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Paediatric Cerebral palsy orthoses

Discussion in 'Pediatrics' started by Trent Baker, Aug 16, 2011.

  1. Trent Baker

    Trent Baker Active Member

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    What are your thoughts on how to engage the first MTP joint of a Child with CP. The unilateral spasticity is moderate. The patient is undergoing Botox therapy and has a reasonable ankle joint range of motion, however the foot is still plantar flexed throughout gait. The 1st MTP joint is therefore functionally limited and we are starting to see the beginnings of a HAV. I want to think out side the box here on how to reduce the 1st MTP joint load and reduce the functional hallux limitus that's occurring with constant fore foot loading. Obviously there is limited heel contact with the supporting surface, so the strategy needs to be focussed on the mid-foot and perhaps fore foot deflections.
  2. Kidsfeet

    Kidsfeet Active Member

    I'm really not sure that without addressing the spastic equinus there are many options to get that forefoot in a rectus attitude. With splinting and bracing you may be able to limit the progression along with the botox treatment, but that won't get that FF to the position you want it in.

    My guess would be that the only real way to do this is a tendo achilles advancement procedure with a Gasrto-soleal resection and then slow rehab to get the FF into position.
  3. Daniel Bagnall

    Daniel Bagnall Active Member

    Hi Trent

    As a result of the foot being plantar flexed throughout gait is the patient toewalking?

    I’m no sure what you mean by reasonable ankle joint ROM. Is this based on the passive non-weightbearing assessment? If the foot is still plantarflexed throughout gait and is not due to an equinus deformity have you determined what is causing the foot to remain plantarflexed? Is there an osseous impingement which is prohibiting ankle joint dorsiflexion?

    Trent, how have you determined that there is a functional hallux limitus during gait if the foot isn’t plantigrade during gait? Is this what you observe dynamically? What would your estimation be with regards to hallux dorsiflexion during the propulsive phase of gait?

    What parameters are you trying to alter with regards to the FnHL? Are there timing tissues or force issues, or both?

    Due to the limited information there is perhaps you could design an orthoic which has an arch which conforms well to MLA and use either a 2-5 reverse mortons extension or possibly a forefoot valgus extension. Theses modifications may help reduce the magnitude of the pronation moment or increase the external supination moment. As a result, this may reduce the magnitude of the forefoot dorsiflexion moment, which will increase the forefoot plantarfexion moment, therefore, reducing 1st MTPJ dorsiflexion stiffness.


  4. BAMBLE1976

    BAMBLE1976 Active Member


    If this patient is presenting with a spastic equinus then they should be referred to an orthotist for assessment. The forefoot problem will be coming from a more proximal problem either at the ankle/knee/hip. This can not be treated with a foot orthosis when dynamic equinus and probably hamstring tightness/increased tone is present I would guess. Please refer on!!!!

  5. Daniel Bagnall

    Daniel Bagnall Active Member

    Hi BAMBLE1976

    I've never had any interaction with an Orthotist before. Could you please expand a little more on what an Orthotist would do differently as far as assessment and treatment is concerned.

    I cant speak for, Trent, because I don't know what the extent of his tx plan is, but as a Podiatrist, I would most certainly be looking at it from this perspective too and incorporate a multidisciplinary approach.


  6. Bug

    Bug Well-Known Member

    Similar to what Barry and Daniel. This is something that needs more than an orthotic at the foot. The muscle tone changes won't just be at the gastroc/soleus.

    They are botoxing one muscle so the other muscles learn to work better while the botoxed muscle isn't able to work. As soon as the botox wears off, the tone will return therefore the equinus will return. Hopefully not as impacting though as the dorsiflexors will have learnt to work more effectively without being overpowered by the gastroc/sol. The equinus is also due to the triad of tightness inte hamstrings and hip flexors, with or without adductor tightness - the dynamic equinus that Barry is talking about. Quite often you need something that crosses the ankle joint and this is where the orthotist comes in.

