Pain on the outside of one leg, inside of the other. 

Whenever you see this pattern of discomfort, compensation is almost always at play and it is your job to sort it out. 

This patient presents with with right sided discomfort lateral aspect of the right fibula and in the left calf medially. Pain does not interfere with sleep.  He is a side sleeper 6 to 8 hours. His shoulders can become numb; left shoulder bothers him more than right.

PAST HISTORY: L shoulder surgery, rotator cuff with residual adhesive capsulitis. 

GAIT AND CLINICAL EVALUATION: see video. reveals an increased foot progression angle on the right side. Diminished arm swing from the right side. A definite body lean to the right upon weight bearing at midstance on that side.

He has external tibial torsion bi-lat., right greater than left with a right short leg which appears to be at least partially femoral. Bi-lat. femoral retrotorsion is present. Internal rotation approx. 4 to 6 degrees on each side. He has an uncompensated forefoot varus on the right hand side, partially compensated on the left. In standing, he pronates more on the left side through the midfoot. Ankle dorsiflexion is 5 degrees on each side. 

trigger points in the peroneus longus, gastroc (medial) and soles. 

Weak long toe extensors and short toe flexors; weak toe abductors. 

pathomechanics in the talk crural articulation b/l, superior tip/fib articulation on the right, SI joints b/l

WHAT WE THINK:  

1.    This patient has a leg length discrepancy right sided which is affecting his walking mechanics. He supinates this extremity as can be seen on video, especially at terminal stance/pre swing (ie toe off),  in an attempt to lengthen it; as a result, he has peroneal tendonitis on the right (peroneus is a plantar flexor supinator and dorsiflexor/supinator; see post here). The left medial gastroc is tender most likely due to trying to attenuate the midfoot pronation on the left (as it fires in an attempt to invert the calcaneus and create more supination). see here for gastroc info

2.    Left shoulder:  Frozen shoulder/injury may be playing into this as well as it is altering arm swing.

WHAT WE DID INITIALLY (key in mind, there is ALWAYS MORE we can do):    

  •  build intrinsic strength in his foot in attempt to work on getting the first ray down to the ground; EHB, the lift/spread/reach exercises to perform.
  • address the leg length discrepancy with a 3 mm sole lift
  • address pathomechanics with mobilization and manipulation. 
  • improve proprioception: one leg balancing work
  • needled the peroneus longus brevis as well as medial gastroc and soles. 
  • follow up in 1 week to 10 days.

Pretty straight forward, eh? Look for this pattern in your clients and patients

People tend to forget about the peroneal muscles. This is what it looks like when the brain forgets.

This client came to see us for obvious reasons but the case details are not what we are focusing on today. Gait gets pretty messed up when a critical component or phase is lost or forgotten.  

In last weeks teleseminar on www.onlineCE.com we discussed several gait cases. In these cases 5 things kept coming up when it came to looking at (specifically) neurologic gait compensations:

  1. slowing of gait
  2. wider based gait
  3. increased ancillary movements 
  4. utilizing support when needed or available
  5. shorted step length and stride length

In this video, it is clear that this person has some serious neurologic problems engaging the peroneal muscles and controlling ankle and foot function and as a consequence you see evidence of some of the itemized issues above, namely, calculated movements, nearly zero arm swing and step length from left to right is abbreviated. 

It can go both ways. The neurologic problem can affect one’s gait, but one’s resultant gait can then affect cortical function, driving an endless loop. Recently, five studies presented at the Alzheimer’s Association International Conference in Vancouver Canada provided striking evidence that when a person’s walk gets slower or becomes more variable or less controlled, his cognitive function is also suffering.(2)  

A person’s gait and their neurologic function cannot be separated. The stuff just run’s too deep.  This is why we love gait so much, because to fully understanding someone’s clinical problems we must understand how and why they move.  There are clues in everyone’s gait that can help you clinically. The question is, will you notice them ? Do you know what normal gait is to begin with ? Will you understand what you are seeing and realize it is a compensation? Will you fix what you see or look deeper to find the cause of what you see ? 

Shawn and Ivo,

The Gait Guys

Gait Posture. 2013 Jul;38(3):549-51. doi: 10.1016/j.gaitpost.2013.02.008. Epub 2013 Mar 11.

Altered gait termination strategies following a concussion.

Buckley TA1, Munkasy BATapia-Lovler TGWikstrom EA.

