• Title/Summary/Keyword: Neuropathic Pain

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Synthesis and Two Electrode Voltage Clamp Assay of PPADS Derivatives as the P2X Antagonists

  • Lee, Jung-Sun;Moon, Hyun-Duck;Park, Chul-Seung;Kim, Yong-Chul
    • 대한약학회:학술대회논문집
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    • 대한약학회 2003년도 Proceedings of the Convention of the Pharmaceutical Society of Korea Vol.2-2
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    • pp.178.3-178.3
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    • 2003
  • P2X receptors are ligand gated cation channels activated by the binding of extracellular adenosine 5'-triphosphate (ATP) and classified into 7 subtype families. $P2X_1$ receptors are abundantly expressed in smooth muscle mediates blood vessel and mediate constriction upon binding of neuronal ATP. The activation of $P2X_3$ receptor by ATP has been known to initiate the pain signaling in the peripheral nervous system, which is involved in chronic inflammatory nociception and neuropathic pain by nerve injury. (omitted)

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복합부위통증증후군 환자에서의 전기경련요법 (Electroconvulsive Therapy for CRPS)

  • 이종하;고영훈;양종윤;김용구;한창수;윤현철
    • 생물정신의학
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    • 제18권3호
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    • pp.163-167
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    • 2011
  • Complex regional pain syndrome (CRPS) is a disease that causes chronic spontaneous pain and hyperesthesia of one or more parts of legs and arms, which is accompanied with problems of the automatic nervous system or the motor nervous system. However, up to date, it is unclear what causes the syndrome and how to diagnose and treat it. Although several treatments including medication and sympathetic nerve block are performed against CRPS, the therapeutic effect of the treatments is limited. The electroconvulsive thera-py (ECT), of which the mechanism is not clarified, is a treatment used for treatment-resistant depression. ECT is also reported to be effective against pain. Therefore, we performed the ECT for a 24-year-old female patient who has been diagnosed as CRPS. Her pain had not been much improved by medications and interventional procedures. At admission to a psychiatric ward for ECT, she com-plained of over 8 points of pain on visual analogue scale and the constrained movement around the painful part. Eight ECTs-three times a week-were performed for three weeks in hospital and then the ECT once a week was performed after her leaving the hospital. During the ECTs, pain had been reduced and the range of movement in the constrained parts had increased. Further systematic re-search is needed to confirm the effect of electroconvulsive therapy against CRPS.

대상포진후 신경통에서 Gabapentin의 효과 (Gabapentin for the Treatment of Postherpetic Neuralgia)

  • 이두익;김동옥;김건식;권무일;신광일;강화자
    • The Korean Journal of Pain
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    • 제12권2호
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    • pp.188-190
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    • 1999
  • Background: The goal of this study was to evaluate the effects of gabapentin on postherpetic neuralgia. Gabapentin is a known anti-seizure medication, whose cellular mechanism of action is not well understood. Unlike other anticonvulsant, gabapentin has the advantage of a low toxicity and favorable side effect profile. If has been recently recommended for use in treatment of neuropathic pain. Methods: Twelve patients with a diagnosis of postherpetic neuralgia were prescribed gabapentin after failure of routine therapeutic regimens. The dose of gabapentin ranged 300~1800 mg per day, in three divided doses. If initial dose was ineffective and no side effects were noted, the dosages was increased by 300 mg a day in divided doses, to the maximum level for 2 weeks. Patients were evaluated for analgesia using visual analogue scale (VAS) pain score (0; no pain, 10; worst possible pain) and possible side effects. Results: A significant decrease in pain scores with gabapentin were noted. There were several mild side effects such as dizziness, somnolence, dry mouth, constipation and facial edema, without need of special treatment. Conclusions: Gabapentin may be a useful adjunct for treating intractable postherpetic neuralgia with a minimal side effects.

