• The Korean Journal of Pain
• /
• v.33 no.2
• /
• pp.121-130
• /
• 2020

Background: Transcutaneous electrical nerve stimulation (TENS), manual acupuncture (MA), and spinal cord stimulation (SCS) are used to treat a variety of pain conditions. These non-pharmacological treatments are often thought to work through similar mechanisms, and thus should have similar effects for different types of pain. However, it is unclear if each of these treatments work equally well on each type of pain condition. The purpose of this study was to compared the effects of TENS, MA, and SCS on neuropathic, inflammatory, and non-inflammatory pain models. Methods: TENS 60 Hz, 200 ㎲, 90% motor threshold (MT), SCS was applied at 60 Hz, an intensity of 90% MT, and a 0.25 ms pulse width. MA was performed by inserting a stainless-steel needle to a depth of about 4-5 mm at the Sanyinjiao (SP6) and Zusanli (ST36) acupoints on a spared nerve injury (SNI), knee joint inflammation (3% carrageenan), and non-inflammatory muscle pain (intramuscular pH 4.0 injections) in rats. Mechanical withdrawal thresholds of the paw, muscle, and/or joint were assessed before and after induction of the pain model, and daily before and after treatment. Results: The reduced withdrawal thresholds were significantly reversed by application of either TENS or SCS (P < 0.05). MA, on the other hand, increased the withdrawal threshold in animals with SNI and joint inflammation, but not chronic muscle pain. Conclusions: TENS and SCS produce similar effects in neuropathic, inflammatory and non-inflammatory muscle pain models while MA is only effective in inflammatory and neuropathic pain models.

• Biomolecules & Therapeutics
• /
• v.26 no.3
• /
• pp.255-267
• /
• 2018

Inflammation is one of the main causes of pathologic pain. Knowledge of the molecular links between inflammatory signals and pain-mediating neuronal signals is essential for understanding the mechanisms behind pain exacerbation. Some inflammatory mediators directly modulate the excitability of pain-mediating neurons by contacting the receptor molecules expressed in those neurons. For decades, many discoveries have accumulated regarding intraneuronal signals from receptor activation through electrical depolarization for bradykinin, a major inflammatory mediator that is able to both excite and sensitize pain-mediating nociceptor neurons. Here, we focus on the final effectors of depolarization, the neuronal ion channels, whose functionalities are specifically affected by bradykinin stimulation. Particular G-protein coupled signaling cascades specialized for each specific depolarizer ion channels are summarized. Some of these ion channels not only serve as downstream effectors but also play critical roles in relaying specific pain modalities such as thermal or mechanical pain. Accordingly, specific pain phenotypes altered by bradykinin stimulation are also discussed. Some members of the effector ion channels are both activated and sensitized by bradykinin-induced neuronal signaling, while others only sensitized or inhibited, which are also introduced. The present overview of the effect of bradykinin on nociceptor neuronal excitability at the molecular level may contribute to better understanding of an important aspect of inflammatory pain and help future design of further research on the components involved and pain modulating strategies.

• Korean Journal of Veterinary Research
• /
• v.39 no.4
• /
• pp.715-723
• /
• 1999

Bee venom (BV) has been traditionally applied to relieve pain and to cure inflammatory diseases such as rheumatoid arthritis (RA) and neuritis. While several investigators have evaluated the anti-inflammatory effect of BV treatment, the anti-nociceptive effect of BV treatment on inflammatory pain is not reported. Therefore, we decided to evaluate the analgesic effect of BV treatment using Freund's adjuvant induced chronic arthritis model. Freund's adjuvant-induced arthritis has been used as an experimental animal model for RA in humans to assess the efficacy of the anti-inflammatory/analgesic drugs. In this study, subcutaneous BV treatment (1mg/kg/day) produced significantly reductions of symptoms related to arthritic pain (i.e. mechanical hyperalgesia and thermal hyperalgesia). The anti-nociceptive effect of BV was observed from at least 12 days after BV treatment. Furthermore, BV treatment significantly suppressed adjuvant induced Fos expression in lumbar spinal cord. We also found that local injection of BV into near the inflammatory site (especially Zusanli-acupoint) showed more potent analgesic effect on arthritic pain rather than distant injection of BV from inflammatory site (arbitrary side of back). The present study demonstrates that BV treatment has anti-nociceptive effect on arthritis induced inflammatory pain. The analgesic effect of BV on RA is probably mediated by the effect of BV itself or possible other mechanism such as counter-irritation. Furthermore, it is possible that BV acupuncture is one of the promising candidates for long-term therapy of RA.

