERATE to ADVANCED, the walking aids used often progress into quad walkers.  Wheelchairs are needed in more difficult places or when fatigue is growing factor.  As the gait challenges progress, the careful observer will note a more obvious reduction in step and stride length, a head down posture, less dual tasking engagement during gait execution, slowed walking speed, reduced foot-floor clearance, shuffling gait (keeping the feet more engaged to the ground, this can be a Parkinsonian-type gait mis-read, there will be no tremor or rigidity), searches for stable external cues (reaching for railings, a kind arm or hand, touching walls etc), widening of the feet (broad based stance), and fears of falling backward.

In the most ADVANCED gait impairments, the fear of falling can become too great. There may even be an inability to engage sit-stand-walk motor patterns and the fatigue of the limbs may be too advanced to even stand let along walk. This stage is referred to as Hydrocephalic astasia-abasia (Ropper).  

Normopressure Hydrocephalus is a serious issue if left unrecognized and untreated.  NPH must be diagnosed early on since a delay in reducing the pressure on the cortical tissues can lead to permanency of disease and dysfunction.  According to Poca there can be a wide range of successes and failures in symptom remediation, but there is clearly a time dependency on early diagnosis. Thus, clearly recognizing any early gait changes and behaviors prior to advancing incontinence and mental decline is paramount.

Dr. Shawn Allen, … one of “the gait guys”

Some of the above was inspired and summarized by this great article, from the Boston Globe.  

References:

1. Marmarou, Anthony; Young, Harold F.; Aygok, Gunes A. (1 April 2007). “Estimated incidence of normal-pressure hydrocephalus and shunt outcome in patients residing in assisted-living and extended-care facilities”. Neurosurgical FOCUS 22 (4): 1–8.

2. Ropper, A.H. & Samuels, M.A. (2009). Adams and Victor’s Principles of Neurology (9th edition). New York, NY: McGraw-Hill Medical.

3. Poca, Maria A.; Mataró, Maria; Matarín, Maria Del Mar; Arikan, Fuat; Junqué, Carmen; Sahuquillo, Juan (1 May 2004). “Is the placement of shunts in patients with idiopathic normal pressure hydrocephalus worth the risk? Results of a study based on continuous monitoring of intracranial pressure”. Journal of Neurosurgery 100 (5): 855–866.

4. Am J Phys Med Rehabil. 2008 Jan;87(1):39-45.
Objective assessment of gait in normal-pressure hydrocephalus.
Williams MA1, Thomas G, de Lateur B, Imteyaz H, Rose JG, Shore WS, Kharkar S, Rigamonti D.

5. Clin Neurophysiol. 2000 Sep;111(9):1678-86.
Gait analysis in idiopathic normal pressure hydrocephalus—which parameters respond to the CSF tap test?
Stolze H1, Kuhtz-Buschbeck JP, Drücke H, Jöhnk K, Diercks C, Palmié S, Mehdorn HM, Illert M, Deuschl G.

6.Rev Neurol (Paris). 2001 Nov;157(11 Pt 1):1416-9.
[Postural and locomotor evaluation of normal pressure hydrocephalus: a case report]. Mesure S1, Donnet A, Azulay JP, Pouget J, Grisoli F.

7.J Neurol Neurosurg Psychiatry. 2001 Mar;70(3):289-97.
Comparative analysis of the gait disorder of normal pressure hydrocephalus and Parkinson’s disease.
Stolze H1, Kuhtz-Buschbeck JP, Drücke H, Jöhnk K, Illert M, Deuschl G.

#normopressure hydrocephalus

#NPH

#gait problems

#balance

#incontinence

#dementia

#parkinsons

#parkinsons disease

#falls

#balance problems

#alzheimers

“If the software in your brain does not acknowledge the change in hardware – the better moving joint, the more elastic muscle, the better firing pattern between your stabilizers and prime movers – it does not matter.” - Gray Cook

We could not agree more. No matter how much table work you do or how much rehab you do, if you do not teach your client how to use the changes in walking, running, locomotion through specific retraining, then the changes are useless. Newly acquired skills that are not made accessible to meaningful locomotion were a waste of time.

A Wobble in the System: The Gait Changes in Normopressure Hydrocephalus

Can you afford to miss this diagnosis ? 

Today, the gait changes in NPH are discussed because as with many neurologic disorders and diseases, subtle gait changes are the first signs. And, in this disorder, you have to catch the gait changes early on in order to give your client the greatest changes of full recovery.   Today we couple this blog post with a great video story of a missed case study of NPH.

