We read with interest of the article by Hellman et al, entitled, Multimodal nociceptive mechanisms underlying chronic pelvic pain, published in the Journal.

The authors found that both experimental assessment of pelvic floor pain thresholds and the measurement of sustained pain are independently associated with pelvic pain phenotypes. Hellman et al believe that observed pressure pain thresholds and aftersensation pain differences imply 2 different alterations may occur in chronic pelvic pain and painful bladder syndrome. The decrease in pressure pain thresholds likely reflects increased excitability in peripheral Aδ fibers, responsible for perception of first pain, whereas the observed aftersensation differences point to aberrant C nerve fiber activity, responsible for the perception of sustained pain, second pain, thus the title multimodal nociceptive mechanisms underlying chronic pain.

However, we believe the title of the authors’ article is somewhat misleading. The notion that nociception involves both Aδ and C fibers has been known for decades. In 1997, in an article entitled “Neurophysiologic and pathologic aspects of acute and chronic pain”, Bonica opined that “new data from single and multiple fiber studies in animals and man support earlier observations and suggest that Aδ and C fibers are essential for pain sensation. Recent work by Swedish investigators using selective blockade of the low-threshold large fibers has confirmed the essentiality of C fiber activity for pain perception in man. The involvement of both fibers explain the phenomenon of double pain (the first pain of pinprick is mediated by the fast-conducting myelinated Aδ fibers), whereas the second pain is medicated by the slow-conducting C axons” (page 752).

The word, multimodal, has been used in pain/anesthesiology literature for decades to imply a therapeutic approach (ie, multimodal analgesia or multimodal approach or multimodal management for pain control).

Multimodal analgesia is achieved by combining different analgesics that act by different mechanisms (eg, opioids, nonsteroidal antiinflammatory drugs, acetaminophen, and local anesthetics), resulting in additive or synergistic analgesia, lower total doses of each analgesic, and fewer side effects.

Although Hellman et al demonstrated that both Aδ and C fibers play a role in the pathogenesis of chronic pelvic pain, their usage of the phrase, multimodal nociceptive mechanisms, appears confusing in light of the fact that the word multimodal has been used in a very different and highly designated way in the pain literature for many years.