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척수강 내로 투여한 Epigallocatechin Gallate이 모르핀의 항침해 작용에 대한 내성 발생에 미치는 효과 (The Effect of Intrathecal Epigallocatechin Gallate on the Development of Antinociceptive Tolerance to Morphine)

  • 김웅모;배홍범;최정일
    • The Korean Journal of Pain
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    • 제22권3호
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    • pp.199-205
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    • 2009
  • Background: A major ingredient of green tea is epigallocatechin-3-gallate (EGCG), and this is known to have many beneficial effects for cancer prevention and also on the cardiovascular system and neurodegenerative diseases through its anti-oxidant, anti-angiogenic, anti-inflammatory, lipid-lowering and neuroprotective properties. Its actions on nociception and the spinal nervous system have been examined in only a few studies, and in these studies EGCG showed an antinociceptive effect on inflammatory and neuropathic pain, and a neuroprotective effect in motor neuron disease. This study was performed to investigate the effect of EGCG on acute thermal pain and the development of morphine tolerance at the spinal level. Methods: The experimental subjects were male Sprague-Dawley rats and the Hot-Box test was employed. A single or double-lumen intrathecal catheter was implanted at the lumbar enlargement for drug administration. An osmotic pump was used to infuse morphine for 7 days for induction of morphine tolerance. EGCG was injected repeatedly for 7 days at twice a day through the intrathecal catheter. Results: Intrathecal EGCG increased the paw withdrawal latency (PWL) after repeated administration for 7 days at twice a day, but this did not happen with administering on single bolus injection of EGCG. In addition, the antinociceptive effect of intrathecal morphine was not affected by co-administration with EGCG. A continuous 7-day infusion of morphine caused a significant decrease of the PWL in the control group (M + S, morphine plus saline). In contrast, intrathecal EGCG injection over 7 days blocked the decrease of the PWL in the experiment group (M + E, morphine plus EGCG). Conclusions: Intrathecal ECGC produced a weak antinociceptive effect for acute thermal pain, but it did not change the morphine's analgesic effect. However, the development of antinociceptive tolerance to morphine was attenuated by administering intrathecal EGCG.

Therapeutic Effect of Epidurally Administered Lipo-Prostaglandin E1 Agonist in a Rat Spinal Stenosis Model

  • Park, Sang Hyun;Lee, Pyung Bok;Choe, Ghee Young;Moon, Jee Yeon;Nahm, Francis Sahngun;Kim, Yong Chul
    • The Korean Journal of Pain
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    • 제27권3호
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    • pp.219-228
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    • 2014
  • Background: A lipo-prostaglandin E1 agonist is effective for the treatment of neurological symptoms of spinal stenosis when administered by an oral or intravenous route. we would like to reveal the therapeutic effect of an epidural injection of lipo-prostaglandin E1 on hyperalgesia in foraminal stenosis. Methods: A total of 40 male Sprague-Dawley rats were included. A small stainless steel rod was inserted into the L5/L6 intervertebral foramen to produce intervertebral foraminal stenosis and chronic compression of the dorsal root ganglia (DRG). The rats were divided into three groups: epidural PGE1 (EP) (n = 15), saline (n = 15), and control (n = 10). In the EP group, $0.15{\mu}g{\cdot}kg-1$ of a lipo-PGE1 agonist was injected daily via an epidural catheter for 10 days from postoperative day 3. In the saline group, saline was injected. Behavioral tests for mechanical hyperalgesia were performed for 3 weeks. Then, the target DRG was analyzed for the degree of chromatolysis, chronic inflammation, and fibrosis in light microscopic images. Results: From the fifth day after lipo-PGE1 agonist injection, the EP group showed significant recovery from mechanical hyperalgesia, which was maintained for 3 weeks (P < 0.05). Microscopic analysis showed much less chromatolysis in the EP group than in the saline or control groups. Conclusions: An epidurally administered lipo-PGE1 agonist relieved neuropathic pain, such as mechanical hyperalgesia, in a rat foraminal stenosis model, with decreasing chromatolysis in target DRG. We suggest that epidurally administered lipo-PGE1 may be a useful therapeutic candidate for patients with spinal stenosis.