Normopressure hydrocephalus (NPH) consists of the triad of :

1. gait disturbance
2. urinary incontinence
3. dementia or mental decline

In the most general terms, Normal pressure hydrocephalus (NPH), also referred to as symptomatic hydrocephalus, is caused by a decreased absorption of cerebrospinal fluid (CSF). The resultant increased intracranial pressure can cause ventriculomegaly.  In NPH patients, the pressure remains just slightly elevated, but enough to create pressure on the cortical tissues of the brain causing the symptoms above. The vagueness of this problem and its seemingly random symptoms is primarily why this disorder is often missed or misdiagnosed as dementia, Parkinson’s or Alzheimers disorders.

As discussed previously, many early neurological diseases and disorders softly present with early gait changes. And, as in NPH, gait changes may be the earliest symptom of the 3 mentioned earlier. One’s ability to know, observe and recognize abnormal gait patterns coupled with a good historical interview and physical exam can often tease out the earliest manifestation of NPH.

Here is what you need to know about the gait presentation in NPH:

The gait changes are often subtle and progress as NPH progresses because of the changes in the brains ventricular tissues eventually compromising the sensory-motor tracts.
Early gait changes, MILD, may show a cautious gait. Steps length and stride length may be slowed and shortened. The gait may begin to show signs of being deliberate and calculated, less fluid and free. The appearance of unsteadiness or balance challenges may prevail. Once simple environmental obstacles may now present as challenges, things like curbs, stairs, weaving between tables in restaurants or wide open spaces where there is nothing to grasp onto for stability. Weakness and tiredness of the legs may also be part of the complaint, although examination discloses no paresis or ataxia. (Ropper)  A walking aid such as a cane may add comfort but often appears to be rarely used.

As the gait changes progress into the more MODERATE to ADVANCED, the walking aids used often progress into quad walkers.  Wheelchairs are needed in more difficult places or when fatigue is growing factor.  As the gait challenges progress, the careful observer will note a more obvious reduction in step and stride length, a head down posture, less dual tasking engagement during gait execution, slowed walking speed, reduced foot-floor clearance, shuffling gait (keeping the feet more engaged to the ground, this can be a Parkinsonian-type gait mis-read, there will be no tremor or rigidity), searches for stable external cues (reaching for railings, a kind arm or hand, touching walls etc), widening of the feet (broad based stance), and fears of falling backward.

In the most ADVANCED gait impairments, the fear of falling can become too great. There may even be an inability to engage sit-stand-walk motor patterns and the fatigue of the limbs may be too advanced to even stand let along walk. This stage is referred to as Hydrocephalic astasia-abasia (Ropper).  

Normopressure Hydrocephalus is a serious issue if left unrecognized and untreated. Here is yet another reason why you must be familiar with this problem:

“Patients with dementia who are confined to a nursing home and may have undiagnosed NPH can possibly become independent again once treated. So far only one study was able to evaluate the prevalence of NPH, both diagnosed and undiagnosed, among residents of assisted-living facilities, showing a prevalence in 9 to 14% of the residents.” - Marmarou

One’s lack of awareness and knowledge, are one’s greatest enemies. If you don’t know something exists, because you’ve never studied or learned it, how can you be aware of it ? If you’re not spending enough time examining a client, you might be unaware of an issue even though you may be knowledgeable about the issue. One must have both awareness and knowledge. One must also be aware that compensations are the way of the body. What you see is not your client’s problem. It is their strategy to cope.

NPH must be diagnosed early on since a delay in reducing the pressure on the cortical tissues can lead to permanency of disease and dysfunction.  According to Poca there can be a wide range of successes and failures in symptom remediation, but there is clearly a time dependency on early diagnosis. Thus, clearly recognizing any early gait changes and behaviors prior to advancing incontinence and mental decline is paramount.

Bonus: here is a little bonus tidbit for my fellow neuro gait friends. 

Stolze (7) study conclusion: “The gait pattern in normal pressure hydrocephalus is clearly distinguishable from the gait of Parkinson’s disease. As well as the basal ganglia output connections, other pathways and structures most likely in the frontal lobes are responsible for the gait pattern and especially the disturbed dynamic equilibrium in normal pressure hydrocephalus. Hypokinesia and its responsiveness to external cues in both diseases are assumed to be an expression of a disturbed motor planning.”

Dr. Shawn Allen, … one of “the gait guys”

Some of the above was inspired and summarized by this great article, from the Boston Globe.  

References:

1. Marmarou, Anthony; Young, Harold F.; Aygok, Gunes A. (1 April 2007). “Estimated incidence of normal-pressure hydrocephalus and shunt outcome in patients residing in assisted-living and extended-care facilities”. Neurosurgical FOCUS 22 (4): 1–8.

