• Journal of Dental Anesthesia and Pain Medicine
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• v.21 no.6
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• pp.479-506
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• 2021

Background: Chronic neuropathic pain (NP) presents therapeutic challenges. Interest in the use of cannabis-based medications has outpaced the knowledge of its efficacy and safety in treating NP. The objective of this review was to evaluate the effectiveness of cannabis-based medications in individuals with chronic NP. Methods: Randomized placebo-controlled trials using tetrahydrocannabinol (THC), cannabidiol (CBD), cannabidivarin (CBDV), or synthetic cannabinoids for NP treatment were included. The MEDLINE, Cochrane Library, EMBASE, and Web of Science databases were examined. The primary outcome was the NP intensity. The risk of bias analysis was based on the Cochrane handbook. Results: The search of databases up to 2/1/2021 yielded 379 records with 17 RCTs included (861 patients with NP). Meta-analysis showed that there was a significant reduction in pain intensity for THC/CBD by -6.624 units (P < .001), THC by -8.681 units (P < .001), and dronabinol by -6.0 units (P = .008) compared to placebo on a 0-100 scale. CBD, CBDV, and CT-3 showed no significant differences. Patients taking THC/CBD were 1.756 times more likely to achieve a 30% reduction in pain (P = .008) and 1.422 times more likely to achieve a 50% reduction (P = .37) than placebo. Patients receiving THC had a 21% higher improvement in pain intensity (P = .005) and were 1.855 times more likely to achieve a 30% reduction in pain than placebo (P < .001). Conclusion: Although THC and THC/CBD interventions provided a significant improvement in pain intensity and were more likely to provide a 30% reduction in pain, the evidence was of moderate-to-low quality. Further research is needed for CBD, dronabinol, CT-3, and CBDV.

• The Korean Journal of Pain
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• v.29 no.3
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• pp.153-157
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• 2016

Tapentadol is a novel oral analgesic with a dual mode of action as an agonist of the ${\mu}$-opioid receptor (MOR), and as a norepinephrine reuptake inhibitor (NRI) all in a single molecule. Immediate release (IR) tapentadol shows its analgesic effect quickly, at around 30 minutes. Its MOR agonistic action produces acute nociceptive pain relief; its role as an NRI brings about chronic neuropathic pain relief. Absorption is rapid, with a mean maximal serum concentration at 1.25-1.5 h after oral intake. It is present primarily in the form of conjugated metabolites after glucuronidation, and excretes rapidly and completely via the kidneys. The most common adverse reactions are nausea, dizziness, vomiting, and somnolence. Constipation is more common in use of the ER formulation. Precautions against concomitant use of central nervous system depressants, including sedatives, hypnotics, tranquilizers, general anesthetics, phenothiazines, other opioids, and alcohol, or use of tapentadol within 14 days of the cessation of monoamine oxidase inhibitors, are advised. The safety and efficacy have not been established for use during pregnancy, labor, and delivery, or for nursing mothers, pediatric patients less than 18 years of age, and cases of severe renal impairment and severe hepatic impairment. The major concerns for tapentadol are abuse, addiction, seeking behavior, withdrawal, and physical dependence. The presumed problem for use of tapentadol is to control the ratio of MOR agonist and NRI. In conclusion, tapentadol produces both nociceptive and neuropathic pain relief, but with worries about abuse and dependence.

• Korean Journal of Psychosomatic Medicine
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• v.18 no.2
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• pp.57-61
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• 2010

The complex regional pain syndrome(CRPS) is a painful and disabling disorder that can affect one or more extremities. Unfortunately, knowledge concerning its natural history and mechanism remains very limited. Many current rationales in treatment of CRPS are mainly dependent on efficacy originate in other common conditions of neuropathic pain. This article introduces various treatments for CRPS, but few studies of high methodological quality have been carried out into the effects of those treatments. I think early recognition and a multidisciplinary approach to management seems important in obtaining a good outcome.

• Journal of Acupuncture Research
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• v.37 no.3
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• pp.193-201
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• 2020

This case report describes a 60-year-old female patient diagnosed with intercostal neuropathy and vertebral compression fractures which occurred following an electric shock injury. The patient received acupuncture, pharmacopuncture, and herbal medicine administration between February 10^th, 2020 and April 25^th, 2020. The pain level in the thoracic and left intercostal areas was assessed using the Numerical Rating Scale. The Self-report of the Leeds Assessment of Neuropathic Symptoms and Signs Pain Scale were used to diagnose neuropathic pain. The Neuropathic-Pain -Scale was used to evaluate the degree of neuropathic symptoms. The Oswestry Disability Index and the European Quality of Life-5 Dimensions were used to assess quality of life scales and functional disorder. Following combined Korean medicine treatment, the patient exhibited reduced levels of pain and significant improvement in functional disorder symptoms and quality of life.

