Spasticity in children with cerebral palsy: what are we treating?
Evelina London Children’s Hospital, London, UK.
This commentary is on the original article by Willerslev-Olsen et al. on
pages 672–679 of this issue.
Spasticity is a central concept in the management of chil-
dren with cerebral palsy (CP) but the term can be difﬁcult
to deﬁne. A systematic review of interventions for children
concluded that botulinum toxin and selective
dorsal rhizotomy were effective in reducing muscle spastic-
ity, but did not provide a deﬁnition of spasticity. The term
spasticity is frequently used without deﬁnition, suggesting
an agreed deﬁnition shared by clinicians, but the evidence
for this is limited.
It has recently been suggested that
spasticity is too restrictive a concept to be functionally rel-
evant and may be distracting us from a deeper understand-
ing of motor control.
Our current clinical model would seem to suggest that
spasticity is both a clinical sign and a form of patho-
physiological entity in the muscles of children with CP
which limits muscle excursion and results in impaired
muscle growth and function. As a result, interventions
which reduce sensory input from a limb or cause muscle
denervation are recommended to improve muscle growth
and function. Spasticity appears to be viewed as an entity
in itself rather than as a concept which we use as part
of our clinical model, although it strictly exists in the
mind of the examiner rather than in the limbs of the
How then can we be sure that we are treating the child
rather than our clinical model? The most effective way
may be to appreciate that we use a model to deal with a
complex phenomenon, and then assess the robustness of
this model and the implications for intervention. The
paper by Willerslev-Olsen et al.
builds on previous
investigations by this group on muscle characteristics in
children with CP to help us to consider the clinical
model we use. Typically developing children and children
with CP between birth and the age of 4 years had mea-
surements of medial gastrocnemius muscle volume and
triceps surae stiffness, with electromyographic recording
to assess muscle activity. The authors noticed an early
difference in muscle volume between both groups which
preceded a difference in passive stiffness. They noted that
a reﬂex response to stretch, which would have been seen
if the underlying muscle stiffness was related to active
muscle contraction rather to than an alteration in the pas-
sive qualities of the muscle, was seen in only a small
number of children with CP. There are some limitations
to the study: muscle volume was not normalized to body
mass, and because of the difﬁculties in data collection in
very young children, not all children had both ultrasound
and stiffness data collected. The paper does however raise
a signiﬁcant question about our existing clinical model. If
increased passive stiffness in the absence of muscle activ-
ity is an early and intrinsic feature of muscles in children
with CP, what do we mean when we say we are treating
argued that the conﬁdence individuals have
in their beliefs depends mostly on the quality of the story
the beliefs tell, and that the amount and quality of the data
on which the story is based is largely irrelevant. The chal-
lenge that we face as clinicians working with children with
CP and their families is to develop a clinical model that is
useful and valid. Any model we construct will be a simpliﬁ-
cation of a complex reality, but this does not mean that
our clinical model cannot develop and improve over time,
with resulting functional beneﬁts for children with CP.
The study by Willerslev-Olsen et al.
is an important step
in this process.
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638 Developmental Medicine & Child Neurology 2018, 60: 636–644