Recent evidence suggests that alterations in ionic conductances in spinal motoneurones, specifically the manifestation of persistent inward currents, may be partly responsible for the appearance of hyperexcitable reflexes following spinal cord injury (SCI). We hypothesized that such alterations would manifest as temporal facilitation of stretch reflexes in human SCI. Controlled, triangular wave, ankle joint rotations applied at variable velocities (30-120 deg s-1) and intervals between stretches (0.25-5.0 s) were performed on 14 SCI subjects with velocity-dependent, hyperexcitable lantarflexors. Repeated stretch elicited significant increases in plantarflexion torques and electromyographic (EMG) activity from the soleus (SOL) and medial gastrocnemius (MG).At higher velocities (≥90 deg s-1), reflex torques declined initially, but subsequently increased to levels exceeding the initial response, while mean EMG responses increased throughout the joint perturbations. At lower velocities (≤60 deg s-1), both joint torques and EMGs increased gradually.Throughout a rangeof angular velocities, reflex responses increased significantly only at intervals ≤1 s between stretches and following at least four rotations. Ramp-and-hold perturbations used to elicit tonic stretchreflexes revealed significantly prolonged EMG responses following one or two triangular stretches, as compared to single ramp-and-hold excursions. Post hoc analyses revealed reduced reflex facilitation in subjects using baclofen to control spastic behaviours. Evidence of stretch reflex facilitation post-SCI may reflect changes in underlying neuronal properties and provide insight into the mechanisms underlying spastic reflexes.
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