Date(s) - 01/06/2014
Although a variety of injury mechanisms are hypothesized to cause pain, a clear mechanical understanding of injuries and the tissue loading scenarios that produce and mediate radicular pain remain largely undefined. Our work incorporates the simultaneous measurement of tissue biomechanics, behavioral sequelae (pain) and neuronal molecular and physiological cascades that contribute to the onset and maintenance of pain from the nerve root compression, which is common during disc herniation and spinal trauma. We utilize in vivo and in vitro modeling to define a mechanistic understanding of how pain can be initiated and maintained, even for subfailure loading of neural tissue. We are defining the spatio-temporal regulatory mechanisms by which mechanical signals from loading to the cervical nerve root regulate local responses in that tissue, as well as those cellular systems in the DRG, spinal cord and brain that contribute to persistent pain. We integrate findings from that work with application of novel imaging techniques to identify and test a variety of different approaches to treat pain. Using these coordinated studies we have been able to begin to define mechanical thresholds for tissue tolerance, pain, and cellular dysfunction; and are able to determine mechanical and physiological meanings for injuries in the spine.