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Differential drug effects on spontaneous and evoked pain behavior in a model of trigeminal neuropathic pain

1 , 2

Journal of Pain Research

Dove Medical Press

trigeminal, infraorbital, neuropathic, allodynia, chronic, grooming

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      Abstract

      Purpose

      Baclofen and morphine have shown efficacy against mechanical allodynia after infraorbital nerve chronic constriction injury (IoN-CCI). No drug effects have yet been reported on spontaneous trigeminal neuropathic pain. It has been proposed that the directed face grooming behavior that also develops following IoN-CCI offers a measure of spontaneous trigeminal neuropathic pain.

      Subjects and methods

      We examined the effects of a continuous 1-week infusion of 30 mg/day carbamazepine (the first-line drug treatment for trigeminal neuralgia), 1.06 mg/day baclofen, 4.18 mg/day clomipramine, and 5 mg/day morphine on spontaneous and mechanically evoked pain behavior (ie, directed face grooming and von Frey testing) in IoN-CCI rats.

      Results

      Isolated face grooming was significantly reduced in rats receiving carbamazepine and baclofen but not in clomipramine- or morphine-treated rats. All drugs showed significant antiallodynic effects; carbamazepine showed the strongest effects, whereas clomipramine had only minor efficacy.

      Conclusion

      The tested drugs have differential effects in the IoN-CCI model, and different neuropathological mechanisms may underlie the different somatosensory symptoms in this model. A mechanism-based approach may be needed to treat (trigeminal) neuropathic pain. The present data support IoN-CCI as a model of trigeminal neuralgia in which isolated face grooming is used as a measure of spontaneous neuropathic pain.

      Related collections

      Most cited references 52

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      Ethical guidelines for investigations of experimental pain in conscious animals.

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        A peripheral mononeuropathy in rat that produces disorders of pain sensation like those seen in man.

         Gary Bennett,  Y. Xie (1988)
        A peripheral mononeuropathy was produced in adult rats by placing loosely constrictive ligatures around the common sciatic nerve. The postoperative behavior of these rats indicated that hyperalgesia, allodynia and, possibly, spontaneous pain (or dysesthesia) were produced. Hyperalgesic responses to noxious radiant heat were evident on the second postoperative day and lasted for over 2 months. Hyperalgesic responses to chemogenic pain were also present. The presence of allodynia was inferred from the nocifensive responses evoked by standing on an innocuous, chilled metal floor or by innocuous mechanical stimulation, and by the rats' persistence in holding the hind paw in a guarded position. The presence of spontaneous pain was suggested by a suppression of appetite and by the frequent occurrence of apparently spontaneous nocifensive responses. The affected hind paw was abnormally warm or cool in about one-third of the rats. About one-half of the rats developed grossly overgrown claws on the affected side. Experiments with this animal model may advance our understanding of the neural mechanisms of neuropathic pain disorders in humans.
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          Neuropathic pain: diagnosis, pathophysiological mechanisms, and treatment.

          Neuropathic pain develops as a result of lesions or disease affecting the somatosensory nervous system either in the periphery or centrally. Examples of neuropathic pain include painful polyneuropathy, postherpetic neuralgia, trigeminal neuralgia, and post-stroke pain. Clinically, neuropathic pain is characterised by spontaneous ongoing or shooting pain and evoked amplified pain responses after noxious or non-noxious stimuli. Methods such as questionnaires for screening and assessment focus on the presence and quality of neuropathic pain. Basic research is enabling the identification of different pathophysiological mechanisms, and clinical assessment of symptoms and signs can help to determine which mechanisms are involved in specific neuropathic pain disorders. Management of neuropathic pain requires an interdisciplinary approach, centred around pharmacological treatment. A better understanding of neuropathic pain and, in particular, of the translation of pathophysiological mechanisms into sensory signs will lead to a more effective and specific mechanism-based treatment approach. Copyright 2010 Elsevier Ltd. All rights reserved.
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            Author and article information

            Affiliations
            [1 ]Department of Medicine, Laboratory for Pain Research, University of Antwerp, Wilrijk
            [2 ]Multidisciplinary Pain Center, Antwerp University Hospital, Edegem, Belgium
            Author notes
            Correspondence: K Deseure, Department of Medicine, Laboratory for Pain Research, University of Antwerp, Universiteitsplein 1, 2610 Wilrijk, Belgium, Tel +32 3 265 2561, Email kristof.deseure@ 123456uantwerp.be
            Journal
            J Pain Res
            J Pain Res
            Journal of Pain Research
            Journal of Pain Research
            Dove Medical Press
            1178-7090
            2017
            27 January 2017
            : 10
            : 279-286
            5291328 10.2147/JPR.S124526 jpr-10-279
            © 2017 Deseure and Hans. 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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