• Journal of Korean Neurosurgical Society
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• 제29권7호
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• pp.877-885
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• 2000

Objective : The NOS inhibitors exhibit antinociceptive activity in rat model of neuropathic pain. NOS activity increases in the dorsal root ganglia(DRG) in neurop-athic pain. However, NOS activity decreases in the dorsal horn of spinal cord in the nerve injury models of neuropathic pain. To investigate whether the mechanism of decrease of NOS expression in the dorsal horn is related to a secondary effect resulting from increased NO production and likewise in the spinal DRG in the spinal nerve ligation model of neuropathic pain. Methods : We conducted behavioral tests for neuropathic pain, and nNOS immunohistochemistry and NADPH-diaphorase histochemistry after tight ligation of the 5th lumbar(L5) and 6th lumbar(L6) spinal nerves and L5 dorsal rhizotomy. Results : Typical neuropathic pain behaviors occurred 7 days after post-ligation in the neuropathic surgery group, but neuropathic pain behaviors in the dorsal rhizotomy group were absent or weak 7 days after post-operation. There was a decrease in the number of nNOS immunoreactive dorsal horn neurons on the both side(especially ipsilateral side) 7 days after post-ligation. The number of nNOS immunoreactive neurons in both side of the dorsal horn was not decreased 7 days after L5 dorsal rhizotomy. Conclusion : These data indicate that the changes in the injured DRG is essential for development and maintenance of neuropathic pain, and mechanism of decrease of nNOS expression in the dorsal horn is a secondary effect against the changes in the DRG including increased NO production in the spinal nerve ligation model of neuropathic pain.

• The Korean Journal of Pain
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• 제37권2호
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• pp.107-118
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• 2024

Nociplastic pain by the "International Association for the Study of Pain" is defined as pain that arises from altered nociception despite no clear evidence of nociceptive or neuropathic pain. Augmented central nervous system pain and sensory processing with altered pain modulation are suggested to be the mechanism of nociplastic pain. Clinical criteria for possible nociplastic pain affecting somatic structures include chronic regional pain and evoked pain hypersensitivity including allodynia with after-sensation. In addition to possible nociplastic pain, clinical criteria for probable nociplastic pain are pain hypersensitivity in the region of pain to non-noxious stimuli and presence of comorbidity such as generalized symptoms with sleep disturbance, fatigue, or cognitive problems with hypersensitivity of special senses. Criteria for definitive nociplastic pain is not determined yet. Eight specific disorders related to central sensitization are suggested to be restless leg syndrome, chronic fatigue syndrome, fibromyalgia, temporomandibular disorder, migraine or tension headache, irritable bowel syndrome, multiple chemical sensitivities, and whiplash injury; non-specific emotional disorders related to central sensitization include anxiety or panic attack and depression. These central sensitization pain syndromes are overlapped to previous functional pain syndromes which are unlike organic pain syndromes and have emotional components. Therefore, nociplastic pain can be understood as chronic altered nociception related to central sensitization including both sensory components with nociceptive and/or neuropathic pain and emotional components. Nociplastic pain may be developed to explain unexplained chronic pain beyond tissue damage or pathology regardless of its origin from nociceptive, neuropathic, emotional, or mixed pain components.

• The Korean Journal of Pain
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• 제12권2호
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• pp.242-245
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• 1999

Gabapentin is an oral antiepileptic agent with an unknown mechanism of action. There have been many proposed uses for gabapentin, including neuropathic pain, reflex sympathetic dystrophy, postherpetic neuralgia, midscapular pain secondary to radiation myelopathy and migraine prophylaxis. This report presents patients who were treated with gabapentin when other pharmacologic interventions failed to relieve neuropathic pain 3 patients with neuropathic pain were included among these cases. All patients were started on 200 mg gabapentin. The maximum dose required for pain relief was between 800 mg and 2400 mg. Gabapentin may be a useful adjunct for treating neuropathic pain with minimum of side effects.

