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Foot to jaw problems

Discussion in 'General Issues and Discussion Forum' started by drkeller, Oct 19, 2010.

  1. Footproman

    Footproman Member

    The subject of FHL's affect on gait mechanics and posture can be found in any number of basic texts, including a few that have been referenced on this very forum! ( http://www.podiatry-arena.com/podiatry-forum/showthread.php?t=46711 ). It's simply a waste of time if your intent is to simply be contrary to any number of references I could give. I have better thing to do than :bash:

    Think I'll just use this forum for info and mild entertainment from hear on out. The interactions seem to be pretty hostile.
     
  2. David Wedemeyer

    David Wedemeyer Well-Known Member

    Beau hello again,

    I know who you are Beau and I believe that you also know who I am from a past encounter. I would urge you to consider that this is an academic site for mainly the podiatric profession that allows allied practitioners to participate. I would not characterize that as elitist or hostile. It only seems that way because it is frustrating not to have had previous exposure to this level of understanding via the pedorthics course. I have been there myself.

    When I first found this board, I observed for a while to gain a lay of the land if you will. I found that I was way out of my depth of understanding (and often still am) considering some of the very finest minds in pedal biomechanics in the world contribute here. You can look at it two ways; either as an affront to your own personal level of knowledge about the subject or as a learning experience beyond most anything that you could gain beyond becoming a podiatrist or PhD candidate in a college environment.

    I saw your post regarding the case you were seeking advice on.
    http://www.podiatry-arena.com/podiatry-forum/showthread.php?t=56201

    It was not inappropriate to ask (it was in fact a good question on a relevant topic) but many here are physicians or doctors in clinical practice (and many others are researchers) they speak a different lexicon. In practice their presentation of such a patient follows a logical established history and examination of the complaint that is standardized. Hopefully the chiropractor that you work for follows this same protocol. You were not taught this method to my knowledge but that does not mean that you cannot benefit from learning it. It will in fact make you a better pedorthist and I know because I am a C.Ped and have to document my care of patients, especially with regard to Medicare.

    I am extending to you the olive branch of sorts, if you want to discuss any of this I am easily found on the web, email me and I will try and point you in the right direction. Most of all though PA is a great resource to learn and I advise you to consider that much of what you will learn from here is well above the level you can gain working in the typical chiropractic office. I know because I am also a chiropractor.

    Regards,
     
  3. So, to be clear, you'll not put up any of your sources because you think I'll disagree with them. Well that makes for a stimulating debate then. Its not a waste of your time to discuss opinion but it IS a waste of your time to discuss literature.

    I put it to you that the "any number of references" which support a predictable and positive link between orthoses and treating TMJ don't exist. That you are reluctant to admit that what you state as fact is in fact merely opinion based on opinion with no actual evidence, nor proper rationale.

    The papers discussed on that thread, fascinating though they are, are mostly simple opinion. Dr Danenburg is a very clever man, but I'm sure he'd be the last to say that nobody is allowed to disagree with him, nor that opinion constitutes evidence and is beyond disputation. And I don't recall him discussing treatment of TMJ dysfunction with orthoses by the way.

    I see the standard bait and switch. The thread is about foot to jaw problems. In particular, do we understand the relationship well enough to predict the effect of orthoses on the TMJ. From here we have somewhat dropped the bar to the effect of insoles on posture more generically.

    So what would you have of me, anonymous? Am I to agree with you because you say you are right? Am I to disagree purely on the basis of my personal and unsupported opinion? You don't seem to want to provide evidence to back your case so it seems this is the end of the debate. I think you're wrong, anonymous, that's not aggression, nor a crime.

    This is a discussion forum. That means if you state an opinion, someone might ask you to support it. If you don't want to discuss, why join in?
     
  4. Clifton Bradeley

    Clifton Bradeley Active Member

    I would value what you guys think about this? I’ve been looking at the effects of LLI of pelvic function for a few years now, which is what motivated me to do my PhD research. The most common pathway (MSK compensation chain) for a LLI is what I call a “Single Femoral Pathway, P.I (posterior inferior) long side (see the image below). During a SFP P.I ilium long side, the inominate of the longer limb travels in a posterior and inferior direction to lower the acetabulum, whilst maintaining a normal inominate orientation on the shorter limb side. This pathway often occurs in the ectomorphic body type, where there is insufficient core strength present to prevent inominate motion, and less COM shift to the short side. A pathway occurs less in the endomorphic body type and rarely in mesomorphic body types due to greater core strength, where the inominates are less able to move. This process occurs in order for the body to maintain a stable COM I the presence of postural asymmetry and gravity (vestibular balance). I call this need to maintain a horizontal eye line, The ‘Hunter-gatherer gait efficiency rules’, which we all still operate today. This compensation mechanism was an instantaneous adaptation to varying terrain for millions of years unshod. The problem is we put concrete everywhere and now modern town dwellers get stuff in one of seven functional pathways, the SFP P.I ilium long limb is just one of them. This compensation mechanism leads to many MSK changes in the kinetic chain in an ascending and descending manner (GRF and gravity), but often leads to pelvic torsion.

