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Special Issue "Recent Advances in Pain Research"

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A special issue of Brain Sciences (ISSN 2076-3425). This special issue belongs to the section "Neuroscience of Pain".

Deadline for manuscript submissions: 5 November 2023 | Viewed by 2974

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Special Issue Editor

Dr. Magdalena Kocot-Kępska

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Guest Editor

Department of Pain Research and Treatment, Jagiellonian University Medical College, 31-531 Krakow, Poland
Interests: neuropathic pain; mechanisms of pain; postoperative pain; pain management; pain treatment; pain research; pharmacotherapy of acute and chronic pain

Special Issue Information

Dear Colleagues,

Pain is a complex phenomenon based on the sensitization of the peripheral and central nervous systems, together with the release of many biochemical pain modulators, and although pain management techniques have improved a lot in recent years, pain still has a substantial influence on patients' quality of life. It is widely known that current pain treatments are burdened with limited effectiveness and numerous adverse effects induced by pharmacotherapy. Therefore, many researchers are seeking novel pain management opportunities to improve pain relief efficiency with the simultaneous reduction in opioid administration, limitation of peripheral and central sensitization, and the prevention of chronic pain development.

The goal of this Special Issue is to highlight and publicize excellent pain research extending the knowledge of pain pathophysiology and leading to the development of more efficient and safe pain treatments. We encourage the submission of original research and review articles or short communications on topics including (but not limited to) the following:

The characterization of current pain management concepts, including pharmacological and nonpharmacological treatments;
The neurobiology of various pain types (neuropathic pain, postoperative pain, nociplastic pain, etc.);
Preclinical pain studies;
Translational studies.

Dr. Magdalena Kocot-Kępska
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Brain Sciences is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2000 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

pain pathophysiology, pain management
multimodal therapy
pain neurobiology
acute pain
chronic pain
neuropathic pain
postoperative pain
persistent pain

Published Papers (4 papers)

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Research

Open AccessArticle

Phenytoin Decreases Pain-like Behaviors and Improves Opioid Analgesia in a Rat Model of Neuropathic Pain

Magdalena Kocot-Kępska

Anna Przeklasa-Muszyńska

and

Joanna Mika

Brain Sci. 2023, 13(6), 858; https://doi.org/10.3390/brainsci13060858 - 25 May 2023

Viewed by 281

Abstract

Neuropathic pain remains a clinical challenge due to its complex and not yet fully understood pathomechanism, which result in limited analgesic effectiveness of the management offered, particularly for patients with acute, refractory neuropathic pain states. In addition to the introduction of several modern therapeutic approaches, such as neuromodulation or novel anti-neuropathic drugs, significant efforts have been made in the repurposing of well-known substances such as phenytoin. Although its main mechanism of action occurs at sodium channels in excitable and non-excitable cells and is well documented, how the drug affects the disturbed neuropathic interactions at the spinal cord level and how it influences morphine-induced analgesia have not been clarified, both being crucial from a clinical perspective. We demonstrated that single and repeated systemic administrations of phenytoin decreased tactile and thermal hypersensitivity in an animal model of neuropathic pain. Importantly, we observed an increase in the antinociceptive effect on thermal stimuli with repeated administrations of phenytoin. This is the first study to report that phenytoin improves morphine-induced antinociceptive effects and influences microglia/macrophage activity at the spinal cord and dorsal root ganglion levels in a neuropathic pain model. Our findings support the hypothesis that phenytoin may represent an effective strategy for neuropathic pain management in clinical practice, particularly when combination with opioids is needed. Full article

(This article belongs to the Special Issue Recent Advances in Pain Research)

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Open AccessArticle

Comparison of Analgesic Efficacy between Epidural and Perineural Administration of Autologous Conditioned Serum in the Conservative Treatment of Low Back Pain Due to Lumbar Degenerative Disc Disease: A Randomized, Open-Label, Controlled Clinical Trial

Piotr Godek

Beata Szczepanowska-Wolowiec

and

Dominik Golicki

Brain Sci. 2023, 13(5), 749; https://doi.org/10.3390/brainsci13050749 - 30 Apr 2023