• The Korean Journal of Pain
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• 제29권3호
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• pp.164-171
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• 2016

Background: Nefopam has been known as an inhibitor of the reuptake of monoamines, and the noradrenergic and/or serotonergic system has been focused on as a mechanism of its analgesic action. Here we investigated the role of the spinal dopaminergic neurotransmission in the antinociceptive effect of nefopam administered intravenously or intrathecally. Methods: The effects of intravenously and intrathecally administered nefopam were examined using the rat formalin test. Then we performed a microdialysis study to confirm the change of extracellular dopamine concentration in the spinal dorsal horn by nefopam. To determine whether the changes of dopamine level are associated with the nefopam analgesia, its mechanism was investigated pharmacologically via pretreatment with sulpiride, a dopaminergic D2 receptor antagonist. Results: When nefopam was administered intravenously the flinching responses in phase I of the formalin test were decreased, but not those in phase II of the formalin test were decreased. Intrathecally injected nefopam reduced the flinching responses in both phases of the formalin test in a dose dependent manner. Microdialysis study revealed a significant increase of the level of dopamine in the spinal cord by intrathecally administered nefopam (about 3.8 fold the baseline value) but not by that administered intravenously. The analgesic effects of intrathecally injected nefopam were not affected by pretreatment with sulpiride, and neither were those of the intravenous nefopam. Conclusions: Both the intravenously and intrathecally administered nefopam effectively relieved inflammatory pain in rats. Nefopam may act as an inhibitor of dopamine reuptake when delivered into the spinal cord. However, the analgesic mechanism of nefopam may not involve the dopaminergic transmission at the spinal level.

• 대한추나의학회지
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• 제5권1호
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• pp.1-9
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• 2004

The purpose of this article is to contribute to study on visceral referred pain. Recently it is getting more interest in measurement of pain degree and effective treatment. We have researched on specific character of visceral referred pain, oriental medical referred pain, and some theories of the mechanism of the visceral referred pain. But therapeutics of visceral referred pain is not yet known. It will be necessary of additional study later.

• BMB Reports
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• 제35권4호
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• pp.420-427
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• 2002

Partial nerve injury is the main cause of neuropathic pain disorders in humans. Acupuncture has long been used to relieve pain. It is known to relieve pain by controlling the activities of the autonomic nervous system. Although the mechanism of neuropathic pain and analgesic effects of electroacupuncture (EA) have been studied in a rat model system, its detailed mechanism at the molecular level remains unclear. To identify genes that might serve as either markers or explain these distinct biological functions, a cDNA microarray analysis was used to compare the expression of 8,400 genes among three sample groups. Messenger RNAs that were pooled from the spinal nerves of 7 normal. 7 neuropathic pain, and 7 EA treatment rat models were compared. Sixty-eight genes were differentially expressed more than 2-fold in the neuropathic rat model when compared to the normal, and restored to the normal expression level after the EA treatment. These genes are involved in a number of biological processes, including the signal transduction, gene expression, and nociceptive pathways. Confirmation of the differential gene expression was performed by a dot-blot analysis. Dot-blotting results showed that the opioid receptor sigma was among those genes. This indicates that opioid-signaling events are involved in neuropathic pain and the analgesic effects of EA. The potential application of these data include the identification and characterization of signaling pathways that are involved in the EA treatment, studies on the role of the opioid receptor in neuropathic pain, and further exploration on the role of selected identified genes in animal models.

• The Korean Journal of Pain
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• 제2권2호
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• pp.145-154
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• 1989

