• Annals of Clinical Neurophysiology
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• v.23 no.1
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• pp.46-52
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• 2021

Background: We aimed to investigate candidates for serological biomarkers of neuropathic pain in individuals with neuromyelitis optica spectrum disorder (NMOSD). Methods: We analyzed 38 sera samples from 38 participants with NMOSD in National Cancer Center. Neuropathic pain was evaluated using the painDETECT questionnaire. Pain with neuropathic components (painDETECT score ≥ 13) was observed in 22 participants, among whom 17 had definite neuropathic pain (painDETECT score ≥ 19). The remaining 16 participants had non-neuropathic pain (painDETECT score < 13). Serum glial fibrillary acidic protein (GFAP) levels were assessed using a single-molecule array assay. Several cytokines, including tumor necrosis factor-alpha (TNF-α), interleukin (IL)-6, IL-10, and IL-17A, were measured by a multiplex bead-based immunoassay. Results: In comparison of NMOSD participants with neuropathic pain components (or definite neuropathic pain) and those with non-neuropathic pain, the absolute values of serum GFAP, TNF-α, IL-6, and IL-10 levels were higher in participants with neuropathic pain components (or definite neuropathic pain), but these findings did not reach statistical significance. Conclusions: Further larger-scale investigations to find reliable serological biomarkers for neuropathic pain in NMOSD are warranted.

• Journal of the Korean Society of Physical Medicine
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• v.8 no.1
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• pp.79-89
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• 2013

PURPOSE: To identify the effects of single trial transcutaneous electrical nerve stimulation (TENS) application on chronic neuropathic pain and the repeated TENS application to development of neuropathic pain following peripheral nerve injury. METHODS: First, 20 rats were given the median nerve ligation to induce chronic neuropathic pain. After the ligation, neuropathic pain was assessed by measuring the forepaws withdrawal threshold to von Frey filaments for 3 weeks. Afterward, rats were randomly divided into TENS group and placebo-TENS group. TENS (frequency 100Hz, pulse width $200{\mu}s$) was applied to the forearm for 20 minutes. Second, 34 rats were randomly allocated into two group after median nerve ligation: TENS group and placebo-TENS group. Both interventions were applied to the forearm for 20 minutes from 1 day to 3 weeks after injury. Neuropathic pain to mechanical was measured on each rat for 3 weeks. RESULTS: Exeprimental rats showed a clear neuropathic pain-like behaviors, such as reduced forepaw withdrawal threshold to mechanical stimulation for 3 weeks, after median nerve ligation. And, TENS decreased effectively the chronic neuropathic pain originated from median nerve injury. TENS also diminished the development of neuropathic pain after nerve injury. CONCLUSION: Our animal model studying for neuropathic pain following median nerve injury may be useful to investigate peripheral neuropathic pain in human. Also, TENS may be used to mediate chronic neuropathic pain and to prevent the development of neuropathic pain following median nerve injury.

• The Korean Journal of Pain
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• v.28 no.4
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• pp.231-235
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• 2015

Damage to peripheral nerves or the spinal cord is often accompanied by neuropathic pain, which is a complex, chronic pain state. Increasing evidence indicates that alterations in the expression and activity of gap junction channels in the spinal cord are involved in the development of neuropathic pain. Thus, this review briefly summarizes evidence that regulation of the expression, coupling, and activity of spinal gap junction channels modulates pain signals in neuropathic pain states induced by peripheral nerve or spinal cord injury. We particularly focus on connexin 43 and pannexin 1 because their regulation vastly attenuates symptoms of neuropathic pain. We hope that the study of gap junction channels eventually leads to the development of a suitable treatment tool for patients with neuropathic pain.

• Korean Journal of Medicinal Crop Science
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• v.16 no.3
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• pp.183-187
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• 2008

Nerve injury can lead to neuropathic pain, which is often resistant to current analgesics and interventional therapeutic methods. Extracellular signal-regulated kinase (ERK) plays important role in the induction of neuropathic pain. We explored the antinociceptive effect of curcumin and its effect on ERK in the spinal cord in the neuropathic pain model of rats induced by chronic constriction injury (CCI) of the sciatic nerve. In injured rats, mechanical allodynia, which is one of characteristics of neuropathic pain developed and the activation of ERK in spinal cord significantly increased compared with control group. However, administration of curcumin (50 mg/kg/day p.o) for 7 days started from one day before the injury prevented the development of mechanical allodynia and increase of ERK phosphorylation. These results indicate that curcumin can be a new therapeutic agent in the treatment of neuropathic pain.

