While not traditionally associated with epilepsy or seizures, the cerebellum is a potentially key node in seizure networks, as cerebellar manipulations can attenuate seizures, and cerebellar alterations occurring with chronic epilepsy can predict comorbidities and negative outcomes, including sudden unexplained death in epilepsy (SUDEP). We are examining how cerebellar neurons interact with seizure networks, including how the activity of different populations can be modulated to inhibit seizures, how chronic seizures impact cerebellar structure and function, and how these alterations lead to comorbidities and negative outcomes like SUDEP.

Spinocerebellar ataxia type 1 is one of the most rapidly progressing forms of ataxia, is characterized by progressive cerebellar atrophy and motor dysfunction, and is ultimately fatal.  A major challenge in understanding the full pathophysiology of SCA1 is that while motor symptoms can emerge prior to overt cell death, little is known about how alterations in cerebellar ataxia underlie symptoms of the disease. In collaboration with the Orr lab, we are interrogating cerebellar network dynamics during clinically relevant tasks in order to understand how cerebellar population activity contributes to disease progression and symptoms, as well as the contributions of key cell populations to disease pathophysiology.