New Insights on Neuropathic Pain Mechanisms as a Source for Novel Therapeutical Strategies

Abstract

Injuries affecting either the peripheral or the central nervous system (PNS, CNS) leads to neuropathic pain characterized by spontaneous pain and distortion or exaggeration of pain sensation. Peripheral nerve pathologies are considered generally easier to treat compared to those affecting the CNS, however peripheral neuropathies still remain a challenge to thera‐ peutic treatment. Animal models such as denervation/neuroma formation [1], chronic constriction injury (CCI) by loose ligatures around the sciatic nerve [2], partial tight ligation of the sciatic nerve trunk (partial sciatic nerve ligation, PNL) [3]; tight ligature of L5 and L6 spinal nerves (spinal nerve ligation, SNL) [4]; section of one or two components of the sciatic nerve (spared nerve injury, SNI) [5]; streptozocin induced diabetic neuropathy [6] and peripheral neuropathy induced by vincristine or by anti-retroviral nucleoside analogue AIDS therapy drugs [7, 8] have been designed to mimic different neuropathic syndromes and reproduce in laboratory neuropathic pain main symptoms. Indeed all the mentioned neuropathic pain models show increased responses to thermal or mechanical nociceptive stimulation (hyperalgesia), hypersensitivity to innocuous tactile or cold stimuli (allodynia) which lead to withdrawal behaviour.