    This is my take on the TMJ connection not to foot function but to pelvic dysfunction (which actually affects the foot massively). Sacral rotation due to pelvic torsion creates tension in the dural tube, which is transmitted up through the spinal column to the dura mater causing muscle imbalance of the upper torso muscles altering the posture of the atlas and axis (C1 and C2) vertebrae because of the dorsal attachments to C1, C2 and C3. This can create muscle imbalance of the facial muscles creating mandibular dysfunction; malocclusions that produce bruxing; TMJ dysfunction and head tilt through the dura’s attachment around the foramen magnum. Disturbances of the dural tube may be the source of neuromuscular and physiological dysfunction throughout the body because of motor and sensory nerves association and biofeedback mechanisms from one part of the body to another.
    Forward and lateral head position changes the mandible, hyoid bone, and tongue. It compresses the upper cervical facet joints causing muscular nerve entrapments. One common entrapment is the greater or lesser suboccipital nerves that pass between the occiput and atlas. This may cause headaches or refer pain to the facial region.
    Some believe however, that the body works reciprocally in that imbalances in the upper body can also have a marked influence on lower body MSK and physiological systems. The pelvis i.e. acetabular position has a greater influence on foot function than the other way round. Roberts I don’t have the evidence however my twenty-two years in biomechanics is evidence enough for me.
    A growing entourage of medical practitioners now accept that a condition called Dental Stress Syndrome (DSS) may be a dominant stressor of the body and responsible for a range of aetiological unknowns that cause symptoms like headaches, dizziness, hearing loss, insomnia, sinusitis, fatigue, indigestion, constipation, ulcers, dermatitis, allergies, frequent urnination, kidney and bladder complication, etc. The descending nature of DSS is also said to be implicated in pelvic and sacral dysfunction creating pelvic torsion through the dural connection described above. This requires further definition as the forces required to creates such changes, have to be greater than that, which influence the acetabulum in a ascending manner from GRF’s, in order for DSS take effect. I’m investigating this connection with Dr. Parag Patel, a dentist in study we are due to start.
    The action of mastication is a vital daily function, which is as old as mammalian life itself, and hundreds of millions of years older that bipedalism. It involves more structures than any other function in the body and is the starting point of every physiological system, which sustains life. What requires consideration by those like this author who are interested in the holistic multisegmental functional relationship between mastication and vestibular balance, is what are the mechanisms of dysfunction. Where there is dysfunction in the structures involved with mastication there has to be a logical and traceable functional pathway of pathomechanics, rather than the neuromuscular explanation often dispensed. Even the neuromuscular cause has an origin and a route, which requires more precise explanation but sadly is lacking in the literature.
    How can such a vital system be allowed to create such bodily devastation as described about in DSS, in the presence of such small forces as those created during mastication. The nervous system is complex primary system ultimately controlling MSK function and so the catalyst to its dysfunction requires definition.
    The link between lower limb, pelvic function and dental structures cannot be overemphasized. There is a reciprocal relationship, which is in the whole mainly misunderstood and over looked by most practitioners involved in these fields. Yet the rewards to both patient and practitioner can be enormous when a balance relationship between structures in the kinetic chain is achieved. Biomechanics of the future will enhance the whole kinetic chain; sadly I will not be around to see it practiced well! Your thoughts please!
     
  5. Clifton Bradeley

    Clifton Bradeley Active Member

    Image of SFP P.I ilium long leg.
     

    Attached Files:

  6. musmed

    musmed Active Member

    Dear Clifton
    Hi and thanks for your post.
    Like you I practice holistic musculoskeletal medicine and I agree with all your comments.
    Like you I do not have data...where would one start but after 45 years of hands-on I too see what you have written about.
    You know these things occur and I do too. Once one ebraces what others have found their patient outcomes improve dramatically.

    An aside. As regards pelvis torsions and flexions. I agree that they can be reflected in the feet as the skull.
    As for gluteal weakness: it usually is not a weakness but muscle inhibition due to a dysfunctional sacro-iliac joint. The muscle acts weakly ut is not weak.

    A dysfunctional SI joint is seen as an upslip on the affected side and once this is corrected the apparent weakness of the gluteals has gone upon retesting.

    An interesting thing is that 90% of pelvic dysfunctions are sacral flexions and 90% occur on the left side.

    I like your mentioning of the hyoid bone. Embryologically it is a cranial bone and a hyoid dysfunction here affects the whole musculoskeletal system. I assume in everyone who ahs had a seatbelt injury has a hyoid dysfunction.

    Good luck with your research.
    Regards
    Paul Conneely
     
  7. for anyone who did the little testing - what did you find ?

    as the amount of knee flexion increased so did the dorsiflexion stiffness - yes-no?

    Yes

    the we add the hip flexion and the dorsiflexion stiffness increases again - yes-no

    Yes

    So what this says to me is that the reason for FnHL is from proximal mechanics not the other way round.

    ie the FnHL does not cause the increase in knee and hip flexion seen in the classic sagittial plane papers of Dananberg - but the proximal increase in knee flexion being the cause of the functional hallux limitus. The comes about through joint coupling which results in increase tension in the plantar fascia which will result in a plantarflexion moment at the 1st MTPJ (well all MTPJ´s) and then we have increased dorsiflexion stiffness. This has been discussed here as well.

    So my point about the whole chicken and egg is that we can not link FnHL to TMJ problems as a simple 1,2,3,4 step process. Especially if the FnHL is the result of mechanical changes not the cause.

    Something to think about- and maybe some of you will see why I don´t see the link.
     
  8. Clifton Bradeley

    Clifton Bradeley Active Member

    Paul,

    We seriously need to talk, Where are you based. Thank god! someone gets it throughout the whole kinetic chain. For the last few years I am seeing a regular pattern of dysfunction through that left SIJ. But there is a really good reason for this, which I will discuss later. I will release more on the forum over the next few weeks on a new thread. I am now ready to take my theory to the MSK world: there are Seven 'Functional Pathways' to all repetitive injury associated with leg length inequality, during stance and gait. It is a massive subject but very logical. Each functional pathways has three phases, which are laid down over many years from childhood until the pathway is interrupted. I have a patient now but will share more later. Look at the affects of axial rotation on the sphenoid bone, when pelvic torsion is present. It can create malocclusions via the push on the Maxilla. Most people with LLI have some degrees of occlusion, just look at their facial postures.

