Treatment of Spastic Forelimb Hypertonia through Cognitive Muscle Reinnervation in Upper Motor Neuron Syndrome in a Rat Model
Olga Politikou, MD1, Silvia Muceli, PhD2, Leopold Harnoncourt, cand. med.1, Udo Maierhofer, MD1, Vlad Tereshenko, MD1, Matthias Luft, MD1, Christopher Festin, MD1, Gregor Laengle, MD1, Konstantin D Bergmeister, MD, PhD3, Dario Farina, PhD4 and Oskar C. Aszmann, MD, PhD5, (1)Medical University of Vienna, Vienna, Austria, (2)Chalmers University of Technology, Gothenburg, Sweden, (3)Department of Surgery/ CD Laboratory for Restoration of Extremity Function, Medical University of Vienna, Vienna, Austria, (4)Imperial College London, London, United Kingdom, (5)CD Laboratory for Restoration of Extremity Function, Division of Plastic and Reconstructive Surgery, Medical University of Vienna, Vienna, Austria
Introduction: Development of limb spasticity is one of the "positive" features of upper motor neuron syndrome (UMNS). A novel approach to reduce spasticity and increase functionality through contralateral C7 nerve root transfer has been recently published. However, the effect of distal nerve transfers on spasticity has never been explored. We established a new animal model to investigate the electrophysiological, molecular-biological and histological outcomes of denervation-cognitive reinnervation of spastic muscles in the rat's forelimb.
Materials-Methods: We perform unilateral pyramidotomy on the brainstem level to create spastic hemiplegia in the rat. In the treatment group, we carry out a transfer of the contralateral ulnar nerve to the pathological ulnar nerve of the spastic side. Final experiments are conducted 12 weeks after spasticity induction. Electrophysiological assessments to the abductor digiti minimi muscle evaluate changes in muscle excitability, while biopsies from spastic and reinnervated muscles are obtained for histological and molecular-biological studies. A naïve group serves as control.
Preliminary results: Spasticity leads to fibrotic changes in muscle and switches the muscle fiber type. Early cognitive reinnervation may protect the muscle against these adverse events and reverse the pathological muscle hyperexcitability.
Conclusions: This animal model introduces a novel surgical treatment of UMNS spasticity encompassing the concept of cognitive nerve transfers. This study will broaden our understanding of spasticity pathophysiology in UMNS and help us to better predict, prevent and treat this disabling stroke sequela.
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