Nociceptive withdrawal reflexes as a model for spinal nociceptive transmission

Abstract

Pain and analgesia in animals are usually inferred from changes in motor and autonomic responses. In particular, the withdrawal reflexes have been extensively used to study spinal pro­ cessing of nociceptive information and to gauge the efficacy of supraspinal analgesic descending systems. Often, a decreased magnitude or increased latency of the withdrawal reflex is taken as evidence for analgesia, whereas the opposite pattern of change is taken as a sign of hyperalgesia. Unfortunately, such interpretations may be erroneous, as Schomburg points out in his Focus article, because different nociceptive withdrawal reflexes exhibit different functional and pharmacologic properties and are under differential supraspinal and segmental control. I entirely agree with this view and have expressed similar cautions over the last years; however, provided that proper controls are made, as listed by Schomburg in his Focus article, I believe that nociceptive withdrawal reflexes will continue to be a useful model for spinal nociceptive transmission. Although I find Schomburg's Focus article excellent in many respects, it is based on the assumption that withdrawal reflexes are organized as reflexes. As new findings in the rat, indicating a modular organi­ zation of the nociceptive withdrawal reflexes, have challenged the traditional flexion reflex concept and the associated flexor reflex afferent (FRA) terminology, I discuss the difference between these two views and the implications for pain research. Some recent findings on nociceptive inhibitory input to withdrawal reflex path­ ways are also commented on.