Browsing by Subject "Lidocaine"

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    Effective spread and timecourse of neural inactivation caused by lidocaine injection in monkey cerebral cortex.
    (J Neurosci Methods, 1997-06-06) Tehovnik, EJ; Sommer, MA
    We studied the effective spread of lidocaine to inactivate neural tissue in the frontal cortex of the rhesus monkey. Injections of 2% lidocaine at 4 microl/min were made while units were recorded 1 or 2 mm away. To inactivate units 1 mm away from the injection site 100% of the time, 7 microl of lidocaine had to be injected. To inactivate units 2 mm away from the injection site 100% of the time, 30 microl of lidocaine were required. Units were maximally inactivated around 8 min after the start of a lidocaine injection, and they gradually recovered, regaining most of their initial activity by around 30 min after the start of an injection. The volume of lidocaine required to inactivate neurons > 90% of the time could be estimated by the spherical volume equation, V = 4/3 pi (r)3. To prolong the inactivation, a slower infusion of lidocaine subsequent to an initial bolus was effective. Saline control injections had no effect. These results allow both a prediction of the timecourse of neural inactivation and an estimate of the spread of neural inactivation following injection of lidocaine into the monkey cerebral cortex.
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    Intravenous Lidocaine Does Not Improve Neurologic Outcomes after Cardiac Surgery: A Randomized Controlled Trial.
    (Anesthesiology, 2019-06) Klinger, Rebecca Y; Cooter, Mary; Bisanar, Tiffany; Terrando, Niccolò; Berger, Miles; Podgoreanu, Mihai V; Stafford-Smith, Mark; Newman, Mark F; Mathew, Joseph P; Neurologic Outcomes Research Group of the Duke Heart Center

    Background

    Cognitive decline after cardiac surgery occurs frequently and persists in a significant proportion of patients. Preclinical studies and human trials suggest that intravenous lidocaine may confer protection in the setting of neurologic injury. It was hypothesized that lidocaine administration would reduce cognitive decline after cardiac surgery compared to placebo.

    Methods

    After institutional review board approval, 478 patients undergoing cardiac surgery were enrolled into this multicenter, prospective, randomized, double-blinded, placebo-controlled, parallel group trial. Subjects were randomized to lidocaine 1 mg/kg bolus after the induction of anesthesia followed by a continuous infusion (48 μg · kg · min for the first hour, 24 μg · kg · min for the second hour, and 10 μg · kg · min for the next 46 h) or saline with identical volume and rate changes to preserve blinding. Cognitive function was assessed preoperatively and at 6 weeks and 1 yr postoperatively using a standard neurocognitive test battery. The primary outcome was change in cognitive function between baseline and 6 weeks postoperatively, adjusting for age, years of education, baseline cognition, race, and procedure type.

    Results

    Among the 420 allocated subjects who returned for 6-week follow-up (lidocaine: N = 211; placebo: N = 209), there was no difference in the continuous cognitive score change (adjusted mean difference [95% CI], 0.02 (-0.05, 0.08); P = 0.626). Cognitive deficit (greater than 1 SD decline in at least one cognitive domain) at 6 weeks occurred in 41% (87 of 211) in the lidocaine group versus 40% (83 of 209) in the placebo group (adjusted odds ratio [95% CI], 0.94 [0.63, 1.41]; P = 0.766). There were no differences in any quality of life outcomes between treatment groups. At the 1-yr follow-up, there continued to be no difference in cognitive score change, cognitive deficit, or quality of life.

    Conclusions

    Intravenous lidocaine administered during and after cardiac surgery did not reduce postoperative cognitive decline at 6 weeks.
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    Lidocaine patch for acute pain management: a meta-analysis of prospective controlled trials.
    (Curr Med Res Opin, 2015-03) Bai, Yaowu; Miller, Timothy; Tan, Mingjuan; Law, Lawrence Siu-Chun; Gan, Tong Joo
    BACKGROUND: Local anesthetic is one of the cornerstones of multimodal analgesia. We investigated the efficacy of the lidocaine patch for acute pain management. METHODS: We searched MEDLINE, CINAHL, Scopus, and the Cochrane Controlled Trials Register for published prospective controlled clinical trials that evaluated the analgesic effect of the lidocaine patch for acute or postoperative pain management (1966--2014). The outcomes were postoperative opioid consumption, pain intensity and length of hospital stay. RESULTS: Five trials comparing the lidocaine patch with control (no treatment/placebo) for acute or postoperative pain treatment/management were included in this meta-analysis. Data was analyzed on 251 patients. Between the lidocaine patch group and the control group, no significant difference was found for all three outcomes (all p > 0.05). For postoperative opioid consumption, mean difference (MD) was -8.2 mg morphine equivalent (95% CI -28.68, 12.24). For postoperative pain intensity, MD was -9.1 mm visual analog scale or equivalent (95% CI -23.31, 5.20). For length of hospital stay, MD was -0.2 days (95% CI -0.80, 0.43). CONCLUSION: Application of a lidocaine patch may not be an effective adjunct for acute and postoperative pain management, in terms of pain intensity, opioid consumption and length of hospital stay. LIMITATIONS: The limitations were a small number of included studies, potential biases from some unblinded studies, clinical heterogeneity between studies, and incomplete reported data for adjunct analgesics.
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    Neuroanesthesia Guidelines for Optimizing Transcranial Motor Evoked Potential Neuromonitoring During Deformity and Complex Spinal Surgery: A Delphi Consensus Study.
    (Spine, 2020-07) Walker, Corey T; Kim, Han Jo; Park, Paul; Lenke, Lawrence G; Weller, Mark A; Smith, Justin S; Nemergut, Edward C; Sciubba, Daniel M; Wang, Michael Y; Shaffrey, Christopher; Deviren, Vedat; Mummaneni, Praveen V; Chang, Joyce M; Mummaneni, Valli P; Than, Khoi D; Berjano, Pedro; Eastlack, Robert K; Mundis, Gregory M; Kanter, Adam S; Okonkwo, David O; Shin, John H; Lewis, Jason M; Koski, Tyler; Hoh, Daniel J; Glassman, Steven D; Vinci, Susan B; Daniels, Alan H; Clavijo, Claudia F; Turner, Jay D; McLawhorn, Marc; Uribe, Juan S

