Literature DB >> 24680197

Asymmetries in vestibular evoked myogenic potentials in chronic stroke survivors with spastic hypertonia: evidence for a vestibulospinal role.

Derek M Miller1, Cliff S Klein2, Nina L Suresh2, William Z Rymer3.   

Abstract

OBJECTIVE: Indirect evidence suggests that lateralized changes in motoneuron behavior post-stroke are potentially due to a depolarizing supraspinal drive to the motoneuron pool, but the pathways responsible are unknown. In this study, we assessed vestibular evoked myogenic potentials (VEMPs) in the neck muscles of hemispheric stroke survivors with contralesional spasticity to quantify the relative levels of vestibular drive to the spastic-paretic and contralateral motoneuron pools.
METHODS: VEMPs were recorded from each sternocleidomastoid muscle in chronic stroke survivors. Side-to-side differences in cVEMP amplitude were calculated and expressed as an asymmetry ratio, a proxy for the relative amount of vestibular drive to each side.
RESULTS: Spastic-paretic VEMPs were larger than contralateral VEMPs in 13/16 subjects. There was a strong positive relationship between the degree of asymmetry and the severity of spasticity in this subset of subjects. Remaining subjects had larger contralateral responses.
CONCLUSION: Vestibular drive to cervical motoneurons is asymmetric in spastic stroke survivors, supporting our hypothesis that there is an imbalance in descending vestibular drive to motoneuron pools post-stroke. We speculate this imbalance is a consequence of the unilateral disruption of inhibitory corticobulbar projections to the vestibular nuclei. SIGNIFICANCE: This study sheds new light on the underlying mechanisms of post-stroke spasticity.
Copyright © 2014 International Federation of Clinical Neurophysiology. Published by Elsevier Ireland Ltd. All rights reserved.

Entities:  

Keywords:  Chronic stroke subjects; Hemispheric stroke; Human; Motoneuron; Post-stroke spasticity; Vestibular evoked myogenic potentials; Vestibulospinal

Mesh:

Year:  2014        PMID: 24680197      PMCID: PMC4162855          DOI: 10.1016/j.clinph.2014.01.035

Source DB:  PubMed          Journal:  Clin Neurophysiol        ISSN: 1388-2457            Impact factor:   3.708


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