Sound-evoked biceps myogenic potentials reflect asymmetric vestibular drive to spastic muscles in chronic hemiparetic stroke survivors

Derek M. Miller*, William Z. Rymer

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

2 Scopus citations


Aberrant vestibular nuclear function is proposed to be a principle driver of limb muscle spasticity after stroke. We sought to determine whether altered cortical modulation of descending vestibulospinal pathways post-stroke could impact the excitability of biceps brachii motoneurons. Twelve chronic hemispheric stroke survivors aged 46-68 years were enrolled. Sound evoked biceps myogenic potentials (SEBMPs) were recorded from the spastic and contralateral biceps muscles using surface EMG electrodes. We assessed the impact of descending vestibulospinal pathways on biceps muscle activity and evaluated the relationship between vestibular function and the severity of spasticity. Spastic SEBMP responses were recorded in 11/12 subjects. Almost 60% of stroke subjects showed evoked responses solely on the spastic side. These data strongly support the idea that vestibular drive is asymmetrically distributed to biceps motoneuron pools in hemiparetic spastic stroke survivors. This abnormal vestibular drive is very likely to be a factor mediating the striking differences in motoneuron excitability between the clinically affected and clinically spared sides. This study extends our previous observations on vestibular nuclear changes following hemispheric stroke and potentially sheds light on the underlying mechanisms of post-stroke spasticity.

Original languageEnglish (US)
Article number535
JournalFrontiers in Human Neuroscience
StatePublished - Nov 10 2017


  • Biceps brachii
  • Motoneuron
  • Spastic hypertonia
  • Stroke
  • Vestibular evoked myogenic potential
  • Vestibular reflexes
  • Vestibulospinal

ASJC Scopus subject areas

  • Neuropsychology and Physiological Psychology
  • Neurology
  • Psychiatry and Mental health
  • Biological Psychiatry
  • Behavioral Neuroscience


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