title: Differential effect of ketamine and lidocaine on spontaneous and mechanical evoked pain in patients with nerve injury pain.
abstract: BACKGROUND
  The mechanisms underlying neuropathic pain are incompletely understood. Targeting specific molecular mechanisms in the pain signaling system may assist in understanding key features in neuropathic pains such as allodynia. This study examined the effect of systemically administered ketamine, an N-methyl-D-aspartate receptor antagonist and lidocaine, a sodium channel blocker, on spontaneous pain, brush-evoked pain, and pinprick-evoked pain in patients with nerve injury pain.
  
  
  METHODS
  Twenty patients participated in two randomized, double-blinded, placebo-controlled, crossover experiments in which they, on four different days, received a 30-minute intravenous infusion of ketamine (0.24 mg/kg), lidocaine (5 mg/kg), or saline. Ongoing pain, pain evoked by brush and repetitive pinprick stimuli, and acetone was measured before, during, and after infusion.
  
  
  RESULTS
  Ketamine significantly reduced ongoing pain and evoked pain to brush and pinprick, whereas lidocaine only reduced evoked pain to repetitive pinprick stimuli. In individual patients, there was no correlation between the pain-relieving effect of lidocaine and ketamine on ongoing or mechanically evoked pains.
  
  
  CONCLUSIONS
  N-methyl-D-aspartate receptor-linked systems and sodium channels are involved in generation and maintenance of pain in patients with peripheral nerve injury. It is likely that ongoing pain as well as mechanical hyperalgesia in individual patients is dependent on several separate molecular mechanisms.
authors.affiliation: Danish Pain Research Center, Department of Neurology, University of Aarhus, Aarhus, Denmark. gottrup.friis@stofanet.dk
authors.forename: Hanne
authors.initials: H
authors.lastname: Gottrup
authors.forename: Flemming W
authors.initials: FW
authors.lastname: Bach
authors.forename: Gitte
authors.initials: G
authors.lastname: Juhl
authors.forename: Troels S
authors.initials: TS
authors.lastname: Jensen
mesh_terms: D000328:Adult; D000368:Aged; D018592:Cross-Over Studies; D004311:Double-Blind Method; D005260:Female; D006801:Humans; D007649:Ketamine / Q000009:adverse effects / Q000097:blood / Q000627:therapeutic use*; D008012:Lidocaine / Q000009:adverse effects / Q000097:blood / Q000627:therapeutic use*; D008297:Male; D008875:Middle Aged; D010146:Pain / Q000188:drug therapy*; D010147:Pain Measurement; D010523:Peripheral Nervous System Diseases / Q000188:drug therapy* / Q000503:physiopathology; D011930:Reaction Time; D016194:Receptors, N-Methyl-D-Aspartate / Q000502:physiology; D015222:Sodium Channels / Q000502:physiology
chemical_list: D016194:Receptors, N-Methyl-D-Aspartate; D015222:Sodium Channels; D007649:Ketamine; D008012:Lidocaine