Welcome to the Podiatry Arena forums

You are currently viewing our podiatry forum as a guest which gives you limited access to view all podiatry discussions and access our other features. By joining our free global community of Podiatrists and other interested foot health care professionals you will have access to post podiatry topics (answer and ask questions), communicate privately with other members, upload content, view attachments, receive a weekly email update of new discussions, access other special features. Registered users do not get displayed the advertisements in posted messages. Registration is fast, simple and absolutely free so please, join our global Podiatry community today!

  1. Everything that you are ever going to want to know about running shoes: Running Shoes Boot Camp Online, for taking it to the next level? See here for more.
    Dismiss Notice
  2. Have you considered the Critical Thinking and Skeptical Boot Camp, for taking it to the next level? See here for more.
    Dismiss Notice
  3. Have you considered the Clinical Biomechanics Boot Camp Online, for taking it to the next level? See here for more.
    Dismiss Notice
Dismiss Notice
Have you considered the Clinical Biomechanics Boot Camp Online, for taking it to the next level? See here for more.
Dismiss Notice
Have you liked us on Facebook to get our updates? Please do. Click here for our Facebook page.
Dismiss Notice
Do you get the weekly newsletter that Podiatry Arena sends out to update everybody? If not, click here to organise this.

Which muscle is most important ?

Discussion in 'Biomechanics, Sports and Foot orthoses' started by mike weber, Sep 12, 2009.

  1. Members do not see these Ads. Sign Up.
    I was thinking on just starting a discussion but thought I would create a scene...

    Your partner has been getting more and more upset with the time you spend on Podiatry Arena.....
    Your sitting on the computer looking at PA and you hear a loud noise all of a sudden 3 masked figures appear grab you pull a bag over your head and inject you with a muscle relaxant.

    You wake up with a bag over your head tired to a chair. You feel very groogy and soon you are covered in cold water, you yell and scream a man with a strange accent tells you to shut up. He then explains that his group are Podiatry Arena deprogrammers and that your loved ones are paying for this to get you back... You yell and scream some more this gets you a punch in the stomach...

    This man then tells you that you need to answer some questions to work out your mental level of addicton to PA. He then asks you which muscle which has it origin above the talocural joint and inserts on the foot would be the best to lose functon of and what would be the worst and why ?.

    You then start laughing and say that´s pretty ironic that they ask you a podiatry question when your family feel your addicted to PA ( and not the Alanis Morreset version which bascially means you had bad luck god I hate that song . ) This gets you another hit to the stomach so you know this is serious.

    (sorry for the long post cant sleep this morning)
  2. heres my thoughts

    best to lose Plantaris ( hope your not one of the few that dont have one)

    worst to lose function of Peroneus Longus... you get lateral deviation of the STJ, reduced 1st ray function, reduced balance and some lose of plantarflexion ability of the ankle
  3. I'd agree on the plantaris but I'd have to say I think I'd miss my triceps surae somewhat more! Technically two muscles but hey...

    Oh and I'd say to that foreign gentleman that the answer is on the arena on the why did the chicken cross the road or the things you don't want to hear from patients thread. I'd then wait for him to check it and make good my escape as the familier glazed expression came over his features.

    You scare me Dr weber. You've been reading too much Tom Clancy.;) Great thread idea though.:drinks

  4. In a foot with a medially deviated STJ axis, it would be worse to lose the posterior tibial muscle. In a foot with a laterally deviated STJ axis, it would be worse to lose either the peroneus longus or peroneus brevis muscle. Since the gastrocnemius-soleus has more combined muscle mass than all the combined masses of all the other muscles of the leg, then certainly losing the triceps surae would be very problematic.....the result of a loss of the triceps surae is a cavus foot, clawtoe deformities and a calcaneus gait and basically no propulsion.

    Anyone want to venture a guess why a cavus foot, a calcaneus gait and clawtoe deformities result from loss of the triceps surae over time?
  5. mgrig

    mgrig Active Member

    Is it due to FHL, FDL and Tib Post attempting to replace to plantar flexion moment what would have been present with triceps surae?

    Is the calc gait an adaption to reduce ff loading thus reducing to force needed to plantar flex/ resist dorsiflexion?
  6. Which other important muscle may contribute to this ankle joint plantarflexion moment other than the FHL, FDL and posterior tibial muscle?

    Not likely. Do you, or anyone else for that matter, have any better guesses?
  7. mgrig

    mgrig Active Member

    Peroneus Longus...could explain an increase in the transverse arch
  8. Yes.

    Now, why does a calcaneus deformity/gait occur with loss of triceps surae function? By the way, it isn't because of the extensor muscles of the ankle!

