Voluntary ankle flexor activity and adaptive coactivation gain is decreased by spasticity during subacute spinal cord injury.

Although spasticity has been defined as an increase in velocity-dependent stretch reflexes and muscle hypertonia during passive movement, the measurement of flexor muscle paresis may better characterize the negative impact of this syndrome on residual motor function following incomplete spinal cord injury (iSCI). In this longitudinal study Tibialis Anterior (TA) muscle paresis produced by a loss in maximal voluntary contraction during dorsiflexion and ankle flexor muscle coactivation during ramp-and-hold controlled plantarflexion was measured in ten patients during subacute iSCI. Tibialis Anterior activity was measured at approximately two-week intervals between 3-5 months following iSCI in subjects with or without spasticity, characterized by lower-limb muscle hypertonia and/or involuntary spasms. Following iSCI, maximal voluntary contraction ankle flexor activity was lower than that recorded from healthy subjects, and was further attenuated by the presence of spasticity. Furthermore the initially high percentage value of TA coactivation increased at 75% but not at 25% maximal voluntary torque (MVT), reflected by an increase in TA coactivation gain (75%/25% MVT) from 2.5+/-0.4 to 7.5+/-1.9, well above the control level of 2.9+/-0.2. In contrast contraction-dependent TA coactivation gain decreased from 2.4+/-0.3 to 1.4+/-0.1 during spasticity. In conclusion the adaptive increase in TA coactivation gain observed in this pilot study during subacute iSCI was also sensitive to the presence of spasticity. The successful early diagnosis and treatment of spasticity would be expected to further preserve and promote adaptive motor function during subacute iSCI neurorehabilitation.