Case of the Week 13/08/98 (ESMAC conference, Belfast 1998): What people said... Thanks very much to Richard & Andreas for putting together the new Case of the Week, which as Richard mentioned, will be presented at the ESMAC conference in September. Feedback from the expert speakers at the meeeting is here. My initial impression, I must say, is that this child's problem might not related to his hamstrings. If you look at the clinical findings, you'll see that he has no static contracture (or very little) at the knee. I wonder whether his problems may be arising from his ankles, which are markedly spastic and prevent the ground reaction vector from going anterior to his knees in order to provide a plantarflexor-knee extensor couple, as described by Jim Gage. Instead the vector would likely be posterior to the knee and be responsible for their collapse. Difficult to be sure, of course, without knowing the joint moment. Was there any reason why you didn't get kinetics, by the way, Richard? Chris Kirtley MD, PhD Assistant Professor Department of Rehabilitation Sciences The Hong Kong Polytechnic University Hung Hom Hong Kong Special Administrative Region of the People's Republic of China Tel.: +852 2766 6755 Fax +852 2330 8656 ------------------------------------------------------------------------ Its amazing how quickly discussion can move away from the actual patient. Chris asks why no kinetics. Superficial answer is that he walks with crutches. Our policy is not to take force plate data for crutch walkers. Now its clear that if the crutch hits a force plate then the force data is invalid, but what if it doesn't? This is a good example of a patient who has his crutches well out to the side and they do not hit the force plates. What does the kinetic data tell us under these circumstances? I think (but would be grateful for confirmation) that a joint moment based on this force data would faithfully represent the external moment applied at the joints. There seems to me to be a little loose thinking about how the weightbearing crutch influences the data. We have no problem with the opposite leg bearing load in double support when working out joint moments so why should the crutch bearing load cause us any concern. It seems to me that the data is valid. The sticking point is that we are unsure how to interpret the data. I am sure in this particular case that we would see no external extending moment at the knee through the gait cycle and am sure as Chris points out that this adds to the subject's problems. I'd still like to hear from him the mechanism of how this gives such a characteristic pattern of pelvic movement. Richard Baker Gait Analysis Service Manager Musgrave Park Hospital Stockman's Lane Belfast BT9 7JB Tel: +1232 669501 ext 2155/2830 Fax: +1232 683816 ------------------------------------------------------------------------ Richard, Your assumption is correct. As long as the crutch does not interfere with (ie. contact) the force platform, joint force and moment of force calculations are valid (or as valid as inverse dynamic estimation can be). If there are any lingering doubts, draw a free body diagram of the leg where the force platform measures the input force at the foot and your unknown force/moment is at the knee (or hip). Unless the crutch (or walking aid in general) is attached to the leg, it does not enter the equations of motion. Because the force platform is a dynamometer, the influence of the crutch is seen in magnitude and direction of the force measured at the foot. Calculating shoulder moment would of course be a different story because the walking aid exerts a force directly on the hand and arm. We like to attach a force tranducer to the crutch or cane to measure it's reaction force separately. Chris A. McGibbon, PhD MGH Biomotion Lab Boston MA ------------------------------------------------------------------------ Thanks to Chris and Andreas for the interesting case. It should provoke some interesting discussions, especially the thread concerning kinetics. We had a long discussion here in our lab about this subject and even broke down to collect data on a norm using crutches. To answer some of the specific questions, I do think that C needs to extend his knees more in gait. I would like to have seen what he looked like while under the effects of the botox, but my feeling is that he needs hamstring lengthenings. I am a bit concerned with popliteal angles of only -50 R and -40 L that other causes may be influencing his knee flexion, such as hip flexor spasticity (both the iliopsoas and the proximal rectus--hence the double bump pelvis) but more importantly his triceps surae weakness. Has he tried rigid or ground reaction braces? Would he tolerate braces with those feet? If this improves his crouch then his somewhat tight and quite spastic hamstrings are not the only cause of his crouch. What is his