• Korean Journal of Acupuncture
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• v.31 no.4
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• pp.195-207
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• 2014

Objectives : The purpose of this study is to examine the effects of laser acupuncture according to the wavelength(532 nm, 650 nm, 830 nm, 904 nm, and 1064 nm) at the acupoint of GB34 GB39 on neuropathic pain rat induced by tibial and sural nerve transection(TST). Methods : Neuropathic pain in rats was induced by tibial nerve and sural nerve transection. The rats were divided into the intact group, the TST control group, and the laser acupuncture therapy group. The laser acupuncture therapy groups were then divided into subgroups with 532 nm(L532), 650 nm(L650), 830 nm(L830), 904 nm(L904), and 1064 nm(L1064) laser acupuncture therapy. The acupoint of GB34 GB39 was selected, and laser acupuncture therapy was provided on both sides alternatively twice a week in a total of 6 sessions. Results : All the laser acupuncture groups showed a significant decrease in reaction time and force intensity. L532, L904, and L1064 groups showed a significant decrease in Bax, the L532 group showed a significant increase in Bcl-2, L532 and L1064 groups showed a significant decrease in the Bax/Bcl-2 ratio, and L532 and L650 groups showed a significant increase in mGluR5, as compared with the TST control group, among nerve tissue reaction. Conclusions : These results showed that laser acupuncture therapy at each of the wavelengths had some significance on neuropathic pain.

• The Academic Congress of Korean Shoulder and Elbow Society
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• 2003.03a
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• pp.113-121
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• 2003

• The Korean Journal of Pain
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• v.34 no.2
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• pp.176-184
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• 2021

Background: Diabetes-related neuropathic pain frequently occurs, and the underpinning mechanism remains elusive. The periaqueductal gray (PAG) exhibits descending inhibitory effects on central pain transmission. The current work aimed to examine whether inflammatory cytokines regulate mechanical allodynia and thermal hyperalgesia induced by diabetes through the phosphoinositide 3-kinase (PI3K)-mammalian target of rapamycin (mTOR) pathway in the PAG. Methods: Streptozotocin (STZ) was administered intraperitoneally to mimic allodynia and hyperalgesia evoked by diabetes in rats. Behavioral assays were carried out for determining mechanical pain and thermal hypersensitivity. Immunoblot and ELISA were performed to examine PAG protein amounts of interleukin-1β (IL-1β), IL-6, and tumor necrosis factor-α (TNF-α), as well as their corresponding receptors in STZ rats, and the expression of PI3K/protein kinase B (Akt)/mTOR signaling effectors. Results: Increased PAG p-PI3K/p-Akt/p-mTOR protein amounts were observed in STZ-induced animals, a PI3K-mTOR pathway inhibition in the PAG attenuated neuropathic pain responses. Moreover, the PAG concentrations of IL-1β, IL-6, and TNF-α and their receptors (namely, IL-1R, IL-6R, and tumor necrosis factor receptor [TNFR] subtype TNFR1, respectively) were increased in the STZ rats. Additionally, inhibiting IL-1R, IL-6R, and TNFR1 ameliorated mechanical allodynia and thermal hyperalgesia in STZ rats, alongside the downregulation of PI3K-mTOR signaling. Conclusions: Overall, the current study suggests that upregulated proinflammatory cytokines and their receptors in the PAG activate PI3K-mTOR signaling, thereby producing a de-inhibition effect on descending pathways in modulating pain transmission, and eventually contributing to neuropathic pain.

• The Korean Journal of Pain
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• v.27 no.3
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• pp.301-302
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• 2014

• Proceedings of the Korean Society for Emotion and Sensibility Conference
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• 2004.11a
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• pp.44-44
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• 2004

• Biomolecules & Therapeutics
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• v.24 no.5
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• pp.489-494
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• 2016

Neuropathic pain (NPP) is the main culprit among chronic pains affecting the normal life of patients. Procaine is a frequently-used local anesthesia with multiple efficacies in various diseases. However, its role in modulating NPP has not been reported yet. This study aims at uncovering the role of procaine in NPP. Rats were pretreated with procaine by intrathecal injection. Then NPP rat model was induced by sciatic nerve chronic compression injury (CCI) and behavior tests were performed to analyze the pain behaviors upon mechanical, thermal and cold stimulations. Spinal expression of Janus kinase 2 (JAK2) and signal transducer and activator of transcription 3 (STAT3) was detected by qRT-PCR and western blot. JAK2 was also overexpressed in procaine treated model rats for behavior tests. Results showed that procaine pretreatment improved the pain behaviors of model rats upon mechanical, thermal and cold stimulations, with the best effect occurring on the $15^{th}$ day post model construction (p<0.05). Procaine also inhibited JAK2 and STAT3 expression in both mRNA (p<0.05) and protein levels. Overexpression of JAK2 increased STAT3 level and reversed the improvement effects of procaine in pain behaviors (p<0.01). These findings indicate that procaine is capable of attenuating NPP, suggesting procaine is a potential therapeutic strategy for treating NPP. Its role may be associated with the inhibition on JAK2/STAT3 signaling.