    Study design

    Expert opinion-modified Delphi study.

    Objective

    We used a modified Delphi approach to obtain consensus among leading spinal deformity surgeons and their neuroanesthesiology teams regarding optimal practices for obtaining reliable motor evoked potential (MEP) signals.

    Summary of background data

    Intraoperative neurophysiological monitoring of transcranial MEPs provides the best method for assessing spinal cord integrity during complex spinal surgeries. MEPs are affected by pharmacological and physiological parameters. It is the responsibility of the spine surgeon and neuroanesthesia team to understand how they can best maintain high-quality MEP signals throughout surgery. Nevertheless, varying approaches to neuroanesthesia are seen in clinical practice.

    Methods

    We identified 19 international expert spinal deformity treatment teams. A modified Delphi process with two rounds of surveying was performed. Greater than 50% agreement on the final statements was considered "agreement"; >75% agreement was considered "consensus."

    Results

    Anesthesia regimens and protocols were obtained from the expert centers. There was a large amount of variability among centers. Two rounds of consensus surveying were performed, and all centers participated in both rounds of surveying. Consensus was obtained for 12 of 15 statements, and majority agreement was obtained for two of the remaining statements. Total intravenous anesthesia was identified as the preferred method of maintenance, with few centers allowing for low mean alveolar concentration of inhaled anesthetic. Most centers advocated for <150 μg/kg/min of propofol with titration to the lowest dose that maintains appropriate anesthesia depth based on awareness monitoring. Use of adjuvant intravenous anesthetics, including ketamine, low-dose dexmedetomidine, and lidocaine, may help to reduce propofol requirements without negatively effecting MEP signals.

    Conclusion

    Spine surgeons and neuroanesthesia teams should be familiar with methods for optimizing MEPs during deformity and complex spinal cases. Although variability in practices exists, there is consensus among international spinal deformity treatment centers regarding best practices.

    Level of evidence

    5.
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    Rationale and design of a multicenter randomized clinical trial of vestibulodynia: understanding pathophysiology and determining appropriate treatments (vestibulodynia: UPDATe).
    (Annals of medicine, 2022-12) Carey, Erin T; Geller, Elizabeth J; Rapkin, Andrea; Farb, Debbie; Cutting, Haley; Akaninwor, Jasmyn; Stirling, Christopher; Bortsov, Andrey; McNulty, Steven; Merrill, Peter; Zakroysky, Pearl; DeLaRosa, Jesse; Luo, Sheng; Nackley, Andrea G

    Background

    Limited data are available to establish evidence-based management protocols for vestibulodynia (VBD), a chronic vulvar pain condition that affects approximately 14 million women in the U.S. For the purposes of the study, our group subdivided VBD subtypes that may benefit from different types of treatment: 1) VBD peripheral (VBD-p), characterized by pain localized to the vulvar vestibule and 2) VBD central (VBD-c), characterized by VBD alongside one or more other chronic overlapping pain conditions (e.g. irritable bowel syndrome, temporomandibular disorder, and fibromyalgia syndrome) that affect remote body regions. Here, we describe the rationale and design of an NIH-funded multicenter clinical trial comparing the effectiveness of topical and/or systemic medication for alleviating pain and normalizing pain- relevant biomarkers among women with VBD-p and VBD-c.

    Methods

    Participants will be randomly assigned to one of four parallel arms: peripheral treatment with 5% lidocaine + 0.5 mg/ml 0.02% oestradiol compound cream + oral placebo pill, 2) central treatment with the tricyclic antidepressant nortriptyline + placebo cream, 3) combined peripheral cream and central pill treatments, or 4) placebo cream and placebo pill. The treatment phase will last 16 weeks, with outcome measures and biomarkers assessed at 4 time points (0, 8, 16, and 24 weeks). First, we will compare the efficacy of treatments in alleviating pain using standardized tampon insertion with a numeric rating scale and self-reported pain on the short form McGill Pain Questionnaire. Next, we will compare the efficacy of treatments in improving perceived physical, mental, and sexual health using standardized questionnaires. Finally, we will measure cytokines and microRNAs in local vaginal and circulating blood samples using multiplex assays and RNA sequencing, and determine the ability of these biomarkers to predict treatment response.

