Inhibitory kinesiotaping has no effect on post-stroke spasticity: Prospective, randomised, controlled study.

OBJECTIVE: Motor neuron pool activity is high in spasticity. The effect of inhibitory kinesiotaping (KT) on spasticity is unclear. The aim of this study is to investigate the effect of inhibitory KT on spasticity after stroke. METHODS: Fifty stroke patients with ankle plantarflexor spasticity were randomised to intervention (27) and control (23) groups. Inhibitory KT was applied to the triceps surae muscle in the intervention group and sham KT to the Achilles tendon in the control group. Inhibitory and sham KT were applied for 72 h with a combined conventional rehabilitation programme. Spasticity was assessed at baseline and 72 h after KT using three instruments: Modified Ashworth Scale (MAS), Homosynaptic Post-Activation Depression (HPAD) reflecting the level of motor neuron pool activity, and joint torque as a measure of resistance to passive ankle dorsiflexion. RESULTS: The baseline MAS score, HPAD levels and dorsiflexion torque of the two groups were not significantly different. The change in MAS score was -3.7 ± 17.5 (p = 0.180) in the intervention group and 3.6 ± 33.3 (p = 0.655) in the control group. The change in dorsiflexion torque was -0.3 ± 16.1 kg m (p = 0.539) in the intervention group and 8.0 ± 24.1 kg m (p = 0.167) in the control group. The change in mean HPAD was 8.7 ± 34.7 (p = 0.911) in the intervention group and 10.1 ± 41.6 (p = 0.609) in the control group. CONCLUSIONS: The present study showed that inhibitory KT has no antispastic effect in stroke patients.

The effect of whole-body vibration on spasticity in post-stroke hemiplegia: A prospective, randomized-controlled study.

Objectives: This study aims to investigate whether whole-body vibration (WBV) has an anti-spastic effect on the ankle plantar flexors. Patients and methods: This single-blind, prospective, randomized-controlled clinical study included a total of 48 patients with chronic stroke (33 males, 15 females; mean age: 60.7±10.9 years; range, 25 to 80 years) between May 2019 and February 2020. They were randomized into two groups: WBV group (n=24) and sham WBV group (n=24). A training program of 12 sessions (three days a week for four weeks) was applied regularly in both groups. The spasticity degree of the plantar flexors was evaluated by using both a subjective assessment method (modified Ashworth scale [MAS]) and several objective assessment methods (Hmax/Mmax, homosynaptic post-activation depression [HPAD], and torque) before and after the training program. Results: There were no significant changes in the torque values, Hmax/Mmax, and HPAD level after the training program in both groups (p>0.05). However, the MAS score in the WBV group significantly decreased (-9.0%), but no change in the control group was observed (0.7%) (p=0.027, effect size = 0.32). Conclusion: The objective assessment methods for spasticity show that WBV has no anti-spastic effect.

A new method to determine stretch reflex latency.

INTRODUCTION/AIMS: Motion artifact signals (MASs) created by the relative movement of intramuscular wire electrodes are an indicator of the mechanical stimulus arrival time to the muscle belly. This study proposes a method that uses wire electrodes as an intramuscular mechanosensor to determine the stretch reflex (SR) latency without lag time. METHODS: Gastrocnemius SR was induced by tendon tap, heel tap, and forefoot tap. The MASs recorded by intramuscular wire electrodes were extracted from background electromyographic activity using the spike-triggered averaging technique. Simultaneous recordings were obtained from multiple sites to validate the MAS technique. RESULTS: Using intramuscular wire electrodes, the MASs were successfully determined and extracted for all stimulus sites. In the records from the rectus femoris, MASs were also successfully extracted; thus, the reflex latency could be calculated. DISCUSSION: Wire electrodes can be used as an intramuscular mechanosensor to determine the mechanical stimulus arrival time to the muscle belly.

A stimulus rate that is not influenced by homosynaptic post-activation depression in chronic stroke.

PURPOSE: To determine a stimulus rate that is not influenced by homosynaptic post-activation depression for H-reflex studies in patients with chronic spasticity. MATERIALS AND METHODS: A cohort of 15 chronic stroke patients with soleus spasticity who received inpatient treatment at our rehabilitation centre participated in this study. The effect of stimulus frequency related depression on H-reflex size was tested using four different stimulus rates (0.1, 0.2, 0.3 and 1 Hz). The affected sides stibial nerve was stimulated by a bipolar electrode. The H-reflex was recorded from the affected sideed sidee sidehe affected smine stimulus frequency related depression of H-reflex size, amplitude of the first H-reflex response (H1) was used as control and amplitude of the second H-reflex response (H2) as test. RESULTS: H2 amplitude for frequency of 1 Hz, 0.3 Hz, 0.2 Hz and 0.1 Hz were 74.3, 84.1, 85.5 and 92.7% of H1, respectively. Depression of H2 amplitude was statistically significant for 1 Hz, 0.3 Hz and 0.2 Hz (p < 0.001, p = 0.002, p = 0.024, respectively). CONCLUSIONS: Higher frequency stimulation of Ia afferents than 0.1 Hz induced a stimulus frequency-related depression of H-reflex size in patients with chronic spasticity. The optimal stimulus rate for H-reflex was found to be 0.1 Hz.