Abstract

The purpose was to examine the immediate effects of dry needling to spastic finger muscles in chronic stroke. Ten chronic stroke patients with spasticity in finger flexors participated in this experiment. Dry needling to the flexor digitorum superficialis (FDS) muscle was performed under ultrasound guidance for about 30 s (about 100 times). Clinical assessment and intramuscular needle EMG readings were made before and immediately after dry needling. Immediately after needling, the FDS muscle was felt less tight to palpation and the proximal phalangeal joint rested in a less flexed position (p = 0.036). The MAS score decreased for FDS (p = 0.017) and flexor digitorum profundus (FDP) (p = 0.029). Motor unit action potential (MUAP) spikes decreased from 41.6 ± 5.5 to 6.7 ± 2.2 spikes/s (p = 0.002), an 84% reduction after dry needling. However, the pre-needling spike frequency was not correlated to MAS or resting position of the FDS muscles. Dry needling to the spastic finger flexors leads to immediate spasticity reduction, increased active range of motion, and decreased frequency of motor unit spontaneous firing spikes. The results suggest that latent trigger points possibly exist in spastic muscles and they contribute partly to spastic hypertonia of finger flexors in chronic stroke.

Highlights

  • Spasticity is a common disabling motor impairment after stroke

  • The modified Ashworth scale (MAS) score decreased for flexor digitorum superficialis (FDS) (2.3 ± 0.4 vs. 1.2 ± 0.4, p = 0.017) and flexor digitorum profundus (FDP) (2.2 ± 0.5 vs. 1.3 ± 0.5, p = 0.029), but no changes in MAS for the metacarpal phalangeal (MCP) joint (1.8 ± 0.5 vs. 1.3 ± 0.4, p = 0.17)

  • The needle EMG recordings showed that the spikes of spontaneous Motor unit action potential (MUAP) decreased from 41.6 ± 5.5 spikes/s to 6.7 ± 2.2 spikes/s (p = 0.002), an 84% reduction after dry needling (Figures 1A,D)

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Summary

Introduction

Spasticity is a common disabling motor impairment after stroke. Spasticity is a result of disinhibited descending excitatory inputs to spinal reflex circuitry, adaptive changes in intraspinal network and peripheral changes in spastic muscles (1). These excitatory inputs at least in part lead to hyperexcitable or spontaneous firing of motor units of spastic muscles (2). Adaptive changes occur in parallel, such as muscle fiber shortening and stiffening (3). Spasticity amplifies other motor impairments, e.g., weakness, and imposes significant limitations in patient’s mobility and activities of daily living (5)

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