Cerebellar injury: clinical relevance and potential in traumatic brain injury research

A treatment for traumatic brain injury (TBI) remains elusive despite compelling evidence from animal models for a variety of therapeutic targets. Numerous animal models have been developed to address the wide spectrum of mechanisms involved in the progression of secondary injury after TBI. Evidence from well-established models such as the fluid percussion injury (FPI) device, cortical impact model, and the impact acceleration model has demonstrated diffuse pathophysiological mechanisms throughout various brain structures. More specifically, we have recently extended characterization of the FPI model to include pathophysiological changes in the cerebellum following unilateral fluid percussion. Data suggest that the cerebellum is susceptible to selective Purkinje cell loss as well as white matter dysfunction. Despite the cerebellum's low profile in TBI research, there is evidence to warrant further study of the cerebellum to examine mechanisms of neuronal death and traumatic axonal injury. Furthermore, evidence from clinical literature and basic science suggests that some components of TBI pathophysiology have a basis in cerebellar dysfunction. This review highlights some of the recent findings in cerebellar trauma and builds an argument for including the cerebellum as a model to assess mechanisms of secondary injury and its potential contribution to the pathology of TBI.