6533b7cffe1ef96bd1258dda

RESEARCH PRODUCT

Multiple mechanisms of secondary hyperalgesia

subject

description

Publisher Summary This chapter discusses the multiple mechanisms of secondary hyperalgesia. The chapter defines the minimal conditions of complexity that must be fulfilled by a model of plasticity of spinal nociceptive transmission in order to explain clinical and psychophysical observations in humans. Secondary hyperalgesia is characterized by a leftward shift of the stimulus-response function for noxious mechanical stimuli. In order to define the afferent pathways involved in inducing central sensitization and in mediating the hyperalgesia to noxious mechanical stimuli, several psychophysical experiments using selective nerve block techniques is performed. Secondary hyperalgesia is likely to result from sensitization of nociceptive neurons in the spinal cord dorsal horn. Most diagrams of central sensitization are simplified single-neuron models in which a critical target neuron, namely the nociceptive projection neuron is thought to be sensitized by the concerted action of neurokinins and excitatory amino acids. The observations in experimentally induced secondary hyperalgesia are reminiscent of the different types of mechanical hyperalgesia seen in patients with neuropathic pain.