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      Prolongation of greater occipital neural blockade with 10% lidocaine neurolysis: a case series of a new technique

      ,

      Journal of Pain Research

      Dove Medical Press

      pain relief, migraines, occipital neuralgia, intractable headaches, injections

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          Abstract

          Introduction

          Greater occipital nerve blocks (GONB) have been used for headache but their benefit may be short. Ready et al performed intrathecal injections on rabbits and reported neurologic/histologic changes that required concentrations of at least 8%. Our study tests the hypothesis that the neurolytic effects of GONB with 10% lidocaine can prolong relief.

          Methods

          After an approval from Henry Ford Hospital Institutional Review Board, a chart review was performed for patients who had GONB with 10% lidocaine. Patients received 10% lidocaine after short response (<1 month / >50% relief) to GONB with 1 cc of a solution containing 9 mL 0.5 % bupivacaine and 40 mg methylprednisolone. They received a block with 10% lidocaine with volume given at <80% of the maximum dose of 4 mg/kg. Injections were performed under fluoroscopic guidance after injection of 0.1 cc of contrast (isovue or magnevist). All patients had intravenous access and were given fentanyl and midazolam. The visual analog scale (VAS) scores were recorded on follow-up, and the duration of response was noted. VAS changes with 10% lidocaine and comparison of duration with methylprednisolone were performed using paired t-test.

          Results

          Thirteen patients were reviewed; 12 were female and the mean age was 47. Ten were diagnosed with migraine, and three with occipital neuralgia; 12 had bilateral symptoms. Baseline VAS prior to 10% lidocaine averaged 86.92 mm. The mean volume injected per nerve was 1.096 mL. There was significant decrease in mean% VAS with 10% lidocaine at 60.4% (mean: −52.69 mm) ( P=0.001). The mean duration of relief was significantly higher with 10% lidocaine at 148.05 days ([standard deviation]=98.87) versus methylprednisolone at 6.33 days (standard deviation=5.01) ( P=0.001). No complications or side effects were reported.

          Conclusion

          Ten percent lidocaine may be a useful neurolytic agent in prolonging the duration of GONB.

          Related collections

          Most cited references 37

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          Greater occipital nerve injection in primary headache syndromes--prolonged effects from a single injection.

          Most patients with primary headache syndromes who have frequent attacks of pain have tenderness in the sub-occipital region. Injection of the greater occipital nerve (GON) with local anesthetic and corticosteroids has been widely used in clinical practice for many years, yet there is no clear understanding of its mechanisms of action. Moreover, there is no current gold-standard of practice regarding GON injections in the management of headache. We audited of our practice to generate hypotheses about the range of primary headaches that might benefit, to determine response rates to power future studies, and to assess whether we should continue to do this procedure. Twenty-six of fifty-seven injections in 54 migraineurs yielded a complete or partial response that lasted for the partial response a median of 30 days. For cluster headache 13 of 22 injections yielded a complete or partial response lasting for a median of 21 days for the partial response. Tenderness over the GON was strongly predictive of outcome, although local anesthesia after the injection was not. The presence or absence of medication overuse did not predict outcome. Apart from two patients with a small patch of alopecia the injection was well tolerated. GON injection is a useful tool in some patients that provides interim relief while other approaches are explored. It is remarkable that in all conditions in which an effect is observed the response time so much exceeds the local anesthetic effect that the mechanism of action may well be through changes in brain nociceptive pathways.
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            The International classification of headache disorders, 2nd edn (ICDH-II).

             J Olesen,  T Steiner (2004)
            Better classification of headache disorders enables better headache research, understanding of headache, communication, and, ultimately, management of a set of disabling neurological disorders.
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              • Article: not found

              Irreversible conduction block in isolated nerve by high concentrations of local anesthetics.

              Delivery of large doses of local anesthetics for spinal anesthesia by repeated injections or continuous infusion could expose the cauda equina to concentrations of drug that may be neurotoxic per se. We studied this possible neurotoxic effect by assessing recovery from conduction blockade of desheathed peripheral nerves after exposure to some of the local anesthetic solutions commonly used for spinal anesthesia. The reversibility of conduction blockade was studied in desheathed bullfrog sciatic nerves, using the sucrose-gap method for recording compound action potentials, before and during exposure to local anesthetics and during drug washout. The nerves were exposed for 15 min to 5% or 1.5% lidocaine, with or without 7.5% dextrose; 0.5% tetracaine; or 0.75% bupivacaine (the latter two without dextrose). Some nerves were also bathed in 7.5% dextrose (without local anesthetic) or in 0.06% tetracaine, which in this preparation is equipotent to 5% lidocaine. After 15 min in the drug, the nerves were washed for 2-3 h and soaked in Ringer's solution overnight. Nerves exposed only to Ringer's solution served as controls. We also studied neuronal uptake and washout of radiolabeled lidocaine. Exposure of nerves to 5% lidocaine, with or without 7.5% dextrose, or to 0.5% tetracaine resulted in irreversible total conduction blockade, whereas 1.5% lidocaine or 0.75% bupivacaine caused 25-50% residual block after the 2-3 h wash. Nerves exposed to Ringer's solution, 7.5% dextrose or 0.06% tetracaine had 0-10% residual block after 2-3 h wash. The action potential of all nerves declined after overnight soak to between 30-60% of the control value, except for those nerves exposed to 5% lidocaine or 0.5% tetracaine, which showed no activity. Exposure to 5% lidocaine for periods of only 4-5 min produced total, irreversible loss of conduction. The uptake by and washout of radiolabeled lidocaine from the nerves indicate that the maximum amount of residual drug after 2-4 min of exposure to 5% lidocaine and a 3-h wash should cause at most only 50% conduction block. Solutions of 5% lidocaine and 0.5% tetracaine that have been associated with clinical cases of cauda equina syndrome after continuous spinal anesthesia caused irreversible conduction block in desheathed amphibian nerve. Whether these in vitro actions also occur in mammalian nerves in vivo is an important, clinically relevant question now under investigation in our laboratory.
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                Author and article information

                Journal
                J Pain Res
                J Pain Res
                Journal of Pain Research
                Journal of Pain Research
                Dove Medical Press
                1178-7090
                2016
                29 September 2016
                : 9
                : 721-725
                Affiliations
                Department of Anesthesiology/Pain Medicine Division, Henry Ford Hospital, Detroit, MI, USA
                Author notes
                Correspondence: David Daewhan Kim, Department of Anesthesiology/Pain Medicine Division, Henry Ford Hospital (I-3 Pain Clinic), 2799 W Grand Blvd, Detroit, MI 48208, USA, Tel +1 248 344 8000, Email Dkim1@ 123456hfhs.org
                Article
                jpr-9-721
                10.2147/JPR.S112947
                5047742
                27729811
                © 2016 Kim and Sibai. This work is published and licensed by Dove Medical Press Limited

                The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License ( http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed.

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                Original Research

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