    Regards

    Clifton
     
  9. musmed

    musmed Active Member

    Dear Mr Weber
    Have a think of this,
    As the knee flexes the tension on the popliteus changes.

    I propose that Functional hallucis limitis is due to a non functioning popliteus.

    I know it to be so. Can I prove it...yes.
    Unfortunately this little secret will be revealed in the near future.

    TMJ=OA=SI what a thought.

    Regards
    Paul Conneely
     
  10. Look forward to seeing the proof , seems like you and Clifton are talking the same talk - so I will say bye for now .
     
  11. musmed

    musmed Active Member

    Dear Mr Weber

    There is no reason for feeling you should leave the forum.
    It is only just that I have been allowed to conduct whatever I wished outside the raillines of medicine.
    So many practitioners of whatever, say podiatry, chiropractic etc, are bound by their guild.
    I do not and will not be bound by such an idium.

    I was lucky to spend a fortune in the 90's seeing many of the worlds greats before they retired and learnt many a thing from them.

    We can enlighten you and others from this thread. Hopefully it will make others start to think outside the square.
    Relax and enjoy life as I do.

    Regards
    Paul Conneely
    for private emails here is my address:

    My email address is: paul@musmed.com.au
     
  12. Mr C.W.Kerans

    Mr C.W.Kerans Active Member

    Phew! Such a lot of foolishness and hot air when its really quite simple; the toe-bone is connected to the foot-bone, the foot-bone is connected to the ankle-bone, the ankle-bone is connected to the leg-bone, the leg-bone.................is connected to the jaw-bone. There. Q.E.D.
     
  13. Clifton Bradeley

    Clifton Bradeley Active Member

    Paul,
    I was fortunate enough twenty-two years ago to get in to full time biomechanics working with athletes after my international athletes career finished. I’ve conducted approximately 15,000 assessment. I only bore you with this fact because I started to see a few interested MSK patterns associated with LLI, which could not be explained by lower limb dysfunction or excessive pronation etc., alone. Here are some regular injury patterns I have frequently seen over the last few years: early right heel lift; more right plantar fasciitis; delayed left heel lift; more Achilles tendinosis left; left foot medial column over load (medial deviation of the COP); late contact phase abduction twist of the right heel (inc risk of right HAV); increased internal leg rotation left (& associated injuries); increase risk of right inversion ankle sprains; more P.I iliums left with corresponding sacral nutation left side (& associated injuries); more A.S iliums right with corresponding counter-nutation (& associated injuries); decrease in patient vertical height with P.I ilium (due to sacral nutation- anterior inferior motion); increased patient vertical height with an A.S ilium ( due to counter-nutation-posterior superior motion); weak left gluteus medius (inc piriformis sciatica); increased tone erector spinae and QL on right; shortened left hamstrings; decreased eccentric load strength right quad (increased left); axial rotation through the spine more TMJ dysfunction left; facial asymmetry etc etc. There are dozens more, as the pathways are incredibly complex. These appear like a random selection of MSK changes however, there is a very logical and repeatable pattern associated with LLI, which I have formulated into seven pathways for my PhD. They occur over many years and can actually be identified in very young children clearly developing in layers. Think of these layers like the layers of an onion, becoming more layered and complex over many years until the MSK dysfunction from natural asymmetry is interrupted by clinical intervention. If you use the pathway theory clinical protocol and use Kevin’s tissue stress theory to off load forces from structures, the patient success rate shoots through the roof. This can be monitored (and evidence based to satisfy the practitioners who want evidence before they believe anything), by taking a sagittal plane inclination between the PSIS and ASIS before and after foot platform therapy with a DPI (digital pelvic inclinometer). I.e. when the patient presents to the clinic the most common Functional pathway (42% of LLI patients) is the: ‘Single Femoral Pathway, P.I ilium long side’ (SFP PI long side). This is more common in ectomorphic, endomorphic body types (almost never in a mesomorph). What happens is to achieve vestibular balance the torso over the longer limb pushes back down on the iliac crest, simultaneous the longer leg is pushing back upwards due to GRF’s. These descending and ascending forces meet at the acetabulum in what I call the Newtonian phase (three phases to each pathway), the axis in the acetabulum for sagittal motion lies posterior for the meeting of forces and the ilium rotates backwards. Also this is due to the auricular nature of the SIJ it will move backwards and inferior easier than forwards especially if the core strength is weak (hence why this would rarely occur in a mesomorph like a footballer. They would maintain relative innominate position but develop more sagittal plane facilitation in the cantilever ability of the legs i.e. flex the longer leg more increasing eccentric load strength on the quad on the longer side, but decrease the eccentric load quad strength on the shorter side. Practitioners traditionally only identify part of the pathway. Some Chiro’s and osteopaths are identifying their part of the pathway and often concluding that the mal-position and torsion is the primary site of dysfunction and adjusting compensation mechanism repeatedly, which without realizing what they have assumed as dysfunction is actually part of a more global (holistic) MSK mechanism. All that inexperienced practitioners do is shift the torque to another part of the kinetic chain to be picked by an allied profession. Hence the patient walks down the road and the ilium slips out again. Dentists see Dental stress syndrome (DSS) and again consider TMJ dysfunction to be the route cause of cranial pathomechanics again without looking at the whole clinical picture. What concerns me is that podiatry is doing the same, e.g. supporting an excessively pronated left foot back to the relative symmetry of the right, without identifying the P.I ilium above. A P.I ilium drops and internally rotates the acetabulum, increasing pronation moment. When the STJ axes are accessed they would be similar but the function is very asymmetrical because it come from the pelvis. Shifting torque like this without understand the functional pathway present is a risky strategy.
     
