Chronic pain is one of the most stubborn and least understood consequences of nerve injury and disease. Our lab investigates why pain persists long after a nerve is damaged — whether by physical trauma, chemotherapy, or an autoimmune attack like the one seen in multiple sclerosis (MS). Understanding the biology behind this is the first step toward treatments that address the cause of the pain, rather than just masking it. We study this question across three complementary models: traumatic peripheral nerve injury, chemotherapy-induced peripheral neuropathy, and experimental autoimmune encephalomyelitis (EAE), a mouse model that mirrors the autoimmune attack on the nervous system seen in MS. Together, these models let us ask whether pain arising from a physical injury, a toxic drug exposure, or an ongoing autoimmune disease shares common underlying mechanisms.

A central theme running through all three models is the degeneration and regeneration of axons, the long fibers nerve cells use to send signals. Whether triggered by trauma, chemotherapy, or autoimmune attack, damaged axons can degenerate, attempt to regrow, or fail to reconnect properly. How well (or poorly) these processes unfold has a direct bearing on whether pain develops and how long it lasts. We’ve shown that immune cells (including macrophages and microglia) and the molecules they release can drive pain by making neurons overly excitable. But the same immune response is also essential for clearing damaged tissue and supporting nerve repair. A major focus of our current work is teasing apart these two faces of the immune response: when and how it promotes pain, and when and how it instead promotes healing and pain resolution. Overall, our goal isn’t to shut down the immune response, but to understand how to tip it towards repair.

To tackle this, we combine animal behaviour studies, electrophysiology, molecular and cellular biology, and imaging. This allows us to move fluidly between what an animal is experiencing and what’s happening inside individual axons, cells, and circuits. Our research is supported by funding from CIHR and the MS Society of Canada, among others. Ultimately, our goal is to pinpoint the specific cellular and molecular events that determine whether an injury or disease resolves or turns into chronic pain, so that new treatments can be designed to tip the balance toward repair and recovery.