가미쌍화탕으로 호전된 뇌졸중 후 중추성 통증 환자 치험 1례 (A Case Report of Central Post-stroke Pain Improved by Gami SSanghwa-tang)

  • 신희연;이상화;이형민;양승보;조승연;박성욱;고창남;박정미
    • 대한중풍순환신경학회지
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    • 제18권1호
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    • pp.77-86
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    • 2017
  • ■ Objectives The purpose of this case study is to report the effect of Gami SSanghwa-tang on a patient with central post-stroke pain. ■ Methods The patient was treated with herbal medicine Gami SSanghwa-tang, acupuncture, pharmaco-acupuncture, and moxibustion. The treatment effect was evaluated by Numerical Rating Scale(NRS), Neuropathic Pain Symptom Inventory(NPSI), and 36-item Short-form Health Survey(SF-36). ■ Results After the treatment, the NRS score of pain intensity was reduced from moderate to mild degree. The total NPSI score and subscores also decreased, as the various features of the pain were relieved. The SF-36 score increased, as the patient's quality of life improved. ■ Conclusion This case study suggests that Gami SSanghwa-tang, could be effective in reducing pain and improving quality of life of patients suffering from central post-stroke pain.

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척추신경결찰 흰쥐에서 척수강내로 투여한 Lamotrigine의 기계적 항이질통 효과 (The Mechanical Antiallodynic Effect of Intrathecal Lamotrigine in Rats with Spinal Nerve Ligation)

  • 송준걸;전인구;권미영;박종연
    • The Korean Journal of Pain
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    • 제18권2호
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    • pp.118-123
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    • 2005
  • Background: A nerve ligation injury may produce a tactile allodynia. The effects of intrathecally delivered lamotrigine on allodynia induced due to fifth and sixth lumbar spinal nerves ligation in rats, using lumbar intrathecal catheters were examined. Methods: Sprague-Dawley rats (body weight 160-180 g) were prepared by tightly ligating the fifth and sixth left lumbar spinal nerves, with the implantation of a chronic intrathecal catheter for drug administration. Mechanical allodynia and allodynic threshold were measured using von Frey filaments and the updown method, respectively. After the baseline hind paw withdrawal thresholds had been obtained, lamotrigine (10, 30, 100 and $300{\mu}g$) was administered intrathecally. Thereafter, the dose-response curves and 50% effective dose ($ED_{50}$) were obtained. Motor dysfunction was assessed by observing the righting/stepping reflex responses and abnormal weight bearing. Results: Intrathecal administration of lamotrigine produced a dose-dependent antiallodynic action ($ED_{50}=61.7{\mu}g$). Mild motor weakness was observed with $300{\mu}g$ lamotrigine, but no severe motor impairment was found. Conclusions: It is suggested that intrathecal lamotrigine could produce moderate antagonism of mechanical allodynia at the spinal level in a rat neuropathic pain model with minimal motor weakness.

Etifoxine for Pain Patients with Anxiety

  • Choi, Yun Mi;Kim, Kyung Hoon
    • The Korean Journal of Pain
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    • 제28권1호
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    • pp.4-10
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    • 2015
  • Etifoxine (etafenoxine, $Stresam^{(R)}$) is a non-benzodiazepine anxiolytic with an anticonvulsant effect. It was developed in the 1960s for anxiety disorders and is currently being studied for its ability to promote peripheral nerve healing and to treat chemotherapy-induced pain. In addition to being mediated by $GABA_A{\alpha}2$ receptors like benzodiazepines, etifoxine appears to produce anxiolytic effects directly by binding to ${\beta}2$ or ${\beta}3$ subunits of the $GABA_A$ receptor complex. It also modulates $GABA_A$ receptors indirectly via stimulation of neurosteroid production after etifoxine binds to the 18 kDa translocator protein (TSPO) of the outer mitochondrial membrane in the central and peripheral nervous systems, previously known as the peripheral benzodiazepine receptor (PBR). Therefore, the effects of etifoxine are not completely reversed by the benzodiazepine antagonist flumazenil. Etifoxine is used for various emotional and bodily reactions followed by anxiety. It is contraindicated in situations such as shock, severely impaired liver or kidney function, and severe respiratory failure. The average dosage is 150 mg per day for no more than 12 weeks. The most common adverse effect is drowsiness at the initial stage. It does not usually cause any withdrawal syndromes. In conclusion, etifoxine shows less adverse effects of anterograde amnesia, sedation, impaired psychomotor performance, and withdrawal syndromes than those of benzodiazepines. It potentiates $GABA_A$ receptor-function by a direct allosteric effect and by an indirect mechanism involving the activation of TSPO. It seems promising that non-benzodiazepine anxiolytics including etifoxine will replenish shortcomings of benzodiazepines and selective serotonin reuptake inhibitors according to animated studies related to TSPO.

