• Korean Journal of Otorhinolaryngology-Head and Neck Surgery
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• v.61 no.11
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• pp.567-572
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• 2018

The sensory function of the trigeminal nerve is to provide tactile, proprioceptive, and nociceptive afference by chemical stimulation. Various physical responses of the trigeminal nerve to stimuli help to defend against harmful substances. Recently, many studies have been conducted on solitary chemoreceptor cells innervated by trigeminal nerve. Most volatile organic compounds stimulate both the olfactory and trigeminal nervous systems. In general, the trigeminal nervous system is less sensitive than the olfactory nervous system. Studies have shown that sensation of the trigeminal nerve by chemical stimulation results in inhibition of olfaction. This indicates that the olfactory and trigeminal nerves interact with each other in the central nervous system. It is important to study various noxious stimuli acting on the trigeminal nerve in modern society where environmental concerns are intensifying.

• Journal of Korean Neurosurgical Society
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• v.65 no.5
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• pp.640-651
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• 2022

Clinical studies on neuromodulation intervention for trigeminal neuralgia have not yet shown promising results. This might be due to the fact that the pathophysiology of chronic trigeminal neuropathy is not yet fully understood. Chronic trigeminal neuropathy includes trigeminal autonomic neuropathy, painful trigeminal neuropathy, and persistent idiopathic facial pain. This disorder is caused by complex abnormalities in the pain processing system, which is comprised of the affective, emotional, and sensory components, rather than mere abnormal sensation. Therefore, integrative understanding of the pain system is necessary for appropriate neuromodulation of chronic trigeminal neuropathy. The possible neuromodulation targets that participate in complex pain processing are as follows : the ventral posterior medial nucleus, periaqueductal gray, motor cortex, nucleus accumbens, subthalamic nucleus, globus pallidus internus, anterior cingulate cortex, hypothalamus, sphenopalatine ganglion, and occipital nerve. In conclusion, neuromodulation interventions for trigeminal neuralgia is yet to be elucidated; future advancements in this area are required.

• International Journal of Oral Biology
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• v.34 no.3
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• pp.157-164
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• 2009

We recently described a novel animal model of trigeminal neuropathic pain following compression of the trigeminal ganglion (Ahn et al., 2009). In our present study, we adapted this model using male Sprague-Dawley rats weighing between 250-260 g and then analyzed the behavioral responses of these animals following modified chronic compression of the trigeminal ganglion. Under anesthesia, the rats were mounted onto a stereotaxic frame and a 4% agar solution ($10{\mu}L$) was injected in each case on the dorsal surface of the trigeminal ganglion to achieve compression without causing injury. In the control group, the rats received a sham operation without agar injection. Air-puff, acetone, and heat tests were performed at 3 days before and at 3, 7, 10, 14, 17, 21, 24, 30, 40, 55, and 70 days after surgery. Compression of the trigeminal ganglion produced nociceptive behavior in the trigeminal territory. Mechanical allodynia was established within 3 days and recovered to preoperative levels at approximately 60 days following compression. Mechanical hyperalgesia was also observed at 7 days after compression and persisted until the postoperative day 40. Cold hypersensitivity was established within 3 days after compression and lasted beyond postoperative day 55. In contrast, compression of the trigeminal ganglion did not produce any significant thermal hypersensitivity when compared with the sham operated group. These findings suggest that compression of the trigeminal ganglion without any injury produces prolonged nociceptive behavior and that our rat model is a useful system for further analysis of trigeminal neuralgia.

• The Korean Journal of Physiology and Pharmacology
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• v.5 no.3
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• pp.213-221
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• 2001

The amygdala is known as a site for inducing analgesia, but its action on the trigeminal nucleus has not been known well. Little information is available on the effect of dynorphin on NMDA receptor-mediated electrophysiological events in the trigeminal nucleus. The purpose of this study was to investigate the changes in the single neuron spikes at the trigeminal nucleus caused by the amygdala and the action of dynorphin on the trigeminal nucleus. In the present study, extracellular single unit recordings were made in the dorsal horn of the medulla (trigeminal nucleus caudalis) and the effects of microiontophoretically applied compounds were examined. When [D-Ala2, N-Me-Phe4, Glys5-ol]enkephalin (DAMGO, 10-25 mM), a ${\mu}-opioid$ receptor agonist, was infused into the amygdala, the number of NMDA-evoked spikes at the trigeminal nucleus decreased. However, the application of naloxone into the trigeminal nucleus while DAMGO being infused into the amygdala increased the number of spikes. Low dose (1 mM) of dynorphin in the trigeminal nucleus produced a significant decrease in NMDA-evoked spikes of the trigeminal nucleus but the NMDA-evoked responses were facilitated by a high dose (5 mM) of dynorphin. After the ${\kappa}$ receptors were blocked with naloxone, dynorphin induced hyperalgesia. After the NMDA receptors were blocked with AP5, dynorphin induced analgesia. In conclusion, dynorphin A exerted dose-dependent dual effects (increased & decreased spike activity) on NMDA-evoked spikes in the trigeminal nucleus. The inhibitory effect of the dynorphin at a low concentration was due to the activation of ${\kappa}$ receptors and the excitatory effect at a high concentration was due to activation of NMDA receptors in the trigeminal neurons.

