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      Topical loperamide for the treatment of localized neuropathic pain: a case report and literature review

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          Abstract

          Peripheral nerve damage can result in neuronal hyperexcitability, resulting in neuropathic pain. Localized neuropathic pain is confined to a specific area not larger than a letter-size piece of paper. Topical analgesics are increasingly popular for the treatment of localized neuropathic pain because systemic agents for managing neuropathic pain often produce undesirable and intolerable side effects. Commonly used agents for topical use are amitriptyline, baclofen, ketamine and lidocaine; however, these agents do not always give the desired analgesic effect in some patients. We report for the first time a patient with chronic idiopathic axonal polyneuropathy and intractable localized neuropathic pain treated successfully with loperamide 5% cream. After application of loperamide 5% cream, the patient reported a complete reduction of pain within 30 mins, lasting for 2.5 hrs. Subsequently, the patient was able to reduce his daily intake of oxycodone, while using topical loperamide for pain relief. Loperamide is a nonprescription opioid agonist, commonly used against diarrhea. As a topical formulation, it is preferable over other opioids due to its low systemic bioavailability and low risk of crossing the blood–brain barrier. Peripheral upregulation and sensitization of opioid receptors at peripheral nerve endings and perhaps at other cell populations in the epidermis might be targets of topical loperamide.

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          Most cited references 22

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          Neuropathic Pain: Central vs. Peripheral Mechanisms.

          Our goal is to examine the processes-both central and peripheral-that underlie the development of peripherally-induced neuropathic pain (pNP) and to highlight recent evidence for mechanisms contributing to its maintenance. While many pNP conditions are initiated by damage to the peripheral nervous system (PNS), their persistence appears to rely on maladaptive processes within the central nervous system (CNS). The potential existence of an autonomous pain-generating mechanism in the CNS creates significant implications for the development of new neuropathic pain treatments; thus, work towards its resolution is crucial. Here, we seek to identify evidence for PNS and CNS independently generating neuropathic pain signals.
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            Modulation of peripheral sensory neurons by the immune system: implications for pain therapy.

            The concept that the immune system can communicate with peripheral sensory neurons to modulate pain is based mostly on documented interactions between opioid ligands and receptors. Such findings may have broad implications for the development of safer pain medication. Innovative strategies take into account that analgesics should be particularly active in pathological states rather than producing a general suppression of the central nervous system, as with conventional morphine- or cannabinoid-like drugs. Inflammation of peripheral tissue leads to increased functionality of opioid receptors on peripheral sensory neurons and to local production of endogenous opioid peptides. In addition, endocannabinoids were detected in leukocytes, but their role in pain modulation has yet to be addressed. Future aims include the development of peripherally restricted opioid agonists, selective targeting of opioid-containing immune cells to sites of painful injury, and the augmentation of peripheral ligand and receptor synthesis (e.g., by gene therapy). Similar approaches may be pursued for cannabinoids. The ultimate goal is to avoid detrimental side effects of currently available analgesics such as respiratory depression, cognitive impairment, addiction, gastrointestinal bleeding, and thromboembolic complications.
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              High doses of topical amitriptyline in neuropathic pain: two cases and literature review.

              Severe chronic neuropathic pain is a challenge to treat, and due to adverse effects of classical oral medication, optimal and effective dose levels are difficult to reach. Therefore, administration of topical analgesics might be an option, due to reduced adverse effects, and increased patient compliance. The aim of this article is to describe two cases treated effectively with topical amitriptyline 5% and 10%, the highest dosage described to date. The first patient was a 39-year-old man, suffering from severe intractable neuropathic pain in feet and hands, due to diabetes mellitus type II (DM-II). After application of amitriptyline 5% the patient experienced a complete relieve only in the hands, whereas after application of amitriptyline 10%, a total reduction of pain occurred within 20 minutes, lasting the whole day. The second patient was a 57-year-old man, suffering for 10 years from progressive sensory disturbances in both feet and increasing pain due to chronic idiopathic axonal polyneuropathy (CIAP). Amitriptyline 5% cream reduced pain in the toes nearly completely, but this was not the case in the heels. Amitriptyline 10% reduced pain in the feet, however, systemic adverse effects occurred, mainly drowsiness. The patient decided to stop topical treatment because of these adverse effects. These two cases suggest an analgesic dose-response effect of topical amitriptyline in painful neuropathy. Systemic adverse effects should be taken into account. © 2011 The Authors. Pain Practice © 2011 World Institute of Pain.
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                Author and article information

                Journal
                J Pain Res
                J Pain Res
                JPR
                jpainres
                Journal of Pain Research
                Dove
                1178-7090
                29 April 2019
                2019
                : 12
                : 1189-1192
                Affiliations
                [1 ]Institute for Neuropathic Pain , Amsterdam, the Netherlands
                [2 ]Pain Management Centre, Charing Cross Hospital Imperial Healthcare NHS Trust , London, UK
                [3 ]Anesthesiology and Pain Department, Westfriesgasthuis , Hoorn, the Netherlands
                [4 ]Institute for Neuropathic Pain , Bosch en Duin, the Netherlands
                Author notes
                Correspondence: DJ KopskyInstitute for Neuropathic Pain , Vespuccistraat 64-III, 1056 SN, Amsterdam, the NetherlandsTel +3 162 867 1847Email info@ 123456neuropathie.nu
                Article
                196927
                10.2147/JPR.S196927
                6503502
                © 2019 Kopsky et al.

                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. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms ( https://www.dovepress.com/terms.php).

                Page count
                Tables: 1, References: 25, Pages: 4
                Categories
                Case Report

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