    This equipment is also generally provided as a post-botox intervention in VIC as part of the FAHCSIA or SWEP funding (both Federal programs for kids with disabilities) so not sure about how it is administered in the NSW system but I would have thought it was similar, but I would check that out prior to considering a costly device.
  7. BAMBLE1976

    BAMBLE1976 Active Member


    An orthotists is trained on assessing, measuring and fitting orthoses for any part of the body using a full biomechanical assessment of the upper and lower limbs including the trunk. We are trained in dealing with patients with neurological problems and specifically provide orthoses for not just distal control but also more proximal control in order to influence the distal aspect i.e. control the hip/knee in order for the foot to be placed correctly at initial contact.

    In children with neurological problems, more specifically CP of which the majority present with spastic CP, you need to control the kinematics of the foot/knee/ankle in order to influence the hindfoot/forefoot during stance. When there is gastrocnemius spasticity the patient will be either toe walking or walking with a hyperextending knee at midstance. In mostly all of these cases an ankle foot orthoses of some description will be used not just to keep the ankle at plantigrade or similar but also to influence more proximal kinematics as these children tend to develop knee and hip flexion contractures due to the poor kinetics of gait because of lack of normal foot phases in stance phase.

    Hopefully this has cleared it up a bit. It is sometimes as important not to treat and know who to refer to as to try to treat everything.


  8. BAMBLE1976

    BAMBLE1976 Active Member


    forgot to add generally the orthotist will be working in an mdt setting with the childs physio.

  9. Daniel Bagnall

    Daniel Bagnall Active Member


    Thank you. I found that information very helpful.


  10. RobinP

    RobinP Well-Known Member


    I think the main thing to take from this is that 1st MPJ kinetics are probably the tip of the iceberg as far as this situation is concerned.

    I would think it highly unlikely that there will be a normal functioning Windlass mechanism with the degree of spasticity that would warrant botox intervention.

    As such, the advice from Barry and Cylie is definately worth following.

    Pass it on and be part of the ongoing treatment so that if the same thing comes up again, you will have a better understanding of why the proximal control is a necessity
  11. Agreed.

    Sounds like an AFO job to me. How can you have FnHL in a toe walking child?
  12. Daniel Bagnall

    Daniel Bagnall Active Member

    Thats what I was trying to figure out?
  13. Kerrie

    Kerrie Active Member

    Yup refer to an orthotist is my opinion too, if you have a good department that is ;)
  14. Kidsfeet

    Kidsfeet Active Member

    How is an AFO going to address this child's progressive deformity?
  15. BAMBLE1976

    BAMBLE1976 Active Member

    What is his progressive deformity???

  16. Robin, you want this one or shall I take it?
  17. dhodgkin

    dhodgkin Member

    Another orthotist here. Treating a child with CP is always a complex issue, depending on the degree of involvement, the child's and parent's wishes, the physio's desired outcomes, and so on. CP is essentially a static condition neurologically speaking; In its commonest form, spastic CP, progressive effects such as contractures come from hypertonus and altered gait dynamics.

    Orthotists' main role is usually in keeping a child walking as efficiently as possible. The largest factor in reduction of mobility is the development of contractures in the calf muscles, caused by the dynamic spastic response of the muscles through gait. An ankle foot orthosis aims to retain (and potentially, improve) muscle length by, as Bamble said, influencing the GRF in gait and hence the alignment of the limbs through the different phases of the gait cycle.

    If that sounded all a bit text-booky, sorry! Big subject - best I could come up with between patients.

  18. Kidsfeet

    Kidsfeet Active Member

    I digress, my apologies. Progressive in that it is not very amenable to permanent correction. The spasticity will persist regardless of attempts to correct the actual deformity, even with surgical intervention, therefore the deformity will progress to what it was initially if not careful with the treatment modality. Also if left to it's own vices, the spasticity will cause a progression of the equinus, which is why bracing is so difficult and it most situations like the one described, simple bracing to reposition the FF will likely not work, and the patient will need surgical intervention. Potentially in stages to relieve the spastic nature of the equinus and assure that the foot maintains it's corrected position.

    Brain infarct wise, there is no progression, but the LE spasticity will cause the deformity like equinus to persist and get worse with time (i.e more spastic and rigid).
  19. Kidsfeet

    Kidsfeet Active Member

    I'm the new guy, so I guess I should expect some hazing, but really??
  20. Respectfully, I beg to differ. Surgery can be effective in lengthening the TA, although in my area botox with serial casting is much the preferred option. As you rightly say, surgery cannot affect the spasticity so any release of tension can, and often does, return in time. AFOs are rather effective at maintaining tension on the TA, reducing shortening. By encouraging / enabling heel strike they can also somewhat improve the spasticity.

