Involvement of the reticulospinal tract in the pathogenesis of spasticity after stroke and spinal cord injury.

Spasticity occurs due to central nervous system (CNS) injuries such as stroke, spinal cord injury, cerebral palsy, or multiple sclerosis. Following CNS injury, spasticity does not appear immediately but emerges several days to weeks later and is believed to be the result of maladaptive changes due to neuroplastic alterations. Previously, research on the pathophysiology of spasticity has primarily focused on the spinal cord, leading to the elucidation of its mechanisms. Although the involvement of upper motor neurons has been suggested, definitive studies on the underlying pathophysiology have not been reported. In recent years, brainstem reticular formation has been identified as a region undergoing active plastic changes following a CNS injury. Although evidence remains limited and controversial, increasing numbers of studies suggest that plastic changes in brainstem reticular formation may be involved in the onset of spasticity. This review outlines the pathophysiological similarities and differences in spasticity between stroke and spinal cord injury, while summarizing recent studies on plastic changes in brainstem reticular formation and the onset of spasticity, including studies of humans and primates, as well as rodents. It organizes and examines the points of contention regarding the differences in outcomes between these two groups.