  14. Footproman

    Footproman Member

    No, I'll not do that because I feel it's a waste of time, given that you "remain unconvinced." I don't know you personally or professionally, but I've been in debates of this kind before (mostly theological). You appear to have a belief system to which you are (possibly adamantly) tied. Therefore, little could, or would, possibly convince you in my opinion. Have you personally read all of the literature and found them wanting?

    On the matter of opinion, yes I did render my opinion, which you immediately disregarded. From my estimation the OP's question was with regard to the connection between TMJD and FHL. My answer was simply, "Yes, there appears to be one based upon some research and gait analysis; and based upon my own experience." Conclusive? No. Anecdotal? Sure. But that is no reason to discount or discredit any or all of the work that's been done on the subject.

    When I took my pedorthics training I remember the instructor saying, "Never say never and never say always." Every patient is different, so one must not assume that a certain modality will never work on patients with a particular pathology. Conversely one must not assume that a certain modality will always work. When dealing with kinetic chain issues I don't believe that there is a "one size fits all" solution. Neither do I believe personally that traditional modalities driven by belief systems are the absolute answer.

    Now, logically to me, some TMJD symptoms are related to posture. Posture is likewise affected by FHL. Therefore, some TMJD symptoms could be caused by FHL. This has not only been postulated in literature on the subject, it's been clinically observed. It's also been clinically observed that treatment of FHL can affect posture and therefore alleviate neck, shoulder and jaw pain.
     
  15. Footproman

    Footproman Member

    So logically one might see FHL being more prominent in athletes that run on varying height surfaces, such as long-distance runners who run on inclines - both up and down. Am I following this correctly? Seems that if popliteal dysfunction is a cause of FHL, then we'd see it typical among some athletes and not others. Is that right?
     
  16. Footproman

    Footproman Member

    I'm giving it another shot. Unfortunately I do not remember you from any past encounter. I hope that encounter was positive, though. Care to refresh my memory?
     
  17. Hi Don´t mix up the posts Ive never mentioned Popliteal that was musmed -Paul.

    Go back to my orginal experiment question and try the 4 stages and see what happens.

    we can discuss after you have tried it, if you want.
     
  18. Footproman

    Footproman Member

    Initially I suppose propulsion, but I would have to check. Will get back with you on this. Question remains for Paul, though.
     
  19. Hiya the experiment got nothing to do with propulsion remember the patients standing in mdstance they are not moving forward. you are just changing the knee and then hip position with increased flexion.
     
  20. musmed

    musmed Active Member

    Dear Mr Weber
    Please explain your statement.

    I have videoed athletes at 200 frames a second and I have never seen one stand still.
    Regards
    Paul Conneely
    www.musmed.com.au
     
  21. Paul it´s a static experiment - if you understand anything about sagittial plane theory, the claim is that FnHL is the cause of changes in gait patterns. In this discussion people have made claims that FnHL is the link to TMJ problems what I´m trying to show if anyone is intersted is that FnHL maybe the result of mechanical changes at the knee,hip and ankle with through joint coupling and changes in muscle and fascia tension leads to the FnHL.

    This link is somewhat explained in the experiement - if anyone takes the 3 minutes.

    As for you video got nothing to do with anything that I talking about which Why I wanted to leave because in my option you just make up stuff to get an arguement out of people and I don´t need to spend my time on it, it never ends well. But footproman asked about something you wrote another left of field statement I jumped back in to say that I didn´t say that that you had.
     
  22. musmed

    musmed Active Member

    Dear Sir
    Que sera sera.
    I know you do not like my thoughts, but I can back up all.
    Regards
    PauL Conneely
     
  23. David Wedemeyer

    David Wedemeyer Well-Known Member

    Clifton are you saying that the PI ilium produces a long leg on the affected side more frequently here assuming that it is the cause or is this a finding rather than the etiology?

    This is an interesting statement Clifton. I assume you are referring to manipulation not resolving the primary issue? Let's assume that a patient walks into a chiropractic or osteopathic office with a SI joint and possibly low back complaint and that the etiology of that complaint is primarily a function of a bony misrelationship. I believe that what you are saying is that this complex problem is not readily solved by the 'inexperienced practitioner' who merely adjusts or manipulates the ilium or sacrum? I wouldn't necessarily agree with that statement and ask what is your protocol for evaluating and treating this patient subset?

    At the end of the day though, Michael's original question was how do we get to the jaw from the foot?

    Regrards,
     
  24. Thing is Paul I don´t think you can.

    We have been down this road before where I asked you to back up your claims.

    http://www.podiatry-arena.com/podiatry-forum/showthread.php?t=44368 Never got an answer with any evidence or even mechancial discription which does not break the laws of physics or mechanical knowledge.

    So
    show me the evidence or explain the mechancial pathways. You claim a non-functioning popliteus will cause a Functional Hallux limiutus. Below is a basic action summary of the popliteus.

    As part of the mechancial joint coupling I´m discussing with knee flexion there is internal rotation of the tibia - ie one of the actions of the popliteus is to internally rotate the tibia on the femur during knee flexion- so if it´s non functioning the tibia would not internal rotate on the femur as much as if it was functioning well and all things being equal lead to less FnHL or in better terms a reduction in dorsiflexion stiffness at the 1st MTPJ not an increase as you claim.

    So it seems to me the evidence is that you have it back to front - the same as the action of the gastroc at the knee - linked above.

    Now if you had of said spasm of the popliteus which could lead to an increase in internal rotation of the tibia - whole different idea - this may lead to an increase in FnHL.

    P s happy Halloween for all those in North America
     
  25. musmed

    musmed Active Member

    Dear Mr Weber
    Just prior to heel strike the knee is going from knee flexion to extendion. This is the time the popliteus is working to make certain that the knee is stable.

