Photonic evaluation of hypertonic muscles in patients with post-stroke spasticity.
Muscle hypertonia may have an extrinsic component resulting from altered neural mechanisms acting on muscles, and an intrinsic component that refers to changes in the soft tissues composing muscles, tendons and joints. These components often coexist in the same patient, making it necessary to enable distinct interventions directed at the underlying impairments. While the quantification of extrinsic hypertonia is best performed by clinical neurophysiology, that of intrinsic hypertonia requires a wide range of skills ranging from biomechanics to US- or RM-based techniques. Having a reliable indicator of the overall state of the hypertonic muscle that complements both neural and not-neural components would certainly help in planning, performing and monitoring specific patient's treatment.
Recently, we set up a photonic-based, easy-to-apply, bed-side procedure able to provide a surrogate marker of the current biological state of the living muscle. A small-sized, portable, spectrophotometer is used to collect reflectance spectra from muscles in the near infrared region that are subjected to chemiometric analysis. In healthy subjects, this procedure distinguished upper limb flexors from extensors, and was sensitive to anthropometric variables (sex, age, and body mass index).
In this research project we will apply reflectance spectroscopy to patients with post-stroke spasticity and hypertonia who undergo periodical botulinum toxin treatment. We will acquire spectra in the visible short-wave infrared regions from the upper limb flexors and extensors before, one-, and three- months after the injection of incobotulinumA in the biceps muscle. Spectra off-line analysis will include PCA aimed to spectral grouping, PLS-DA for implementing discrimination/prediction models, correlation with clinical data. We aim to see whether photonic evaluation distinguish normal from affected muscles, affected from unaffected muscles in patients, muscle changes induced by chemo-denervation.