New insights into the pathophysiology of post-stroke spasticity

Abstract

Spasticity is one of many consequences after stroke. It is characterized by a velocity-dependent increase in resistance during passive stretch, resulting from hyperexcitability of the stretch reflex. The underlying mechanism of the hyperexcitable stretch reflex, however, remains poorly understood. Accumulated experimental evidence has supported supraspinal origins of spasticity, likely from an imbalance between descending inhibitory and facilitatory regulation of spinal stretch reflexes secondary to cortical disinhibition after stroke. The excitability of reticulospinal (RST) and vestibulospinal tracts (VSTs) has been assessed in stroke survivors with spasticity using non-invasive indirect measures. There are strong experimental findings that support the RST hyperexcitability as a prominent underlying mechanism of post-stroke spasticity. This mechanism can at least partly account for clinical features associated with spasticity and provide insightful guidance for clinical assessment and management of spasticity. However, the possible role of VST hyperexcitability cannot be ruled out from indirect measures. In vivo measure of individual brainstem nuclei in stroke survivors with spasticity using advanced fMRI techniques in the future is probably able to provide direct evidence of pathogenesis of post-stroke spasticity.

Keywords: brainstem; pathophysiology; reticulospinal pathways; spasticity; stroke.

FIGURE 1

Brunnstrom stages of motor recovery after stroke (at the end of the manuscript).

FIGURE 2

Illustration of supraspinal control of spinal stretch reflex. CST, cortical spinal tract; RST, reticulospinal tract; VST, vestibular spinal tract; (+), facilitation; (-), inhibition. Other descending pathways, such as rubrospinal tract, tectospinal tract, medial CST are not shown here.

FIGURE 3

A representative electromyography (EMG) of flexor digitorum superficialis (FDS) and extensor digitorum communis (EDC) before and 10 days after botulinum toxin injection. The subject was asked to grip as soon and as hard as possible after the “grip signal” and relax after the “release signal” (dash lines). The release delay time decreases after injection, along with shortened EDC activities. Modified from Chang et al. (2012, with permission).