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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.
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.
The patient is undergoing Botox therapy and has a reasonable ankle joint range of motion, however the foot is still plantar flexed throughout gait.
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?
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Originally Posted by Trent Baker
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
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.
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!!!!
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 present I would guess. Please refer on!!!!
Barry
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.
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Originally Posted by BAMBLE1976
This can not be treated with a foot orthosis when dynamic equinus and probably hamstring tightness/increased tone present I would guess. Please refer on!!!!
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.
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.
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Cylie.... in a permanent state of confusion
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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.
Regards
Barry
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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.
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
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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.
Dan
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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).
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.
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Potentially in stages to relieve the spastic nature of the equinus and assure that the foot maintains it's corrected position.
I just can't see this. As you said
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The spasticity will persist regardless of attempts to correct the actual deformity
How can any intervention assure that the foot maintains its new position?
I'm the new guy, so I guess I should expect some hazing, but really??
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.
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?
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.
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.
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?
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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?
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.
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!
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.
Robin
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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?
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.
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.
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I see you girls checkin' out my trunks
I see you girls checkin' out the front of my trunks
I see you girls lookin' at my junk, then checkin' out my rump, then back to my sugarlumps
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?
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!!!!
Paediatric Cerebral palsy orthoses
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