• Biomedical Science Letters
• /
• v.25 no.3
• /
• pp.247-255
• /
• 2019

Curcuma longa L. (C.L), Curcuma aromatica Salisb. (C.A) and Zingiber officinale Rosc. (Z.O) of Zingiberaceae plants which are well known as effects of natural anti-oxidant, anti-cancer and anti-inflammatory. We examined that the Zingiberaceae plants are involved in development and modulation of orofacial pain in rats. Male, 7- to 8-week-old, Sprague-Dawley rats weighing 240~280 g were used in this study. Experiments were performed using acute pain model that was caused by the injection of 5% formalin into the right vibrissa pad. The number of scratching or rubbing to the injection site was recorded for 9 consecutive 5-minute intervals following injection of formalin. The experimental groups were acute orofacial inflammatory pain; control group (formalin, 5%), vehicle group (5% formalin after sodium carboxymethyl cellulose), single administration group, single mixed administration group, repeated administration group. The experiments were performed various concentrations of Zingiberaceae plants extract. Therefore, oral administration of C.L, C.A, and Z.O (p.o., concentrations of 12.5, 25 mg/mL) in orofacial inflammatory pain model substantially decrease the nociceptive behavior in a concentration dependent manner. And it tended to decrease at low concentration (12.5 mg/mL) of single mixed and repeated administration more than single administration. This result means that Zingiberaceae plants extract affects the modulation of acute orofacial inflammatory pain. Thus, Zingiberaceae plants extract may be a potential therapeutic treatment for orofacial inflammatory pain.

• Journal of Haehwa Medicine
• /
• v.18 no.1
• /
• pp.109-116
• /
• 2009

Objective: The objective of this study is to observe the effect of anti-inflammatory herbal acupuncture on the Complex Regional Pain Syndrome Methods : Anti-inflammatory herbal acupuncture, A-Shi Point, Sa-am acupunture were used to treat shoulder pain & ROM(range of movement)disorder, chest pain, finger's causalgic pain. We evaluated the patient through VAS(Visual Analog Scale) daily and Physical Examinations Results & Conclusions : After 42days of treatment, shoulder pain was decreased from VAS10 to VAS3, chest pain was decreased from VAS10 to VAS1.5, finger's causalgic pain was decreased from VAS10 to VAS2.5. and the patient showed that the ROM(range of movement) of shoulder was better, oriental treatment is good method for pain relief and better movement.

• Journal of Haehwa Medicine
• /
• v.18 no.2
• /
• pp.89-94
• /
• 2009

Objective : This study was designed to evaluate the effect of treatment of Bell's palsy patients with postauricural pain by Anti-inflammatory pharmacopuncture Methods : The clinical comparison studies were carried out 30 cases of Bell's palsy patient with postauricular pain. Anti-inflammatory pharmacopuncture. We divided into two groups. One was control group that was treated only Acupuncture and Herbal therapy and The other was a Anti-inflammatory pharmacopuncture group and the conclusions for treatment are as follows. Results : 1. Regarding alleviation of pain by VAS, Anti-inflammatory pharmacopuncture Group II showed significant decrease of VAS in the 5days treatment. 2. They were not significant score within two groups after 5th days treatment. 3. As a result of evaluation by using Yanagihara score, they were not significant score within two groups after final treament.

• The Korean Journal of Pain
• /
• v.33 no.2
• /
• pp.108-120
• /
• 2020

From the perspective of the definition of pain, pain can be divided into emotional and sensory components, which originate from potential and actual tissue damage, respectively. The pharmacologic treatment of the emotional pain component includes antianxiety drugs, antidepressants, and antipsychotics. The anti-anxiety drugs have anti-anxious, sedative, and somnolent effects. The antipsychotics are effective in patients with positive symptoms of psychosis. On the other hand, the sensory pain component can be divided into nociceptive and neuropathic pain. Non-steroidal anti-inflammatory drugs (NSAIDs) and opioids are usually applied for somatic and visceral nociceptive pain, respectively; anticonvulsants and antidepressants are administered for the treatment of neuropathic pain with positive and negative symptoms, respectively. The NSAIDs, which inhibit the cyclo-oxygenase pathway, exhibit anti-inflammatory, antipyretic, and analgesic effects; however, they have a therapeutic ceiling. The adverse reactions (ADRs) of the NSAIDs include gastrointestinal problems, generalized edema, and increased bleeding tendency. The opioids, which bind to the opioid receptors, present an analgesic effect only, without anti-inflammatory, antipyretic, or ceiling effects. The ADRs of the opioids start from itching and nausea/vomiting to cardiovascular and respiratory depression, as well as constipation. The anticonvulsants include carbamazepine, related to sodium channel blockade, and gabapentin and pregabalin, related to calcium blockade. The antidepressants show their analgesic actions mainly through inhibiting the reuptake of serotonin or norepinephrine. Most drugs, except NSAIDs, need an updose titration period. The principle of polypharmacy for analgesia in case of mixed components of pain is increasing therapeutic effects while reducing ADRs, based on the origin of the pain.