    Failure here will lead to the trashing of the knee cartilages.
    So,
    the knee is extended rqapidly
    the foot hits the ground rapidly
    you can hear them coming
    the FLH is now pulling the great toe into the ground
    there is dropping and int rotn of the tibia and thus int. rotn of the talus and navicular the medial cun and th 1st MET.
    the forefoot stays on the ground longer.

    Next functional hallucis you see try testing the popliteus and see if it is working
    and sitting at the foot of the bed
    try
    with your inner hand grasp the 1MET at the level of the prox joint.'
    with your outer hand grasp 2-3MET heads
    now keeping 2-3 METs still
    try moving the 1stMET up and down
    it should move
    a. no effort about 6-8mm
    b. move upwards and downwards equally
    I bet the popliteus wont work and the 1st MET motion is dysfunctional which is simply a reflection of midfoot mechanics.

    Regards
    Paul Conneely
    www.musmed.com.au
    ps thanks for the anatomy lession, I actually do know my anatomy extremely well, jsut ask any one who has been to my workshops
     
  26. I´m not really sure what you saying here Paul as you claim that you understand Biomechanics while 99% of the words make sense most of the sentances do not.

    If this was written by a student I would send it back saying I will give you the chance to proof read it and look at what you have written - think about what you are trying to say and rewrite it, because if you hand this in now you would not pass. Think about correct biomechancial terms.

    as an example of what I mean
    all Hallux are functional unless they have been removed.

    So from my side of things I will move on, back to the foot to Jaw if anyones in.
     
  27. musmed

    musmed Active Member

    Dear Mr Weber

    ...you see.. is referring to you
    maybe a re read will suffice.

    Hopefully your quest will be solved
    but just try what I wrote
    Regards froma wet Australia
    Paul Conneely
     
  28. Actually, FnHL is caused by a dysfunction of the Tib Post.

    Tib post creates supination moments
    Supination reduces 1st met dorsiflexion moments
    High external 1st met dorsi moments create high internal Hallux plantarflexion moments
    High internal Hallux Plantarflexion moments.

    Test any patient who's Tib post does not work, they all have FnHl

    Or...

    That could be a grotesque oversimplification! As is

    Just because it might feel right don't make it so.

    And that is the point of this debate. Aside from that to ascribe a poorly defined section of a functional continuum (FnHl) as being due to any one factor is frankly, toilet (Simon has been schooling me in the art of "call it what it is"). We've no firm definition of FnHl, its not a binary state anyway, Muscles cannot be properly described in terms of "not working" unless completely paralysed or absent. In the same way whilst I can believe that there is a link between posture and foot function I can practically guarentee its not as simple as "FnHl causes TMJ dysfunction". To pretend it is is at best disingenuous, at worst dishonest.


    I'm not so arrogant as to believe I've read anything. But answer me this. Do you beleive in atlantis? No. Have you personnally read all of the literature and found it wanting? No. Will you start beleiving in atlantis if I tell you its real IMO? No.

    What I have on Foot to jaw is not a beleif system, its a lack of belief. I'm open to be proven wrong, but I'm not swayed by the crys of "I believe".
    No. I disagreed.

    Show me the evidence and gait analysis.

    I've discredited nothing I've not seen. What I have, I've done because I found it wanting, not because of the nature of the conclusions.
     
  29. Graham

    Graham RIP

    This is a good point! While I have seen two clients with TMJ report significant improvement post Orthoses when all else has failed, the reasons for this improvement are unclear. I have seen more clients with un-resolved TMJ who I have treated with CFOs, after explaining that these "MAY" help, but haven't!

    As much as " I believe" there may be a link in "some" cases of TMJ to foot mechanics, I can't identify who and why! I only offer treatment if clients have been seen and treated by the usual conventional methods first!

    Sometimes a last resort may be useful. If they have tried everything else It's something to try as long as you explain the non-science behind the theory!
     
  30. :good:

    Or even if you don't, but remain AWARE of the non science behind the theory. If you want a placebo effect it is not always wise to explain too much. What troubles me is when we make up science to fit our desires (to make patients better). Placebos should be for patients, not us.

    I've used types of orthoses I didn't understand. I've used devices where I could not plot the course between cause and effect. I've even used "alternative" therapies and methods. But I've never pretended, to myself or anyone else, that these things are other than they are, and I've never tried to stretch science over belief.

    Heres a question. Hands up who beleives that placebo / psychology CAN'T affect posture?

    Hands up who thinks Occams Razor (when you have two competing theories that make exactly the same predictions, the simpler one is the better) is a bad concept.

