Abstract
Pain receptors, nociceptors inputs to the spinal cord and supra spinal structures triggering a prolonged but reversible increase in the excitability and synaptic efficacy of neurons in central nociceptive pathways, is the phenomenon of central sensitization. Key processes for pain memory stabilizing could be considering processes of peripheral and central sensitizations. Mechanical hypersensitivity and allodynia to light touch after central sensitization are pathologic in that they are evoked by Aβ low threshold mechanoreceptors, which normally do not produce painful sensations. Peripheral sensitization allows low-intensity stimuli to produce pain by activating Aδ and C nociceptors whereas central sensitization allows normal low-threshold Aβ mechanoreceptors to produce pain as a result of changes in sensory processing in the spinal cord. During peripheral and central sensitization, the receptive fields of dorsal horn neurons expand beyond the site of injury into surrounding non-injured tissue. The clinical result of all above changes is hyperalgesia, allodynia, spontaneous pain, referred pain and sym-pathetically maintained pain. Therefore, these persistent sensory responses to noxious stimuli are a form of memory, the memory for pain. Long lasting synaptic plasticity as the long-term potentialtion at spinal and supra-spinal levels could undergo hyperalgesia and allodynia. The latter could be providing neuronal basis for persistent pain and pain memory. Thus, it will be particularly important to know how to regulate long-lasting plastic changes in spinal cord, thalamus and cortex. Molecular mechanisms of these plastic processes could be main targets for new therapeutic drugs in pain relief.
Highlights
Each of us remembers pain experience in case of illness
Mechanical hypersensitivity and allodynia to light touch after central sensitization are pathologic in that they are evoked by Aβ low threshold mechanoreceptors, which normally do not produce painful sensations
The central nervous system (CNS) pathway was seen to constitute particular anatomical connections in the spinal cord, brain stem, thalamus and cortex, linking the sensory inflow generated in high threshold primary afferents with those parts of the cortex that leads to the conscious awareness of painful sensations [1]
Summary
Each of us remembers pain experience in case of illness. Anyone who has ever got electric shock, broken a leg or an arm, or have had a kidney colic remembers it all his life span and never forgets it. Since 30 years ago, the prevailing view on pain processing in the central nervous system (CNS) was of a largely passive neural relay that conveyed by encoded action potentials, information on the onset, duration, intensity, location and quality of peripheral noxious stimuli, from one site to another. Many of neural mechanisms mobilized in vertebrates’ nervous system by painful stimuli are present in neurons of mollusks. These same mechanisms (ion channels, second messengers, gene expression, etc.) mediate hyperresponsiveness of the mollusk to an electrical shock delivered at the site of a previous shock a day before. Mollusks and vertebrates evolved from a common ancestor (probably a small worm) 600 million years ago. Augmentation of responses to successive nociceptive stimuli has been a biological truth for at least this time [2]
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