    I've found that Bracing with a good AFO will arrest progression of the deformity in many cases and slow it in the rest. Although a few cases do progress to require the botox / casting and even fewer to TA lengthening, these are a very small number of cases.

    I just can't see this. As you said

    How can any intervention assure that the foot maintains its new position?
  21. That's not hazing. That's Robin is an orthotist and thus knows more about AFOs than me. I disagree with elements of your post, I suspected he would to, so I thought it would be polite to see if he wanted to try an answer to your question.

    Chill ;). Its all love.
  22. Kidsfeet

    Kidsfeet Active Member

    In my first post I suggested a tendo achilles advancement procedure along with a gastroc recession. The achilles advancement shortens the moment arm at which the achilles can have it's plantar flexory affect and serial gatroc recessions can eventually have the desired effect.

    As you said, there are no guarantees, but the OP's query doesn't seem to me to have a non surgical solution.

    I did have a question. Do we really know what the long term effects are of serial botox injections are? This is definitely something that has been used in this instance for some time, but is it reasonable to have these injections for years and years?
  23. Kidsfeet

    Kidsfeet Active Member

    Point taken.
  24. You may be right at that. But it would appear that there are still a lot of non surgical options which have not been tried. Given the high success rates of non surgical management of spastic CP should this not always be the first avenue we explore?
    No. But that's not what I said. The use of Botox is to paralyse the muscle for long enough for the serial casting to acheive the lengthening. Once lengthened, the AFO, Night splints and / or good physiotherapy can maintain the length. Its a short term, non surgical way to increase the range, I've seen 20 degrees or more achieved in 6 weeks this way.

    You seem knowledgeable and informed Kidsfeet. Might I ask the courtesy of your name? Its nice to know who we're talking to.
  25. BAMBLE1976

    BAMBLE1976 Active Member


    it's been shown that persistant use of botox seems to increase the tolerance to it i.e. it seems to be less effective each time.

    The AFO is cast in the quiet zone of the spastic range. This is where there is no dynamic catch present or the 'cog wheel effect' if you like.

    As robert said, the botox/serial cast regime works well and I have been using that as part of the MDT team setting I work in for a number of years with good success. Any TA release will only last as long as the child growing as the problem with spastic muscle is that the muscle does not catch up when the bones grow due to the dynamic component. I don't know if you have much dealings with orthotists or ankle foot orthoses but we see hundreds of this type of thing so are talking through actual experience and research via people like elaine owen and barry meadows at strathclyde university in glasgow, scotland!


  26. RobinP

    RobinP Well-Known Member

    I did have a full copy of this a few years back but it has been a while since I specialise in paeds. Not sure how current this is as I haven't done much reading round the subject recently but out did influence the treatment modality at the hospital I worked in at the time.


    One of the things about AFO usage its that, although a rigid AFO is not dynamic, the GRV can be tuned to maintaining it's position in front of the knee even into terminal stance. This can create a considerable stretch of gastrocnemius and I'm sure (although I could be very wrong) that elaine owen had some figures on this to demonstrate an increased talocrural ROM . Apologies for this not being well written but I am doing it on my mobile as this is the first chance to reply.

  27. Daniel Bagnall

    Daniel Bagnall Active Member

    Hi Kidsfeet

    I've been trying to do gain a bit more of an understanding on this subject.

    Your suggestion re: surgical lengthening of the Achilles tendon is probably better suited for Idiopathic Toe Walkers (ITW) in conjunction with intramuscular Botox injections and casting. This is based on the best current evidence.

    Due to the hypertonus and hypotonus issues in patients with CP, I'm not sure how beneficial surgery is long term? How do you go about determining who's suitable for this procedure and who's not? How successful are these procedures in patients with CP?

    Im unsure as to what the best current evidence is pertaining to the management of CP from a lower limb perspective? I would assume it would be along the lines of intramuscular Botox injections, AFO's and paediatic physiotherapy/orthotist intervention which has already been outlined in this thread.


