Neurophysiologie clinique = Clinical neurophysiology · 2026
Neurophysiological mechanisms of extracorporeal shock wave therapy in post-stroke spasticity.
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Caronni Antonio, Brevi Elena, Scarano Stefano, Lamonica Antonella, Perucca Laura, Malfitano Calogero
Аннотация
OBJECTIVES: Focal extracorporeal shock wave therapy (ESWT) reduces post-stroke spasticity, yet its mechanisms, whether neural (modulation of spinal excitability) or peripheral (rheological changes), remain debated. This study aims to investigate the neurophysiological effects of ESWT on upper-limb spasticity using a within-subject, controlled design.
METHODS: Twelve chronic stroke patients underwent a protocol of three weekly ESWT sessions. The treatment targeted the spastic muscles of the upper limb, including the Flexor Carpi Radialis (FCR). Clinical (Modified Ashworth Scale (MAS); Functional Assessment Test for Upper Limb (FAST-UL)), ultrasonographic and neurophysiological assessments were performed at baseline, during the first and third treatment sessions, and at 1- and 3-month follow-ups. Key neurophysiological outcomes were the H-reflex/M-wave ratio (Hmax/Mmax) and Post-activation Depression (PoD) of the FCR. Both the affected and unaffected upper limbs were evaluated. Data were analysed using Bayesian linear mixed-effects models.
RESULTS: Clinical outcomes showed credible improvements: MAS scores decreased, and upper-limb dexterity (FAST-UL) increased after treatment compared with baseline. Conversely, neurophysiological analysis revealed no credible modulation in spinal excitability. The 95% Credible Intervals for changes in Hmax/Mmax and PoD in the treated limb excluded any clinically relevant effect, falling entirely within the range of spontaneous fluctuations observed in the unaffected limb.
CONCLUSION: Clinical hypertonia improved after ESWT without inducing detectable changes in the excitability of the spinal phasic stretch reflex. The observed dissociation between clinical improvement and stable neurophysiology suggests that ESWT acts primarily via peripheral rheological mechanisms rather than by modulating the spinal circuitry, whose dysfunction underlies the pathophysiology of spasticity.
METHODS: Twelve chronic stroke patients underwent a protocol of three weekly ESWT sessions. The treatment targeted the spastic muscles of the upper limb, including the Flexor Carpi Radialis (FCR). Clinical (Modified Ashworth Scale (MAS); Functional Assessment Test for Upper Limb (FAST-UL)), ultrasonographic and neurophysiological assessments were performed at baseline, during the first and third treatment sessions, and at 1- and 3-month follow-ups. Key neurophysiological outcomes were the H-reflex/M-wave ratio (Hmax/Mmax) and Post-activation Depression (PoD) of the FCR. Both the affected and unaffected upper limbs were evaluated. Data were analysed using Bayesian linear mixed-effects models.
RESULTS: Clinical outcomes showed credible improvements: MAS scores decreased, and upper-limb dexterity (FAST-UL) increased after treatment compared with baseline. Conversely, neurophysiological analysis revealed no credible modulation in spinal excitability. The 95% Credible Intervals for changes in Hmax/Mmax and PoD in the treated limb excluded any clinically relevant effect, falling entirely within the range of spontaneous fluctuations observed in the unaffected limb.
CONCLUSION: Clinical hypertonia improved after ESWT without inducing detectable changes in the excitability of the spinal phasic stretch reflex. The observed dissociation between clinical improvement and stable neurophysiology suggests that ESWT acts primarily via peripheral rheological mechanisms rather than by modulating the spinal circuitry, whose dysfunction underlies the pathophysiology of spasticity.