Roland Staud, M.D.

Roland Staud, M.D.

Professor of Medicine

College of Medicine

2009 Awardee

Roland Staud’s research over the last ten years has focused on central nervous system (CNS) pain processing abnormalities as important factors for Fibromyalgia (FM) pain. Chronic widespread pain is very prevalent in the United States (25% of the population). It afflicts predominantly women and is not only associated with disability but also with increased mortality.

FM represents the extremes of widespread pain in the general population and is characterized by mechanical tenderness, fatigue, and distress. Despite extensive investigations, no consistent tissue abnormalities have been detected in FM patients. Generally, clinical tests, including neurological evaluations are normal in most FM patients. It is well established that almost all FM patients lack evidence of primary hyperalgesia (peripheral mechanisms) but show widespread secondary hyperalgesia to mechanical, heat, cold, electrical, and chemical stimuli (central mechanisms).

The Staud laboratory was the first to report that FM patients have abnormal temporal summation of second pain or windup (WU), a phenomenon which is highly relevant for chronic pain. WU is dependent on a central N-methyl-D-aspartate (NMDA) receptor mechanism within the dorsal horn of the spinal cord and is not only increased in FM participants compared to normal controls (NC) but also results in prolonged WU after sensations, indicating stimulus dependent as well as stimulus independent central sensitization. The Staud laboratory determined that that the response of WU to several pharmacological manipulations is normal in FM. In addition, using fMRI, Staud determined that although FM subjects required lower stimulus intensities than NC, WU related brain activation did not differ between groups.

The Staud research laboratory has shown that chronic pain sufferers like FM patients demonstrate evidence of nociception dependent and independent central sensitization. These abnormalities represent a mechanism relevant for the widespread pain of FM and similar pain disorders. Further investigations are currently underway to provide additional insights into peripheral and central pain processing abnormalities that contribute to clinical pain in this prevalent syndrome.