title: Intrathecal lidocaine reverses tactile allodynia caused by nerve injuries and potentiates the antiallodynic effect of the COX inhibitor ketorolac.
abstract: BACKGROUND
  Systemic lidocaine and other local anesthetics reduce hypersensitivity states induced by both acute inflammation and peripheral nerve injury in animals and produce analgesia in some patients with chronic pain. The mechanisms underlying the antiallodynic effect of systemic lidocaine are unclear, although most focus is on peripheral mechanisms. Central mechanisms, particularly at the spinal dorsal horn level, are less known. In this study, the authors aimed to determine whether intrathecal lidocaine has an antiallodynic effect on established mechanical allodynia in two well-characterized neuropathic pain rat models: partial sciatic nerve ligation (PSNL) and spinal nerve ligation (SNL).
  
  
  METHODS
  Lidocaine (100-300 micro g) was intrathecally injected in PSNL and SNL rats. The withdrawal threshold of both hind paws in response to mechanical stimulation was measured using a series of calibrated von Frey filaments.
  
  
  RESULTS
  This single injection reduced ongoing tactile allodynia in PSNL and SNL rats. The antiallodynic effect of intrathecal lidocaine lasted longer in PSNL (> 3 days) than in SNL rats (< 3 days). Intraperitoneal lidocaine (300 micro g) had no effect on tactile allodynia in PSNL rats. In SNL rats, prior intrathecal lidocaine (200 and 300 micro g) potentiated the antiallodynic effect of intrathecal ketorolac, a nonselective cyclooxygenase inhibitor. Intrathecal ketorolac alone had no antiallodynic effect on SNL rats. However, prior intrathecal lidocaine (100 micro g) failed to potentiate the antiallodynic effect of intrathecal ketorolac.
  
  
  CONCLUSIONS
  The authors' data suggest that intrathecal lidocaine possibly suppressed the hyperexcitability of the dorsal horn neurons and likely interacted with eicosanoid systems in the spinal dorsal horn.
authors.affiliation: Pain Mechanisms Laboratory, Department of Anesthesiology and Center for the Study of Pharmacologic Plasticity, Wake Forest university School of Medicine, wisnton Salem, North Carolina 27157-1009, USA. wma@wfubmc.edu
authors.forename: Weiya
authors.initials: W
authors.lastname: Ma
authors.forename: Wei
authors.initials: W
authors.lastname: Du
authors.forename: James C
authors.initials: JC
authors.lastname: Eisenach
mesh_terms: D000779:Anesthetics, Local / Q000008:administration & dosage / Q000627:therapeutic use*; D000818:Animals; D001522:Behavior, Animal / Q000187:drug effects; D016861:Cyclooxygenase Inhibitors / Q000008:administration & dosage / Q000627:therapeutic use*; D004305:Dose-Response Relationship, Drug; D004357:Drug Synergism; D007278:Injections, Spinal; D020910:Ketorolac / Q000008:administration & dosage / Q000627:therapeutic use*; D008012:Lidocaine / Q000008:administration & dosage / Q000627:therapeutic use*; D008026:Ligation; D008297:Male; D010146:Pain / Q000188:drug therapy* / Q000209:etiology; D010523:Peripheral Nervous System Diseases / Q000188:drug therapy*; D051381:Rats; D017207:Rats, Sprague-Dawley; D012584:Sciatic Nerve / Q000473:pathology; D020426:Sciatic Neuropathy / Q000188:drug therapy; D013127:Spinal Nerves / Q000473:pathology
chemical_list: D000779:Anesthetics, Local; D016861:Cyclooxygenase Inhibitors; D008012:Lidocaine; D020910:Ketorolac