2. Ropper, A.H. & Samuels, M.A. (2009). Adams and Victor’s Principles of Neurology (9th edition). New York, NY: McGraw-Hill Medical.

3. Poca, Maria A.; Mataró, Maria; Matarín, Maria Del Mar; Arikan, Fuat; Junqué, Carmen; Sahuquillo, Juan (1 May 2004). “Is the placement of shunts in patients with idiopathic normal pressure hydrocephalus worth the risk? Results of a study based on continuous monitoring of intracranial pressure”. Journal of Neurosurgery 100 (5): 855–866.

4. Am J Phys Med Rehabil. 2008 Jan;87(1):39-45.
Objective assessment of gait in normal-pressure hydrocephalus.
Williams MA1, Thomas G, de Lateur B, Imteyaz H, Rose JG, Shore WS, Kharkar S, Rigamonti D.

5. Clin Neurophysiol. 2000 Sep;111(9):1678-86.
Gait analysis in idiopathic normal pressure hydrocephalus–which parameters respond to the CSF tap test?
Stolze H1, Kuhtz-Buschbeck JP, Drücke H, Jöhnk K, Diercks C, Palmié S, Mehdorn HM, Illert M, Deuschl G.

6.Rev Neurol (Paris). 2001 Nov;157(11 Pt 1):1416-9.
[Postural and locomotor evaluation of normal pressure hydrocephalus: a case report]. Mesure S1, Donnet A, Azulay JP, Pouget J, Grisoli F.

7.J Neurol Neurosurg Psychiatry. 2001 Mar;70(3):289-97.
Comparative analysis of the gait disorder of normal pressure hydrocephalus and Parkinson’s disease.
Stolze H1, Kuhtz-Buschbeck JP, Drücke H, Jöhnk K, Illert M, Deuschl G.

Invalid video embed.

Rearfoot to Hip Pathomechanical considerations.

In normal gait, the rearfoot strikes in slight inversion and then quickly moves through eversion in the frontal plane to help with the midfoot through forefoot pronation phases of gait. Some sources would refer this rearfoot eversion as the rearfoot pronatory phase, after all. pronation can occur at the rear, mid or forefoot. As with all pronation in all areas, when it occurs too fast, too soon or too much, it can be a problem and rearfoot eversion is no different.  If uncontrolled via muscles such as through tibialis posterior eccentric capabilities (Skill, endurance, strength) or from a structural presentation of Rearfoot Valgus pain can arise. 

From a scenario like in the video above, where a more rearfoot varus presentation is observed,  where the lateral to medial pronation progression is excessive and extreme in terms of speed, duration and magnitude this can also create too much lateral to medial foot, ankle and knee movement.  This will often accompany unchecked movements of internal spin through the hip. So one should see that these pronation and spin issues can occur and be controlled from the bottom or from the top, and hopefully adequately from both in a normal scenario.  It is when there is a biomechanical limitation or insufficiency somewhere in the chain that problems can arise. And remember, pain does not have to occur where the failure occurs, in fact it usually does not. So when you have knee pain from an apparent valgus posturing knee, make sure you look above and below that knee.  Also, keep in mind that as discussed last week in the blog post on ischiofemoral impingment syndrome (link), these spin scenarios can be quite frequently found with ipsilateral frontal plane lateral deviations (bumping of the hip-pelvis outside the vertical stacking of the foot-knee-hip stacking line). This stacking failure can also be the source of many of the issues discussed above, so be sure you are looking locally and globally. And remember, what you see is not the problem, it is their compensation around their deeper problem quite often.

If you have not read the blog post from last week on ischiofemoral impingement syndrome you might not know where the components of the cross over gait come in to play here nor how a rearfoot problem can present with a hip impingement scenario, so I can recommend that article one more time.

One last thing, just in case you think this stuff is easy to work through, remember that these rearfoot varus and valgus problems, and pronation rates. and limb spin rates are all highly variable when someone has varying degrees of femoral torsion, tibial torsion or talar torsion. Each case is different, and each will be unique in their presentation and in the uniqueness of the treatment recipe. I just thought I would throw that in to make your head spin a little in case it wasn’t already.

For example, a case where the rearfoot is a semi rigid varus, with tibial varum, and frontal plane lateral pelvic drift with components of cross over gait (ie. the video case above) will require a different treatment plan and strategy than the same rearfoot varus in a presentation of femoral torsion challenges and genu valgum. Same body parts, different orientations, different mechanics, different treatment recipe.  

So, you can fiddle with a dozen pair of shoes to find one that helps minimize your pains, you can go for massages and hope for the best, you can go and get activated over and over, you can try yet another new orthotic, you can go to a running clinic and try some form changes, throw in some yoga or pilates, compression wear, voodoo bands and gosh who knows what else. Sometimes they are the answer or stumble across it … or you can find someone who understands the pieces of the puzzle and how to piece a reasonable recipe together to bake the cake just right. We do not always get there, but we try.  

