Abstract
The pathophysiology of pain syndromes refers to two groups of experimental models aimed to mimic inflammatory and neuropathic pain [1]. In the first case, an overstimulation of peripheral nociceptors leads to pain sensation and to abnormal sensory modalities characterized by changes in quality sensation, like allodynia or increased response to painful stimuli such as hyperalgesia. In the second case, a lesion of peripheral or central pain pathways causes persistent pain that also comprises aberrant somatosensory processes, such as the phantom limb. In inflammatory pain, pain fibres are intact and no anatomical rearrangements in spinal and supraspinal tracts are present. In contrast, in neuropathic pain all tracts involved in pain transmission undergo severe anatomical rearrangements that take part in pain syndrome generation and evolution.
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Calzà, L., Pozza, M., Zanni, M. (1999). Neurochemical memory in pain circuits. In: Tiengo, M., Paladini, V.A., Rawal, N. (eds) Regional Anaesthesia Analgesia and Pain Management. Topics in Anaesthesia and Critical Care. Springer, Milano. https://doi.org/10.1007/978-88-470-2240-9_2
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DOI: https://doi.org/10.1007/978-88-470-2240-9_2
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