Viewed by 619

Abstract

Lumbar degenerative disc disease (LDDD) is widely acknowledged as a significant contributor to low back pain (LBP), which is a prevalent and debilitating health condition affecting millions of individuals worldwide. The pathogenesis of LDDD and associated pain mechanisms are thought to be mediated by inflammatory mediators. Autologous conditioned serum (ACS, Orthokine) may be used for symptomatic treatment of LBP due to LDDD. This study aimed to compare the analgesic efficacy and safety of two routes of ACS administration, perineural (periarticular) and epidural (interlaminar), in the conservative treatment of LBP. This study used an open-label, randomized, controlled trial protocol. A group of 100 patients were enrolled in the study and randomly allocated into two comparative groups. Group A (n = 50) received the epidural (interlaminar) approach—2 ultrasound-guided injections as control intervention (each containing two doses of ACS—8 mL). Group B (n = 50) received the perineural (periarticular) approach—2 ultrasound-guided injections as experimental intervention at 7-day intervals (the same volume of ACS). Assessments consisted of an initial assessment (IA) and control assessments at 4 (T1), 12 (T2), and 24 (T3) weeks after the last intervention. Primary outcomes comprised Numeric Rating Scale (NRS), Oswestry Disability Index (ODI), Roland Morris Questionnaire (RMQ), and Euro Quality of Life—5 Dimensions–5 Levels (EQ-5D-5L): Index, Visual Analogue Scale (VAS), and Level Sum Score (LSS). Secondary outcomes included differences between groups in specific endpoints for the above-mentioned questionnaires. In conclusion, this study revealed that both perineural (periarticular) and epidural ACS injections tended to perform in a very similar way. Both routes of Orthokine application show significant improvement in the primary clinical parameters, such as pain and disability, and therefore, both methods can be considered equally effective in managing LBP due to LDDD. Full article

(This article belongs to the Special Issue Recent Advances in Pain Research)

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Open AccessArticle

TET1-TRPV4 Signaling Contributes to Bone Cancer Pain in Rats

and

Brain Sci. 2023, 13(4), 644; https://doi.org/10.3390/brainsci13040644 - 10 Apr 2023

Viewed by 621

Abstract

Bone cancer pain (BCP) is excruciating for cancer patients, with limited clinical treatment options and significant side effects, due to the complex and unclear pathogenesis of bone cancer pain. Peripheral sensitization in dorsal root ganglion (DRG) neurons is a recognized cellular mechanism for bone cancer pain. The pathological mechanism of chronic pain is increasingly being affected by epigenetic mechanisms. In this study, we unbiasedly showed that the DNA hydroxymethylase ten-eleven translocation 1 (TET1) expression was significantly increased in the L4–6 DRG of BCP rats and ten-eleven translocation 2 (TET2) expression did not change significantly. Notably, TET1 inhibition by intrathecal injection of Bobcat339 (a TET1 inhibitor) effectively relieved mechanical hyperalgesia in BCP rats. Peripheral sensitization in chronic pain relies on the activation and overexpression of ion channels on neurons. Here, we demonstrated that TRPV4, one of the transient receptor potential ion channel family members, was significantly elevated in the L4–6 DRG of BCP rats. In addition, TRPV4 inhibition by intrathecal injection of HC067047 (a TRPV4 inhibitor) also significantly attenuated mechanical hyperalgesia in BCP rats. Interestingly, we found that TET1 inhibition downregulated TRPV4 expression in the L4–6 DRG of BCP rats. As a result, these findings suggested that TET1 may contribute to bone cancer pain by upregulating TRPV4 expression in the L4–6 DRG of BCP rats and that TET1 or TRPV4 may become therapeutic targets for bone cancer pain. Full article

(This article belongs to the Special Issue Recent Advances in Pain Research)

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Open AccessArticle

Pharmacological Modulation of the MIP-1 Family and Their Receptors Reduces Neuropathic Pain Symptoms and Influences Morphine Analgesia: Evidence from a Mouse Model

and

Brain Sci. 2023, 13(4), 579; https://doi.org/10.3390/brainsci13040579 - 29 Mar 2023

Cited by 1 | Viewed by 605

Abstract

Neuropathic pain pathophysiology is not fully understood, but it was recently shown that MIP-1 family members (CCL3, CCL4, and CCL9) have strong pronociceptive properties. Our goal was to examine how pharmacological modulation of these chemokines and their receptors (CCR1 and CCR5) influence hypersensitivity after nerve injury in Albino Swiss male mice. The spinal changes in the mRNA/protein levels of the abovementioned chemokines and their receptors were measured using RT-qPCR and ELISA/Western blot techniques in a mouse model of chronic constriction injury of the sciatic nerve. Behavioral studies were performed using the von Frey and cold plate tests after pharmacological treatment with neutralizing antibodies (nAbs) against chemokines or antagonists (CCR1-J113863, CCR5-TAK-220/AZD-5672) alone and in coadministration with morphine on Day 7, when the hypersensitivity was fully developed. Our results showed enhanced protein levels of CCL3 and CCL9 1 and 7 days after nerve injury. The single intrathecal administration of CCL3 or CCL9 nAb, J113863, TAK-220, or AZD-5672 diminished neuropathic pain symptoms and enhanced morphine analgesia. These findings highlight the important roles of CCL3 and CCL9 in neuropathic pain and additionally indicate that these chemokines play essential roles in opioid analgesia. The obtained results suggest CCR1 and CCR5 as new, interesting targets in neuropathy treatment. Full article

(This article belongs to the Special Issue Recent Advances in Pain Research)

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