1991
DOI: 10.1097/00000542-199105000-00020
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Analgesic Concentrations of Lidocaine Suppress Tonic A-delta and C Fiber Discharges Produced by Acute Injury

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Cited by 199 publications
(73 citation statements)
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“…The acute outbreak of zoster may damage the peripheral nerve apparatus from the dorsal root to cutaneous nerve endings [16][17][18] . Surviving but damaged cutaneous nociceptor fibers in the area of pain may have abnormal spontaneous activity and be sensitized to mechanical or other stimuli [19][20][21][22][23] . These changes may in part be due to accumulation of sodium channels at the injury sites [23][24][25] .…”
Section: Discussionmentioning
confidence: 99%
“…The acute outbreak of zoster may damage the peripheral nerve apparatus from the dorsal root to cutaneous nerve endings [16][17][18] . Surviving but damaged cutaneous nociceptor fibers in the area of pain may have abnormal spontaneous activity and be sensitized to mechanical or other stimuli [19][20][21][22][23] . These changes may in part be due to accumulation of sodium channels at the injury sites [23][24][25] .…”
Section: Discussionmentioning
confidence: 99%
“…Therapeutic plasma levels and duration of IVLT for acute pain management are not well defined, although the optimal therapeutic range for acute pain treatment appears to be between 1 and 5 μg/ml [6,24,[117][118][119][120]. Only preservative free formulations should be given intravenously.…”
Section: Myoclonic Jerks Dysphoria/hallucinationsmentioning
confidence: 99%
“…Systemic administration of local anaesthetics provides clinical analgesia in a broad range of neuropathic pain states [23,117,[137][138][139][140]. IVLT induces global analgesia and dampens the neuro-inflammatory response in pain [126,[141][142][143][144].…”
Section: The Rationale For Ivlt In the Management Of Painmentioning
confidence: 99%
See 1 more Smart Citation
“…Electrophysiologic studies aimed at elucidating the site at which lidocaine and tocainide exert their antinociceptive action provide compelling evidence in support of a central site of action. [14][15][16] With regard to a peripheral mechanism, animal models of nerve injury 14,[17][18][19][20] and a model of phantom limb pain in humans 21 seem to indicate that after nerve injury peripheral mechanisms may develop that are responsive to the blockade of sodium channels.…”
Section: Solutionmentioning
confidence: 99%