  28. RobinP

    RobinP Well-Known Member

    I would agree with the latter part Daniel. Not sure about surgery for idiopathic toe walkers. In my experience, the best" cure" for idiopathic toe walking is when the child reaches an age of being socially and physically aware of the the way they walk . some people believe in' breaking the habit' with AFOs. Not so sure myself. for an otherwise normal child, this seems like overkill. In many cases the parents become the person you are treating.
  29. Daniel Bagnall

    Daniel Bagnall Active Member

    Hi Robin

    I can undeerstand now how AFO intervention is an excellent choice in CP cases. However, I've never been able to obtain any decent papers or valid opinions on the management of ITW with AFO intervention. I do know there are some reasonable papers that support casting and Botox therapy though.

    There is evidence to support Achilles tendon lengthening in ITW's but this type of intervention would only be considered appropriate in the more serious cases and the ones that have failed to respond appropriately to conservative management. I know that I certainly wouldn't be in a position to be making judgment calls like that though.

    What are your thoughts on AFO intervention and ITW? Is the AFO meant to apply a gradual dorsiflexion force to the foot and ankle over time until the desired outcome is met?
  30. BAMBLE1976

    BAMBLE1976 Active Member


    For ITW's, If they have a tight calf complex then you would serial cast them.

    You could then use a hinged or jointed afo to block planterflexion at any angle you wish depending on the hinge but allow free dorsiflexion for a more normal gait. You should not have to be stretching them out as you should have acheived this at the serial casting stage. If you apply a hinged afo to someone who is tight, it is very hard to get a stretch at the talo-crural joint without losing the frontal plane control i.e. inv/eversion of the calcaneus and collapsing of the talo-navicular joint.

    That being said I only use this on the worst cases as a long term habit breaker. As you know ITW are notoriously difficult to treat and as Robin said, until they have an understanding of their toe walking habits then it can be hit and miss!!!!

  31. RobinP

    RobinP Well-Known Member

    I think there is an important distinction to be made in the case of idiopathic toe walkers.

    An idiopathic toe walker may not necessarily have an equinous present, although I am sure there is a high percentage correlation.

    If I were being pedantic, I would argue that idiopathic (no known cause) toe walking is an inaccurate diagnosis in the presence of an equinous contracture. It is probably worth talking about ankle joint stiffness as opposed to reduced range of motion(RoM) but I think I will avoid that subject for now

    For the sake of arguement, let's say that there is an equinous present, reducing the equinous may well reduce the toe walking and I would very rarely not advocate a fairly intense stretching programme or building a wedge/ramp to use when brushing teeth etc (Trevor Prior style for those that were at Summer school). In cases where I felt that it was a major issue to the parents and the parents and child were well motivated, I might advocate serial plastering or AFO usage to speed up the process.

    In many cases, if it is the school health visitor that has flagged up the problem, concordance with any treatment modalities carries a much lower success rate than with parents who are well motivated and have actively sought treatment.

    In a true idiopathic toe walker with no equinous/ankle joint stiffness, what am I treating? An unusual gait pattern/parents expectations about their child? In my book that makes treatment pretty difficult to justify, especially when I anecdotally know that success rates with this type of patient are very poor(mainly due to concordance, not the ineffectiveness of treatment). I will generally still advise stretching as less ankle joint stiffness is rarely a bad thing(although i did start a thread on low ankle joint stiffness recently and there appeared to be little evidence of problems)

    I hope this helps

  32. Kidsfeet

    Kidsfeet Active Member

    As far as the lengthening procedure I would agree that in and of itself it is not a great solution.

    Even though there is literature to support the casting/botox solution I'm not sold on the long term benefits of this. Yes this is "conservative" but it doesn't knock out the spasticity issue either. Even if you "lengthen" the Gatro-Soleal complex with botox/casting, we are back to the same issue of the return of deformity due to progressive spasticity. I have not seen good long term results with this, but have had good experience with the tendo-achilles advancement/recession combination. I'm also an advocate of serial lengthenings with time. I believe there was a study that advocated this out of Europe some time ago, but can't seem to locate it:confused:.I have found that the bracing eventually causes irritation and that new braces are required often and many times the parents get tired of this modality and would like to at least try something more definitive.

