Case of the Week 12/5/2005: What people said...

Hello Folks -

                 Before we ask too many questions about Botox effectiveness for this fellow, please red up on the newest research about Botox and
                 contracture and spasticity recurrence.

               Kay RM, Rethlefsen SA, Fern-Buneo A, Wren TA, Skaggs DL.  Botulinum toxin as an adjunct to serial casting treatment in children with cerebral palsy. J Bone Joint Surg Am. 2004 Nov;86-A(11):2377-84

                 The authors compare long-term effects of serial casting compared with serial casting after Botox injection. Their results suggest that Botox
                 accelerates the pathologoc soft tissue transformation process and increases spasticity (i.e. hyperactive stretch reflex). The mechanism appears
                 to be sprouting and proliferation of the peripheral nerves at the injection site.

                 Regards -

               Billi Cusick, PT, MS


The data of this study do not “suggest that Botox accelerates the pathologoc soft tissue transformation process and increases spasticity (i.e.
                 hyperactive stretch reflex)”. Figure 4 clear shows a reduction in spasticity from baseline in both groups at 12 months, the reduction is still
                 statistically significant in the casting group but not in the casting plus injection group. The data thus suggests that the combination of Botox and
                 casting has had little effect on spasticity at the twelve months after injection. From the point of view of the injections, which are known only to last
                 for a period of months, this is exactly what might be expected. Casting on its own, however, works. Applying a mechanical stretch to the muscle
                 increases passive length and reduces Ashworth scores.

                 So the conclusion of this study is not that injections make things worse (casting + injections seem to have had little effect on the patient at 12
                 months) but that they reduce the efficacy of the casting. This might actually be expected. If casting works by applying a stretch against the resting
                 tension in the muscle then anything that reduces that resting tension is likely to reduce the efficacy of casting. This is borne out by the trend in the
                 data showing that reduction in passive range is greater in the injection group at 3 months, while the toxin is still active. I’d suggest that the simplest
                 explanation of these data is that by relaxing the gastroc while casting is applied you reduce the efficacy of casting to reduce fixed contractures.

                 Biomechanically it might be anticipated that injections, by blocking neurotransmission, will have an effect on the dynamic component of muscle
                 shortness and that casting, by applying a mechanical stretch, will have an effect on fixed contractures. This is indeed now borne out by the data of
                 Corry and Flett for dynamic contractures and this study for fixed contractures.

                 Richard
 

                 PS has anyone noticed that despite the changes in passive length, Ashworth scores and gait data, the group with injections + casting showed
                 nearly twice the improvement in GMFM (admittedly not statistically significant) despite, as a group, having a score that was already 10% higher at
                 baseline.
 

               Richard Baker
                 Gait Analysis Service Manager
                 Hugh Williamson Gait Laboratory
                 Royal Children's Hospital
                 Parkville, Victoria 3052, Australia
                 Tel: +613 9345 5354, Fax: +613 9345 5447


Richard,

                 Just a note to say that the authors did not find a significant difference between the groups at any time point for passive dorsiflexion, dorsiflexion in
                 swing and dorsiflexion in stance.

                 It is interesting to note the reduction in the Ashworth score. We are scrabbling around in the dark here to understand a pathopysiological argument
                 that explains how Botox or Casting reduces spasticity (Botox for diminishing hyperreflexia, maybe). More likely they reduce the observed effects of
                spasticity by weakening the muscles. The only mild surprise is that casting appears to weaken the muscle more than botox + casting!
                 And another thing Rich, if the Botox (and not the casting) was affecting the dynamic component of muscle shortness then why do we see similar
                 results at 3 mo for dorsiflexion in stance and swing, and for the Ashworth scale?

