The Use and Method of Action of Intravenous Lidocaine and Its Metabolite in Headache Disorders

Berk, Thomas; Silberstein, Stephen D.

doi:10.1111/head.13298

Cited by 42 publications

(18 citation statements)

References 53 publications

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“…The analgesic benefits of lidocaine also may be mediated indirectly via its primary metabolite, monoethylglycine (MEG) [ 24 , 26 ]. Animal models suggest that MEG attenuates the inflammatory pain response and indirectly regulates the extracellular glycine concentration via competitive inhibition of the glycine transporter, GlyT1 [ 26 ]. Glycine is a major neurotransmitter involved in the descending regulation of pain [ 25 , 26 ].…”

Section: Intravenous Lidocainementioning

confidence: 99%

Beyond the Raskin Protocol: Ketamine, Lidocaine, and Other Therapies for Refractory Chronic Migraine

Mojica

Schwenk

Lauritsen

et al. 2021

Curr Pain Headache Rep

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Purpose of Review The purpose of this review is to discuss the available evidence and therapeutic considerations for intravenous drug therapy for refractory chronic migraine. Recent Findings In carefully monitored settings, the inpatient administration of intravenous lidocaine and ketamine can be successful in treating refractory chronic migraine. Summary Many patients with refractory chronic migraine have experienced treatment failure with the Raskin protocol. The use of aggressive inpatient infusion therapy consisting of intravenous lidocaine or ketamine, along with other adjunctive medications, has become increasingly common for these patients when all other treatments have failed. There is a clear need for prospective studies in this population comprised of patients who have largely been excluded from other studies.

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Section: Intravenous Lidocainementioning

confidence: 99%

Beyond the Raskin Protocol: Ketamine, Lidocaine, and Other Therapies for Refractory Chronic Migraine

Mojica

Schwenk

Lauritsen

et al. 2021

Curr Pain Headache Rep

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show abstract

“…Lidocaine is a local anesthetic that exerts efficacy within 1–3 min after administration, with an anesthetic effect that lasts for 1–3 h ( 6 ). In clinical practice, it is used to treat arrhythmia and is the first line of treatment for patients with ventricular tachycardia and tremor ( 7 , 8 ). The current evidence has demonstrated that treatment with lidocaine eliminates severe arrhythmia and prevents heart death in an in vivo rat model of acute myocardial I/R ( 9 ).…”

Section: Introductionmentioning

confidence: 99%

Lidocaine attenuates hypoxia/reoxygenation‑induced inflammation, apoptosis and ferroptosis in lung epithelial cells by regulating the p38 MAPK pathway

Yan

2022

Mol Med Rep

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Lung ischemia-reperfusion (I/R) injury poses a serious threat to human health, worldwide. The current study aimed to determine the role of lidocaine in A549 cells, in addition to the involvement of the p38 MAPK pathway. Oxygen deprivation/reoxygenation-induced A549 cells were utilized to simulate I/R injury in vitro . Cell viability and apoptosis were detected using MTT and TUNEL assays, respectively. The levels of IL-6, IL-8, TNF-α, malondialdehyde (MDA), superoxide dismutase (SOD), glutathione peroxidase, iron and reactive oxygen species (ROS) were measured using corresponding commercial kits. The corresponding protein expression levels were also measured using western blotting. Moreover, a monolayer cell paracellular permeability assay was performed to determine the permeability of A549 cells. The results demonstrated that, whilst lidocaine had no influence on untreated A549 cells, it significantly increased the viability of hypoxia/reoxygenation (H/R)-induced A549 cells. A549 cell apoptosis and the release of inflammatory cytokines in the H/R group were decreased after the addition of lidocaine. When compared with the H/R group, increased MDA level and decreased SOD level were observed in H/R-induced A549 cells following lidocaine treatment. In addition, the permeability of H/R-induced A549 cells was markedly decreased following lidocaine treatment. Compared with the H/R group, the expression levels of tight junction and ferroptosis-related proteins were significantly upregulated by lidocaine, whereas the expression of transferrin was downregulated. However, p79350, an agonist of p38, reversed the effects of lidocaine on H/R-induced A549 cells. In conclusion, lidocaine exerted a protective role in HR-induced lung epithelial cell injury, which may serve as a potential agent for the treatment of patients with lung I/R injury.

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“…Besides local anesthesia, lidocaine is capable for general anesthesia, intrathecal anesthesia, and antiarrhythmic as well. 12 , 13 In 1961, Bartlett and Hutaserani had firstly shown the efficacy of systemic lidocaine for the relief of postoperative pain. 14 Recent studies have given credit for the strategy that bolus infusion of lidocaine 1~1.5 mg/kg during anesthesia induction followed by a continuous infusion of lidocaine 1.5~2 mg/kg/h until the end of surgery.…”

Section: Introductionmentioning

confidence: 99%

Efficacy of Perioperative Continuous Intravenous Lidocaine Infusion for 72 Hours on Postoperative Pain and Recovery in Patients Undergoing Hepatectomy: Study Protocol for a Prospective Randomized Controlled Trial

Xu¹,

Ye²,

Hong³

et al. 2021

JPR

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Purpose: Many patients develop severe and persistent pain after hepatectomy delaying postoperative rehabilitation. Studies have suggested that intravenous lidocaine infusion relieved postoperative pain and improved overall postoperative outcomes. However, its efficacy on hepatectomy is still masked, due to the postoperative metabolic change of lidocaine by the liver. We hypothesized that intravenous lidocaine infusion in the perioperative period would lead to postoperative pain reduction and improve the overall patient experience. Study Design and Methods: In this prospective double-blind, randomized controlled design trial, 260 adults scheduled for hepatectomy will be allocated to the lidocaine and the placebo groups. The lidocaine group will be administered lidocaine intravenously during intraoperative period and 72 postoperative hours; the placebo group will be administered normal saline at the same volume, infusion rate, and timing. The primary outcome is the incidence of moderate-severe pain (numeric rating scale ≥4) during movement at 24 hours after surgery. The secondary outcomes include the incidence of moderate-severe pain at 24 hours after surgery at rest, the incidence of moderate-severe pain at 48 and 72 hours after surgery at rest and during movement, the cumulative morphine consumption at 24, 48 and 72 hours postoperatively, bowel function recovery, the incidence of postoperative nausea and vomiting, the incidence of postoperative pulmonary complications, the length of hospital stay, levels of inflammatory factors and patient satisfaction scores. Discussion: This is the first prospective trial to shed light on the efficacy of intraoperative period and 72 postoperative hours intravenous lidocaine on postoperative pain and recovery after hepatectomy. The findings will provide a new strategy of perioperative pain management for hepatectomy.

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The Use and Method of Action of Intravenous Lidocaine and Its Metabolite in Headache Disorders

Abstract: Open label and retrospective studies have investigated the use of lidocaine in many headache disorders, primarily via injection or infusion. Further research into the active metabolite of lidocaine may allow for its use as a novel nonopiate treatment of chronic pain.

Cited by 42 publications

References 53 publications

Beyond the Raskin Protocol: Ketamine, Lidocaine, and Other Therapies for Refractory Chronic Migraine

Beyond the Raskin Protocol: Ketamine, Lidocaine, and Other Therapies for Refractory Chronic Migraine

Lidocaine attenuates hypoxia/reoxygenation‑induced inflammation, apoptosis and ferroptosis in lung epithelial cells by regulating the p38 MAPK pathway

Efficacy of Perioperative Continuous Intravenous Lidocaine Infusion for 72 Hours on Postoperative Pain and Recovery in Patients Undergoing Hepatectomy: Study Protocol for a Prospective Randomized Controlled Trial

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