Tatyana Gerachshenko1, W Zev Rymer1, James W Stinear2. 1. Sensory Motor Performance Program, Rehabilitation Institute of Chicago, Suite 1406, 345 E Superior Street, Chicago, IL 60611, USA. 2. Sensory Motor Performance Program, Rehabilitation Institute of Chicago, Suite 1406, 345 E Superior Street, Chicago, IL 60611, USA. Electronic address: j-stinear@northwestern.edu.
Abstract
OBJECTIVE: To assess corticomotor (CM) excitability of the antagonist biceps brachii (BB) post-stroke in preparation for pronator contraction. In healthy subjects, we previously demonstrated that prior to pronator contraction CM excitability of the antagonist BB was suppressed. METHODS: Transcranial magnetic stimulation (TMS) was used to assess pre-contraction changes in motor evoked potential (MEP) amplitude of the BB, when BB was acting either as an antagonist or an agonist. TMS was applied 100-200ms prior to rhythmic isometric BB or pronator contractions in chronic stroke survivors and age/gender matched healthy control subjects. RESULTS: Prior to pronator contraction, MEPs in BB were elicited in the stroke group but were absent in healthy controls indicating that CM excitability of the antagonist BB was increased post-stroke. The extent of the abnormal increase in excitability positively correlated with the extent of upper limb motor impairment. CONCLUSIONS: Our results suggest that an alteration of cortical control mechanisms regulating motor excitability of the antagonist BB may contribute to the impairment of upper limb motor coordination post-stroke. SIGNIFICANCE: This study offers a unique approach to study the potential for a cortical origin of post-stroke motor discoordination.
OBJECTIVE: To assess corticomotor (CM) excitability of the antagonist biceps brachii (BB) post-stroke in preparation for pronator contraction. In healthy subjects, we previously demonstrated that prior to pronator contraction CM excitability of the antagonist BB was suppressed. METHODS: Transcranial magnetic stimulation (TMS) was used to assess pre-contraction changes in motor evoked potential (MEP) amplitude of the BB, when BB was acting either as an antagonist or an agonist. TMS was applied 100-200ms prior to rhythmic isometric BB or pronator contractions in chronic stroke survivors and age/gender matched healthy control subjects. RESULTS: Prior to pronator contraction, MEPs in BB were elicited in the stroke group but were absent in healthy controls indicating that CM excitability of the antagonist BB was increased post-stroke. The extent of the abnormal increase in excitability positively correlated with the extent of upper limb motor impairment. CONCLUSIONS: Our results suggest that an alteration of cortical control mechanisms regulating motor excitability of the antagonist BB may contribute to the impairment of upper limb motor coordination post-stroke. SIGNIFICANCE: This study offers a unique approach to study the potential for a cortical origin of post-stroke motor discoordination.