ABSTRACT
Disruption of upper motor neuron pathways following a traumatic brain injury (TBI) results in a multitude of clinically meaningful sensori-motor limitations, among which is spasticity. As a result, a patient with TBI and spasticity not only has limited functional abilities but also has challenges in participating in a rehabilitation programme to promote recovery. Contracture can occur as early as 14 days in the ankle joint after a severe TBI. Spasticity and contracture usually co-exist in muscles that are shortened in patients with TBI, such as the shoulder adductors and internal rotators, elbow flexors, forearm pronators, and wrist and finger flexors in the upper extremity. Presence of lower extremity spasticity may be used as a clinical marker to predict recovery of ambulation after TBI. Commonly prescribed medications include baclofen, tizanidine, dantrolene, and benzodiazepine. Applications of these medications for spasticity management after TBI have undergone thorough reviewed by Zafonte et al.