                 Seriously though, we can speculate all we like about how a muscle changes in response to casting and botox in electrophysiological and
                 biomechanical terms, and its quite good fun, but we just don't know. For joined-up thinking, we need knowledge of all the levels of a child's problem
                 from the pathophysiological origins to impairment to disability to handicap. If you don't understand the relationship between pathophysiology and
                 impairment you're  left with a one size fits all approach to intervention in a heterogenous group (it's interesting to note the variability in this study).
                 We need to do the studies.

               Anne McNee & Adam Shortland
                 One Small Step Gait Laboratory


Dear CGA subscriber,

                 I would like to do 2 comments about the 'Case of the Week':

                 a. the graphs of normal gait have important deviations in knee valgus/varus and hip
                 rotation. This subject was discussed (positioning of the kad in the Vicon/VCM system), and
                 perhaps exist reference in the CGA web site.

                 b. about 2d gait analysis: if some gait laboratory wants to donate its 3d equipments, old
                 systems, used, with few cameras..., I accept!

                 Thank you for your attention.
                 Best regards.

               Wagner de Godoy
                 Brazil


Dear all,

                        I am in accordance with Wagner the graphs of normal gait are inadequate. If
                        Chris want, I can send data of the normal Brazilians gait who had been
                        presented in congress ESMAC 2003.

                        On the graphs 2D and 3D I believe that Mark had luck in finding similar
                        values. The possibilities of error in the 2D video capture is very great e
                        is very easy to have error of parallaxia.
                        Best Regard

                      Paulo Lucareli


Dear all,

Thanks for the comments so far on this case.

It's always interesting to me what people pick up on when discussing these cases. As far as the normative data is concerned - particularly the knee varus/valgus artefact, I think it's worth pointing out that Mark's peak valgus artefact was only 16 degrees. I wonder what people think the maximum permissible value should be?

Now, to address Mark's suggested questions:

- a good question. Jump knee was described because it looks as if the person is about to jump off a diving board. But really it is simply a consequence of the knee being flexed at contact. It then extends as the limb is loaded. I would venture that this is as a result of the plantarflexor-knee extensor couple, so I would conclude that it originates from the ankle. Am I correct?
  - Recurvatum is, of course, the natural consequence of an overactive plantarflexor-knee extensor couple: either pathological (overactive plantarflexors, over-dependence on the GRF in stabilising the knee) or iatrogenic (secondary to a floor reaction orthosis). I don't see how Botox per se would worsen recurvatum - am I missing something?
  - Good question! I guess it depends whether cosmesis or efficiency is the bottom line, which is not always obvious. I think for someone walking at 0.1 m/s, cosmesis is the least of their worries, whereas to someone walking at 1.2 m/s it may be their (or their parents') highest priority.
  - A messy one! In my view it really relates to loading: has weight shifted to the contralateral limb? If it has then the dragging limb must be deemed to be in swing phase.
  - First I think Mark should be commended for his most impressive videos. I especially liked the one in which the left leg has been computorily disarticulated from the rest of the patient: /archives/12-5-05/Videos/LeftStromotion/LeftStromotion.swf in case you haven't checked it out! I personally think we can still learn a lot from 2D, and the combination of 2D video with 3D has great potential (maybe this is one reason for the recent merger between Peak Performance and Vicon Motion Systems!). Mark only compares the temporospatial parameters - I see no reason why 3D should have any advantages over 2D for these. Moreover, his superimposition of the barefoot and treated videos nicely demonstrates any improvement or deterioration. It would be interesting to know how easily such videos are made. I think lately the output of motion analysis has become rather staid and boring, as everyone uses whatever the manufacturers' provide in their software - it's nice to see some new approaches.

Chris
--
Dr. Chris Kirtley MD PhD
Associate Professor
Dept. of Biomedical Engineering
Catholic University of America
Washington DC 20064
From May 9-June 20 2005 I am at STAPS, University of Reims, France


Hi All

A brief note to Anne's response

I have done hundreds of r-wrap AFOs and Flexcasts to improve and maintain ROM in "spasticity" patients.

