Pain is a complex and subjective experience often associated with noxious stimulation. However, in the past several decades it has become clear that the central nervous system (CNS) can augment or even cause pain in the absence of noxious input. In addition to chronic widespread pain, many patients have increased sensitivity to multiple sensory stimuli (e.g. sound, odor, and light) suggesting a global dysfunction in sensory processing. However, the CNS alterations associated with sensory hypersensitivity in chronic pain patients remain largely unknown. The prospective goal of my research is to identify network mechanisms that contribute to sensory hypersensitivity in chronic pain patients. Combining quantitative sensory testing, neuroimaging and computational data analysis methods, I will measure functional connectivity and network architecture at rest and during presentation of aversive stimuli in patients and healthy participants. These analyses aim to provide novel insight into how multiple brain regions interact and contribute to pain and sensory hypersensitivity. Furthermore, these results will help us to understand the neural signature of and mechanisms involved in multisensory processing in chronic pain.