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Article citations


Latremoliere, A. and Woolf, C.J. (2009) Central sensitization: A generator of pain hypersensitivity by central neural plasticity. The Journal of Pain, 10, 895-926. doi:10.1016/j.jpain.2009.06.012

has been cited by the following article:

  • TITLE: Pain and memory: Do they share similar mechanisms?

    AUTHORS: Merab G. Tsagareli

    KEYWORDS: Allodynia; Analgesia; Hyperalgesia; Nociception; Synaptic Plasticity; Long-Term Potentiation

    JOURNAL NAME: World Journal of Neuroscience, Vol.3 No.1, February 20, 2013

    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.