• Proceedings of the KACD Conference
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• 2001.11a
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• pp.561.2-561
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• 2001

Trigeminal sensory nerves relay mechanical, thermal, chemical and proprioceptive information from craniofacial region. Therefore, it is important of dentistry. Trigeminal sensory nucleus consists of principal sensory trigeminal nucleus, spinal trigeminal nuclei, mesencephalic trigeminal nucleus. Transmission of these sensation depends on function and distribution of ion channels.(omitted)

• The Journal of Korean Medicine Ophthalmology and Otolaryngology and Dermatology
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• v.20 no.3
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• pp.243-250
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• 2007

Trigeminal neuralgia is nerve systematic disease appearing in the distribution scope of trigeminal nerve. It's characterized by extreme pain accompanying with a repeated and simultaneous fit from several seconds to 1-2 minutes. The oriental medical name of trigeminal neuralgia is generally Dootong, Doopoong, Myuntong, Pyundootong, Pyundoopoong, and Myuntong is the nearest in Occidental medicine. So I study for general prescription of Trigeminal neuralgia and point out Galgunhaegui-tang(葛根解肌湯). Trigeminal neuralgia patients were given Galgunhaegui-tang. After taking Galgunhaegui-tang, the patients's Trigeminal neuralgia was improved.

• The Journal of Korean Medicine
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• v.18 no.1
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• pp.58-71
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• 1997

In order to the location and local arrangement of nerve cell bodies and nerve fibers projecting to the meridian points related to facial nerve paralysis in the rat using the neural tracers, CTB and WGA-HRP, labeled neurons the were investigated by immunohistochemical and HRP histochemical methods following injection of 2.5% WGA-HRP and 1% CTB into Hyopko$(S_6)$. Chichang$(S_4)$, Sugu$(GV_{26})$, Sajukkong$(TE_{23})$ and Yangbaek$(G_{14})$. Following injection of Hyopko$(S_6)$, Chichang$(S_4)$, labeled motor neurons were founded in facial nucleus, trigeminal motor nucleus, reticular nucleus and hypoglossal nucleus. labeled sensory neurons were founded in trigeminal ganglia and $C_{1-2}$ spinal ganglia. sympathetic motor neurons were found in superior cervical ganglia. Sensory fibers labeled in brainstem were found in mesencephalic trigeminal tract, sensory root of trigeminal nerve, oral, interpolar and caudal part of trigeminal nucleus, area postrema, nucleus tractus solitarius, lateral reticular nucleus and $C_{1-2}$ spinal ganglia. Following injection of Sugu$(GV_{26})$, labeled motor neurons were founded in facial nucleus. Labeled sensory neurons were founded in trigeminal ganglia and $C_{1-2}$ spinal ganglia. Sympathetic motor neurons were found in superior cervical ganglia. Sensory fibers labeled in brainstem were found in spinal trigeminal tract, trigeminal motor nucleus, mesencephalic trigeminal tract, oral. interpolar and caudal parts of trigeminal nucleus, area postrema, nucleus tractus solitarius, lateral reticular nucleus, dorsal part of reticular part and $C_{1-2}$ spinal ganglia. Following injection of Sajukkong$(TE_{23})$ and Yangbaek$(G_{14})$, labeled motor neurons were founded in facial nucleus, trigeminal motor nucleus. Labeled sensory neurons were founded in trigeminal ganglia and $C_{1-2}$ spinal ganglia. sympathetic motor neurons were found in superior cervical ganglia. Sensory fibers labeled in brainstem were found in oral, interpolar and caudal parts of trigeminal nucleus, area postrema, nucleus tractus solitarius, inferior olovary nucleus, medullary reticular field and lamina I-IV of $C_{1-2}$ spinal cord. Location of nerve cell body and nerve fibers projecting to the meridian points related to the facial nerve paralysis in the rats were found in facial nucleus and trigeminal motor nucleus. Sensory neurone were found in trigeminal ganglia and $C_{1-2}$ spinal ganglia. Sympathetic motor neurons were found in superior cervical ganglia. Sensory fibers labeled in brainstem were found in mesencephalic trigeminal tract, oral, interpolar and caudal parts of trigeminal nucleus, area postrema, nucleus tractus solitarius. lateral reticular nucleus, medullary reticular field.

