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.
Billi Cusick, PT, MS
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
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.
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
Gait Analysis Service Manager
Hugh Williamson Gait Laboratory
Royal Children's Hospital
Parkville, Victoria 3052, Australia
Tel: +613 9345 5354, Fax: +613 9345 5447
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
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
One Small Step Gait Laboratory
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
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.
Wagner de Godoy
I am in accordance with Wagner the graphs of normal gait are inadequate.
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.
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:
Dr. Chris Kirtley MD PhD
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
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
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
Collier Rehab Sys.
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
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
-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
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
-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.
Oslo Movement Lab,
Dept. child neurology, Rikshospitalet
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