Want more ? Try our National Shoe Fit certification program for a starter or try our online teleseminars at www.onlinece.com (we did a one hour course on the RearFoot just the other night, and it was recorded over at onlineCE.com).

Dr. Shawn Allen,  of the gait guys

Reference:

Man Ther.  2014 Oct;19(5):379-85. doi: 10.1016/j.math.2013.10.003. Epub 2013 Oct 29.Clinical measures of hip and foot-ankle mechanics as predictors of rearfoot motion and posture.  Souza TR et al.

Health professionals are frequently interested in predicting rearfoot pronation during weight-bearing activities. Previous inconsistent results regarding the ability of clinical measures to predict rearfoot kinematics may have been influenced by the neglect of possible combined effects of alignment and mobility at the foot-ankle complex and by the disregard of possible influences of hip mobility on foot kinematics. The present study tested whether using a measure that combines frontal-plane bone alignment and mobility at the foot-ankle complex and a measure of hip internal rotation mobility predicts rearfoot kinematics, in walking and upright stance. Twenty-three healthy subjects underwent assessment of forefoot-shank angle (which combines varus bone alignments at the foot-ankle complex with inversion mobility at the midfoot joints), with a goniometer, and hip internal rotation mobility, with an inclinometer. Frontal-plane kinematics of the rearfoot was assessed with a three-dimensional system, during treadmill walking and upright stance. Multivariate linear regressions tested the predictive strength of these measures to inform about rearfoot kinematics. The measures significantly predicted (p ≤ 0.041) mean eversion-inversion position, during walking (r(2) = 0.40) and standing (r(2) = 0.31), and eversion peak in walking (r(2) = 0.27). Greater values of varus alignment at the foot-ankle complex combined with inversion mobility at the midfoot joints and greater hip internal rotation mobility are related to greater weight-bearing rearfoot eversion. Each measure (forefoot-shank angle and hip internal rotation mobility) alone and their combination partially predicted rearfoot kinematics. These measures may help detecting foot-ankle and hip mechanical variables possibly involved in an observed rearfoot motion or posture.

Spinal interneuronal networks linking the forelimbs and hindlimbs

Do the intimate relationships of the upper limbs and lower limbs suggest that quadrupedal skill sets, if not true quadrupedal gait, were a piece of our past locomotion strategies ?  Or is it just representative of the close linkages for gait efficiency? Or maybe both?

In this study below the researchers pondered whether lower limb motor function can be improved after a spinal cord lesion by re-engaging functional activity of the upper limbs. Although this study looked at spinal cord hemisections in adult rats we know there is likely human correlation. This study showed improved hindlimb function when the forelimbs were engaged simultaneously with the hindlimbs during treadmill step-training as opposed to training only the hindlimbs.
As we have proposed here on the gait guys blog many times previously, this study’s results provide strong evidence that actively engaging the forelimbs improves hindlimb function and that one likely mechanism underlying these effects is the reorganization and re-engagement of rostrocaudal spinal interneuronal networks.
“For the first time, we provide evidence that the spinal interneuronal networks linking the forelimbs and hindlimbs are amenable to a rehabilitation training paradigm. Identification of this phenomenon provides a strong rationale for proceeding toward preclinical studies for determining whether training paradigms involving upper arm training in concert with lower extremity training can enhance locomotor recovery after neurological damage.”

This likely has huge implications in rehab measures and gait retraining for those who are not spinal cord impaired as well.  We have discussed many times that making a single limb change merely because the observer/clinician does not like the functional appearance of a limb is a  mistake most of the time. That what we see is a compensation, not the problem.  Go back and review our many “arm swing” blog posts, you should recall that the arms can have a huge impact on the leg function and that many times the arms take their cues from the lower limbs during gait.  This is a topic we have hammered many times in many blog posts and in many courses we have taught.  It is nice to see the literature continue to support the close relationships of the 4 limbs on a neurologic level.


Brain. 2013 Nov;136(Pt 11):3362-77. doi: 10.1093/brain/awt265. Epub 2013 Oct 7.

Use of quadrupedal step training to re-engage spinal interneuronal networks and improve locomotor function after spinal cord injury.

Shah PK1, Garcia-Alias G, Choe J, Gad P, Gerasimenko Y, Tillakaratne N, Zhong H, Roy RR, Edgerton VR.

Gait: sometimes it is about the ear (sort of).

