• Annals of Clinical Neurophysiology
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• 제23권1호
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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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• 제8권1호
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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.

• 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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• 제28권4호
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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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• 제16권3호
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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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• 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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• 제13권1호
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• pp.101-104
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• 2000

Since conventional analgesics have showed limited therapertic value in the treatment of painful neuropathy, the new anticonvulsant gabapentin, has been tried and turned out to be effective and safe in the treatment for various forms of neuropathic pain. The basic pathophysiology of neuropathic pains is abnormal neuronal hyperactivity similar to epileptic seizures. Therefore, we could expect that neuropathic pain would be suppressed by anticonvulsants which inhibit abnormal excessive neuronal output and nerve conduction. This report include effective pain relief in four cases of neuropathic pain with gabapentin without any significant complications.

• The Korean Journal of Pain
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• 제11권2호
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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.

• The Journal of the Korean dental association
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• 제49권6호
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• pp.327-333
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• 2011

Clinically, treatment goal of neuropathic pain focused on not elimination of etiology but management and control of symptoms because we don't know certain about clear etiology of neuropathic pain yet. The drugs used for the management of neuropathic pain were classified as drugs with strong evidence for benefit(antidepressants, anticonvulsants, opioid analgesics etc.), modest evidence for benefit(mexiletine, carbamazepine, clonidine etc.), preliminary evidence for benefit(NSAIDs, dextromethorphan, topiramate etc.). Finally, the treatment for trigeminal neuralgia was outlined separately since this disorder responds to a different group of drugs than other neuropathic pain conditions.

• Journal of Interdisciplinary Genomics
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• 제1권2호
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• pp.15-18
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• 2019

Gaucher disease (GD) is an autosomal recessive inborn error of metabolism resulting from a deficiency in ${\beta}$-glucocerebrosidase (GBA) activity that leads to the accumulation of glucocerebroside in macrophages in multiple organs, such as the bone marrow, liver, spleen, and brain. GD can be classified into three clinical types: type 1 (non-neuropathic form, OMIM #230800); type II (acute neuropathic form, OMIM #230900); and type III (chronic neuropathic form, OMIM #231000). Type III is the subacute form of neuropathic GD. The best available treatment for GD is long-term enzyme (imiglucerase) replacement therapy (ERT) performed every two weeks. This report describes the long-term clinical course of a patient with type III GD who was treated with ERT for 18 years.