    Regards
    Robert
     
  31. Clifton Bradeley

    Clifton Bradeley Active Member

    Hi Dave,
    I’ve been looking at links and patterns in the MSK for many years now, and there is a link throughout the whole kinetic chain created by the complex nature of ascending and descending forces during the process of vestibular balance. I call these the constants of injury – gravity and GRF. During stance and gait our primary basic need is for balance; for our eyes to scan the horizon in plane. With the COM below the head and over the sacral base. In my research I call this basic primary motion pattern the “Hunter-gatherer gait efficiency rules”. All professions allied to medicine are coming at it in our different trained perspectives i.e. the dentists; the osteo/chiros; the podiatrists etc. Experienced practitioners, (old and knackered like me!) who have assessed a large volume of patients, but more importantly during those assessments have spent a little longer looking at the whole MSK (trying to understand anyway how other deal with the same injury). I spent years looking up at the pelvis wondering why one foot excessive pronated more than the other (normally left foot), and why one foot suffered inversion sprains more than the other (normally right foot), in presence of an asymmetrical pelvis and when the STJ axes were symmetrical. I then made a digital pelvic inclinometer and started measuring the PSIS to ASIS relationship on hundreds of patients. It was during this data collection that I found an amazing pattern in pelvic behaviour when a LLI existed, which is most of us.
    Some readers will find this difficult to believe, although some of the more experienced and older MSK practitioners have seen the same thing. My latest results on LLI 52.5% longer left, 42.5% longer right 5% we can’t find. In a recently audit of 22 premiership footballers with Mel Pejik (Bolton Wanders and Welsh senior team physio) THANK YOU MEL FOR PERMISSION TO USE YOUR NAME AND DATA. Results 81% longer left leg, and LLI type repetitive injuries. Obviously, this does not mean that 81% of all premiership footballers have a longer left leg, however over and over again in audits and data collect the left comes out longer. I know many readers would not have seen the same, but that does not mean it is not there. There is a particular method of looking at LLI when you do not have access to CT scanning. Here is part of my protocol below: I use a whole range of tests during a longer than normal assessment process because as you know, to identify motion patterns and reveal the underlying source of the dysfunction takes time. I start with patient standing comparing the frontal plane sacral base position against the sagittal plane inclination between the PSIS and ASIS using a digital pelvic inclinometer. This should marry up i.e if longer left leg and P.I ilium present on the long side as a compensation mechanism created by GRF then the left PSIS will be lower than usual, so the planar relationships between pelvic positions should make sense in stance and gait (E.g. If there is a P.I ilium on the left and it is still higher than the right ilium sitting between 8-12 degrees +ve, then it has to be a longer left leg with a compensation mechanism. Can't be anything else). Then test motion at SIJ in normal way. I do make a token LL measurement with pt supine flat on the couch however if there is any torsion at all the ASIS to medial mallioli will be out (lots of ways in interpreting even this small test, that is for another discussion), then I use board test with 12mm EVA (best response) with pt standing on it with first say right and then left. I'm looking for sacral base and ilia behaviour. Again the motion patterns should make sense as they change from side to side. From this static assessment I move onto functional trials i.e. a raise platform (3mm in FF, 9mm in RF therefore heel raise gradient of 6mm. Works best) in the shoes, first one foot then other. I am looking for motion pattern to appear and settle, then and appear and settle again as you switch it from side to side. This is an important this stage for objective and subjective feedback. This should marry with previous tests (in most people). Then move onto treadmill to do the same again and using motion palpation techniques i.e. hands on pelvis is all three plane, on sacral base looking for the pendular motion that should be there with good function of the innominates, or otherwise. When I settle on a correction in the shoe and I am happy with the motion patterns and pathways occurring in the MSK, have been revealed I place my hand on the top on the patient's head and assess for sinusoidal motion. When this appears the whole body functions better; motion patterns return to normality; the quads and gastrosoleal complex are naturally absorbing shock from GRF's, the sacral base is rocking in the frontal plane; the innominate are moving symmetrically and the sacrum is moving sagitally and efficiently etc. This is a massive subject and there is much more to tell you but this, but will give you an idea of what I do. I then place the patient into a 'pathway' category and break the cycle of abuse functionally.
    To answer your question Dave there is a link between the locomotor unit; pelvis and HaT, however none has correctly mapped it out yet. This is something I am working on with Dr. Stefaan Vossen and Dr Parag Patel (Dentist) for my PhD. This is an amazing functional relationship in the MSK, which will be mapped over the next couple of years I a sure.
    I have, in my own way and to satisfy my own work- mapped out the pelvis and its relationship to LLI and COM behaviour. This is what I take to conference starting in March 2011. I mention a small part of it previously, hence your questions. There appears to be from my work seven pathways to repetitive injury. I call them ‘Functional pathways’. Each pathway is determined by he degree of asymmetry; core strength; body type (Ecto/endo/mesomorphic); age etc There are three stages to each pathway (First The Newtonian stage; second The Pathway stage; third The Pathology stage). We as practitioners see the Pathology stage, but do not necessarily understand how it’s got there. The one I mention early was the Single Femoral Pathway, P.I ilium longer limb (most common pathway in ectomorphs). This is a long pathway but to keep it short, the descending and ascending forces created by gravity and GRF during stance and gait and the need to vestibular balance build in the acetabulum. The axis at the hip joint to these forces lies in the transverse and frontal plane posterior to the where the forces meet and the innominate travels posterior and inferior ward lowering and internally rotating the acetabulum. (The longer leg functionally drops by as much as 6mm, but would measure longer on the couch as the ASIS rises). Hence the pelvis on that side lowers (which is why it can hide the LLI during standing assessment some times); the femur internally rotates creating a longer ground contact phase, delayed heel lift, longer pronation moments at STJ (axes will determine how much torque is dispensed in the foot causing issues). If the STJ is stable the extrinsic torque from the pelvis is dispensed at knee level or groin etc. This simple relationship causes a domino effect throughout the MSK. This is just a small part of this pathway. There are six other pathways, which should when you learn them make sense of every repetitive injury up to he lower back including pathomechanics of the lumbar spine. You find evidence of the pathways and whether the LLI is bony; apparent or only reveals itself during function, by taking a PSIS to ASIS measurement using a DPI (digital pelvic inclinometer) and assessing changes the in pelvic torsion as you correct, exaggerate and test the existence of the LLI. I see the DPI samples of position, much like a geologist would take rock sample to work out where the ectopic plates have moved from over millions of years. The DPI pelvic samples will tell you where the pelvis and come from and where it is going to, and you can make an assessment of injury risk from that. An example is on the image posted above. This is SFP P.I ilium long side. There are rules to the pathways e.g. if a P.I ilium exist on a longer limb and the iliac crest is higher than that of the shorter limb, which sits between 8-12 degrees +ve, then it has to be an anatomical difference with a compensation mechanism and the osteo/chirop/physio should not adjust it unless a mobilization of a lesion is required to reduce the pathway. Because it is a compensation mechanism not a subluxation. Nothing should very be moved on the body mechanically until this paradigm has been followed and established, otherwise a functional time bomb exists which will go off further into the MSK layers, which develop over the years the pathway exists. The whole idea of the Pathways theory is to break the pathway chain of MSK events (compensation) to restore the body back to normal sinusoidal motion when assessed at sacral base and head level.