We have talked on several occasions about the aging population and the high morbidity and mortality rates with falls in this population. We have discussed the eyes, dual tasking, changes in environment and many other factors that play seamlessly into normal gait, things we all take for granted. But the aging population has yet another challenge, declining function of the vestibular apparatus. We often hear about balance, and we tend to treat it without truly thinking that this is a integration of the eyes, ears and proprioceptive systems together. If you have clients with multiple falls for unknown reasons, it is time to send them for a check up of the mechanical components of the vestibular system (and visual check up as well) you should be able to do the functional vestibular assessments in your office for the most part.

Recent studies are showing significant declines in semicircular canal function in each of the canal planes as well as otolith function within the aging population. “These findings suggest that age-related slowing of gait speed is in part mediated by the decreased magnitude of saccular response associated with age. ” -Ferrucci study

While the Agrawal study suggested “an overall decline in semicircular canal as well as otolith function associated with aging, although the magnitude of impairment was greater for the semicircular canals than the otoliths in this elderly population. A better understanding of the specific vestibular deficits that occur with aging can inform the development of rational screening, vestibular rehabilitation, and fall risk reduction strategies in older individuals.”

Dr. Shawn Allen, the gait guys

References:

Otol Neurotol. 2015 Jan 7. [Epub ahead of print]
Association Between Saccular Function and Gait Speed: Data From the Baltimore Longitudinal Study of Aging. Layman AJ1, Li C, Simonsick E, Ferrucci L, Carey JP, Agrawal Y.

Otol Neurotol. 2012 Jul;33(5):832-9. doi: 10.1097/MAO.0b013e3182545061.
Decline in semicircular canal and otolith function with age.
Agrawal Y1, Zuniga MG, Davalos-Bichara M, Schubert MC, Walston JD, Hughes J, Carey JP.

Anterior meniscofemoral impingement syndrome.  Ever heard of it ? Probably not.

Here we have a case of a young fellow with knee pain immediately below the patellae. As you can see here there are a few issues, some of which he will likely grow out of and some of which he may not.  Here we obvious see hyperextension of the knees and increased ankle plantarflexion posturing (I chose that word carefully) that obviously goes hand in hand with this retro-postured knees.

After a few more questions it was clear that the pain had been around for quite some time and was at a specific pencil eraser sized area above the anterior joint line, slightly medially to center and without question not at the joint line proper but directly on the medial femoral condyle.  There was no swelling or fulness to suggest this was involvement of Hoffa’s fat pad. The patellar tendons were not thick. So, do you know what he has ?  You should always suspect this in knees that hyperextend this far or in athlete that have sustained or repetitive hyperextension stressing:

• gymnastics
• kicking sports (martial arts, soccer, swimming etc)
• postural syndrome folks (like this little fella) who have low core tone, anterior pelvic tilt both of which drive knee hyperextension.
• any one who has a loss of ankle rocker dorsiflexion range and who then chooses the knee hyperextension option to regain ankle range in an attempt to normalize progressive gait. Frequently flatter feet/hyperpronators will drive more tibial internal spin resulting in hyperextension as well.
• short quadriceps with a dominant quadriceps strategy to control the hip and knees

This fella has several factors here.

So, clearly understanding these biomechanical factors and coupling a palpatory tenderness at the correct spot on the medial femoral condyle indicates that he has (the youngest we have ever seen)…….drum roll…….

Anterior meniscofemoral impingement syndrome.  Ever heard of it ? Probably not. Why, because it was glazed over in school, and maybe not at all for many doctors to be honest. Go ahead, look it up under Pubmed and see how many referenced papers you find on it.  I see it enough (albeit still rarely) to know that it is frequently diagnosed as a patellar tracking problem but those clients do not have the same risk and anatomy factors that I discussed above. I have had doctor referrals call me back saying they have never even heard of it, most have not to be honest.  Bottom line, if you know your anatomy and your biomechanics you can figure out most things. If you are slim and skinny on either one you might be missing a few things.  I do sometimes as well; we are all students.

Summary:  When the knee hyperextends either too much, too long, or for too many repetitions either statically or in dynamic walking, running or in activity the leading upper edge of the medial meniscus can impinge repeatedly and forcefully into the soft medial femoral articular cartilage and over time create a softening of the cartilage (chondromalacia ).  Do it long enough or enough times and you create an inflammatory reaction with a cartilagenous defect.

This poor little guy was hating walking.  Interestingly, what do you think happened when we had him crouch walk (knees flexed)……yup…..no pain. He looked up at me in wonderment immediately and of course saw me smiling knowing very well he would be pain free.

