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In our early clinical experience of evaluating children with cerebral palsy (CP), it became clear that selective motor control (SMC) was an important but unrecognized prognostic factor for responsiveness to a variety of treatment interventions, such as selective posterior rhizotomy. At the time, there was no consensus definition of SMC or a standardized assessment, which led to our development of the Selective Control Assessment of the Lower Extremity (SCALE).[1] Consensus definitions and the development of a range of clinical assessment tools for movement disorders in CP have substantially moved the field forward. Technological advances now enable direct assessment of brain white matter, affording an exciting opportunity to better understand the relationship between movement disorders and specific neuroanatomical correlates. In this regard, the review by Cahill-Rowley and Rose[2] discusses evidence that rubrospinal tracts (RSTs) are responsible for synergistic movement patterns observed in patients following stroke and this may have important implications for patients with CP. The primary focus of the review is ‘obligatory co-activation of synergist muscles’, which is one feature of SMC impairment attributed to corticospinal tract (CST) damage. Other features include lack of movement, isolated movement through partial range, inability to reverse direction, reduced speed, and obligatory involuntary movement at another joint (including mirror movement).

Research has shown that patients with spastic CP have damage to CSTs and ascending sensory tracts, which correlates with impaired sensorimotor function;[3] however, the specific relationship between severity of SMC impairment and white matter tract damage has not been validated. As noted in the review, RSTs are enhanced in both acute and chronic injuries in adults following stroke. The authors of the review suggest that these tracts may be responsible for obligatory synergistic movement observed in spastic CP and could be a type of ‘imperfect compensation.’ This may prove to be true, but there are fundamental differences between injury to the mature and immature neuromuscular systems. If RST function is enhanced in individuals with CP, is this imperfect compensation or is it a form of maladaptive plasticity? Maladaptive plasticity, in the form of ipsilateral CST preservation, has been identified during early development in the presence of a unilateral brain injury.[4] This is associated with mirror movements, another feature of impaired SMC commonly observed in children with CP. It is possible that retention and enhancement of RSTs is another form of undesirable plasticity which preserves synergistic limb function and may interfere with development of selectivity. If so, can intervention improve SMC, especially in young children who have not yet developed a mature CST system?

While the focus of this review is the lower extremity, more has been learned about skilled voluntary motion of the upper extremity in individuals with CP.[3, 5, 6] Advances in technology that are informative for assessing neuromuscular function in the upper extremity are problematic for the lower extremities. Cortical representation of the upper extremity is larger than that of the lower extremity and is accessible for techniques such as transcranial magnetic stimulation. As humans, we perform most functional activities with our upper extremities and there are many ways to practice skilled voluntary movement. We tend to think of the lower limbs as being limited to gross motor activities. Yet, an infant reaches with their feet prior to their hands[7] and a skilled soccer player or a tightrope walker clearly has highly developed voluntary motion in their feet and ankles. While we are not suggesting a ‘circus camp’ for juggling with one's feet, we could do more to stimulate lower extremity SMC in children with spastic CP. Perhaps wearing ankle foot orthoses all day and splinting all night are forms of constraint that prevent more normal development of motor and sensory systems? Lower extremity robotic and video game interventions are novel concepts that are promising. As proposed by Cahill-Rowley and Rose, we hope that an advanced understanding of SMC impairment will lead to innovative and effective treatment strategies.

References

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  2. References
  • 1
    Fowler EG, Staudt LA, Greenberg MB, Oppenheim WL. Selective Control Assessment of the Lower Extremity (SCALE): development, validation, and interrater reliability of a clinical tool for patients with cerebral palsy. Dev Med Child Neurol 2009; 51: 60714.
  • 2
    Cahill-Rowley K, Rose J. Etiology of impaired selective motor control: emerging evidence and its implications for research and treatment in cerebral palsy. Dev Med Child Neurol. DOI: 10.1111/dmcn.12355.
  • 3
    Rose S, Guzzetta A, Pannek K, Boyd R. MRI structural connectivity, disruption of primary sensorimotor pathways, and hand function in cerebral palsy. Brain Connect 2011; 1: 30916.
  • 4
    Eyre JA. Corticospinal tract development and its plasticity after perinatal injury. Neurosci Biobehav Rev 2007; 31: 113649.
  • 5
    Sukal-Moulton T, Krosschell KJ, Gaebler-Spira DJ, Dewald JPA. Motor impairments related to brain injury timing in early hemiparesis. Part II: abnormal upper extremity joint torque synergies. Neurorehabil Neural Repair 2014; 28: 2435.
  • 6
    Kuhnke N, Juenger H, Walther M, Berweck S, Mall B, Staudt M. Do patients with congenital hemiparesis and ipsilateral corticospinal projections respond differently to constraint-induced movement therapy? Dev Med Child Neurol 2008; 50: 898903.
  • 7
    Heathcock JC, Galloway JC. Exploring objects with feet advances movement in infants born preterm: a randomized controlled trial. Phys Ther 2009; 89: 102738.