A brief noxious stimulus, such as a heat tap at 51°C or percutaneous electrical stimulation of A and C axons, can evoke two distinct pain sensations called, "first" and "second" pain (22,29-31). First pain is usually an immediate sharp sensation, whereas second pain occurs
about a second later and can be a dull, throbbing, or burning sensation depending on the type of stimulus used to evoke it. Second pain often lingers well beyond the brief stimulus that evokes it. VAS scaling methods have been used to analyze the temporal summation found in second pain (30,31). Examples of temporal summation of second pain in normal subjects and fibromyalgia patients are shown in Figure 2. These examples include responses to repeated heat and cold taps, both of which evoke reliable temporal summation. Among normal pain-free subjects, C-fiber-evoked second pain increases in intensity whenever the interstimulus interval is three seconds or less but does not change when the interstimulus interval is five seconds or greater. This slow temporal summation occurs even when the stimulus moves from spot to spot during the train of heat pulses, and even after total blockade of the peripheral impulses in the A axons necessary for first pain (29,30). Temporal summation of second pain usually results in a continuous burning pain after several stimuli and this burning pain often continues for several seconds after termination of the stimuli. This "after-sensation" has long been noted to be a common feature of pain evoked by stimulation of C nociceptive afferent neurons (1,22,24). Temporal summation of second pain reflects early mechanisms that lead to central sensitization, secondary hyperalgesia, and persistent pain states. For example, dorsal horn neurons show temporal summation or "windup" in response to repeated C-fiber stimulation (32,33). There are numerous parallels between "windup" and temporal summation of second pain and there is considerable evidence that enhanced second pain reflects activation of N-methyl-D-aspartate (NMDA) receptors as well as intracellular mechanisms of sensitization in the spinal dorsal horn (6,31,34).
Was this article helpful?