Pain is a common and important clinical symptom, and treatments aimed at relieving pain have a central position in medical practice. Recently Transcutaneous Electrical Nerve Stimulation (TENS) has been effectively used to control acute and chronic conditions that produce pain. But the mechanism of analgesia resulting from TENS remains obscure. In order to investigate the analgesic effect of TENS and it's action mechanism, TENS was applied in 40 rabbits with different frequencies, low frequency (2Hz) and high frequency (100Hz), for 20 minutes. And the pain threshold was measured by the temperature before and after stimulation, and an attempt was made to antagonize the stimulation effect with naloxone pretreatment (0.4 mg/kg) The results are as follows: 1) Both low frequency and high frequency TENS resulted in increasing the pain threshold significantly (Both p<0.01). 2) Naloxone pretreatment could antagonize the effect of increasing the pain threshold with low frequency TENS significantly (p<0.01), but not with high frequency TENS. Plasma beta-endorphin was measured by radioimmunoassay using an Beta-Endorphin Kit (Immunonuclear Corporation, Stillwater, Minnesota, USA) and Automatic Gamma Scintillation Counter (Micromedic System 4/2000) before and after stimulation. An attempt was made to reverse the stimulation effect with naloxone pretreatment (0.4 mg/kg). The results are as follows: 1) Low frequency TENS resulted in increasing the level of plasma beta.endorphin significantly (p<0.01), but high frequency TENS did not. 2) Naloxone pretreatment could reverse the effect of increasing the plasma beta-endorphin level with low frequency TENS significantly (p<0.01).

• The Korean Journal of Pain
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• 제34권4호
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• pp.463-470
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• 2021

Background: Although neuropathic pain is a severe and common pain, its pathophysiology has not been elucidated yet. Studies in recent years have focused on the immune system's role in the pathogenesis of neuropathic pain. The aim of this study was to investigate the role of immunological mechanisms in neuropathic pain and the effect of pregabalin by measuring immunological marker levels in peripheral blood before and after pregabalin treatment in postherpetic neuralgia (PHN) patients with neuropathic pain. Methods: Forty patients diagnosed with PHN were included in the study. CD4, T follicular cells (Tfh: CD4⁺CXCR5⁺PD1⁺), Th17 (CD4⁺CCR6⁺ and CD4⁺IL17A⁺), regulatory T cells (Treg: CD4⁺ CD25⁺foxp3⁺), Th1 (CD4⁺ CXCR3⁺ and CD4⁺ IFN-γ⁺) and Th2 (CD4⁺ IL-4⁺) cell ratios were measured in peripheral blood samples before treatment and after 3 months of treatment. Results: When immunological marker and inflammation parameter levels were compared before and after treatment, the helper T cell ratio (CD3⁺, CD4⁺) was 30.28 ± 12.27% before treatment and 34.93 ± 11.70% after treatment, so there was a statistically significant increase (P = 0.028). Th17 was 4.75 ± 5.02% before treatment and 5.80 ± 3.13% after treatment, and there was a statistically significant increase (P = 0.036). Conclusions: Immunological mechanisms play an essential role in the pathogenesis of neuropathic pain, immunologically based treatment approach will be the critical point of treatment.

• Journal of Dental Anesthesia and Pain Medicine
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• 제16권3호
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• pp.159-163
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• 2016

Orofacial pain is a common complaint of patients that causes distress and compromises the quality of life. It has many etiologies including trauma, interventional procedures, nerve injury, varicella-zoster (shingles), tumor, and vascular and idiopathic factors. It has been demonstrated that the sympathetic nervous system is usually involved in various orofacial pain disorders such as postherpetic neuralgia, complex regional pain syndromes, and atypical facial pain. The stellate sympathetic ganglion innervates the head, neck, and upper extremity. In this review article, the effect of stellate ganglion block and its mechanism of action in orofacial pain disorders are discussed.

• 감성과학
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• 제21권4호
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• pp.3-10
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• 2018

The present study explores two relationships: first, between number of payment and payment option preference, and second, total sum and payment option preference, with pain of payment as a mediator variable. The analyses revealed that consumers who feel higher pain of payment preferred the pennies-a-day pricing to the aggregate pricing when the per-payment price is low. Consumers who experience higher pain of payment prefer to pay in small frequent installments because they feel the small per-payment price can be comparable to daily expense. Consumers who experienced higher pain of payment preferred aggregate pricing to pennies-a-day pricing when the per-payment price was high. When the per-payment price is high, it is no longer comparable to daily expense, thus leading to greater pain of payment among consumers. The study discusses the implications for mechanism of pain of payment on payment option preference.