    Apologies, there is a lot more to this work. This is a fascinating and complex area but I use it every single day and has made me more interested in biomechanics than at any other time in my 22 years of work in this field. The MSK clues to dysfunction are there, but you will not find then on a couch.
     
  32. pebbles

    pebbles Member

    Clifton,

    Can you please explain the sinusoidal motion you are talking about. Is this similar to craniosacral motion?

    Cheers Patrick
     
  33. David Wedemeyer

    David Wedemeyer Well-Known Member

    Clifton I’m not certain that I would call this a need but rather an inherent, developed and subconscious, complex process. Our basic primal need that obviates all others is survival, hence horizontal scanning. I’m not sure how necessary this is anymore unless you live in Detroit though? Interesting..

    There are always those who merely practice and those who aspire to understand deeper or advance the science and art of any profession. I think that the latter is admirable. There is certainly a great deal of overlap in the professions and they all have a different perspective on the proximal vs. distal etiology of complaints such as LLI. It is a complex problem for certain but I am not convinced the answer lies more distally. I do believe that in the rarer cases this occurs though.

    I believe that the incidence of FnLLI (we are discussing functional problems correct?) is over reported. The research supports this (Knutson I believe). I also believe that the vast majority of FnLLI that I have encountered is due to a complex interaction of vertebral body rotation, the iliolumbar ligament, the ilium and the sacrum. I would agree that the majority of patients with symptoms of lumbar or sacroiliac pain exhibit the pattern of an L5 vertebral body rotation on the left and I cannot tell you why. They almost unilaterally have a short functional right leg. I agree that the left leg is more commonly the long leg but for different reasons I suspect. I find that overwhelmingly the PI ilium occurs on the right and is the short leg side but I suspect that that may not make much sense to you initially.

    Think about that and sacral nutation; just as you cannot have side bending of the spine without vertebral body rotation, you cannot have vertebral body rotation without nutation of the ilia and the acetabulum (and therefore the leg) following this motion. Play with (or picture) a model of the skeleton and nutate the ilia PI. Does the leg on the corresponding side become longer or shorter?


    A colleague of mine, Joe Kurnick alerted me to this when I was in clinic and has written on it extensively. I thought in all honestly Joe was completely incorrect but in my years in practice I can validate that his observations were in fact prescient although he found more PI ilia on the left and I on the right (it could be simply the way we develop or are wired, who knows, but I rarely see the same vertebral body rotation pattern on the right). These patients are our miracles, who arrive in a great deal of pain and leave thanking me, require very short treatment encounters and almost all resolve completely including the presenting functional short leg on the right.

    I treated a gentleman with this precise pattern not long ago who was prescribed a lift for the right leg by his podiatrist. He had a very high level of lumbar and sacroiliac pain and I determined a functional short right leg. His iliopsoas on the right was also hypertonic and flexion of the knee prone resulted in the buttocks coming clear off the table at 90 degrees as well Thomas’ test was positive.. I took the lift out of his shoe, did some post-isometric relaxtion on the psoas, reduced the L5 body rotation and posterior sacral base and he walked out on his first visit with good relief. I saw him 8 times as I recall and followed up with him a few months later and he was asymptomatic. The point being that there is a place for manipulation in this patient subset and the etiology is not foot driven. It is the most common pattern of the functional short leg complex that I encounter in daily practice.

    The rest fall into two categories; those with discernable muscular imbalance of the hip flexors and those with gait disturbances (I’m sure there are more but for the sake of this discussion I am limiting it to the main three that I encounter), which less often is evaluated to be pronation related. Either of these is amenable to treatment if the assessment is performed properly and lumbar and/or sacral fixation is ruled out.

    I asked previously if you felt the PI ilium is always the long leg side? Your reference to sinusoidal motion and previous comments about the sphenoid lead me to conclude that you have some experience with cranio-sacral work. I believe that was Upledger’s (D.O.) and sacral-occipital’s Dejarnete’s (D.C.) work? I’m not sold on either of these to be honest with you although I do use the pelvic blocking techniques found in SOT on occasion. I do find it interesting when professions outside of my own or traditional osteopathy foray into these as a treatment modality. I guess it may be no stranger than a chiropractor with an unyielding interest in the lower extremity (of which I am guilty).


    I’d like to read your research when it is available Clifton.
    .
    Could you explain this? Are we going from the inner ear to the hip here and how? What pathway or mechanism links the two? We are diverging from the original question which is the foot to the jaw and how this may be accomplished. No offense but I am waiting for a cogent explanation of this process. I just do not see it Clifton, I need to be convinced as do others and I don’t mean didactic study, RCT’s etc. but clinical observations that make sense based on our knowledge and training that appear reasonable and common sense and that we can test and explore.


    I believe we are on the same page in some part here. The key is to discern between a truly mechanical fixation and FnLLI and a purely muscular one or a pedal distortion. There can of course be myriad permutations of these existing in tandem I hope you will agree; it is not a simple subject. I would offer to you that in my own clinical experience and we are talking about a large number of spines that I have evaluated, that purely mechanical fixations causing FnLLI occur far more frequently than any other single cause. The problem with long term correction lies in the accuracy of the assessment; the precision of the treatment and in addressing any muscular or gait concomitant that is contributing to the presentation.

    I find that frequently the problem is not viewed as the complex beast that it is and practitioners rely on what is in their own scope of practice or toolbag (or dip into that of another profession in a dilettante fashion), rarely refer or defer and want to be all things to all people. You are either patient centric or practice centric I believe. My mantra is “if you’re concerned about income, focus on outcome” and don’t’ shy away from an interdisciplinary approach for a complex problem.

