Quantitative assessment of Muscle stiffness using Tensiomyography before and after Injection of Botulinum toxin Type A in Patients after Stroke

Muscle spasticity after stroke causes pain and decrease of activities of daily living (ADL), and is one of the causes of decreasing Quality of life (QOL) and social participation of the patients. Botulinum toxin is a neurotoxin produced by Clostridium botulinum, and type A is the most stable and toxic [1]. In 1977, Scott [2] first applied botulinum toxin type A (BTA) clinically for strabismus, and was also used for the treatment of blepharospasm, hemifacial spasm, and spastic torticollis. In recent years, BTA has become widely applied as a treatment for muscle spasticity after stroke, and there have been many reports that said BTA treatment is a safe and effective treatment [3-5]. BTA cleaves the SNAP25 protein involved in the release of acetylcholine within nerve endings at the neuromuscular junction. Thereby, the release of acetylcholine is suppressed, and the neuromuscular transmission is suppressed to obtain muscular relaxation. Neurons in which neuromuscular transmission has been inhibited are reopened several months later due to the formation of a nerve branch from the axonal side, and the muscular relaxation disappears [6]. The effect of BTA treatment on muscle spasticity is generally assessed using the modified Ashworth scale (MAS). However, the evaluation by MAS is less objective and has differences among the examiners, and MAS is not highly reliable [7-9]. Therefore, there have been few objective outcome measures regarding the effect of BTA treatment, and the optimal dose, duration of the effect, and the interval of re-administration of BTA have not been clarified.