Effects of Altered Neural Input and Botulinum Toxin on Finger and Wrist Passive Properties in Chronic Hemiparetic Stroke
ABSTRACTBackground and PurposeFollowing a hemiparetic stroke, prolonged altered motor neuron inputs may drive passive mechanical changes within muscle that further amplify brain injury induced motor impairments, reducing optimal recovery. However, due to confounding factors, i.e. muscle hypertonicity and spasticity, and the use of botulinum neurotoxin (BoNT), chemical denervation to reduce their expression, there is no consensus on how altered neural inputs following a stroke affect muscle passive mechanical properties or the extent to which these properties ultimately limit functional recovery. Therefore, the objective of this study is to quantify muscle passive biomechanical properties following chronic hemiparetic stroke and BoNT.MethodsPassive torques about the wrist and metacarpophalangeal (MCP) joints were quantified in both hands of 34 individuals with chronic hemiparetic stroke. Participants’ hand impairments ranged from severe to mild with a subset who previously received BoNT injections. Torques were quantified with subjects in a sleep or near-sleep state, mitigating muscle hyperactivity. EMGs were continuously monitored to ensure no muscle activity during data collection.ResultsParticipants who previously received BoNT injections demonstrated significantly greater passive flexion torques about their paretic wrist and fingers as compared to those who never received BoNT. As a result, only the group who received BoNT demonstrated significant decreases in passive MCP extension.ConclusionsThe results of our thorough investigation of in vivo passive elastic torques at the wrist and fingers in chronic hemiparetic stroke contrast with the increased stiffness and decreased passive ROM observed clinically and in many previous studies. We highlight the need to effective address both stroke-induced muscle hyperactivity and BoNT treatment history as confounds. We conclude that loss of hand function post-stroke is predominantly due to motor impairments post stroke. Adverse effects of BoNT warrant consideration in future studies and rehabilitation interventions.