• Clinical and Experimental Pediatrics
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• v.54 no.9
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• pp.389-393
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• 2011

We present the case of a patient with Epstein-Barr virus (EBV) encephalitis who developed abnormal white matter lesions during the chronic phases of the infection. A 2-year-old-boy was admitted for a 2 day history of decreased activity with ataxic gait. The results of the physical examination were unremarkable except for generalized lethargy and enlarged tonsils with exudates. Brain magnetic resonance imaging (MRI) at admission showed multiple high signal intensities in both basal ganglia and thalami. The result of EBV polymerase chain reaction (PCR) of the cerebral spinal fluid was positive, and a serological test showed acute EBV infection. The patient was diagnosed with EBV encephalitis and recovered fully without any residual neurologic complications. Subsequently, follow-up MRI at 5 weeks revealed extensive periventricular white matter lesions. Since the patient remained clinically stable and asymptomatic during the follow-up period, no additional studies were performed and no additional treatments were provided. At the 1-year follow-up, cranial MRI showed complete disappearance of the abnormal high signal intensities previously seen in the white matter. The patient continued to remain healthy with no focal neurologic deficits on examination. This is the first case of asymptomatic self-limited white matter lesions seen in serial MRI studies in a Korean boy with EBV encephalitis.

• The Korean Journal of Pain
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• v.5 no.2
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• pp.258-262
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• 1992

Herpes zoster is an acute infectious viral disease which affects the posterior spinal root ganglion of the spinal nerve. A single posterior spinal root ganglion or a small number of adjacent ones may be affected, usually on the same side. The corresponding ganglia of the cranial nerve may also be similarly affected. The causative virus, varicella zoster, belongs to the group of host-specific DNA viruses. Postherpetic neuralgia is a continuation of herpes zoster in older patients. Although spontaneous resolution of herpes zoster may be expected in most patients, a significant number experience intractable pain. Postherpetic neuralgia is one of the most difficult problems encountered by physicians. There are many methods for management of postherpetic neuralgia, but there is no method that results in complete remission. Laser has lately come into use to reduce several acute or chronic pains. In order to determine the degree of pain relief by laser, 27 patients of postherpetic neuralgia were irradiated with He Ne, Infrared, and $CO_2$ combine scan moded lasers two to three times per week. The results were as follows: 1) The most frequent site was thoracic vertebral nerve area. 2) Patients younger than 70 years of age showed an improvement rate of 57% vs 27% for those patients older than 70 years of age. 3) Laser therapy proved effective of those patients who received the laser treatment within one month of the onset of the disease. 4) For those patients who received treatment within one month of the disease and reflecting a 50% improvement rate, the average irradiation time was 5.7.

• The Korean Journal of Pain
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• v.22 no.2
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• pp.151-157
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• 2009

Background: We hypothesized that if a fluoroscopic image of the lumbar sympathetic ganglion block (LSGB) showed the spread patterns of contrast at both the L2/3 and L4/5 disc areas, then this would demonstrate a more profound blockade effect because the spread patterns are close to sympathetic ganglia. In addition, we compared the effects of LSGB and transforaminal epidural steroid injection (TFESI) for the patients suffering with spinal stenosis. Methods: Eighty patients were divided into two groups (Group S: the patients treated with TFESI, Group L: the patients treated with LSGB). The patients of group L were classified into three groups (groups A, B and, C) according to their contrast spread pattern. The preblock and postblock temperature difference between the ipsilateral and contralateral great toe ($DT^{pre}$, $DT^{post}$, $^{\circ}C$), and the DTnet were calculated as follows. $DT^{net}$ = $DT^{post}$ - $DT^{pre}$. Results: Both group showed a significant reduction of the visual analogue score (VAS) and the Oswestry disability index (ODI) score. Only the patients of group L showed a significant increase of their walking distance (WD). Group A showed the most significant changes in the $DT^{post}$ ($6.1{\pm}1.2^{\circ}C$, P = 0.021), and the DTnet ($6.0{\pm}1.0^{\circ}C$, p = 0.023), as compared to group C. Conclusions: LSGB showed a similar effect on the VAS, and ODI, and a significant effect, on WD, compared with TFESI. Group A showed a significant sympatholytic effect, as compared to group C.