Solution in a 4 year old.  Slightly flex the knees and place a long strip of tape down the back side of the upper and lower leg.  If he extends the knee he forces the tape taught and is instantly reminded (pseudo biofeedback if you will) that he is approaching the danger zone. As this case and many other find, after a few days the skin gets pretty irritated but that is time to take the tape off and let him go back to his old tricks……. trust us, it is only for a few hours until he will figure it out……meaning….. hyperextension is evil ! Teaching this little guy our now famous “Shuffle walks” (to drive ankle dorsiflexion strength in the tibialis anterior and toe extensors in a posture of knee flexion) was on the menu to improve ankle dorsiflexion and anterior compartment strength and we turned it into a fun game for him to play with mom and dad.

Anterior Meniscofemoral Impingement Syndrome.  Say it 3 times fast with a mouthful of organic chunky peanut butter for fun. 

Hope you never see it in a little one. if you do, smile and reach for some tape and put on some 70’s music and shuffle to some oldies.

Dr. Shawn Allen,  one of the gait guys

Arthroscopy.

1996 Dec;12(6):675-9.Meniscal impingement syndrome.

McGuire DA, Barber, Hendricks

.Plano Orthopedic and Sports Medicine Center, Texas, USA.

Abstract

The meniscal impingement syndrome consists of three elements: impaction on theanterior medial femoral condyle by the leading edge of the medial meniscus, articular cartilage damage of at least Outerbridge grade 3, and knee hyperextension of at least 5 degrees. This report reviews this condition in a series of seven knees with an average follow-up of 39 months. The time from the onset of symptoms until surgery averaged 45 months. Treatment consisted of a thorough arthroscopic knee evaluation and debridement of the articular cartilage fragmentation and any impinging synovitis. Postoperative rehabilitation includes extension block bracing, hamstring strengthening, and closed-chain exercise. With this regimen, there was improvement in the Tegner scores and a reduction in postoperative knee hyperextension. Identification of this uncommon condition requires a complete evaluation of the medial femoral condyle in patients with knee hyperextension.

Ischial-femoral impingement: you have to know what it is to make the diagnosis and know how to treat it.

How many times have you had a client come in with pain high up in the ischial area, often explaining that it feels like a high hamstring pull. Others come in and say they have deep gluteal pain, deep in the buttock near the “sit bones”. Often they do not have a “hamstring-type event” that could be the cause of this injury or pain. I see this “high hamstring” pain often in runners, mostly distance runners but in high velocity cutting sports as well.

I see this one often, and it was a difficult fix until I recognized what it truly was and what was generating the pain and problem. Often the problem is at the quadratus femoris muscle. This muscle has an origin off of the ischial tuberosity and inserts into the trochantric interval. The problem arises when the space, the interval, between these bony prominences is closed causing the quadratus femoris to become compressed or pinched in the small space. This can occur from too much frontal plane drift of the pelvis (side shift/drift) and this is almost always met by a relative adduction of the femur. This adduction narrows the space. Frontal plane drift of the pelvis and adduction of the femur, as either genu valgum or a cross over gait, are highly suspicious culprits in getting to the bottom of this clinical entity.

Do you know how to test and evaluate the quadratus femoris muscle ? How about the similarly functioning obturator externus, upper vastus medialis or iliac division of the gluteus maximus ? Can you reasonably tease them out on your physical examination? If you know the common motion amongst them all you will know why they all can be a culprit of the pain and impinging mechanism, and why in treating this problem you likely will have to evaluate and treat one or more of them since they all support external rotation of the femur especially in varying degrees of hip flexion, and thus are used eccentrically to a significant degree to control the rate and degree of internal rotation of the lower limb during contact phase of gait. Losing this control and compounding frontal pelvis drift (and thus femur adduction) will close off the interval for the ischium of the pelvis moving past the femur’s lesser trochanter.

I know you have seen this problem in your clinics and gyms. Have you missed it and called it a hamstring tendonopathy, or have you nailed it ? It is out there, but you have to know something exists to recognize it, and to fix it. You have to recognize it and understand the pieces of the problem, the anatomy and the pathomechanics and understand what is going on in their gait that could be causing it. This is not a psoas related entity although that should remain on your differential list. This is not to be mistaken for a hamstring tear as I suggested earlier, look at this study’s findings, it is not the same entity, although it is possible to have both simultaneously:

“Abnormalities of the quadratus femoris muscle included edema (100%), partial tear (33%), and fatty infiltration (8%). The hamstring tendons of affected subjects showed evidence of edema (50%) and partial tears (25%).” - Torriani (3)

I cannot find any research out there correlates weakness of the gluteals and of the lateral chains with weakness of this quadratus femoris muscle and its synergists with femur adduction and cross over gait styles in this clinical impingement phenomenon. These components are closely related and functional in my experience.  Certainly I cannot be the first to entertain this conceptual layered idea with the cross over gait /frontal plane drift predisposers. So, please come forward if you have seen the same things and had similar successes, lets compare notes and share your nuances in caring for it. There is something here though, because my clients progress nicely when the multiple muscles that support this spiral-natured external rotation are cleaned up, active, strong and paired nicely in a motor pattern that stacks the foot, knee, hip and pelvis reducing femoral adduction and in the functional components that reduce frontal plane drift which I have discussed here many times on the gait guys blog (type in “cross over gait” in the blog search box).  