2.  http://www.nytimes.com/2012/07/17/health/research/signs-of-cognitive-decline-and-alzheimers-are-seen-in-gait.html?_r=1&

Functional Ankle Instability and the Peroneals 


Lots of links available here with today’s blog post. please make sure to take your time and check out each one (underlined below) 

As you remember, the peroneii (3 heads) are on the outside of the lower leg (in a nice, easy to remember order of longus, brevis and tertius, from top to bottom) and help to stabilize the lateral ankle. The peroneus brevis and tertius dorsiflex and evert the foot while the peroneus longus plantarflexes and everts the foot. We discuss the peroneii more in depth here in this post. It then is probably no surprise to you that people with ankle issues, probably have some degree of peroneal dysfunction. Over the years the literature has supported notable peroneal dysfunction following even a single inversion sprain event. 

Functional ankle instability (FAI) is defined as ” the subjective feeling of ankle instability or recurrent, symptomatic ankle sprains (or both) due to proprioceptive and neuromuscular deficits.” 

Arthrogenic muscle inhibition (AMI) is a neurological phenomenon where the muscles crossing a joint become “inhibited”, sometimes due to effusion (swelling) of the joint (as seen here) and that may or may not be the case with the ankle (see here), or it could be due to nociceptive input altering spindle output or possibly higher centers causing the decreased muscle activity. 

This paper (see abstract below) merely exemplifies both the peroneals and FAI as well as AMI.

Take home message?

Keep the peroneals strong with lots of balance work!

The Gait Guys: bringing you the meat, without the filler!                                                                         

Am J Sports Med. 2009 May;37(5):982-8. doi: 10.1177/0363546508330147. Epub 2009 Mar 6.

Peroneal activation deficits in persons with functional ankle instability.

Source

School of Kinesiology, University of Michigan, 401 Washtenaw Avenue, Ann Arbor, MI 48109, USA. riannp@umich.edu

Abstract

BACKGROUND:

Functional ankle instability (FAI) may be prevalent in as many as 40% of patients after acute lateral ankle sprain. Altered afference resulting from damaged mechanoreceptors after an ankle sprain may lead to reflex inhibition of surrounding joint musculature. This activation deficit, referred to as arthrogenic muscle inhibition (AMI), may be the underlying cause of FAI. Incomplete activation could prevent adequate control of the ankle joint, leading to repeated episodes of instability.

HYPOTHESIS:

Arthrogenic muscle inhibition is present in the peroneal musculature of functionally unstable ankles and is related to dynamic peroneal muscle activity.

STUDY DESIGN:

Cross-sectional study; Level of evidence, 3.

METHODS:

Twenty-one (18 female, 3 male) patients with unilateral FAI and 21 (18 female, 3 male) uninjured, matched controls participated in this study. Peroneal maximum H-reflexes and M-waves were recorded bilaterally to establish the presence or absence of AMI, while electromyography (EMG) recorded as patients underwent a sudden ankle inversion perturbation during walking was used to quantify dynamic activation. The H:M ratio and average EMG amplitudes were calculated and used in data analyses. Two-way analyses of variance were used to compare limbs and groups. A regression analysis was conducted to examine the association between the H:M ratio and the EMG amplitudes.

RESULTS:

The FAI patients had larger peroneal H:M ratios in their nonpathological ankle (0.399 +/- 0.185) than in their pathological ankle (0.323 +/- 0.161) (P = .036), while no differences were noted between the ankles of the controls (0.442 +/- 0.176 and 0.425 +/- 0.180). The FAI patients also exhibited lower EMG after inversion perturbation in their pathological ankle (1.7 +/- 1.3) than in their uninjured ankle (EMG, 3.3 +/- 3.1) (P < .001), while no differences between legs were noted for controls (P > .05). No significant relationship was found between the peroneal H:M ratio and peroneal EMG (P > .05).

CONCLUSION:

Arthrogenic muscle inhibition is present in the peroneal musculature of persons with FAI but is not related to dynamic muscle activation as measured by peroneal EMG amplitude. Reversing AMI may not assist in protecting the ankle from further episodes of instability; however dynamic muscle activation (as measured by peroneal EMG amplitude) should be restored to maximize ankle stabilization. Dynamic peroneal activity is impaired in functionally unstable ankles, which may contribute to recurrent joint instability and may leave the ankle vulnerable to injurious loads.

all material (except for the study); copyright 2013 The Gait Guys/ The Homunculus Group. All rights reserved. Please ask before you lift our stuff. If you are nice and give us credit, we will probably let you use it!