• The Korean Journal of Pharmacology
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• v.24 no.2
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• pp.153-164
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• 1988

The potential role of endogenous opioid peptides (EOPS) in cardiovascular regulation has only recently been entertained. EOPS have been localized in brain, spinal cord, autonomic ganglia, particularly the adrenal gland, and many other peripheral tissues. There are at least five major types of opioid receptors; namely ${\mu},\;{\delta},\;k,\;{\sigma},\;and\;{\varepsilon}$ and Experimental evidence indicates that cardiovascular actions of the peptide are mediated primarily by ${\mu},\;{\delta}$ and k receptors, and that these receptor types may be allosterically coupled. In anesthetized rabbits met-enkephalin decreased blood pressure and heart rate, which closely paralleled a reduction in sympathetic discharge. Naloxone, but not naloxone methobromide, antagonized these effects, which suggests a central site of action of met-enkephalin. A number of autonomic agents, particularly adrenergic ${\alpha}$-and, ${\beta}-agonists$ and antagonists modify the cardiovascular actions of met-enkephalin. Experiments in reserpine-treated and adrenalectomized rats provide no evidence of sympathetic nervous system involvement in the pressor responses to intravenous injection of opioid peptides, but rather suggest a direct peripheral action. Finally, activation of a beta-endorphinergic pathway projecting from the arcuate nucleus to the nucleus tractos solitarii in rats can cause naloxone reversible hypotension and bradycardia. There is evidence to implicate this pathway in antihypertensive drug action and in the modulation of baroreflex activity.

• Molecules and Cells
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• v.21 no.2
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• pp.237-243
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• 2006

Brain-derived neurotrophic factor (BDNF) is a neuromodulator of nociceptive responses in the dorsal root ganglia (DRG) and spinal cord. BDNF synthesis increases in response to nerve growth factor (NGF) in trkA-expressing small and medium-sized DRG neurons after inflammation. Previously we demonstrated differential activation of multiple BDNF promoters in the DRG following peripheral nerve injury and inflammation. Using reporter constructs containing individual promoter regions, we investigated the effect of NGF on the multiple BDNF promoters, and the signaling pathway by which NGF activates these promoters in PC12 cells. Although all the promoters were activated 2.4-7.1-fold by NGF treatment, promoter IV gave the greatest induction. The p38 mitogen-activated protein kinase (MAPK) inhibitor, SB203580, phosphatidylinositol 3-kinase (PI-3K) inhibitor, LY294003, protein kinase A (PKA) inhibitor, H89, and protein kinase C (PKC) inhibitor, chelerythrine, had no effect on activation of promoter IV by NGF. However, activation was completely abolished by the MAPK kinase (MEK) inhibitors, U0126 and PD98059. In addition, these inhibitors blocked NGF-induced phosphorylation of extracellular signal-regulated protein kinase (ERK) 1/2. Taken together, these results suggest that the ERK1/2 pathway activates BDNF promoter IV in response to NGF independently of NGF-activated signaling pathways involving PKA and PKC.

• Tuberculosis and Respiratory Diseases
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• v.63 no.1
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• pp.78-82
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• 2007

Schwannoma represents approximately 40% of neurogenic tumors arising in the mediastinum, and develops along the sympathetic or parasympathetic chain, intercostals nerve, and spinal ganglia. It is usually asymptomatic, and is confronted accidentally but can produce chest pain, cough and dyspnea. However, dyspnea with pleural effusion is rare in patients with benign schwannoma. We encountered two cases of benign schwannoma with pleural effusion. Both cases had similar initial symptoms and the characteristics of a mass but the characteristics of pleural effusion analysis were different. The benign schwannoma was confirmed in two cases using VATS (video-assisted tharawswpic surgery).

• The Korean Journal of Pain
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• v.32 no.3
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• pp.215-222
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• 2019

Background: Several nerve blocks can reduce the incidence of postherpetic neuralgia (PHN) as well as relieve acute zoster-related pain, but the long-term outcome of PHN has not been clearly determined. This study investigated the efficacy of selective nerve root block (SNRB) for herpes zoster (HZ) on the long-term outcome of PHN. Methods: We prospectively conducted an interview of patients who had undergone an SNRB for HZ from January 2006 to December 2016 to evaluate their long-term PHN status. The relationship between the time from HZ onset to the first SNRB and the long-term outcome of PHN was investigated. Results: The data of 67 patients were collected. The patients were allocated to acute ($SNRB{\leq}14days$, n = 16) or subacute (SNRB > 14 days, n = 51) groups. The proportions of cured patients were 62.5% and 25.5% in the acute and subacute groups (P = 0.007), respectively. In logistic regression, an SNRB >14 days was the significant predictor of PHN (adjusted odd ratio, 3.89; 95% confidence interval, 1.02-14.93; P = 0.047). Kaplan-Meier analysis revealed that time from the SNRB to the cure of PHN was significantly shorter in the acute group ($2.4{\pm}0.7yr$) than in the subacute group ($5.0{\pm}0.4yr$; P = 0.003). Conclusions: An early SNRB during the acute stage of HZ (within 14 days) appears to decrease the incidence and shorten the duration of PHN, with a median of 5.0 years of follow-up.