It is my feeling that because the voluntary muscles are weak underneath the spasticity, casting helps.

Serial casts will not work when there is pain, so what does work is control with comfort. It is controlling the involuntary muscles motions comfortably
that improves the ROM, not stretching. An unusual thing, serial cast or flexcast only works well or 100% the first time, but if they lose ROM again
then after that you will never get full ROM. (by serial cast)

The dynamic synergy foot does better than the constant tone high R2 foot.

Just my two cents
 

John Russell
Collier Rehab Sys.


Dear Dr. Kirtley,

I will try to comment on the valgus/varus (my old friend) - after all, I went the 'insane' that mentioned this subject.
 

1. my comment was restricted to the reference data (normal graphs) - a motion range of 20
degrees (-4 to 16) is a flaw in normal samples - Dr. Paulo Selber commented valgus/varus
and hip rotation fails when the normal sample was sent for CGA (Dr. Richard Baker
indicated this fact in that time).

2. in pathologic exams, I don't know which is the acceptable varus/valgus, but I believe
that the best solution is a redundancy of methods: KAD, minimum range variation of
varus/valgus (Dr. R. Baker), "pure" cinematic analysis (Dr. Michael Schwartz - Gillette
Childrens), complementary graphs (hip/rotation absolute angle, in relation to the sagittal
plane of the laboratory).

We used a method similar to the Dr. Baker, and, in this case, I would try to minimize the
valgus/varus range, that would probably increase the hip rotation (> external rotation) on
both sides (perhaps exist part of the knee flexion in the valgus/varus, because this
curves  oscillates synchronized with the knee flexion).

3. on clinical subjects I am an illiterate.
 

Thank you again for your attention.
Best regards from Brazil,

Wagner de Godoy
Brazil


Hi there!
                 Have I missed something or are the ankle dorsiflexion(DF) angles largely overestimated? Looking at
                 the barefoot kinematics in sagittal plane it seems impossible that L ankle during midstance is in
                 15 degrees of DF while the knee is hyperextended . Although there is no kinetic data it can
                 clearly be seen from the video that there is forefoot loading and not heel walk during stance! Following
                 the dicussion concerning jump knee pattern and talking about PF-KE couple I guess it is implicated
                 that there is an error in marker placement which has not been edited in the software?!

                 Is the improvement afforded by the AFOs worth a reduction in velocity?
                 In general, AFO's are rarely used for cosmetic reasons. It is important to stay focused on what
                 you want to achieve by using an orthosis and to evaluate whether the means you have to measure the
                 outcome of orthotic treatment are appropriate. If the objective f.ex. is to stabilize the ankle,
                 subtalar and/or midtarsal joints in the frontal plane it may be very difficult to measure the effect
                 of an orthosis by way of 3D gait analysis using simplified foot models. However, it doesn't mean
                 that the orthosis is not working!

                 In this weeks case, the AFO's seem to have an effect at both knees in sagittal plane;
                 -Left knee is less hyperextended during stance. Theoretically this should be due to AFO providing
                 PF stop and ankle in neutral to dorsiflexed position, heel height in shoes included.
                 -Right knee achieves better extension during stance. This again should be due to DF
                 stop/restriction in the AFO and GRAFO effect at the knee. Once again I'm suspicious about those ankle joint
                 angles...
                 In addition there is better extension in R hip. The patient looks relaxed and it seems to me as if
                 the moments acting at hip, knee and ankle joints are better balanced by the use of AFO's. Yes,I
                 would accept a slight reduction in gait velocity.

                 Does the jump knee pattern originate from the knee joint or the ankle joint?
                 -Concerning R knee; it probably originates from the ankle as it is difficult to achieve knee
                 extension with AFO's in the presence of Hamstrings spasticity/tightness.

                 Regards,
                 Ingrid Skaaret
                 CPO
                 Oslo Movement Lab,
                 Dept. child neurology, Rikshospitalet
                 Oslo, Norway

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