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      Journal of Pain Research (submit here)

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      Postdural puncture headache and pregabalin

      case-report
      Journal of pain research
      Dove Medical Press
      postdural puncture headache, spinal anesthesia, pregabalin

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          Abstract

          Background:

          Even if carried out under optimal conditions, postdural puncture headache is still a frustrating and unpleasant complication in spinal anesthesia. This syndrome has an estimated incidence from less than 1% to about 5% of patients undergoing spinal anesthesia, even in the highest risk subset, the young, female, and pregnant population.

          Case presentation:

          In our two female cases, headaches started following spinal anesthesia on the 11th and 14th hours, respectively. No response was obtained from patients diagnosed with postdural puncture headache with classical treatments such as bed rest, hydration, oral analgesic, and caffeine combination as well as intravenous theophylline application. The treatment of oral pregablin, commonly used for cases that rejected epidural blood patch, caused a significant decrease in headache severity. Later, the two cases whose headaches were completely resolved were discharged from the hospital on the post-operative 7th day.

          Conclusion:

          Postdural puncture headache is one of the most common complications of spinal anesthesia. Cerebral spinal fluid leakage into the epidural space has been proposed as the main mechanism responsible for this syndrome. Multiple methods of treatment have been applied with wide-ranging results. We detected that oral pregabalin application caused a significant decrease in the difficult and severe postdural puncture headaches of both our cases who did not respond to conventional treatments.

          Most cited references21

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          The International Classification of Headache Disorders: 2nd edition.

          (2004)
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            Pregabalin: its pharmacology and use in pain management.

            Pregabalin is a new synthetic molecule and a structural derivative of the inhibitory neurotransmitter gamma-aminobutyric acid. It is an alpha2-delta (alpha2-delta) ligand that has analgesic, anticonvulsant, anxiolytic, and sleep-modulating activities. Pregabalin binds potently to the alpha2-delta subunit of calcium channels, resulting in a reduction in the release of several neurotransmitters, including glutamate, noradrenaline, serotonin, dopamine, and substance P. In this review, I will discuss the pharmacology of pregabalin and available efficacy studies in pain management. This review will focus on the advances in pregabalin pharmacology since my previous review in 2005.
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              Inhibition of neuronal Ca(2+) influx by gabapentin and pregabalin in the human neocortex.

              Gabapentin and pregabalin (S-(+)-3-isobutylgaba) produced concentration-dependent inhibitions of the K(+)-induced [Ca(2+)](i) increase in fura-2-loaded human neocortical synaptosomes (IC(50)=17 microM for both compounds; respective maximal inhibitions of 37 and 35%). The weaker enantiomer of pregabalin, R-(-)-3-isobutylgaba, was inactive. These findings were consistent with the potency of these drugs to inhibit [(3)H]-gabapentin binding to human neocortical membranes. The inhibitory effect of gabapentin on the K(+)-induced [Ca(2+)](i) increase was prevented by the P/Q-type voltage-gated Ca(2+) channel blocker omega-agatoxin IVA. The alpha 2 delta-1, alpha 2 delta-2, and alpha 2 delta-3 subunits of voltage-gated Ca(2+) channels, presumed sites of gabapentin and pregabalin action, were detected with immunoblots of human neocortical synaptosomes. The K(+)-evoked release of [(3)H]-noradrenaline from human neocortical slices was inhibited by gabapentin (maximal inhibition of 31%); this effect was prevented by the AMPA receptor antagonist NBQX (2,3-dioxo-6-nitro-1,2,3,4-tetrahydro[f]quinoxaline-7-sulphonamide). Gabapentin and pregabalin may bind to the Ca(2+) channel alpha 2 delta subunit to selectively attenuate depolarization-induced Ca(2+) influx of presynaptic P/Q-type Ca(2+) channels; this results in decreased glutamate/aspartate release from excitatory amino acid nerve terminals leading to a reduced activation of AMPA heteroreceptors on noradrenergic nerve terminals.
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                Author and article information

                Journal
                J Pain Res
                Journal of Pain Research
                Journal of pain research
                Dove Medical Press
                1178-7090
                2010
                25 February 2010
                : 3
                : 11-14
                Affiliations
                Department of Anesthesiology and Reanimation, Mostas Private Health Hospital, Kahramanmaras, Turkey
                Author notes
                Correspondence: Beyazit Zencirci, Department of Anesthesiology and Reanimation, Mostas Private Health Hospital, Kahramanmaras, Turkey, Email bzencirci@ 123456fastmail.fm
                Article
                jpr-3-011
                3004652
                21197305
                f81bcc35-1e32-4fb3-ba71-8d3ea3e6ff22
                © 2010 Zencirci, publisher and licensee Dove Medical Press Ltd.

                This is an Open Access article which permits unrestricted noncommercial use, provided the original work is properly cited.

                History
                : 25 February 2010
                Categories
                Case Report

                Anesthesiology & Pain management
                postdural puncture headache,spinal anesthesia,pregabalin
                Anesthesiology & Pain management
                postdural puncture headache, spinal anesthesia, pregabalin

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