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      Minocycline for Controlling Neuropathic Pain: A Systematic Narrative Review of Studies in Humans

      1 , 2 , 3

      Journal of Pain Research


      minocycline, microglia, neuropathic pain, pain, review

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          Minocycline is known to reduce microglial activation, suggesting that it may reduce neuropathic pain. We reviewed studies in humans that evaluated the effectiveness of minocycline in alleviating neuropathic pain.


          We searched the PubMed, Embase, Cochrane library, and SCOPUS databases for papers published before January 06, 2021, using the search words minocycline and pain. The inclusion criteria for the selection of articles were (1) minocycline administered to humans and (2) minocycline administered to control neuropathic pain.


          The primary literature search yielded 2299 relevant papers. Based on the assessment of the titles, abstracts, and full-text, nine publications were selected for this review. Only four of the nine studies showed a positive pain-reducing outcome after minocycline administration. Two of the three studies on chemotherapy-induced neuropathic pain showed a positive pain-reducing effect. Minocycline was effective in controlling pain from diabetic and leprotic neuropathies. However, minocycline was not effective in controlling lumbar radicular pain and pain resolution after carpal tunnel release.


          Our review provides evidence that minocycline may have some potential for reducing neuropathic pain. Further high-quality studies need to be conducted to validate this potential.

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          Most cited references 33

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          Minocycline: far beyond an antibiotic.

          Minocycline is a second-generation, semi-synthetic tetracycline that has been in therapeutic use for over 30 years because of its antibiotic properties against both gram-positive and gram-negative bacteria. It is mainly used in the treatment of acne vulgaris and some sexually transmitted diseases. Recently, it has been reported that tetracyclines can exert a variety of biological actions that are independent of their anti-microbial activity, including anti-inflammatory and anti-apoptotic activities, and inhibition of proteolysis, angiogenesis and tumour metastasis. These findings specifically concern to minocycline as it has recently been found to have multiple non-antibiotic biological effects that are beneficial in experimental models of various diseases with an inflammatory basis, including dermatitis, periodontitis, atherosclerosis and autoimmune disorders such as rheumatoid arthritis and inflammatory bowel disease. Of note, minocycline has also emerged as the most effective tetracycline derivative at providing neuroprotection. This effect has been confirmed in experimental models of ischaemia, traumatic brain injury and neuropathic pain, and of several neurodegenerative conditions including Parkinson's disease, Huntington's disease, amyotrophic lateral sclerosis, Alzheimer's disease, multiple sclerosis and spinal cord injury. Moreover, other pre-clinical studies have shown its ability to inhibit malignant cell growth and activation and replication of human immunodeficiency virus, and to prevent bone resorption. Considering the above-mentioned findings, this review will cover the most important topics in the pharmacology of minocycline to date, supporting its evaluation as a new therapeutic approach for many of the diseases described herein. © 2013 The Authors. British Journal of Pharmacology © 2013 The British Pharmacological Society.
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            Inhibition of microglial activation attenuates the development but not existing hypersensitivity in a rat model of neuropathy.

            Microglia, the intrinsic macrophages of the central nervous system, have previously been shown to be activated in the spinal cord in several rat mononeuropathy models. Activation of microglia and subsequent release of proinflammatory cytokines are known to play a role in inducing a behavioral hypersensitive state (hyperalgesia and allodynia) in these animals. The present study was undertaken to determine whether minocycline, an inhibitor of microglial activation, could attenuate both the development and existing mechanical allodynia and hyperalgesia in an L5 spinal nerve transection model of neuropathic pain. In a preventive paradigm (to study the effect on the development of hypersensitive behaviors), minocycline (10, 20, or 40 mg/kg intraperitoneally) was administered daily, beginning 1 h before nerve transection. This regimen produced a decrease in mechanical hyperalgesia and allodynia, with a maximum inhibitory effect observed at the dose of 20 and 40 mg/kg. The attenuation of the development of hyperalgesia and allodynia by minocycline was associated with an inhibitory action on microglial activation and suppression of proinflammatory cytokines at the L5 lumbar spinal cord of the nerveinjured animals. The effect of minocycline on existing allodynia was examined after its intraperitoneal administration initiated on day 5 post-L5 nerve transection. Although the postinjury administration of minocycline significantly inhibited microglial activation in neuropathic rats, it failed to attenuate existing hyperalgesia and allodynia. These data demonstrate that inhibition of microglial activation attenuated the development of behavioral hypersensitivity in a rat model of neuropathic pain but had no effect on the treatment of existing mechanical allodynia and hyperalgesia.
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              Central sensitization: a generator of pain hypersensitivity by central neural plasticity.

              Central sensitization represents an enhancement in the function of neurons and circuits in nociceptive pathways caused by increases in membrane excitability and synaptic efficacy as well as to reduced inhibition and is a manifestation of the remarkable plasticity of the somatosensory nervous system in response to activity, inflammation, and neural injury. The net effect of central sensitization is to recruit previously subthreshold synaptic inputs to nociceptive neurons, generating an increased or augmented action potential output: a state of facilitation, potentiation, augmentation, or amplification. Central sensitization is responsible for many of the temporal, spatial, and threshold changes in pain sensibility in acute and chronic clinical pain settings and exemplifies the fundamental contribution of the central nervous system to the generation of pain hypersensitivity. Because central sensitization results from changes in the properties of neurons in the central nervous system, the pain is no longer coupled, as acute nociceptive pain is, to the presence, intensity, or duration of noxious peripheral stimuli. Instead, central sensitization produces pain hypersensitivity by changing the sensory response elicited by normal inputs, including those that usually evoke innocuous sensations. In this article, we review the major triggers that initiate and maintain central sensitization in healthy individuals in response to nociceptor input and in patients with inflammatory and neuropathic pain, emphasizing the fundamental contribution and multiple mechanisms of synaptic plasticity caused by changes in the density, nature, and properties of ionotropic and metabotropic glutamate receptors.

                Author and article information

                J Pain Res
                J Pain Res
                Journal of Pain Research
                26 January 2021
                : 14
                : 139-145
                [1 ]Department of Neurosurgery, Yonsei University, College of Medicine , Seoul, Republic of Korea
                [2 ]Department of Physical Medicine and Rehabilitation, College of Medicine, Dankook University , Cheonan, Republic of Korea
                [3 ]Department of Physical Medicine and Rehabilitation, College of Medicine, Yeungnam University , Taegu, Republic of Korea
                Author notes
                Correspondence: Min Cheol Chang Department of Physical Medicine and Rehabilitation, College of Medicine, Yeungnam University , 317-1, Daemyungdong, Namku, Taegu705-717, Republic of KoreaTel +82-53-620-4682 Email wheel633@ynu.ac.kr
                © 2021 Shin 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
                Figures: 1, Tables: 2, References: 36, Pages: 7
                This research was supported by the 2020 Joint Research Project of Institutes of Science and Technology.

                Anesthesiology & Pain management

                review, minocycline, microglia, neuropathic pain, pain


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