Abstract
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.
Highlights
Muscle tone regulation helps to maintain normal posture and to facilitate movement [1]
There are many uncertainties regarding the contribution of spasticity to hypertonia and, in particular, its contribution to the gait abnormalities seen in cerebral palsy (CP)
We summarize the state of the art on instrumented spasticity assessment in this population and review the parameters developed to quantify its contribution to muscle hypertonia
Summary
Muscle tone regulation helps to maintain normal posture and to facilitate movement [1]. Spasticity is manifested by increased stretch reflex which is intensified with movement velocity [3] This results in excessive and inappropriate muscle activation which can contribute to muscle hypertonia. Hypertonia is assessed as the “resistance to passive stretch while the patient maintains a relaxed state of muscle activity” [5]. Different stretch velocities can be incorporated and the increase in stretch reflex due to velocity is thereby subjectively evaluated. In reality, this clinical interpretation oversimplifies the fundamental physiological mechanisms of spasticity. Nonneural mechanical muscle properties such as stiffness and viscosity are often altered in children with CP [7] and can contribute to the feeling of increased resistance to passive motion (Figure 1). We consider the impact of quantification of these parameters on clinical decision-making and discuss recommendations for future clinical and research investigations
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