방사열 자극실험쥐에서 Ketorolac과 Morphine의 병용투여 효과 (The Analgesic Interaction between Ketorolac and Morphine in Radiant Thermal Stimulation Rat)

  • 노장호;최동훈;이윤우;윤덕미
    • The Korean Journal of Pain
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    • 제18권1호
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    • pp.10-14
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    • 2005
  • Background: Previous studies have suggested synergistic analgesic drug interactions between NSAIDs and opioids in neuropathic and inflammatory pain models. The aim of this study was to investigate the analgesic drug interaction between intraperitoneal (IP) ketorolac and morphine in radiant thermal stimulation rat. Methods: Initially, we assessed the withdrawal latency time of the hindpaw to radiant thermal stimulation every 15 min for 1 hour and every 30 min for next 1 hour after IP normal saline 5 ml (control group). The latency time was changed into percent maximal possible effect (%MPE). Next, IP dose response curves were established for the %MPE of morphine (0.3, 1, 3, 10 mg/kg) and ketorolac (3, 10, 30 mg/kg) to obtain the $ED_{50}$ for each agent. And we confirmed that the IP morphine effect was induced by opioid receptor through IP morphine followed by IP naloxone. At last, we injected three doses of IP ketorolac (3, 10, 30 mg/kg) mixed with one dose of morphine (2 mg/kg) for fixed dose analysis. Results: IP morphine delayed the paw withdrawal latency time dose dependently, but not ketorolac. $ED_{50}$ of IP morphine was 2.1 mg/kg. And the IP morphine effect was reversed to control level by IP naloxone. IP ketorolac + morphine combination showed no further additional effects on paw withdrawal latency time over morphine only group. Conclusions: IP ketorolac did not produce antinociceptive effect during radiant thermal stimulation. There was neither additional nor synergistic analgesic interaction between IP morphine and ketorolac in thermal stimulation rat.

The antinociceptive effect of artemisinin on the inflammatory pain and role of GABAergic and opioidergic systems

  • Dehkordi, Faraz Mahdian;Kaboutari, Jahangir;Zendehdel, Morteza;Javdani, Moosa
    • The Korean Journal of Pain
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    • 제32권3호
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    • pp.160-167
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    • 2019
  • Background: Pain is a complex mechanism which involves different systems, including the opioidergic and GABAergic systems. Due to the side effects of chemical analgesic agents, attention toward natural agents have been increased. Artemisinin is an herbal compound with widespread modern and traditional therapeutic indications, which its interaction with the GABAergic system and antinoniceptive effects on neuropathic pain have shown. Therefore, this study was designed to evaluate the antinociceptive effects of artemisinin during inflammatory pain and interaction with the GABAergic and opioidergic systems by using a writhing response test. Methods: On the whole, 198 adult male albino mice were used in 4 experiments, including 9 groups (n = 6) each with three replicates, by intraperitoneal (i.p.) administration of artemisinin (2.5, 5, and 10 mg/kg), naloxone (2 mg/kg), bicuculline (2 mg/kg), saclofen (2 mg/kg), indomethacin (5 mg/kg), and ethanol (10 mL/kg). Writhing test responses were induced by i.p. injection of 10 mL/kg of 0.6% acetic acid, and the percentage of writhing inhibition was recorded. Results: Results showed significant dose dependent anti-nociceptive effects from artemisinin which, at a 10 mg/kg dose, was statistically similar to indomethacin. Neither saclofen nor naloxone had antinociceptive effects and did not antagonize antinociceptive effects of artemisinin, whereas bicuculline significantly inhibited the antinocicptive effect of artemisinin. Conclusions: It seems that antinocicptive effects of artemisinin are mediated by $GABA_A$ receptors.