Dr. Shawn Allen,

the gait guys

references:

1. Am J Orthop (Belle Mead NJ). 2014 Dec;43(12):548-51.Ischiofemoral Impingement and the Utility of Full-Range-of-Motion Magnetic Resonance Imaging in Its Detection.Singer A1, Clifford P, Tresley J, Jose J, Subhawong T.

2. Magn Reson Imaging Clin N Am. 2013 Feb;21(1):65-73. doi: 10.1016/j.mric.2012.08.005. Epub 2012 Oct 13.Ischiofemoral impingement.Taneja AK1, Bredella MA, Torriani M.

3. AJR Am J Roentgenol. 2009 Jul;193(1):186-90. doi: 10.2214/AJR.08.2090.Ischiofemoral impingement syndrome: an entity with hip pain and abnormalities of the quadratus femorismuscle.Torriani M1, Souto SC, Thomas BJ, Ouellette H, Bredella MA.

4. J Bone Joint Surg Br. 2011 Oct;93(10):1300-2. doi: 10.1302/0301-620X.93B10.26714. Ischiofemoral impingement. Stafford GH1, Villar RN.

Pain at toe-off; Stopping Big Toe Impingement with the extensor hallucis capsularis.

Photo: note the AET coming off the EHL tendon in the diagram

What if there was a mechanism in place by which to pull structures out of the way of a joint moving to end range ? If you know your biomechanics, you know this is a true phenomenon on several levels. We know of one at the knee, the articularis genu has been written about having function of drawing the suprapatellar bursa and joint capsule/synovial tissue cephalad (upward) during knee extension preventing an impingement phenomenon during full quadriceps contraction in knee extension loading. 

What if there were a similar mechanism in the big toe ? When teaching we are sometimes asked what joint, that when it goes sour, creates more devastation to the entire biomechanical chain than any other joint. I like to choose the big toe/1st metatarsophalangeal joint because failure to fully push off the big toe at full joint range impairs hip extension, stride and step lengths, and creates compensations far and wide ipsilaterally and contralaterally in the body. Most everyone knows about bunions, turf toe, hallux valgus, sesamoiditis and the like, but there are many other things that can make this joint painful. Today we bring you another “clearing mechanism” that acts to pull synovial and capsular tissues out of a joint that is nearing end range.
As seen in the anatomy dissection photo above, the extensor hallucis capsularis (EHC) is an accessory tendon slip off of the extensor hallucis longus (EHL). Interestingly, one study found that 8% of the dissections showed the EHC came off of the tibialis anterior tendon slip. This EHC accessory slip typically originates off the long extensor tendon (EHL) and traverses medially to the dorsomedial joint capsule region. Some studies suggest it is found in 80-98% of people. We propose it is most likely present in everyone because of the critical nature of its function. We propose that perhaps it may be missed on traditional dissections because of its blending with fascial tissues and because of its sometimes trivial size and girth. Just like when we fully extend our knee we want to be sure the articularis genu will draw the synovial capsular tissue up and out of the patellar/femoral approximation, the EHC has been shown on intra-operative testing to exert a pretension on the metatarsophalangeal (MTP) joint capsule similarly pulling the synovial-capsular tissue free from the end range dorsiflexing toe. Without this function, synovial-capsular impingement can occur and create pain and an inhibitory arthrogenic reflex to the EHL, tibialis anterior or any other muscles around the joint for that matter. This can act and feel like an acute “turf toe” (hyper-dorsiflexion event) and yet, not be true turf toe osseous impingement.
So if your client has pain at the dorsal joint on end range extension of the great toe, meaning things like toe-off, doing push ups from the ball of the foot, jumping, kneeling or squatting with the hallux in forced dorsiflexion etc, this tendon slip (and its origin, the EHL muscle) should be on your mind and assessment of the anterior compartment for S.E.S. must commence (S.E.S.= skill, endurance and strength, our Gait Guys mantra). This is why you need to intimately understand this important video (link) and need to know how to do this exercise, the shuffle walks (video link) and build clean ankle rocker ranges of motion via S.E.S. of the anterior compartment.  Pulling on the great toe, twisting it like a radio knob, and forcing end range shouldn’t be the biggest guns in your arsenal, logically restoring all the dysfunctional components should be.

