In a study that melds the interrelated domains of spinal surgery and pain medicine, researchers have discovered that in the transition from acute inflammatory pain to chronic neuropathic pain, neurons undergo molecular changes.
Team leader Mohammed Farid Shamji, MD, PhD, FAANS, presented the study's findings today during the 82nd Annual Scientific Meeting of the American Association of Neurological Surgeons (AANS). Titled 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 basis of neuropathic pain that persists after apparently successful surgery.
Dr. Shamji noted, "It is extremely novel to learn that an autoimmune neuroinflammatory radiculopathy that we clinically manage in most patients as being self-limited has the potential to cause permanent structural changes to neurons and functional sensitivity in the pain experience."
Understanding the molecular changes that occur, said Dr. Shamji, could help researchers develop appropriate treatments. "If we can minimize the disability caused by this pain syndrome, we may be able to prevent it from occurring upon onset of the acute inflammatory pain, potentially even reversing it once established."