2012
Volume 12, Number 4, pp. 174–181
Pain as memory: neuroplasticity of central sensitization as a therapeutic target
Merab G. Tsagareli
Department of Neurophysiology, Ivane Beritashvili Centre of Experimental Biomedicine, 0160 Tbilisi, Georgia
One of the crucial cellular processes for major symptoms of pain, like hyperalgesia and allodynia, is considered as a phenomenon of sensitization. Key processes for pain memory stabilizing are peripheral and central sensitizations. Mechanical hypersensitivity and allodynia to light touch after central sensitization are pathologic in that they are evoked by Ab low threshold mechanoreceptors, which normally do not produce painful sensations. Peripheral sensitization allows low-intensity stimuli to produce pain by activating Ad and C nociceptors whereas central sensitization allows normal low-threshold Ab 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 uninjured tissue. The clinical result of all above changes is hyperalgesia, allodynia, spontaneous pain, referred pain and sympathetically maintained pain. These persistent sensory responses to noxious stimuli are a form of memory, the memory for pain. Long-lasting synaptic plasticity as long-term potentiation at spinal and supraspinal levels could be providing the neuronal basis for persistent pain and pain memory. Thus, it will be particularly important to know how to regulate long-lasting plastic changes in the spinal cord, thalamus and cortex. Molecular mechanisms of these plastic processes could be main targets for new therapeutic drugs in pain relief. This review presents findings from recent studies that examined the possibility of relations between pain and memory.
Keywords: allodynia, analgesia, hyperalgesia, long-term potentiation, nociception, synaptic plasticity