  9. there is an increase in ankle dorsiflexion as talus is displaced upward & as os calcis rotates under and into a more verticle position;
    - patient will be noted to maintain heel contact during the terminal stance phase;
    - forefoot develops equinus position, therby creating cavus deformity;
    Thats a quote from the article

    Before I read the article I was going to say because of the elastic properties of the plantarfascia which I still beleive will have a role in creating the ff equinus.
  10. Much too much in the way of action type books.
    Sort of got the idea from reading the links Simon Spooner put up about preferred pathways in the orthoses thread . Thinking that we as a profession should look more closley at muscle-joint relationship not joint-muscle relationship.

    ps no DR too much time doing other much more fun things so mike is my preferred title
  11. Interesting Link. I'll be honest, I've not heard of a "calcaneal deformity" and I'm just off to run a birthday party for about 15 3 year olds so I don't have time to look it up.

    However I would think that without the TS to exert planterflexion moments on the foot throughout stance phase the person would have to alter their posture to keep their centre of gravity more posterior, directly over the STJ, and shorten their stride so that their tibia did not advance much beyond vertical. Otherwise they would have a tendancy to fall over forward. As per this helpful diagram I stole. Don't tell the original artist, I'm hoping he won't spot that its his ;).


    In which case, given the lever arms being shorter posterior (pivot to heel) than anterior (pivot to forefoot) and the fact that the COP could not advance much past the ankle there would have to be a hell of a lot more force on the calc.

    But thats a very quick guess. I'm just off to purgatory.

  12. Mike:

    I copied the article to let everyone know what "calcaneus" deformity was, since it is not very common. The explanation from the article doesn't make sense to me so it is not the one I was looking for. In addition, it is quite unlikely that the plantar fascia is the primary culprit.
  13. Robert:

    You are getting very warm, Robert. However, the calcaneus deformity not only causes increased pressure under the calcaneus but also results in the cavus foot/hammertoe deformity. Why would loss of the gastroc-soleus complex cause all of these problems?
  14. In that case I'd have to say it was a balance of forces style of thing. Presuming the calc pivots around the talus / stj it will be pulled down (towards the transverse plane) by the ts and up (toward the frontal) by the short flexors and the plantar apeurneurosis. Remove the tension on one side of the equation and I would expect , over time, the PLantar structures to pull the calc into a more vertical position - cavus foot.

    Kinda like a tent pole with two equally tense guy ropes. Cut one, the other will be unapposed.

    But my brain is fried from 2 hours of sugared up kids so I might be babbling.

  15. David Wedemeyer

    David Wedemeyer Well-Known Member

    - deformity occurs as a result of unopposed dorsiflexor function combined with attenuation of of the triceps surae;

    - when the triceps surae is weak, the tibialis posterior, peronei, and long toe flexors are ineffective hind foot plantarflexors;

    The action of tibialis anterior would be unopposed and since this muscle inserts on the 1st met and cuneiform there is a strong dorsiflexion moment produced antagonistic to the now deficient triceps surae (which also renders the other plantar flexors deficient) which will eventually alter the foots shape as well. Clawtoes ensue in attempt to balance the foot that has lost its rotational component about the STJ, especially a supination moment in late midstance.

    Since the STJ joint is dependant upon several muscles that would be affected by the loss of antagonistic plantarflexors, the STJ would no longer function as a roatational unit that produces torque and converts linear energy to rotational torque. Essentially these linear moments would be just that, linear and directed in dorsiflexion thus creating a cavus arch and the rest follows???
  16. Mike, Robert and David:

    Thanks to you all for making a stab at my theoretical question. Here is how I would explain the development of clawtoe deformities, calcaneus deformity and cavus foot with patients that have a loss of triceps surae function.

    The ankle joint plantarflexors include the triceps surae, posterior tibial (PT), flexor digitorum longus (FDL), flexor hallucis longus (FHL) and peroneus longus (PL). Of these muscles, the triceps surae is the only muscle that inserts posterior to the ankle joint axis so, as a result, it has, by far, the greatest ability to generate ankle joint plantarflexion moments during gait. In addition, with more contractile force in the triceps surae, more tensile force will be present with the plantar fascia since triceps surae contractile activity will cause a rearfoot plantarflexion moment and a forefoot dorsiflexion moment [as a result of increase in ground reaction force plantar to the forefoot].

    Since the remainder of the ankle joint plantarflexors (i.e. FDL, FHL, PT and PL) all insert plantar to the foot and distal to the ankle joint, when they exert contractile force, they will cause a forefoot plantarflexion moment and a rearfoot dorsiflexion moment, tending to raise the longitudinal arch of the foot. In fact, in a normal foot with normal muscle function, the arch height is maintained as a result of the triceps surae exerting an arch-flattening moment while the FDL, FHL, PT and PL are all exerting an arch-raising moment. Arch-raising moments are also being exerted by the plantar fascia, plantar ligaments and plantar instrinsics which also help the FDL, FHL, PT and PL prevent arch collapse during weightbearing activities.

    When the triceps surae ceases to function, for whatever reason, these muscles, which are vitally important at generating ankle joint plantarflexion moment, are lost. The strong ankle joint plantarflexion moment from triceps surae contractile activity is critical to generating the forefoot ground reaction force (GRF) that will help decelerate ankle joint dorsiflexion in late midstance of walking to help slow the descent of the center of mass (CoM) during the latter half of stance phase.