strength like? I am concerned about his apparent midfoot break and assume that most of the dorsiflexion seen on the kinematics comes through his midfoot. This would compound his weak ankle plantarflexor even more, reducing his plantarflexion/knee extension couple, and resulting in increased knee flexion. I assume that the botox had a significant effect on his crouch (why else would one continue injections) then I would be inclined to conclude that the cause of his crouch is a combination of weak plantarflexors unable to overcome his spastic hamstrings, combined with spastic hip flexors. Did his pelvic tilt or hip motion change with the botox? With this much apparent spasticity and limited contractures would selective dorsal rhizotomy be an appropriate treatment? I would need to see his strength scores before I could recommend that intervention. We generally do SDR only on free walkers. So, to fully stick my neck out I would recommend hamstring lengthenings and subtalar fusions with possible iliopsoas lengthenings. I am concerned that his pelvic tilt would become very anterior if only his hamstrings were lengthened. I assume that his hamstrings and iliopsoas are balanced now at reasonable high force. If he is pretty strong (4s at least) then I would consider SDR. The goals would be to increase his knee extension in stance and improve his foot position to tollerate bracing. I look forward to other responses and hope I can convince our lab to collect kinetics on patients with crutches. Sincerely, Michael Michael Orendurff, MS Clinical Biomechanist Gait Analysis Laboratory Portland Shriners Hospital ------------------------------------------------------------------------ I certainly agree with Ronny's assertion that the lower-limb joint kinetics are faithfully recorded when using crutches (providing the crutch doesn't hit the plate). As he points out, bottom-up inverse dynamics doesn't care about what's going on higher up (i.e. in the upper-limbs). It all comes out in the wash, so to speak, from the force platform input to the foot segment model. Having said, that we've also just started to measure crutch forces with a Berme-type (Strathclyde) pylon tri-axial transducer (3 forces, 3 moments), as designed for use in lower-limb prostheses. I confess I'm not looking forward to resolving the various components. If your transducer is similar, Michael, I'd be grateful for a few modelling tips. About the case, Michael says... I am a bit concerned with popliteal angles of only -50 R and -40 L that other causes may be influencing his knee flexion, such as hip flexor spasticity (both the iliopsoas and the proximal rectus--hence the double bump pelvis) but more importantly his triceps surae weakness. Well, it seems to me that a negative Thomas test pretty well rules out hip flexor problems - in fact there appear to be very little in the way of static contractures, which still leads me suspect weakness as the main problem. I realise that he could have dynamically tight hamstrings and hip flexors, but I'd have thought you'd pick up some degree of static contracture on the physical exam if that were the case. I would be inclined to conclude that the cause of his crouch is a combination of weak plantarflexors unable to overcome his spastic hamstrings, combined with spastic hip flexors. Yes - this confirms what I was suggesting, and I agree that a floor (ground) reaction orthosis might work wonders. I wonder how many people are using these around the world. My impression is that they are not well studied by young clinicians - I have a suspicion that since modern plastics (which I don't believe are rigid enough to make an effective GRO) have replaced steel in most AFOs, the principle of the GRO has been lost. As usual, I'm being controversial to see what people think! I'd love to see some pictures of the orthoses people are using (please send GIFs or JPGs). I'll cc this message to the P&O list and hope someone responds. So, to fully stick my neck out I would recommend hamstring lengthenings and subtalar fusions with possible iliopsoas lengthenings. I'd have a try with the GRO first! Chris Kirtley MD, PhD Assistant Professor Department of Rehabilitation Sciences The Hong Kong Polytechnic University ------------------------------------------------------------------------ Two questions that Chris has posted to me personally but would probably interest others: What exactly did his "splints" consist of? Were they, in fact, GROs? Splints were (what we consider) standard plastic shell AFOs. I'd agree with Chris that AFO prescription is poorly understood in relation to CP. I'd suggest that, in a great many young kids with diplegia, AFOs designed to prevent excessive plantarflexion are actually functioning to prevent excessive dorsiflexion in stance consequent to weak extensor musculature (not just in plantarflexors). You can see this from the fact