Hyperalgesia fibers

Centrally mediated hyperalgesia involves the hyperexcitability of second-order sensory neurons in the dorsal horn of the spinal cord. In the case of severe or persistent tissue injury, C fibers fire action potentials... 

NGF has effects on the physiological responses of mature neurons. NGF acts as a target-derived trophic factor for pain neurons, which innervate peripheral tissues such as the skin. Inflammation of these peripheral tissues leads to local elevation of NGF synthesis and abundance. Elevated concentartions of NGF are responsible for the enhanced sensitivity to pain that accompanies inflammation. This is due to the ability of NGF to lower the sensory threshold of the pain fibers, leading to hyperalgesia. Nocioceptive sensory neurons mediating pain sensation are entirely dependent upon NGF for their survival as these cells are selectively lost in animal in which either the NGF or TrkA genes have been knocked out. These animals are insensitive to pain and live only a few weeks. 

Shir, Y., and Seltzer, Z. (1990). A-fibers mediate mechanical hyperesthesia and allodynia and C-fibers mediate thermal hyperalgesia in a new model of causalgiform pain disorders in rats. Neurosci. Lett. 115, 62-67. 

Baumann TK, Simone DA, Shain CN, LaMotte RH (1991) Neurogenic hyperalgesia the search for the primary cutaneous afferent fibers that contribute to capsaicin-induced pain and hyperalgesia. J Neurophysiol 66 212-227... 

PAIN NSAIDs usually are classified as nuld analgesics. However, consideration of the type of pain, as well as its intensity, is important in the assessment of analgesic efficacy. NSAIDs are particularly effective when inflammation has caused sensitization of pain receptors to normally painless mechanical or chemical stimuli. Pain that accompanies inflammation and tissue injury probably results from local stimulation of pain fibers and enhanced pain sensitivity (hyperalgesia), in part a consequence of increased excitability of central neurons in the spinal cord. 

The affective motivational component is mediated by slowly conducting c-fibers, and polysynaptic transmission to the limbic cortex [10,12]. It is responsible for continued pain perception, suffering, pain-related behaviors, hyperalgesia, reflex spasm (splinting behavior). It is also responsible for immobilization, and protection of the injury site. 

Hyperalgesia is defined by the International Association for the Study of Pain (lASP) as an increased response to a stimulus which is normally painful . Primary hyperalgesia or peripheral sensitization reflects the activation and sensitization of nociceptive A delta and polymodal C-fiber terminal endings within the injured area. Secondary hyperalgesia, or central sensitization, involves spinal neuroplasticity and facilitation... 

A-fiber nociceptors mediate secondary hyperalgesia to punctate stimuli through a second pathway. 

Capsaican is a TRPV-1 agonist. TRPVl (also termed the capsaican receptor) is a polymodal nociceptor exhibiting a dynamic threshold of activation that is markedly reduced in inflammatory conditions [3]. TRPVl knock-out mice are devoid of post-inflammatory thermal hyperalgesia. TRPV receptors are in abundance on unmyelinated C fiber peripheral endings and respond to a variety of noxious mediators. Once activated these fibers transmit localized and... 

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