Mechanisms of neuropathic pain

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Mechanisms of neuropathic pain D. Bridges, S.W.N. Thompson, A.S.C. Rice British Journal of Anaesthesia Volume 87, Issue 1, Pages 12-26 (July 2001) DOI: 10.1093/bja/87.1.12 Copyright © 2001 British Journal of Anaesthesia Terms and Conditions

Fig 1 Graphical representation of hyperalgesia and allodynia: stimulus intensity vs response relationship for noxious and innocuous stimuli. British Journal of Anaesthesia 2001 87, 12-26DOI: (10.1093/bja/87.1.12) Copyright © 2001 British Journal of Anaesthesia Terms and Conditions

Fig 2 Schematic drawing of the partial sciatic nerve ligation (tight ligation of 33–50% of the sciatic nerve trunk), CCI (loose ligations of the sciatic nerve trunk), and SNL (tight ligation and transection of the L5 and L6 spinal nerves) animal models of neuropathic pain. British Journal of Anaesthesia 2001 87, 12-26DOI: (10.1093/bja/87.1.12) Copyright © 2001 British Journal of Anaesthesia Terms and Conditions

Fig 3 Summary of the phenomena which have been observed in the central and peripheral nervous system after experimental peripheral nerve injury, which may contribute to neuropathic pain. British Journal of Anaesthesia 2001 87, 12-26DOI: (10.1093/bja/87.1.12) Copyright © 2001 British Journal of Anaesthesia Terms and Conditions

Fig 4 Tyrosine hydroxylase immunoreactivity within the DRG showing post-ganglionic sympathetic fibre invasion after sciatic nerve axotomy (a) and intrathecal administration of NGF (b). Higher power magnification shows the distinct ‘basket’ structures surrounding sensory cell bodies (c), (d) Adapted from Jones and colleagues.62 British Journal of Anaesthesia 2001 87, 12-26DOI: (10.1093/bja/87.1.12) Copyright © 2001 British Journal of Anaesthesia Terms and Conditions

Fig 5 Schematic representation of reorganization of the spinal dorsal horn which is observed after peripheral nerve injury. After the peripheral nerve injury the unmyelinated primary afferent neurones which normally sub-serve nociception and terminate in the superficial dorsal horn degenerate. This allows the larger myelinated primary afferent neurones, which normally sub-serve innocuous sensory modalities, to sprout into the superficial dorsal horn from the laminae deeper in the dorsal horn which normally receive their central terminations. This observation allows some insight into the mechanisms of allodynia. (Adapted with permission from Woolf and Mannion.145) British Journal of Anaesthesia 2001 87, 12-26DOI: (10.1093/bja/87.1.12) Copyright © 2001 British Journal of Anaesthesia Terms and Conditions

Fig 6 Mechanisms of opioid resistance in neuropathic pain: comparison of the effects of inflammation and nerve injury on features of the opioid system. British Journal of Anaesthesia 2001 87, 12-26DOI: (10.1093/bja/87.1.12) Copyright © 2001 British Journal of Anaesthesia Terms and Conditions

Fig 7 Preservation of cannabinoid CB1 receptors in the dorsal horn after dorsal rhizotomy: sections A and B are transverse sections of rat lumbar spinal cord taken from animals which had undergone dorsal rhizotomy. Section A was immunostained for cannabinoid CB1 receptors and there is no significant effect of dorsal rhizotomy. Section B was immunostained for the lectin IB4 (a marker of the GDNF dependent class of primary afferent nociceptor), the loss of IB4 staining ipsilateral to the dorsal rhizotomy indicates adequate degeneration of primary afferent nociceptors. After similar nerve injury, there is a considerable loss of μ-opioid receptor binding (scale bar 100 μm). Adapted from Farquhar-Smith and colleagues.40 British Journal of Anaesthesia 2001 87, 12-26DOI: (10.1093/bja/87.1.12) Copyright © 2001 British Journal of Anaesthesia Terms and Conditions