that the tibial strap leaves a mark on the skin if the splint is removed after walking. If the splint is resisting plantarflexion then there is no need for the splint to apply a force on the proximal anterior tibia. This isn't a problem for the kids (it helps them to walk!) but it does lead to some woolly thinking when thinking about the biomechanics of gait and sometimes on the follow through of this analysis to a consideration of the surgical options. As the kids get heavier the such splints get less effective at withstanding the larger forces which are applied, they're not designed for this. What should be happening is that the prescription should be changing to something actually designed to do the job, proper anterior floor reaction splints. However because it has never been appreciated that this is the kid's requirement in the first place this is seldom done. I'm not sure that the limitations of the materials is significant if the correct design is used. The problems are firstly of cosmesis and secondly that these kids generally develop rotational deformities which prevent the AFR from working in the required plane. Why did you do the new analysis with crutches when he's now walking without them? Another point for general discussion. Technically C can "walk" but is very unstable. He does not have sufficient control either to stop himself or to turn around. It is our feeling that his gait with crutches is a much better indication of his basic motor abilities than his independent "walking". Do other labs have a policy on selecting which form of ambulation to assess if a subject can walk with different levels of support with different levels of competence. Obviously you could analyse all forms of walking but this takes time. Richard Baker Gait Analysis Service Manager Musgrave Park Hospital Stockman's Lane BELFAST BT9 7JB Tel: 01232 669501 ext 2155 Fax: 01223 683816 ------------------------------------------------------------------------ In response to the discussion so far, we'd like to make the following comments: We would agree with Richard that it is not possible/practical to fully analyse gait with and without all aids and orthoses. Our policy is to look for the most repeatable gait pattern and we find that borderline walkers without aids (as in this case) are more repeatable with support. If gait patterns are similar with and without aids we would prefer to measure without aids so that we can collect kinetics more easily. Only if the patient's endurance is very good would we collect 3D data both with and without aids but would usually video all walking methods. We note in the discussion so far that there seems to be an assumption that dynamic contracture always accompanies a static contracture on clinical examination. This is not our experience and we are not surprised to see a double bump pattern at the pelvis which could be caused by dynamically tight/overactive hamstrings. Similarly the hamstrings could also be responsible for the increased knee flexion at initial contact. We would therefore expect the Botulinum Toxin to reduce the range of the double bump pattern at the pelvis and reduce knee flexion in stance. In order to consider long term treatment we would like dynamic EMG data, particularly rectus femoris in view of his positive Duncan Ely test. Similarly we would like some indication of the child's underlying muscle power and selective control, this would help in deciding whether any surgery would further weaken him and whether he has good potential for rehabilitation. One last comment - we would not be able to reproduce the clinical examination with such precision!! We look forward to the discussion at ESMAC. Nicky Thompson Oxford Gait Laboratory Team Nuffield Orthopaedic Centre Headington Oxford tel: 01865 227609 OX3 7LD fax: 01865 744277 ------------------------------------------------------------------------ Hello CGA members, This is the first time for me to mail you. Nice to meet you. I have several questions... I would like to ask what kind of mechanism would work on the double bump of pelvic tilt curve by the dynamic and static hamstring tightness. The least ant. tilted pelvis on the initial contact point may be explained with hamstring tightness. But why would the pelvis tilt anteriorly during the loading response? To hold upright with one leg support, the hip should flex to compensate the flexed knee which is caused by hamstring tightness. Would this compensatory hip flexion cause the GRF far ant. to the hip and make the trunk and pelvis tilt forward? The hamstring is two joint muscle which encompass the hip and knee, and the hamstring's lever arm for the hip joint is longer than that for the knee. So, the simultaneous extension of hip and knee may cause the hamstring to go slack (only assumption not solid fact). Would a little bit slack hamstring release the pelvis to tilt forward? If