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BioMed Research International
Volume 2015 (2015), Article ID 317047, 10 pages
Review Article

Spasticity and Its Contribution to Hypertonia in Cerebral Palsy

1KU Leuven Department of Rehabilitation Sciences, 3000 Leuven, Belgium
2Clinical Motion Analysis Laboratory, University Hospital Leuven, 3212 Pellenberg, Belgium
3KU Leuven Department of Development and Regeneration, 3000 Leuven, Belgium
4Department of Orthopedics, University Hospital Leuven, 3212 Pellenberg, Belgium
5KU Leuven Department of Mechanical Engineering, 3000 Leuven, Belgium
6KU Leuven Department of Neurosciences, 3000 Leuven, Belgium
7Department of Neurosurgery, University Hospital Leuven, 3000 Leuven, Belgium

Received 20 June 2014; Accepted 15 December 2014

Academic Editor: Derek G. Kamper

Copyright © 2015 Lynn Bar-On et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Spasticity is considered an important neural contributor to muscle hypertonia in children with cerebral palsy (CP). It is most often treated with antispasticity medication, such as Botulinum Toxin-A. However, treatment response is highly variable. Part of this variability may be due to the inability of clinical tests to differentiate between the neural (e.g., spasticity) and nonneural (e.g., soft tissue properties) contributions to hypertonia, leading to the terms “spasticity” and “hypertonia” often being used interchangeably. Recent advancements in instrumented spasticity assessments offer objective measurement methods for distinction and quantification of hypertonia components. These methods can be applied in clinical settings and their results used to fine-tune and improve treatment. We reviewed current advancements and new insights with respect to quantifying spasticity and its contribution to muscle hypertonia in children with CP. First, we revisit what is known about spasticity in children with CP, including the various definitions and its pathophysiology. Second, we summarize the state of the art on instrumented spasticity assessment in CP and review the parameters developed to quantify the neural and nonneural components of hypertonia. Lastly, the impact these quantitative parameters have on clinical decision-making is considered and recommendations for future clinical and research investigations are discussed.