    Conclusion

    This is the first multicenter randomized controlled trial to evaluate the efficacy of peripherally and centrally acting medications currently used in clinical practice for treating unique VBD subtypes based on distinct clinical and biological signatures.

    Administrative information

    Vestibulodynia UPDATe is a multi-centre, two-by-two factorial designed randomized, double-blind, placebo-controlled trial registered at clinical trials.gov (NCT03844412). This work is supported by the R01 HD096331 awarded to Drs. Nackley, Rapkin, Geller and Carey by the Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD).Key messagesPeripheral lidocaine and oestradiol and centrally-targeted nortriptyline medications are used for the treatment of pain in women with VBD, but there is a lack of data from well-powered RCTs.This two-by-two factorial RCT will test the efficacy of these medications in VBD subtypes characterized by distinct clinical characteristics and biomarker profiles.We hope that results will provide clinicians with scientific evidence of therapeutic efficacy in distinct VBD subtypes in an effort to direct and optimize treatment approaches.
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    Reversible inactivation of macaque dorsomedial frontal cortex: effects on saccades and fixations.
    (Exp Brain Res, 1999-02) Sommer, MA; Tehovnik, EJ
    Neural recording and electrical stimulation results suggest that the dorsomedial frontal cortex (DMFC) of macaque is involved in oculomotor behavior. We reversibly inactivated the DMFC using lidocaine and examined how saccadic eye movements and fixations were affected. The inactivation methods and monkeys were the same as those used in a previous study of the frontal eye field (FEF), another frontal oculomotor region. In the first stage of the present study, monkeys performed tasks that required the generation of single saccades and fixations. During 15 DMFC inactivations, we found only mild, infrequent deficits. This contrasts with our prior finding that FEF inactivation causes severe, reliable deficits in performance of these tasks. In the second stage of the study, we investigated whether DMFC inactivation affected behavior when a monkey was required to make more than one saccade and fixation. We used a double-step task: two targets were flashed in rapid succession and the monkey had to make two saccades to foveate the target locations. In each of five experiments, DMFC inactivation caused a moderate, significant deficit. Both ipsi- and contraversive saccades were disrupted. In two experiments, the first saccades were made to the wrong place and had increased latencies. In one experiment, first saccades were unaffected, but second saccades were made to the wrong place and had increased latencies. In the remaining two experiments, specific reasons for the deficit were not detected. Saline infusions into DMFC had no effect. Inactivation of FEF caused a larger double-step deficit than did inactivation of DMFC. The FEF inactivation impaired contraversive first or second saccades of the sequence. In conclusion, our results suggest that the DMFC makes an important contribution to generating sequential saccades and fixations but not single saccades and fixations. Compared with the FEF, the DMFC has a weaker, less directional, more task-dependent oculomotor influence.
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    Reversible inactivation of macaque frontal eye field.
    (Exp Brain Res, 1997-09) Sommer, MA; Tehovnik, EJ
    The macaque frontal eye field (FEF) is involved in the generation of saccadic eye movements and fixations. To better understand the role of the FEF, we reversibly inactivated a portion of it while a monkey made saccades and fixations in response to visual stimuli. Lidocaine was infused into a FEF and neural inactivation was monitored with a nearby microelectrode. We used two saccadic tasks. In the delay task, a target was presented and then extinguished, but the monkey was not allowed to make a saccade to its location until a cue to move was given. In the step task, the monkey was allowed to look at a target as soon as it appeared. During FEF inactivation, monkeys were severely impaired at making saccades to locations of extinguished contralateral targets in the delay task. They were similarly impaired at making saccades to locations of contralateral targets in the step task if the target was flashed for < or =100 ms, such that it was gone before the saccade was initiated. Deficits included increases in saccadic latency, increases in saccadic error, and increases in the frequency of trials in which a saccade was not made. We varied the initial fixation location and found that the impairment specifically affected contraversive saccades rather than affecting all saccades made into head-centered contralateral space. Monkeys were impaired only slightly at making saccades to contralateral targets in the step task if the target duration was 1000 ms, such that the target was present during the saccade: latency increased, but increases in saccadic error were mild and increases in the frequency of trials in which a saccade was not made were insignificant. During FEF inactivation there usually was a direct correlation between the latency and the error of saccades made in response to contralateral targets. In the delay task, FEF inactivation increased the frequency of making premature saccades to ipsilateral targets. FEF inactivation had inconsistent and mild effects on saccadic peak velocity. FEF inactivation caused impairments in the ability to fixate lights steadily in contralateral space. FEF inactivation always caused an ipsiversive deviation of the eyes in darkness. In summary, our results suggest that the FEF plays major roles in (1) generating contraversive saccades to locations of extinguished or flashed targets, (2) maintaining contralateral fixations, and (3) suppressing inappropriate ipsiversive saccades.