yes, why the pelvis starts to tilt backward just after the loading response (after the contralat. foot off), although the hip and knee still extends simultaneously? Why would the pelvis tilt posterior during the single limb support? Does he use the backward movement of his trunk and pelvis to initiate swing and advance his incoordinated limb? Because the kinematic data may be the tip of the iceberg, we should assume or imagine other factors to contribute his gait. This case does not seem to show much about the iceberg under the water by the kinetic data. His co-contraction as we see in the video and the crutch he uses may not fit to inverse dynamic approach. What, do you think, would be the other factors? I am afraid that the double bump has been discussed away already. If then, I hope some kind member would send me the discussion. About the rigid, solid or ground reaction type AFO, I completely agree with Dr. Kirtley, that the ankle must solid and rigid enough not to give up the ground reaction force especially the mid and terminal stance phase. We use more than 4 mm thick plastic material but the material may become thinner during molding. So, we should often reinforce the ankle part of AFO with metal pieces. I have a question to Dr. Kirtley. Which point do you cut the ant. end of the foot shell of the rigid AFO, just proximal to the MP joint or just distal to the toe end (foot shell meets entire foot)? And why? I hope my words make sense. Sincerely, Sun G. Chung M.D., Ph.D. Dept Rehab Med Seoul National University College of Medicine Chong Ro Ku YeonGeon Dong, Seoul South Korea (TEL) 82-2-760-2619 (FAX) 82-2-743-7473 ------------------------------------------------------------------------ Dear all, Dr. Chung reminds me that we're supposed to explain the double bump in the pelvic tilt curve. Before proposing an explanation, it occurs to me to recap on the normal pelvic tilt curve (in dotted lines at /archives/13-08-98/both.gif). There isn't much movement in the normal, it's true (and the coefficient of variation on this parameter is large), but as Inman pointed out in his 'determinants of gait' (see /faq/determinants.html) the pelvis tilts anteriorly just before toe-off to lengthen the trailing limb and thereby reduce the droop in the body CoM (of course, this also shortens the advancing limb - which rather defeats the object, and this is one of the criticisms of the 'determinants'!). This harks back a little to our discussion of step length ( /teach-in/step ). C seems to be reversing the determinants, with posterior tilt (relatively) during terminal swing. Could he then, I wonder, be trying to help swing advancement? As corollary evidence, note that his First Determinant (external pelvic rotation in terminal stance to help with contralateral reach) is accentuated. Isn't it interesting just how many paradigms we can use to explain pathological movement! Wouldn't it be nice if we can find a universal approach? Dr. Chris Kirtley MD PhD Dept. of Rehabilitation Sciences The Hong Kong Polytechnic University Hong Kong ------------------------------------------------------------------------ There is no doubt in my mind that a for many CPs the pelvic double bump is as much about lengthening step in late swing phase, for those with limitations in hamstring function, as it is about hip flexor function. It has proved incredibly difficult to provide any supporting evidence though due to the fact that pelvic data is in laboratory co-ordinates and therefore is as dependent on CoG control, via the contralateral stance limb, as it is directly on the hamstrings function of the swing leg (I am talking specifically here about CPs with exaggerated double bumps). We do not have the vast numbers of patients it would take to perform the multivariate analysis necessary to sort this out. Returning to pelvic tilt in normals I have a couple of comments. Firstly about the CoV, again related the to fact that pelvic kinematics are in laboratory co-ordinates. I think that much of the variation is due to the fact that subjects tend to wander i.e. do not often walk consistently in a perfect straight line - We have data from a significant minority of subjects whose CoV for pelvic tilt is extremely small indeed. The second point ("my theory chris"!!!!!!) is that anterior pelvic tilt at toe off occurs primarily to take the strain of the anterior structures of the hip which is obviously extended, but also further strained by pelvic retraction as step length and adductor function are optimised. I am not wanting to deflect the discussion away from the case (which is stimulating) but would find comments on this interesting. Jeremy Linskell Manager, Gait Analysis Laboratory Co-Ordinator, Electronic Assistive Tehcnology Service Dundee Limb Fitting Centre Dundee, DD5 1AG, Scotland tel +1382-730104, fax +1382-480194 web: http://www.dundee.ac.uk/orthopaedics/dlfc/gait.htm ------------------------------------------------------------------------ Hello CGA members This is the first time to mail you. Re; C is a 6 1/2 year old boy with a diagnosis of spastic diplegia Answering this from the OandP list. The main focus here will be braces. no external extending moment at the knee through the gait cycle I did see the knee extends after foot flat, I felt that was the main reason for the double bump pelvis. Leads me to believe that his gait involves spasticity, and not weakness. I done tons of floor reaction orthosis, but have not been satisfied with the results. They only slowed down the progression towards surgery. With the idea of spastic reduction, the needs are, make the device as comfortable as possible, do not restrict the foot and ankle in a abnormal way, but allow the most motion. I use the word serial to refer to serial cast, that can reduce spasticity consistently. The properties of serial cast just needs to be in an AFO. Once you have that idea, we can start to understand that what works is using packaging not three point pressure systems. AFO's are only a tool to help orthotist to make the AFO comfortable, one of the main points that we miss is no AFO can guarantee comfort. So, to reduce the spasticity, you can not use three point pressure systems, but packaging with thin modern plastics. That's all for now. High price research equals high price solutions. John G. Russell Jr. 3161 Putnam Blvd. Pleasant Hill, CA. 94523 Phone 510-943-1119 Fax 510-943-24-93 ------------------------------------------------------------------------ Dear Jeremy, I agree with some of you comments but respectfully differ with others. On Mon, 24 Aug 1998 18:29:18 +0800 (WST) Jeremy Linskell wrote: There is no doubt in my mind that a for many CPs the pelvic double bump is as much about lengthening step in late swing phase, for those with limitations in hamstring function, as it is about hip flexor function. It has proved incredibly difficult to provide any supporting evidence though due to the fact that pelvic data is in laboratory co-ordinates and therefore is as dependent on CoG control, via the contralateral stance limb, as it is directly on the hamstrings function of the swing leg (I am taling specifically here about CPs with exaggerated double bumps). We do not have the vast numbers of patients it would take to perform the multivariate analysis necessary to sort this out. It is my assumption that the pelvis tilts anteriorly to initiate swing in this type of ambulator. This allows the iliopsoas to remain isometric and results in lower motor control requirements (no spasticity to overcome with eccentric contraction). The tight hamstrings pull the pelvis posterior again after foot strike has occurred. After surgical lengthening of the hamstrings only, increased anterior pelvic tilt occurs, suggesting that there had been a balance between the hip flexors (iliopsoas and rectus, the anterior pelvic tilters!?) and the hip extensors (hamstrings, the posterior pelvic tilters!?). This dynamic interplay of poorly controlled and possibly weak muscles is what drives the pelvis through so much arc. I have evaluated the effects of various kinematic and kinetic parameters on the stride length and velocity of both normals and CPs. For the sake of brevity let me say that the near-holy Determinants of Gait paper would be a wonderful resource if it contained any data whatsoever. Pelvic tilt in the sagittal plane contributed an insignificant amount to the stride length and velocity of both normals and of CPs. Other factors were easily able to make up for deviations here. The posterior tilt of the pelvis in late swing did not contribute significantly to stride length. (see Orendurff, et al., Limits to passive range of motion and the effect on crouch gait in children with cerebral palsy. (1998) Gait and Posture, 7 (2) 165.; Orendurff, et al., Predictors of stride length barefoot and with ankle foot orthoses for children with cerebral palsy. (1998) Gait and Posture, 7 (2) 148.; Orendurff, et al., Stride length changes following surgical hamstring lengthenings in individuals with cerebral palsy. American Society of Biomechanics Conference Proceedings, (1997).; Orendurff, et al., Kinematic and kinetic determinants of stride length in children with cerebral palsy. (1997) Developmental Medicine and Child Neurology, 39(S75), 3.) This is not to say that the function of the pelvis in gait is contrary to our present understanding (reducing CoM excursion to an appropriate level, increasing stride length, reducing anterior hip structure stress, increasing adductor function, etc.) but rather that its contribution is lower than other factors (hip, knee and ankle motion for example). Returning to pelvic tilt in normals I have a couple of comments. Firstly about the CoV, again related the to fact that pelvic kinematics are in