Spasticity is a common occurrence in patients with spinal cord injury (SCI). Indeed almost ~80% of those with SCI experience spasticity a few months after the initial injury1. Spasticity may worsen residual motor function and hamper spontaneous motor recovery. It also contributes to pain and sleep disturbances and significantly interferes with daily activities and rehabilitation, dramatically reducing the patients’ quality of life. The previous study has implicated plateau potentials in the development of spasticity. It has been shown that reduction in plateau potentials via inhibition of Cav1.3 L-type calcium channels correlates strongly with the alleviation of spastic phenotypes. Nimodipine, an L-type Calcium channel blocker, has been shown to prevent the development of plateau potentials and spasticity after sacral SCI through its interaction with Cav1.3. However, sacral transection injuries are not a common clinical occurrence. The overall objective of this project is to examine the therapeutic efficacy of nimodipine to mitigate the spasticity, promote motor recovery and preserve the integrity of the lumbar locomotor-related motoneurons in a clinically relevant model of cervical SCI (cSCI). Immediately following injury, a six-week regimen of daily nimodipine (10mg/kg) or vehicle solution administration was coupled with electrophysiology and detailed behavioral analysis to assess spasticity and locomotor function. Our data indicate that early and prolonged treatment with nimodipine not only produced a reduction in the development of spasticity following injury, but it also resulted in a significant improvement in locomotor recovery when compared to vehicle control. Our results indicate for the first time that nimodipine is a potential therapeutic to prevent the development of spasticity and to promote locomotor recovery in cases of cervical spinal cord injury.

Key Words: spinal cord injury, neuroprotection, spasticity