    Because the central nervous system (CNS) now senses that the forefoot can no longer use the triceps surae to generate GRF on the forefoot to decelerate the fall of the CoM during late midstance, it will recruit the only other ankle joint plantarflexors it has available (i.e. the FDL, FHL, PT and PL) in an attempt to generate adequate forefoot GRF to decelerate the fall of the CoM during late midstance.

    As a result of this overactivity of the FDL, FHL, PT and PL, the arch will start to raise which will result in a cavus foot deformity over time. In addition, the increased forefoot plantarflexion moment from the FDL, FHL, PT and PL overactivity also results in a decrease in tensile force within the plantar fascia and a loss of the important stablizing force on the digit from the MPJ plantarflexion moment from the plantar fascia. The combination of the loss of plantar fascial tensile force and the increase in tensile force at the FDL/FHL results in the gradual development of clawtoe deformity over time. Finally, the calcaneus type of gait is caused by the inability of the FDL, FHL, PT and PL to generate adequate ankle joint plantarflexion moment to properly oppose the ankle joint dorsiflexion moments from the ankle joint dorsiflexors, including the anterior tibial, extensor hallucis longus, extensor digitorum longus, peroneus tertius, and peroneus brevis.

    Hope this all makes sense. If not, when I am done with completing my lectures on Biomechanics of Subtalar Arthroereisis, and on Effects of First Ray Dorsiflexion Stiffness on Foot Biomechanics, for an upcoming lecture in San Diego, I should have more time to provide some illustrations that better describe the important biomechanical concepts that I have attempted to describe above.:drinks
  17. David Wedemeyer

    David Wedemeyer Well-Known Member

    Excellent description and thank you Kevin. Would you say though that the most dramatic influence on the foot and changes would present as a result of the above or am I just way off? :craig:

  18. Dave:

    I thought you were very close.

    However, the point that I feel is most important is that the deep flexors and peroneus longus, all in their attempt to cause a deceleration in the CoM in late midstance when the triceps surae is weak or absent, will cause an arch raising/clawtoe effect while the gastrocnemius and soleus cause a arch flattening/toe flattening effect. Hope that makes sense.
  19. It makes a lot of sense what you said for the above occurance.

    I Hope this makes sense it does in my head...

    Ive been thinking about ff equinus for a little while now and considering what Kevin wrote would this be true?

    Kevin and others would you say that a garden variety FF equinus is a developed position change ie plantarflexing of the forefoot against the rearfoot due to this muscle imbalance that you wrote about above ( ie the relationship between the triceps surea and the FDL, FHL, PT and PL muscles)

    I´m also thinking the deformitly would also be made worse by a thickening in the platar fascia this would occur over time from the increased bow stringing effect which I beleive would also occur from the muscle imbalance .

    As time goes on the fascia would store more elastic energy and therefore be able to shorten the distance between the calc and met heads, but due to the above muscle imbalance a plantarflexion moment of the forefoot occurs and therefore a FF equinus.

    ie a soft tissue contracture similar to a FF supinatus ?
  20. Donnchadhjh

    Donnchadhjh Active Member

    Thank you Kevin, Mike et al.

    This thread made it worthwhile logging in to PA - I am also glad my patient didnt turn up so I could learn something.
  21. Phil Wells

    Phil Wells Active Member


    Very interesting work - thanks.
    Do you think it would possible for the CNS to adapt in an alternative way via sagittal knee movement.
    Delayed knee flexion could keep the COM posterior to the ankle joint (momentarily) then accelerate the COM via rapid knee flexion resulting in decreased forefoot dorsiflexion load under the mets then into proulsion - would this reduced the need for the PTT, FDL etc activity.
    I assume it does not do as this would take more energy but if this type of approach can be mimicked via clinical intervention - e.g. heel strike modification to footwear - then could we reduce the onset of a cavoid foot? (diabetics pathomechanics etc)

    Hope I got this right.


  22. David Wedemeyer

    David Wedemeyer Well-Known Member

    I aspire to one day answering one of Kevin's mind-bending questions with resounding clarity and correctness. Until then......

    I know this isn't part of the thread but I want to thank everyone who contributes to The Arena, especially those who teach their superior skills and knowledge to the rest of us. There is nothing like this available to the chiropractic or pedorthic professions. Simply brilliant!
  23. HansMassage

    HansMassage Active Member

    I wish to add my thanks for this thread as educational exercise.
    I find direct correlation between trigger points in the planter muscles and position of trigger points in the soleus and secondarily the gastrocnemius. My impression is that the CNS prefers to continue lateral balancing forces through the calcaneus as if it is a pulley while preserving its use as an anchor in propulsion.
    Hans Albert Quistorff, LMP
    Antalgic Posture Pain Specialist
  24. Interestingly enough, this came up recently. Saw a patient with idiopathic motor neuropathy. All his muscles were a bit weak but his tib ant and hallux flexors and extensors were completely inactive! Also lost all proprioception in these muscles.

    He often found himself falling / walking backward without realising he was doing it until his inner ear balance told him! Fascinating stuff.

    So you can get by without tib ant. Stop press.

Share This Page