• International Journal of Oral Biology
• /
• v.42 no.3
• /
• pp.129-135
• /
• 2017

The present study investigated the role of spinal glutamate recycling in the development of orofacial inflammatory pain or trigeminal neuropathic pain. Experiments were carried out on male Sprague-Dawley rats weighing between 230 and 280 g. Under anesthesia, a polyethylene tube was implanted in the atlanto-occipital membrane for intracisternal administration. IL-$1{\beta}$-induced inflammation was employed as an orofacial acute inflammatory pain model. IL-$1{\beta}$ (10 ng) was injected subcutaneously into one vibrissal pad. We used the trigeminal neuropathic pain animal model produced by chronic constriction injury of the infraorbital nerve. DL-threo-${\beta}$-benzyloxyaspartate (TBOA) or methionine sulfoximine (MSO) was administered intracisternally to block the spinal glutamate transporter and the glutamine synthetase activity in astroglia. Intracisternal administration of TBOA produced mechanical allodynia in naïve rats, but it significantly attenuated mechanical allodynia in rats with interleukin (IL)-$1{\beta}$-induced inflammatory pain or trigeminal neuropathic pain. In contrast, intracisternal injection of MSO produced anti-allodynic effects in rats treated with IL-$1{\beta}$ or with infraorbital nerve injury. Intracisternal administration of MSO did not produce mechanical allodynia in naive rats. These results suggest that blockade of glutamate recycling induced pro-nociception in na?ve rats, but it paradoxically resulted in anti-nociception in rats experiencing inflammatory or neuropathic pain. Moreover, blockade of glutamate reuptake could represent a new therapeutic target for the treatment of chronic pain conditions.

• The Korean Journal of Pain
• /
• v.22 no.1
• /
• pp.1-15
• /
• 2009

Neuropathic pain is often refractory to intervention because of the complex etiology and an incomplete understanding of the mechanisms behind this type of pain. Glial cells, specifically microglia and astrocytes, are powerful modulators of pain and new targets of drug development for neuropathic pain. Glial activation could be the driving force behind chronic pain, maintaining the noxious signal transmission even after the original injury has healed. Glia express chemokine, purinergic, toll-like, glutaminergic and other receptors that enable them to respond to neural signals, and they can modulate neuronal synaptic function and neuronal excitability. Nerve injury upregulates multiple receptors in spinal microglia and astrocytes. Microglia influence neuronal communication by producing inflammatory products at the synapse, as do astrocytes because they completely encapsulate synapses and are in close contact with neuronal somas through gap junctions. Glia are the main source of inflammatory mediators in the central nervous system. New therapeutic strategies for neuropathic pain are emerging such as targeting the glial cells, novel pharmacologic approaches and gene therapy. Drugs targeting microglia and astrocytes, cytokine production, and neural structures including dorsal root ganglion are now under study, as is gene therapy. Isoform-specific inhibition will minimize the side effects produced by blocking all glia with a general inhibitor. Enhancing the anti-inflammatory cytokines could prove more beneficial than administering proinflammatory cytokine antagonists that block glial activation systemically. Research on therapeutic gene transfer to the central nervous system is underway, although obstacles prevent immediate clinical application.

• The Korean Journal of Pain
• /
• v.18 no.1
• /
• pp.69-73
• /
• 2005

This report describes a case of spinal nerve root compression due to an acute inflammatory granuloma after lumbar surgery. A 39 year-old man with a history of increasing back pain with a 3-week duration was diagnosed with a herniated intervertebral disc (HIVD). The diagnosis of a HIVD was confirmed by magnetic resonance imaging (MRI) with indications for surgery. A discectomy and a partial laminectomy was performed and the symptoms were alleviated immediately after surgery for a five-day period. However, a slowly progressing pain was subsequently noted along a different dermatome. There was no pain relief despite the patient being given pharmacological treatments, combined with an epidural steroid injection. The follow up MRI images showed severe compression of the nerve roots by a epidural lesion. Another procedure was performed 17 days after the initial operation. The lesion responsible for the compression of the nerve roots was found to be an acute inflammatory granuloma. The pain was relieved after the second procedure and there were no other symptoms or neurological problems. This case is remarkable in that a granuloma formed relatively quickly and grew to such a size that it was able to severely compress the surrounding nerve roots.