Electromyography measurements for the assessment of the effect of botulinum toxin-A in spasticity of the wrist

• Autor(a) principal: Baptista, Miguel Mafra
• Data de Publicação: 2023
• Tipo de documento: Dissertação
• Idioma: eng
• Título da fonte: Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos)
• Texto Completo: http://hdl.handle.net/10362/163647
• topic: Spastic paresis; Spasticity; Surface electromyography; Botulinum neurotoxin A; NeuroFlexor; Domínio/Área Científica::Engenharia e Tecnologia::Outras Engenharias e Tecnologias

This study addresses the growing impact of spastic paresis resulting from conditions like stroke, with a focus on wrist spasticity assessment, and treatment using Botulinum neurotoxin A (BoNT). Spasticity, a velocity-dependent increase in muscle tone in response to passive stretching, remains acomplex andinsufficiently understoodchallenge in medical care. While the NeuroFlexor (NF) device offers a means to quantify spasticity, it is proposed that combining electromyography (EMG) with NF data could provide a more comprehensive understanding. The study aims to determine the value of incorporatingEMGalongsideNFfor assessing BoNT’s impact on wrist spasticity. By evaluating EMG’s validity and role in detecting spasticity changes pre- and post-BoNT injection, the study seeks to enhance predictive models for BoNT treatment outcomes, ultimately improving the diagnosis and therapy of wrist spasticity. In this study, patients who had experienced a stroke or had cerebral palsy were included if they were eligible for BoNT injections at the wrist and were able to follow instructions. This study involved 18 patients and three evaluation sessions: before BoNT treatment for spasticity of the wrist joint, and at 6 and 12 weeks after treatment. EMG data was recorded from the flexor carpi radialis (FCR) and extensor carpi radialis (ECR) muscles alongside NF data (neural and non-neural contributors of wrist hyper-resistance to passive movement), and the surface EMG signals were processed and normalised. The EMG outcomes were defined as the short- (M1) and long- (M2) latency responses to passive wrist extension, andwere detected using a threshold method. Clinical scales, such as the modified Ashworth scale and the Tardieu scale, and NF data provided outcome measurements, with the neural force component (NC) being a representative of spasticity. TheM1of the FCR, but not the M2, correlated significantly with theNCof theNF. There were no significant correlations with the clinical scales. There was a significant decrease in M1-related parameters for the FCR after BoNT. EMG parameters correlated strongly with BoNT dose, with higher doses resulting in a larger decrease of EMG parameters. The accuracy, precision and sensitivity were higher for prediction models that included EMG. The construct validity of EMG with respect to the NF was proven as was the effect of BoNT in treating wrist spasticity. The addition of EMG shows an increase in predictive power between responders and non-responders to BoNT. The extra effort in using EMG might not justify the small increase in the goodness of the model.