The development of chronic pain after spinal cord injury or in diseases such as multiple sclerosis (MS) is a major clinical concern. The main focus of research in my laboratory is aimed at addressing the cellular mechanisms that generate neuropathic pain in these conditions. My research uses two primary animal models: a clinically relevant spinal contusion injury model and a mouse model of autoimmune demyelination that resembles MS, experimental autoimmune encephalomyelitis (EAE). My research aims to understand the specific pathways and cellular changes that arise in response to direct trauma or in chronic disease states that may promote the development of neuropathic pain. The lab employs a number of different strategies that include analysis at the cell and molecular levels, as well as systems level approaches to address this complex biological problem.