The Analgesic Response to Intravenous Lidocaine in the Treatment of Neuropathic Pain

Abstract

This study was performed in order to determine concentration-effect, and graded and quantal dose-response relationships for the clinical administration of intravenous (IV) lidocaine to patients with neuropathic pain. Thirteen patients were administered 500 mg of IV lidocaine at a rate of 8.35 mg/min over 60 min. Visual analog pain scores and venous blood samples were obtained concomitantly at 10 min intervals for 60 min. Blood samples were also obtained for determination of serum and serum water lidocaine concentrations at the onset of analgesia and at the time complete pain relief was attained. Lidocaine concentrations were determined by gas chromatography. Graded dose-response curves were prepared individually and for the group as a whole, and a quantal dose-response curve was prepared for the entire group. The dose-response relationship for IV lidocaine was characterized by large increases in pain relief for concomitant minimal increases in dosage. The difference between the ED50 (372.0 mg) and the ED90 (416.5 mg) was 44.5 mg of lidocaine (5.3 min of infusion). The concentration-effect relationship was also steep with pain scores abruptly decreasing over a range of 0.62 microgram/mL of lidocaine. Interestingly, the free concentration of lidocaine had no better correlation with the onset of analgesia or the attainment of complete analgesia than the serum concentration of lidocaine. This suggests that the mechanism of analgesia to IV lidocaine may not be based upon a conventional concentration-effect relationship. In conclusion, the results of this study suggest that the analgesic response to IV lidocaine is best characterized by a precipitous "break in pain" over a narrow dosage and concentration range.

Effect of Intravenous Lidocaine on the Neuropathic Pain of Failed Back Surgery Syndrome

“…The analgesic effects of lidocaine observed in our patients did not different among 1 mg/kg and 5 mg/kg of lidocaine.Results of the present study which VAS was decreased correspond with the results of earlier studies [6,7,16,17]. This suggests that lidocaine produces a dose-related reduction of afferent activity from dorsal root ganglion [8-10].…”

“…Moreover, the free concentration of lidocaine showed no better correlation with the onset of analgesia or the attainment of complete analgesia than the serum concentration of lidocaine. Ferrante et al [17] suggested that the mechanism of analgesia from IV lidocaine is not being based upon a conventional concentration-effect relationship and there was not a direct relationship between total or free lidocaine levels and the effect on neuropathic pain [15]. However, we did not determine the blood levels of lidocaine.…”

Antinociceptive effect of ambroxol in rats with neuropathic spinal cord injury pain

“…Clinical use of non-selective Na + channel blockers lidocaine and its analogue mexiletine appear to be effective on some neuropathic pain symptoms, the efficacy being non-dose dependent and the centrally-mediated side-effects are not well tolerated (Attal et al, 2004; Ferrante et al, 1996; Finnerup et al, 2005; Wallace et al, 2000). In a previous study, the highest tested dose of mexiletine (75 mg/kg) did not ameliorate either mechanical or heat hypersensitivity in SCI rats (Hama and Sagen, 2007).…”

“…Ambroxol’s effect on mechanical hypersensitivity was restricted to the highest tested dose, similar to that observed in peripheral nerve-injured rats (Gaida et al, 2005). The all-or-none effect with Na + channel blocking drugs has also been clinically observed (Ferrante et al, 1996). The high dose-only effect could be related to the limited distribution of Na v 1.8 in large-diameter mechano-sensitive primary afferents in contrast to the abundant expression of Na v 1.8 in small-diameter nociceptors.…”

Lidocaine priming reduces tourniquet pain during intravenous regional anesthesia: A preliminary study☆

“…15 In the second study, pain in 5 patients with various neuropathic syndromes was reduced when toxic lidocaine levels (Ͼ3 g/mL) were achieved following a total dose of 3 mg/kg. 16 Non-sodium channel mechanisms are also plausible explanations for the antihyperalgesic actions of lidocaine, including inhibition of substance P, 17 NMDA receptors, 18 and glutamate activity. 19 A study using the isolated arm technique in humans 20 supports a peripheral analgesic effect of regional intravenous infusion of lidocaine on the development of mechanical-induced hyperalgesia and histamine-induced itching, but not touch perception and heat-induced nociception.…”