• The Korean Journal of Pain
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• v.13 no.2
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• pp.232-236
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• 2000

Bilateral trigeminal neuralgia is uncommon and usually occurs in 1% to 11% of patients with trigeminal neuralgia. There has been no report of a patient with bilateral trigeminal neuralgia in Korea. Based on our review, the incidence of bilateral trigeminal neuralgia among the trigeminal neuralgia patients who visited our pain clinic numbered 0.7% (4 out of 531). This is much lower than those of other previous studies. This lower incidence might be explained by the fact that we excluded those patients with mild bilateral trigeminal neuralgia which did not require treatment and also patients whose symptom on controlateral side was relieved by injection of local anesthetics for that side. Among the four patients with bilateral trigeminal neuralgia, three patients received alcohol block of the branches of trigeminal nerve and one refused the treatment. Overall, three patients maintained good or excellent pain relief without any serious complications throughout the follow-up period.

• Journal of the korean academy of Pediatric Dentistry
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• v.25 no.1
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• pp.249-256
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• 1998

Glial fibrillary acidic proteins (GFAP) are a group of intermediate filaments that are distributed in the cytoplasm of glial cells. GFAP immunoreactivity (GFAP-IR) increase after central and peripheral nerve injuries. The purpose of this study was to determine change of GFAP-IR in rat trigeminal ganglion satellite cells following the axotomy of inferior alveolar nerve(IAN). The immunohistochemistry was carried out using the avidin-biotin-peroxidase complex(ABC) method. 1. Control group : Astrocytes in central root of trigeminal ganglion had strong GFAP-IR, but satellite cells of trigeminal ganglion occasionally had GFAP-IR. The patterns of reactivity in satellite cells of trigeminal ganglion were not concenturated in any specific region of trigeminal ganglion. 2. Three day group after IAN axotomy : There were highly GFAP-IR in satellite cells of trigeminal ganglion in mandibular region. GFAP-IR in maxillary and ophthalmic regions were less intense compared to mandibular region. 3. Seven day group after IAN axotomy : GFAP-IR that were increased compared to control group were seen in the mandibular region. But GFAP-IR were less intense compared to three day group. These results suggest that GFAP-IR increase in specific region of trigeminal ganglion following peripheral axotomy. therefore we suppose that GFAP study offer research tool in trigeminal neuralgia.

• The Korean Journal of Pain
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• v.31 no.3
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• pp.174-182
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• 2018

Background: The trigeminal nucleus caudalis (Vc) is a primary central site for trigeminal transmitting. Noxious stimulation of the trigeminal nociceptors alters the central synaptic releases and neural expression of some inflammatory and trophic agents. Orexin-A and the orexin 1 receptor (OX1R) are expressed in pain pathways including trigeminal pain transmission. However, the the mechanism(s) underling orexin-A effects on trigeminal pain modulation have not been fully clarified. Methods: Trigeminal pain was induced by subcutaneous injection of capsaicin in the upper lip in rats. The effect of trigeminal pain on cyclooxygenase-2 (COX-2) and brain-derived neurotrophic factor (BDNF) expression in the Vc of animals was determined by immunofluorescence. Subsequently, OX1R agonist (orexin-A) and antagonist (SB-334867-A) was administrated in the Vc to investigate the possible roles of the Vc OX1R on changes in COX-2 and BDNF levels following pain induction. Results: The data indicated an increase in COX-2 and decrease in BDNF immuno-reactivity in the Vc of capsaicin, and capsaicin- pretreated with SB-334867-A (80 nM), groups of rat. However, the effect of capsaicin on COX-2 and BDNF expressions was reversed by a Vc microinjection of orexin-A (100 pM). Conclusions: Overall, the present data reveals that orexin-A can attenuate capsaicin-induced trigeminal pain through the modulation of pain effects on COX-2 and BDNF expressions in the Vc of rats.