Abstract
Equinovarus/equinus foot is a pattern most commonly treated with botulinum toxin type A in patients with post-stroke spasticity involving the lower limbs; the gastrocnemius is the muscle most frequently injected. Spastic equinovarus/equinus can present a mixture of conditions, including spasticity, muscle/tendon shortening, muscle weakness and imbalance. In this study, we wanted to determine whether botulinum toxin treatment affects the ultrasonographic characteristics of post-stroke spastic equinus. The same dose of AbobotulinumtoxinA was injected into the gastrocnemius medialis and lateralis of 21 chronic stroke patients with spastic equinus. Clinical (Ashworth scale and ankle range of motion) and ultrasound (conventional and sonoelastography) evaluation of the treated leg was carried out before and 4 weeks after injection. No significant effects of botulinum toxin treatment on the ultrasonographic characteristics of spastic equinus were observed. As expected, there were significant improvements in ankle passive dorsiflexion range of motion and calf muscle spasticity at 1 month after treatment. There was a direct association between Achilles tendon elasticity and calf muscle spasticity at baseline evaluation. Larger studies with a long-term timeline of serial evaluations are needed to further investigate the possible effects of botulinum toxin injection on spastic muscle characteristics in patients with post-stroke spasticity.
Highlights
Botulinum toxin type A (BoNT-A) injection is a first-line treatment for post-stroke spasticity (PSS) [1]
We investigated whether BoNT-A treatment affects the ultrasonographic characteristics of post-stroke spastic equinus
We wanted to determine whether botulinum toxin treatment, and the progression of PSS over time, can affect the ultrasonographic characteristics of spastic equinus
Summary
Botulinum toxin type A (BoNT-A) injection is a first-line treatment for post-stroke spasticity (PSS) [1]. Spastic equinovarus/equinus can present with a mix of calf muscle spasticity, tricep surae/Achilles tendon shortening, ankle dorsiflexor weakness and tibialis anterior/peroneus muscle imbalance [3]. This group of conditions may require combined treatment with drugs, physical therapy, orthoses, surgery and other rehabilitation procedures [3,4,5,6]. Increased intramuscular connective tissue and fat content can cause progressive enhancement of muscle echogenicity in post-stroke spastic equinus [7], resulting in gradual loss of response to BoNT-A. Muscle structure changes due to PSS can lead to a progressive decrease in muscle thickness and posterior pennation angle in patients with spastic equinus [7]
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