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Diagnostic Nerve Block to Guide Botulinum Neurotoxin Type A Injection for Clonus in Spastic Equinovarus Foot: A Retrospective Study
Diagnostic Nerve Block to Guide Botulinum Neurotoxin Type A Injection for Clonus in Spastic Equinovarus Foot: A Retrospective Study
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Diagnostic Nerve Block to Guide Botulinum Neurotoxin Type A Injection for Clonus in Spastic Equinovarus Foot: A Retrospective Study
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Diagnostic Nerve Block to Guide Botulinum Neurotoxin Type A Injection for Clonus in Spastic Equinovarus Foot: A Retrospective Study
Diagnostic Nerve Block to Guide Botulinum Neurotoxin Type A Injection for Clonus in Spastic Equinovarus Foot: A Retrospective Study

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Diagnostic Nerve Block to Guide Botulinum Neurotoxin Type A Injection for Clonus in Spastic Equinovarus Foot: A Retrospective Study
Diagnostic Nerve Block to Guide Botulinum Neurotoxin Type A Injection for Clonus in Spastic Equinovarus Foot: A Retrospective Study
Journal Article

Diagnostic Nerve Block to Guide Botulinum Neurotoxin Type A Injection for Clonus in Spastic Equinovarus Foot: A Retrospective Study

2024
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Overview
Clonus is characterized by involuntary, rhythmic, oscillatory muscle contractions, typically triggered by rapid muscle stretching and is frequently associated with spastic equinovarus foot (SEVF), where it may increase risk of falls and cause discomfort, pain, and sleep disorders. We hypothesize that selective diagnostic nerve block (DNB) of the tibial nerve motor branches can help identify which muscle is primarily responsible for clonus in patients with SEVF and provide useful information for botulinum neurotoxin type A (BoNT-A) treatment. This retrospective study explored which calf muscles contributed to clonus in 91 patients with SEFV after stroke (n = 31), multiple sclerosis (n = 21), and cerebral palsy (n = 39), using selective DNB. We found that SEVF-associated clonus was most commonly driven by the soleus muscle, followed by the gastrocnemius lateralis and medialis, tibialis posterior, and flexor digitorum longus, and that frequency differed according to SEVF etiology. Our data suggest that identifying the muscles involved in SEVF-associated clonus may aid clinicians in personalizing BoNT-A treatment to single patients. Also, the findings of this study suggest that applying a ‘stroke model’ to treating spasticity secondary to other etiologies may not always be appropriate.