    I'm 100% with you on conservative management attempts, but ultimately I end up seeing the patients whose families are "been there/done that".

    I should have signed up with my real name. I am an Assistant Moderator on another forum that I use "Kidsfeet" on, and can't divulge myself as the other forum can get a little ummm, feisty. Sorry.
  33. Bug

    Bug Well-Known Member

    You really can't compare the treatment between ITW and CP. The conditions originate from different neural changes.

    I am yet to see an ITW child without an equinus and agree with Robin, therefore is not idiopathic. However, they also have a lot of other "stuff" going on, not just at the ankle. Even the major study that used surgical tendon lengthening procedures reported a high percentage of the children still toe walked in the long term. They just had improved dorsiflexion range. Casting, botox, AFO's etc all address any associated equinus only, not the gait style. Therefore there is no successful treatment for ITW. Yes, many get lower with age however, I have shared my view that there are still many ITW adults that adopt instead a bouncy gait style or toe walk only when socially acceptable.

    Back to CP, heaps of good advice here but I think the message is a better understanding of both the condition and long term implications are needed before looking at the treatment options.
  34. Daniel Bagnall

    Daniel Bagnall Active Member

    Hi Bug

    I brought up the topic of ITW as, Kidsfeet, brought up the suggestion of Achilles tendon lengthening. I thought that it might be worth mentioning that Achilles tendon lengthening would probably be more effective in ITW than CP patients as there is evidence to support it.

    Are you implying that the majority of ITW cases you have seen are not idiopathic due to an equinus being present? How can you know for sure, in ITW cases, whether the equinus is primary or secondary (excluding an osseous equinus of course)?. If there are other gait factors involved in toe walking, what if the calf muscle complex undergoes contracture due to the toe walking gait pattern itself?


  35. How that for Service huh
  36. RobinP

    RobinP Well-Known Member

    Mike, you are a God amongst men

    Interesting study though for those of us that routinely deal with CP.
  37. Bug

    Bug Well-Known Member

    Chicken and egg - did the equinus come first or did the toe walking come first, we just don't know but I am yet to see a child with ITW that does not have equinus.

    It is semantics but idiopathic means "no known cause" if there is equinus, it is easier to toe walk therefore is it really idiopathic? My belief is that the toe walking causes the equinus from prolonged plantar flexed foot position but in the absence evidence it is an educated presumption.

    Really, it's just debating words. I don't believe idiopathic toe walking is really idiopathic anyway but some sort of complex mild neurological change but that is a whole other thread.
  38. Daniel Bagnall

    Daniel Bagnall Active Member

    That was my point. I think in the majority of cases the equinus is generally going to be secondary. As a result, I’d say that it’s more of a contributing factor than an actual “cause”. So I would still say idiopathic is the right term.

    I haven’t come across any literature yet to support what you’re saying, however, this doesn’t mean that I necessarily disagree with your statement. The cause of ITW is largely unknown. I do believe that there has to be a cause but until we are able to determine what that is it will remain unknown.
  39. RobinP

    RobinP Well-Known Member

    Cylie, I'm with you on the mild neuro idea. Nothing but a hunch really. I could count on 1 hand the number of true idiopathic toe walkers that I have seen. More often than not, I think there is something else going on. I have seen an idiopathic toe walker without equinous. no other dismay a diagnosis to give but was never convinced there was nothing else there.
  40. Bug

    Bug Well-Known Member

    Daniel - I think you need to integrate what is out there and known about ITW. While they have normal reflexes etc, we know they tend to toe walk past resolution of equinus, we know there is an association with speech issues, we know there is an issue with some motor development, we know there is anecdotal evidence of sensory concerns. Put them all together and this equals neurological in origin. Sure, there is no one study that proves it all, it would be huge to do but there is plenty of little studies out there that point to a neurological origin.

    I'm at the end of a 4 year study working with kids with ITW, all had some sort of soft neuro signs. Not enough to be given a diagnosis of anything at all, but enough to make you wonder what is going on. I think you also need to use a bit of logic: Why walk on toes, with normal muscle tone, normal muscle strength and normal foot function? It's not an abnormal structure, has to be the brain telling it to do so. Brain = neurological.

    Hope to have something published soon that will help with the thinking as soon as I get this thesis out of the way (mumble grumble).

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