• The Korean Journal of Pain
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• v.12 no.2
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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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• v.11 no.2
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• pp.294-298
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• 1998

The feature of neuropathic pain may occur in the absence of any apparent stimulus and be exaggerated in either amplitude or duration. Peripheral nerve injury may produce neuropathic pain and opioids have been shown to be relatively unsatisfactory for the treatment of most cases of neuropathic pain. The NMDA receptor system is involved in transmission and modulation of nociceptive information. We treated patients with severe pain, hyperaesthesia and allodynia with epidural injection of NMDA receptor antagonist, ketamine (10 mg) and morphine (0.5 mg) or other opioid. The combinations provided effective pain management in 23 patients with neuropathic pain.

• Journal of Korean Neurosurgical Society
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• v.29 no.7
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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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• v.27 no.1
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• pp.54-62
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• 2014

Background: The recently known analgesic action mechanisms of nefopam (NFP) are similar to those of anticonvulsants and antidepressants in neuropathic pain treatment. It is difficult to prescribe high doses of oral neuropathic drugs without titration due to adverse effects. Unfortunately, there are few available intravenous analgesics for the immediate management of acute flare-ups of the chronic neuropathic pain. The aim of this study was to determine the additional analgesic effects for neuropathic pain of NFP and its adverse effects during the titration of oral medications for neuropathic pain among inpatients with postherpetic neuralgia (PHN). Methods: Eighty inpatients with PHN were randomly divided into either the NFP or normal saline (NS) groups. Each patient received a 3-day intravenous continuous infusion of either NFP with a consecutive dose reduction of 60, 40, and 20 mg/d, or NS simultaneously while dose titrations of oral medications for neuropathic pain gradually increased every 3 days. The efficacy of additional NFP was evaluated by using the neuropathic pain symptom inventory (NPSI) score for 12 days. Adverse effects were also recorded. Results: The median NPSI score was significantly lower in the NFP group from days 1 to 6 of hospitalization. The representative alleviating symptoms of pain after using NFP were both spontaneous and evoked neuropathic pain. Reported common adverse effects were nausea, dizziness, and somnolence, in order of frequency. Conclusions: An intravenous continuous infusion of NFP reduces spontaneous and evoked neuropathic pain with tolerable adverse effects during the titration of oral medications in inpatients with PHN.

• Journal of Korean Neurosurgical Society
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• v.57 no.1
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• pp.6-11
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• 2015

Objective : Neuropathic pain causes patients feel indescribable pain. Deep Brain Stimulation (DBS) is one of the treatment methods in neuropathic pain but the action mechanism is still unclear. To study the effect and mechanism of analgesic effects from DBS in neuropathic pain and to enhance the analgesic effect of DBS, we stimulated the ventral posterolateral nucleus (VPL) in rats. Methods : To observe the effect from VPL stimulation, we established 3 groups : normal group (Normal group), neuropathic pain group (Pain group) and neuropathic pain+DBS group (DBS group). Rats in DBS group subjected to electrical stimulation and the target is VPL. Results : We observed the behavioral changes by DBS in VPL (VPL-DBS) on neuropathic pain rats. In our study, the pain score which is by conventional test method was effectively decreased. In specific, the time of showing withdrawal response from painful stimulation which is not used measuring method in our animal model was also decreased by DBS. Conclusion : The VPL is an effective target on pain modulation. Specifically we could demonstrate changes of pain response duration which is not used, and it was also significantly meaningful. We thought that this study would be helpful in understanding the relation between VPL-DBS and neuropathic pain.

• The Korean Journal of Pain
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• v.33 no.4
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• pp.359-377
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• 2020

Background: This study investigated whether current smoking and a higher nicotine dependency were associated with chronic low back pain (LBP), lumbar related leg pain (sciatica) and/or radicular neuropathic pain. Methods: A cross-sectional study was conducted on 150 patients (mean age, 60.1 ± 13.1 yr). Demographic data, the International Association for the Study of Pain (IASP) neuropathic pain grade, STarT Back tool, and the Fagerström test were completed. A control group (n = 50) was recruited. Results: There was a significant difference between current smokers and nonsmokers in the chronic LBP group in the mean pain score (P = 0.025), total STarT Back score (P = 0.015), worst pain location (P = 0.020), most distal pain radiation (P = 0.042), and in the IASP neuropathic pain grade (P = 0.026). There was a significant difference in the mean Fagerström score between the four IASP neuropathic pain grades (P = 0.005). Current smoking yielded an odds ratio (OR) of 3.071 (P = 0.011) for developing chronic LBP and sciatica, and an OR of 4.028 (P = 0.002) for obtaining an IASP "definite/probable" neuropathic pain grade, for both cohorts. The likelihood for chronic LBP and sciatica increased by 40.9% (P = 0.007), while the likelihood for an IASP neuropathic grade of "definite/probable" increased by 50.8% (P = 0.002), for both cohorts, for every one unit increase in the Fagerström score. Conclusions: A current smoking status and higher nicotine dependence increase the odds for chronic LBP, sciatica and radicular neuropathic pain.