We wonder how many of the videos online of people demonstrating big toe mobilizations, toe distractions, fancy exercises and various toe circus tricks to regain motion and function and reduce pain actually truly know about the anatomy and function of the big toe and how ankle rocker and other things can impair its function.  We wonder about these kinds of things.  

Please just remember, the average uneducated viewer is merely looking for solutions to their painful parts. Those in the know have a responsibility to deliver as complete a package as possible, within reason. 

“With great powers (and knowledge) there must also come, great responsibility.”-Stan Lee  

Dr. Shawn Allen

the gait guys

Photo credit link: http://www.wisconsinfootandankleinstitute.com

www.wisconsinfootandankleinstitute.com/img/research/The-Accessory-Extensor-Tendon_fig1.jpg

references:

Foot Ankle Surg. 2014 Sep;20(3):192-4. doi: 10.1016/j.fas.2014.04.001. Epub 2014 Apr 16.
The extensor hallucis capsularis tendon–a prospective study of its occurrence and function.Bayer T1, Kolodziejski N2, Flueckiger G2.

Foot Ankle Int. 2006 Mar;27(3):181-4.
Extensor hallucis capsularis: frequency and identification on MRI.
Boyd N1, Brock H, Meier A, Miller R, Mlady G, Firoozbakhsh K.

Foot Ankle Int. 2004 Jun;25(6):387-90.
The accessory extensor tendon of the first metatarsophalangeal joint.
Bibbo C1, Arangio G, Patel DV.

All about Toe Break.

No, this is not a post about fractures phalanges, but rather where your shoe bends, or should bend.

Toe break is where the shoe bends anteriorly. Ideally, we believe this to be at the 1st metatarsal phalangeal joint and metartarsal phalangeal articulations. This allows for the best “high gear” push off as described by Bojsen-Moller (1) High gear push off means that the pressure goes to the base of the great toe (1st MTP joint) for push off. (for an interesting post on this, see here . 

If we think about rockers of the foot during the gait cycle (need a review? click here), it seems best that we accommodate each of them to the best of our abilities. Since most of us wear shoes, it would make sense that it flex in the right places. With regards to the forefoot, it should (theoretically) be under the 1st metatarsal phalangeal joint. This should provide both optimal biomechanical function (distribution of force to the 1st metatarsal phalangeal joint for push off/ terminal stance) and maximal perceived comfort (2).

If the shoe bends in the wrong place, or DOES NOT bend (ie, the last is too rigid, like a rockered hiking shoe, Dansko clog, etc), the mechanics change. This has biomechanical consequences and may result in discomfort or injury.

If the axis of motion for the 1st metatarsal phalangeal joint is moved posteriorly, to behind (rather than under) the joint, the plantar pressures increase at MTP’s 4-5 and decrease at the medial mid foot. If moved even further posteriorly, the plantar pressures, and contact time in the mid foot and hind foot (3). A rocker bottom shoe would also reduce the plantar pressures in the medial and central forefoot as well (4). It would stand to reason that this would alter gait mechanics, and decrease mechanical efficiency. That can be a good thing or a bad thing, depending on what you are trying to accomplish.

Take home messages:

• Where a shoe flexes will, in part, determine plantar pressures
• Changes in shoe flex points can alter gait mechanics
• More efficient “toe off” will come from a shoe flexing at the 1st metatarsal phalangeal joint and across the lesser metatarsal phalangeal joints
• examine the “toe break” in your clients shoes, especially of they have a foot problem

1. F Bojsen-Møller Calcaneocuboid joint and stability of the longitudinal arch of the foot at high and low gear push off. J Anat. 1979 Aug; 129(Pt 1): 165–176.

2. Jordan C1, Payton C, Bartlett R Perceived comfort and pressure distribution in casual footwear. Clin Biomech (Bristol, Avon). 1997 Apr;12(3):S5.

3. van der Zwaard BC1, Vanwanseele B, Holtkamp F, van der Horst HE, Elders PJ, Menz HB Variation in the location of the shoe sole flexion point influences plantar loading patterns during gait. J Foot Ankle Res. 2014 Mar 19;7(1):20.

4. Schaff P, Cavanagh P Shoes for the Insensitive Foot: The Effect of a “Rocker Bottom” Shoe Modification on Plantar Pressure Distribution Foot & Ankle International December 1990 vol. 11 no. 3 129-140

plantar pressure image above from : Dawber D., Bristow I. and Mooney J. (1996) “The foot: problems in podiatry and dermatology”, London Martin Dunitz Medical Pocket Books.