laboratory co-ordinates. I think that much of the variation is due to the fact that subjects tend to wander i.e. do not often walk consistently in a perfect straight line - We have data from a significant minority of subjects whose CoV for pelvic tilt is extremely small indeed. The second point ("my theory chris"!!!!!!) is that anterior pelvic tilt at toe off occurs primarily to take the strain of the anterior structures of the hip which is obviously extended, but also further strained by pelvic retraction as step length and adductor function are optimised. I am not wanting to deflect the discussion away from the case (which is stimulating) but would find comments on this interesting. It is my hope that we will get to see what this child's gait looks like while under the effects of the botox injections. It may provide some insight into the function of the hamstrings and hip flexors. I am eagerly awating lengthy input from the ESMAC group following their conference. Sincerely ---------------------- Michael Orendurff, MS Clinical Biomechanist Gait Analysis Laboratory Portland Shriners Hospital ------------------------------------------------------------------------ My interpretation is that the double bump is a result of the increased hip and knee flexion during swing phase (necessary for clearance of the plantarflexed ankle) in the presence of hamstring tightness/spasticity causing the posterior element of the curve, double support allows the pelvis to tilt anteriorly again. The spastic gastrocnemius causing the persistent equinus is also acting to flex the knee during stance phase, this action of the 2 joint muscle will be increased if the plantarflexion is blocked with an AFO. Perhaps gasrocnemius should be injected also, this will also help to make orthotic fitting more comfortable. So to an orthotic solution... if an AFO is to manipulate the line of action of the GRF anteriorly to the knee to exert an external extension moment then dynamic knee flexion must be reduced. Botulinum injections to hamstrings may have some effect in this regard, injecting gastronemius as the other main knee flexor would also help as mentioned above. Accomodating a little of the equinus, albeit 3 degrees! (bilaterally to maintain symmetry) will make the orthosis more tolerable without increasing the knee flexing effect of gastroc whilst facilitating correction of the foot deformities and preventing the midfoot break. The shank of the resulting plantarflexed AFO can be tilted into the vertical position using heel raising either attached to the orthosis or by tuning with footwear. Note that 5 degrees of plantarflexion is desirable for effective anterior GRF orthoses, although I can't recall the reference. Let us also remember that the Anterior GRO, Saltiel design was developed for Spina Bifida and Polio patients without knee contractures and more importantly without spastic knee flexors.... a popliteal angle of lees than 30 degrees is ideal. Further to the request for designs of AGRO's I currenly use 3: * Saltiel, one piece proximal entry. * Anterior shell, posterior entry (GROPE !) * Two piece, anterior entry as standard AFO, with polyprop front shell extending from mid tibia to patella tendon. Rigidity can be achieved using the correct thickness of material, incorporating corrugations, bevels or carbon fibre inserts into the design maintains a lightweight finished orthosis. Back to our patient, I would prescribe the 2 piece AGRO as this would provide more foot and ankle control and be easier than the alternatives to put on and take off. Cast in slight equinus as discussed above. The remaining question is where to finsh the distal trim line of the orthosis.... I would suggest that the AFO extends to under and slightly distal to the toe ends to provide the longest lever arm preventing plantarflexion. More critical is where to finish the medial and lateral walls, extending these distal to the MTP joints will block dorsiflexion at the MTP joints... all three rockers of stance phase removed... how will he move? If the trimline remains proximal to the MTP joint then the orthosis will permit some restricted movement due to the flexibility of the plastic. If the AFO is too rigid then the child either falls backwards or flexes his hips excessively in order to achieve forward momentum by shifting his CofG sufficiently anteriorly to allow the heel to rise. The exact desirable rigidity/ flexibility of AFO for optimal gait remains to be established except by trial and error tuning on individual patients. Chris Morris Senior Orthotist NUFFIELD ORTHOPAEDIC CENTRE, OXFORD UK. ------------------------------------------------------------------------ The message that Mr. Morris sent has several answers to my question. I have additional questions about his analysis. My interpretation is that the double bump is a result of the increased hip and knee flexion during