• The Korean Journal of Pain
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• v.34 no.1
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• pp.4-18
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• 2021

Except for carbamazepine for trigeminal neuralgia, gabapentinoid anticonvulsants have been the standard for the treatment of neuropathic pain. Pregabalin, which followed gabapentin, was developed with the benefit of rapid peak blood concentration and better bioavailability. Mirogabalin besylate (DS-5565, Tarlige®) shows greater sustained analgesia due to a high affinity to, and slow dissociation from, the α2δ-1 subunits in the dorsal root ganglion (DRG). Additionally, it produces a lower level of central nervous system-specific adverse drug reactions (ADRs), due to a low affinity to, and rapid dissociation from, the α2δ-2 subunits in the cerebellum. Maximum plasma concentration is achieved in less than 1 hour, compared to 1 hour for pregabalin and 3 hours for gabapentin. The plasma protein binding is relatively low, at less than 25%. As with all gabapentinoids, it is also largely excreted via the kidneys in an unchanged form, and so the administration dose should also be adjusted according to renal function. The equianalgesic daily dose for 30 mg of mirogabalin is 600 mg of pregabalin and over 1,200 mg of gabapentin. The initial adult dose starts at 5 mg, given orally twice a day, and is gradually increased by 5 mg at an interval of at least a week, to 15 mg. In conclusion, mirogabalin is anticipated to be a novel, safe gabapentinoid anticonvulsant with a greater therapeutic effect for neuropathic pain in the DRG and lower ADRs in the cerebellum.

• Korean Journal of Acupuncture
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• v.39 no.4
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• pp.132-141
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• 2022

Objectives : Some acupoints are commonly utilized to treat a variety of diseases. The acupoints appear to have a wide range of effects caused by several mechanisms. The purpose of this study is to investigate into the potential role of microRNAs (miRNAs) in the multipotent effects of individual acupoint stimulation. Methods : We examined the miRNA expressions in the dorsal root ganglia (DRG) of neuropathic or inflammatory pain rats following ST36 and GB34 electroacupuncture (EA) stimulation. Neuropathic pain was induced by L5 spinal nerve ligation. Inflammatory pain was induced by knee joint injection of Complete Freund's adjuvant (CFA). EA was given under gaseous anesthesia with the same parameters (1mA, 2Hz, 30 min) in 5 consecutive days. Pain behaviors and miRNA expressions were analyzed. Results : In rats with neuropathic and inflammatory pain, EA treatments significantly enhanced the paw withdrawal threshold and weight-bearing force. After nerve injury, 36 miRNAs were upregulated in the DRG of neuropathic rats, while EA downregulated 10 of them. Furthermore, 14 miRNAs were downregulated following nerve damage, while one was increased by EA. 15 miRNAs were increased in the DRG of inflammatory rats following CFA injection, while 5 were downregulated by EA. Furthermore, 17 miRNAs were downregulated following CFA injection, while 7 were increased by EA. The miRNAs rno-miR-335, rno-miR-381-5p, rno-miR-1306-3p, and rno-miR-1839-3p were regulated by EA in both models. Conclusions : In two pain models, EA applied to ST36 and GB34 regulated miRNA expression differently. There appeared to be both acupoint-specific and non-specific miRNAs, and miRNA regulation of differential protein expression may modulate a variety of EA mechanisms.

• The Korean Journal of Pharmacology
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• v.26 no.2
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• pp.101-111
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• 1990

The effect of physostigmine (PS), which has been shown to act on the muscarinic receptors in the brains of the rat, dog and cat, on the arterial blood pressure (BP) was investigated in urethane-anesthetized rabbits. Intravenous (iv) PS, $25{\sim}300\;{\mu}g/kg$, caused little change in BP. However, after treatment of rabbits with either of chlorisondamine (CS), hexamethonium, intracerebroventricular (icv) clonidine, icv xylazine and icy reserpine iv PS produced a pressor response. Spinalization of the rabbit also caused iv PS to increase BP. The pressor effect of iv PS in CS-treated rabbits was markedly reduced after prazosin or pirenzepine. Iv PS inhibited the pressor response to McN-A-343 in CS-treated and in spinal rabbits; alternately during the infusion of McN-A-343 iv PS failed to produce the pressor response. The pressor response to DMPP was not affected by iv PS. Icv PS, $12{\sim}200\;{\mu}g/kg$, produced a pressor response which was accentuated after CS-treatment. This pressor effect was inhibited, though not complete, by prazosin or by pirenzepine. A simultaneous treatment of rabbits with both $[Sar^{1},\;Ala^{8}]-angiotensin$ II, an angiotensin II antagonist, and prazosin or pirenzepine almost completely abolished the pressor effect of icv PS, whereas the angiotensin II antagonist did not enhance the inhibitory effect of pirenzepine and prazosin on the pressor response to iv PS . Icv pirenzepine blocked the pressor response to icv PS without affecting that to iv PS. The present results show that the pressor response to iv PS in CS-treated and in spinal rabbits arises from stimulation of the muscarinic receptors in the sympathetic ganglia, whereas the pressor response by icv PS via activation of the muscarinic receptors in the brain which causes an enhancement in the outflow of sympathetic discharge and angiotensin. The results also suggest that iv PS is unable to produce a pressor response in the rabbit unless the sensitivity of the gangionic muscarinic receptors is altered by ganglionic nicotinic blockade, by the decrease of central sympathetic outflow on the sympathetic ganglia or by spinalization.