    .

    Interesting theories Clifton, worthy of further discussion over time I hope. We may not agree all of the time but I am sure that a cooperative effort somewhere along the line may prove productive?

    Now let's get back to the pathway that links the foot to the jaw shall we? Any takers?
     
  34. Clifton Bradeley

    Clifton Bradeley Active Member

    Hi Patrick,
    When gait is working well, which is rare as most people of some degree of dysfunction present or developing, which might not even be symptomatic, the pelvis should have a wave like motion as it moves forward. To be precise it should have an amplitude (amplitude is the magnitude of change in the oscillating variable) and a frequency (frequency is the number of occurrences of a repeating event per unit time). Both amplitude and frequency will increase with speed. The pelvis should not be on a flat plane as it moves forward because it would be absorbing shock. Actually the pelvis always has motion, however sadly most people have some degree of abnormal motion due to he high incidence of LLI and pelvic torsion. To the head: when the pelvis is moving on a nice sinusoidal motion, this is translated to the head obviously moving forward at the same speed as the pelvis, but it moves on a lower sinusoidal curve (less amplitude). This is because our spinal motion sagittally is absorbing shock and reducing the wave so that our brain and senses housed in the head can move more smoothly to scan the horizon and make quick decisions. Going back to the original question in this fascinating forum question: when there is dysfunction in this mechanism; in what I call the ‘Functional pathways’, hundreds of structures respond with logical dysfunction and often upper body pain occurs and DSS (dental stress syndrome). In my mind this can work in an ascending manner due to the magnitude of forces created from GRF and gravity meeting at the pelvis (main effect at the acetabulum) however I am struggling with accepting that descending forces from created mastication and swallowing. Craniosacral motion is a couch-based therapy.

    Hope this helps.
     
  35. Clifton Bradeley

    Clifton Bradeley Active Member

    David,

    I'm going to read your reply later and come back to you, work is called.

    many thanks
     
  36. Clifton Bradeley

    Clifton Bradeley Active Member

    Hi David,
    Your quote: “I would agree that the majority of patients with symptoms of lumbar or sacroiliac pain exhibit the pattern of an L5 vertebral body rotation on the left and I cannot tell you why. They almost unilaterally have a short functional right leg. I agree that the left leg is more commonly the long leg but for different reasons I suspect. I find that overwhelmingly the PI ilium occurs on the right and is the short leg side but I suspect that that may not”
    Dave, these are fascinating observations and I totally agree with this aspect of your comments. I am a podiatrist but have been investigating the effects of LLI on pelvic mechanics for many years, which is what has lead me to my PhD in more recent time. I think I may have found an explanation and want o share it through my research. The reason why you and I and other very experienced MSK practitioners have seen the same patterns is because they are there. I say ‘ very experienced’ because to identify them you have to have seen thousands of MSK patients and had to have looked at the whole kinetic chain. They are present in the largest majority of patients but are sadly and worryingly missed by most practitioners, and you and I know this can be very dangerous to the patients and leave them with many unresolved symptomatic and non-symptomatic issues if not dealt with correctly. I have to say many chiropractors ad osteopaths do not deal with them correctly either.
    The largest majority of humans have a LLI (approx 95%). This LLI on presentation is both apparent due to pelvic torsion and bony. There are three different types of LLI. FnLLI for me is a difference, which only appears during gait, and apparent due to ilia asymmetry caused by pelvic torsion eve if there is an underlying bony LLI. The first graph below show you pelvic torsion before heel raise/foot platform therapy (50% raise of the measured difference). Minutes after the heel raise is used the compensation (pelvic torsion) is reduced (second graph) to reveal the true difference in LLI. A very big proportion of the population have a longer left leg, the ‘Single femoral pathway, P.I ilium – long side’ (From my research) if the most common compensation mechanism and occurs in ectomorphic body types mainly. Core strength and body type etc determines the type of pathway and there are six more in my research. Actually more A.S iliums occur on the right, simply because with a LLI (mainly left side) there is less weight of the CoM over the right ilium and it is free to rotate forward to raise and externally rotate the acetabulum (P.I lowers and internally rotates the acetabulum).


    I look forward to your thoughts on this. Where are you based?
     
  37. Griff

    Griff Moderator

    Hi Clifton,

    Don't want to steer away from the topic under discussion too much but two things you said interested me:

    Are these statements based on your anecdotal findings over the years or the literature review for your PhD? If the latter could you pop the references up on here please?

    Cheers

    Ian
     
  38. Clifton Bradeley

    Clifton Bradeley Active Member

    Hi Ian,
    There is very little available on this particular area, although I have an on-going search for my PhD. This is my observation over many years and am writing a paper on it now. This is the focus of my research. The effects on LLI on pelvic mechanics is of emerging interest in podiatry. Just because there are not lots of papers on this particular area does not mean it does not exist. I will get some references hopefully when I get time later. Ian, where are you based? I would be delighted to show you what we are doing here in our lab before my research is finished. Let me know if this interests you? I tried to post a couple of graphs earlier but struggled, will try again later.
     
  39. Clifton Bradeley

    Clifton Bradeley Active Member

    A invitation to visit our lab is open to anybody wishing to explore what we are researching on the effects of LLI on pelvic mechanics.
     
  40. Griff

    Griff Moderator

    Hey Clifton,

    I appreciate that lack of evidence is not evidence of lack - I just wondered if you were quoting an epidemiological study that I had missed thats all. I'm penning a blog on LLI's and just at the gathering references stage now.

    Thanks for the invite, but I'm down South and my interest in LLI's isn't sufficient enough to travel North for ;)

    All the best

    Ian
     
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