swing phase (necessary for clearance of the plantar flexed ankle) in the presence of hamstring tightness/ spasticity causing the posterior element of the curve, double support allows the pelvis to tilt anteriorly again. I think that the first bump comes from the activity of the other leg and second bump from the ipsilateral leg. I interpret the words causing the posterior element of the curve, as similar idea. Am I right? But if the second bump is a result of the increased hip and knee flexion during swing phase, why does the bump reach the peak just after ipsilateral toe off when the hip and knee are in rather extended position? The spastic gastrocnemius causing the persistent equinus is also acting to flex the knee during stance phase, this action of the 2 joint muscle will be increased if the plantarflexion is blocked with an AFO made in a plantargrade position. Perhaps gasrocnemius should be injected also, this may help to make orthotic fitting more comfortable. I do agree that the AFO will increase the Gastroc's 2 joint action and we should inject it. I do not think that the increased gastroc action would flex the knee in stance phase. It will flex the knee in swing, preswing, loading phase but not during the single limb support. In mid and terminal stance phase, a "significant" load (his weight, more exactly ground reaction force) is applied on the distal end of kinetic chain, so, the gastroc may extend the knee. This kind of idea has been discussed by Dr. Kirtley. If I do not understand it correctly, please let me know. The remaining question is where to finsh the distal trim line of theorthosis.... I would suggest that the AFO extends to under and slightly distal to the toe ends to provide the longest lever arm preventing plantarflexion. More critical is where to finish the medial and lateral walls, extending these distal to the MTP joints will block dorsiflexion at the MTP joints... all three rockers of stance phase removed... how will he move? If the trimline remains proximal to the MTP joint then the orthosis will permit some restricted movement due to the flexibility of the plastic. I also extend the distal trim line to just distal end of toes to avoid focal pressure on plantar surface of MTP joints, which may increase the flexor tone(spasticity) of the limb. I found another reason for the trim line from the above words. Thanks! Thank you Mr. Morris for your sincere answers. Hope to hear from you and the members. Sun G. Chung M.D., Ph.D. Dept Rehab Med Seoul National University College of Medicine Chong Ro Ku YeonGeon Dong Seoul South Korea (TEL)82-2-760-2619 (FAX)82-2-743-7473 ------------------------------------------------------------------------ Feedback from the ESMAC conference. Again discussion of the case veered away from the questions posed towards the suggestions of possible intervention. Speaker A thought the major problems were weakness and spasticity. There is symmetrical involvement of the rectus and hamstrings. The apparent internal rotation may well be a consequence of pelvic rotation. In his centre the subject would be referred to a specialist spasticity evaluation clinic. In the long term, when the subject no longer responded to Botulinum toxin then surgery will be required. Speaker B agreed with particular emphasis on the weakness in the calf muscles. Speaker C recommended Rectus femoris transfers, hamstrings lengthening and femoral derotations. Speaker B would like to see the effect of Botulinum toxin in the hamstrings as a test. He thought it was too early for surgery. He recommended an AFO to prevent foot deformity. Speaker D was worried about the use of rectus femoris transfer in subjects with crouch gait as this weakens the knee extensors. Speaker A thought that the vasti are primarily responsible for support during stance and that the loss of the rectus is not a significant issue. He would assess the anteversion in theatre and de-rotate if this was greater than 45-50 degrees. He would transfer the rectus femoris, fix the pes valgus, and lengthen the gastrocnemius and hamstrings bilaterally. Speaker E commented on the coronal plane and the problem of the apposition of the knees. Speaker F wanted to check on the fixed and dynamic part of the problem and saw a requirement for orthotics with any Botulinum toxin. Speaker B reiterated concerns over weakening the triceps surae. Speakers included Ros Boyd, Reinhold Brunner, Aidan Cosgrove, Jim Gage, Kerr Graham, Tim O'Brien and John Paul. The above account is based on notes I took during the discussion which may well contain misunderstandings and errors which are mine and not those of the speakers. Richard Baker Gait Analysis Service Manager Musgrave Park Hospital Stockman's Lane BELFAST BT9 7JB Tel: 01232 669501 ext 2155 Fax: 01223 683816 ------------------------------------------------------------------------ Back to Case 13-08-98[Image]