The Pain Research Unit focuses on pain, the most common symptom responsible for individuals seeking health care. Pain remains a uniquely personal experience that cannot be measured objectively. The relief of pain remains a largely unmet medical need with high prevalence of poorly controlled pain in chronic diseases and at the end of life. The limitations of analgesic therapy include adverse CNS effects, nausea and vomiting, GI bleeding and ulceration, idiosyncratic cardiovascular events recently attributed to drugs that suppress cyclooxygenase-2, renal toxicity, abuse potential and others that span the spectrum of drug toxicity. This broad range of adverse events is often experienced by patients within the context of toxicities associated with therapeutic modalities used for disease treatment. Cancer patients, for example, commonly develop chemotherapy-induced peripheral neuropathy, cancer-related fatigue, sleep disorders, depression, and cognitive impairment that can result in dose-limiting adverse events. These negative sequelae may lead to diminished quality of life and limitation of underlying disease treatment. The greatest symptom burden often occurs at end of life when the patient is perhaps the most psychologically vulnerable, and when pain management may come at the price of significant morbidity, thereby further diminishing the quality of life. The treatment of intractable pain at end of life has been designated as an orphan drug indication by the Food and Drug Administration (FDA) in recognition of the inability to effectively provide pain relief and sustain quality of life with current medications and therapeutic strategies.

The Pain Research Unit will focus on four areas over the next few years:

• individual responder analyses that could be used in clinical trials to better detect analgesic activity across patient groups and within sub-groups,
• the identification of molecular-genetic mechanisms that contribute to individual variation in pain and analgesia,
• evaluating the reciprocal interplay between inflammation, gene expression and COX inhibitory drugs as mechanisms of individual variability in therapeutic response and adverse events, and
• fibromyalgia, a complex presentation of widespread chronic pain with a poorly understood etiology.