title: Hyperbaric oxygen therapy attenuates neuropathic hyperalgesia in rats and idiopathic trigeminal neuralgia in patients.
abstract: BACKGROUND
  Neuropathic pain after nerve injury is severe and intractable, and current drug and non-drug therapies offer very limited pain relief. Hyperbaric oxygen (HBO 2) has been clinically used for protection of the nervous system after acute injury. We investigated whether HBO 2 treatment could prevent and/or attenuate neuropathic pain in animals and in patients.
  
  
  METHODS
  Mechanical allodynia and thermal hyperalgesia and neurochemical alterations of neuropathic pain were analysed in male, adult, Sprague-Dawley rats with sciatic nerve injury. Clinical trials were conducted in patients with idiopathic trigeminal neuralgia.
  
  
  RESULTS
  Repetitive HBO 2 treatment [a combination of pressure at 3 atmosphere absolute (ATA) and pure oxygen] greatly inhibited behavioural signs of neuropathic pain manifested as thermal hyperalgesia and mechanical allodynia. Such an HBO 2 treatment also inhibited nerve injury-induced induction of c-Fos and activation of astrocytes and increased phosphorylation of NR2B receptor and the subsequent Ca 2+-dependent signals in rats. Neither high pressure (up to 3 ATA) nor pure oxygen alone resulted in analgesic effect. In clinical trials, one course of HBO 2 therapy (10 consecutive days) produced a rapid-onset, dose-dependent and long-lasting analgesic effects evidenced by the decreased doses of carbamazepine required for keeping patient pain at a minimum and decreased scores of visual analogue scales, which was used for patient's self-evaluation.
  
  
  CONCLUSIONS
  These findings support that HBO 2 therapy is an effective approach for treating neuropathic pain in both animals and human beings and suggest that neural protection, anti-inflammation and inhibition of nerve injury-induced altered neural activity may contribute to the analgesic effect of HBO 2 therapy.
authors.affiliation: Department of Anesthesiology, Xijing Hospital, The Fourth Military Medical University, Xi'an, China.
authors.forename: N
authors.initials: N
authors.lastname: Gu
authors.forename: J-Y
authors.initials: JY
authors.lastname: Niu
authors.forename: W-T
authors.initials: WT
authors.lastname: Liu
authors.forename: Y-Y
authors.initials: YY
authors.lastname: Sun
authors.forename: S
authors.initials: S
authors.lastname: Liu
authors.forename: Y
authors.initials: Y
authors.lastname: Lv
authors.forename: H-L
authors.initials: HL
authors.lastname: Dong
authors.forename: X-J
authors.initials: XJ
authors.lastname: Song
authors.forename: L-Z
authors.initials: LZ
authors.lastname: Xiong
mesh_terms: D000818:Animals; D054732:Calcium-Calmodulin-Dependent Protein Kinase Type 2 / Q000378:metabolism; D000242:Cyclic AMP / Q000378:metabolism; D017362:Cyclic AMP Response Element-Binding Protein / Q000378:metabolism; D004305:Dose-Response Relationship, Drug; D048049:Extracellular Signal-Regulated MAP Kinases / Q000378:metabolism; D005260:Female; D006801:Humans; D006930:Hyperalgesia / Q000378:metabolism / Q000628:therapy*; D006931:Hyperbaric Oxygenation; D008297:Male; D009437:Neuralgia / Q000378:metabolism / Q000628:therapy*; D010147:Pain Measurement; D010766:Phosphorylation; D051381:Rats; D017207:Rats, Sprague-Dawley; D016194:Receptors, N-Methyl-D-Aspartate / Q000378:metabolism; D012584:Sciatic Nerve / Q000293:injuries; D013116:Spinal Cord / Q000378:metabolism*; D016896:Treatment Outcome; D014277:Trigeminal Neuralgia / Q000378:metabolism / Q000628:therapy*
chemical_list: D017362:Cyclic AMP Response Element-Binding Protein; C409466:NR1 NMDA receptor; C121001:NR2B NMDA receptor; D016194:Receptors, N-Methyl-D-Aspartate; D000242:Cyclic AMP; D054732:Calcium-Calmodulin-Dependent Protein Kinase Type 2; D048049:Extracellular Signal-Regulated MAP Kinases