A recent study showing that hypersensitivity of peripheral tissues to subthreshold stimuli persists after resolution of neuropathic lesions resulting from acute experimental disc herniation, which is modulated by upregulation of transient receptor potential vanilloid receptor 1 (TRPV1) receptor expression and activity, is expected to shed light on the mechanism of action of neuropathic pain that persists after those apparently successful surgical procedures. The findings were presented as a conference abstract at the 82nd Annual Meeting of the American Association of Neurological Surgeons (AANS) on April 9, 2014. Despite the structural success achieved with spine surgery, postoperative pain persists, and how to figure this out has been a longstanding and perplexing problem for physicians. In a study that blends the interrelated fields of spine surgery and pain medicine, researchers found that molecular changes in neurons occur during the transition from acute inflammatory pain to chronic neuropathic pain. Their findings were presented today at the 82nd Annual Scientific Meeting of the American Association of Neurological Surgeons (AANS) by the head of the research team, Dr. Mohammed Farid Shamji, a member of the Royal Society of Canada. Their presentation was titled, Peripheral Hypersensitivity to Subthreshold Stimuli Persists after Resolution of Neuropathic Lesions Caused by Acute Experimental Disc Herniation and is Modulated by Upregulation of Transient Receptor Potential Vanilloid Receptor 1 (TRPV1) Receptor Expression and Activity (Peripheral Hypersensitivity to Subthreshold). Stimuli Persists after Resolution of Acute Experimental Disc-Herniation Neuropathy and Is Mediated by Heightened TRPV1 Receptor Expression and Activity). The study promises to shed light on the mechanism of action of neuropathic pain that persists after apparently successful surgery. Dr. Shamji noted, “We are extremely novel in recognizing that an autoimmune neuroinflammatory radiculopathy, which clinically we manage as a self-limiting disease in most patients, has the potential to lead to permanent structural changes that occur in the neuronal and functional sensitivity in undergoing pain.” Figuring out what changes occur in these molecules, Dr. Shamji says, could help researchers develop appropriate treatments.” If we can minimize the disability caused by this pain syndrome, we may have the ability to prevent its onset based on acute inflammatory pain, and perhaps even reverse it as soon as it develops.