Selective motor control in spastic cerebral palsy

settings; however, they report a high percentage (26%)
of children in this cohort later diagnosed with autism
spectrum disorder by a specialized autism clinic. This may
not be representative of other GDD cohorts and, as
pointed out by the authors, may have accounted for some
of the variability in the cognitive abilities of this sample.
It may have been beneficial to evaluate this group sepa-
rately.
It is important to note that this study by Riou et al. does
indeed challenge the prevalent hypothesis that all children
with GDD have a cognitive impairment. As noted in this
study, there are at least two subsets of children with GDD,
those with and those without cognitive impairment. This
has important diagnostic, therapeutic, and prognostic
implications for the clinical setting.
REFERENCES
1. Shevell M. Global developmental delay and
mental retardation or intellectual disability:
conceptualization, evaluation, and etiology.
Pediat Clin North Am 2008; 55: 1071–84.
2. Shevell M, Ashwal S, Donley D, et al. Prac-
tice parameter: Evaluation of the child with
global developmental delay. Neurology
2003; 60: 367–80.
3. Riou EM, Ghosh S, Francoeur E, Shevell
MI. Global developmental delay and its rela-
tionship to cognitive skills. Dev Med Child
Neurol 2009; 51: 600–06.
4. Andersson L. Determining the adequacy of
tests of children’s language. Communication
Disorders Quarterly 2005; 26: 207–25.Selective motor control in spastic cerebral palsyJESSICA ROSE PHD
Department of Orthopaedic Surgery, Stanford University School of Medicine;
Motion & Gait Analysis Lab, Lucile Packard Children's Hospital, Stanford, CA,
USA.
See related article5
Gait disorders in children with spastic cerebral palsy (CP)
arise from a set of interrelated motor deficits that include
muscle weakness, spasticity, shortened muscle-tendon
length, and loss of selective motor control.1
These motor
deficits present together with varying degrees of severity in
children with spastic CP, suggesting common neural cor-
relates in the motor tracts of periventricular white matter.2
Sensorimotor and balance impairments also limit mobility
in children with spastic CP, but are thought to have sepa-
rate neural correlates in subcortical nuclei and the cerebel-
lum.3
Clinical manifestations of these motor deficits and
their impact on gait can be challenging to delineate. How-
ever, understanding their etiology can clarify their role in
limiting motor performance and may lead to more effective
treatment. Establishing precise definitions of motor deficits
and developing valid and reliable assessment measures are
essential first steps.
Consensus on definitions of pediatric motor disorders
have recently been published for terms such as weakness,
spasticity, and loss of selective motor control in children
with CP.4
However, to date there are few valid and reliable
clinical measures of these deficits. The study by Fowler
et al. in this issue of DMCN describes a promising new tool
for assessment of loss of selective motor control.5
The
Selective Control Assessment of the Lower Extremity
(SCALE) offers a graded assessment of severity of loss of
selective motor control that is needed to provide more
precise clinical evaluation and to facilitate research that
examines neural correlates, etiology, functional impacts,
and treatment outcome.
Knowledge regarding the etiology of motor deficits in
children with spastic CP is gradually emerging. Muscle
weakness in spastic CP is associated with reduced motor
drive, as evidenced by markedly reduced maximal neuro-
muscular activation6
and related muscle fiber abnormalities
of type-1 fiber predominance, fiber size variability, and
fatty replacement.2
Recently, spastic muscle was also found
to be composed of short and stiff muscle fibers.7
In chil-
dren with spastic CP, shortened muscle-tendon length
may be a consequence of growth rate discrepancies
between muscle and bone, where the slow growth rate of
spastic muscle fails to keep pace with more rapid skeletal
growth, leading to joint contracture. Shortened muscle-
tendon length also exacerbates the effect of muscle spastic-
ity, the velocity-dependent increased sensitivity to stretch,
further contributing to joint contracture and constraints
on mobility. Adding to these biomechanical limitations
there is a loss of selective motor control, which can be
defined as an obligatory coactivation of synergist muscles.8
This imposes abnormal movement during gait that is dom-
inated by synergist muscle activation.
The etiology of loss of selective motor control is not
well understood but may be multifaceted. Several possi-
ble mechanisms have been discussed, such as the release
of primitive flexor and extensor patterns generated from
brain stem regions in the absence of normal inhibitory
578 Developmental Medicine & Child Neurology 2009, 51; 575–579
control or, alternatively, arising from a loss of descending
inhibition to synergists, or a loss of descending excitation
which fails to activate inhibitor...