Pathophysiology

Pain involves release of potent mediators of inflammation, and is modulated by neurocognitive factors resulting in an unpleasant sensory and emotional experience. The peripheral pain system (e.g., nociceptors, C fibers, A-d fibers, free nerve endings) registers the original noxious stimulus and conducts it to the central nervous system (CNS). The primary afferent peripheral nociceptors have poorly differentiated nerve fiber terminals and slow conduction velocities (ranging from C fibers at 2.5 ms-1 to A-d fibers at 2.5 to 20.0 ms-1) and are normally activated by stimuli of strong to noxious intensity. They release several neurotransmitters. Glutamate, an excitatory amino acid (EAA) released from these nociceptors, elicits fast synaptic responses in second-order neurons that are mediated by at least two EAA receptor subtypes. Some primary afferent nerve fibers also express and synthesize neuropeptides (substance P, neurokinin A, and calcitonin gene-related peptide) that are coreleased with glutamate within the spinal cord.3 The dorsal horn of the spinal cord (e.g., dorsal root ganglion, inhibitory interneurons, ascending pain tracts) integrates and modulates pain and other sensory stimuli. Supraspinal centers (e.g., hypothalamic centers, thalamic nuclei, the limbic and reticular activating systems) integrate and process pain information, allowing detection and perception of pain. Cognitive interpretation, localization, and identification of pain and triggering of emotional and physiologic reactions also occur at this site. Parietal pain pathways are more complex and differ in structure from visceral pain pathways, which may explain the poor localization of visceral pain as opposed to parietal pain.

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