• Title/Summary/Keyword: Pain: mechanism

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A Study on the Serotonin Metabolism and the Morphine-related Analgesic Mechanism in Mice Fed Tryptophan Supplemented Deit (II) (트립토판 보강식이를 섭취한 마우스에서 serotonin 대사와 morphine 진통기작 관련성에 대한 연구(II))

  • 권영혜;이윤옥;김해리
    • Biomolecules & Therapeutics
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    • v.9 no.1
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    • pp.20-25
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    • 2001
  • In this study we fed control diet and tryptophan supplemented diets containing 0.35% tryptophan to ICR mice for 2 weeks. The concentrations of serotonin and 5-HIAA were changed by injection of the serotonin synthesis inhibitor, p-CPA and the serotonin precursor, serotoninP and the change of brain serotonin concentration negatively correlated with that of pain sensitivity, and p-CPA and serotoninP also changed the analgesic effect of morphine. The injection of naloxone, the opiate antagonist, resulted in an increase in the writhing frequency, but its antagonistic effect was not significant. The concentration of 5-HIAA elevated in mice brain at least 3hr after administration of morphine hydroxide indicates that the changes in brain serotonin metabolism may be associated with the acute effects of morphine analgesia. In short, these results not only suggest that tryptophan supplemented diet suppress pain sensitivity in mice, but also indicate that at least in part analgesic mechanism of serotonin may be associated with morphine analgesia.

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New Mechanism of Vasovagal Syncope -Trigeminocardiac Reflex- (혈관미주신경실신의 새로운 기전 -삼차신경-심장반사-)

  • Yoon, Ji Young;Kim, Cheul Hong
    • Journal of The Korean Dental Society of Anesthesiology
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    • v.12 no.3
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    • pp.151-155
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    • 2012
  • A vasovagal reaction is defined as the 'development of hypotension and bradycardia associated with the typical clinical manifestations of pallor, sweating and weakness'. The most profound degree of vasovagal reaction results in fainting or syncope. Incidence of vasovagal reactions in the local anesthetic department of a dental hospital is around 2%. The pathophysiology of the hypotension/bradycardia reflex responsible for vasovagal syncope is not completely understood. Central as well as peripheral mechanisms have been implicated in its pathogenesis: however their relative contribution is not fully elucidated. Recently, trigeminocardiac reflex, previously known as oculocardiac reflex, may serve as syncope. The management of vasovagal syncope is evolving. Non-pharmacological treatment options are a fundamental first step of all treatment pathways. In this article, we would like to review new mechanism of vasovagal syncope and hope to be of help to manage the syncopal patients.

The Experience of Open Reduction and Internal Fixation of Mandible Fracture by Acupuncture Method (Acupuncture를 이용한 하악골 골절수술경험 -증례 보고-)

  • Khil, Hong-Mo;Kwak, Ho-Sung;Ro, Shik
    • The Korean Journal of Pain
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    • v.9 no.1
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    • pp.195-199
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    • 1996
  • Based on points of neuroendocrine physiology, stimulus developed at the acupuncture site can pass to the pituitary gland through somatosensory and activated descending inhibitory mechanism which originated in raphe magnus of midbrain. For the operation of mandible fracture, acupuncture anesthesia was performed at 6 points of both forearm and both feet by method taking point on distant segment. Acupuncture anesthesia deals with central analgesic mechanism and the theory of diffuse noxious inhibitory control.

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Conservative Treatment of the Knee Injury and Pain (슬관절 손상과 동통의 보존적 치료)

  • Bin Seoung-I1;Nam Tae-Seok;Ahn Ji-Hyun;Jung Kwang-Whan
    • Journal of Korean Orthopaedic Sports Medicine
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    • v.3 no.2
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    • pp.107-110
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    • 2004
  • Treatment of knee injury and pain consists of conservative and surgical treatment. Although conservative treatment is suffice in many cases, surgical treatment is performed which is not necessary. Therefore, thorough knowledge of injury mechanism and selection of treatment modalities are required. Injury mechanism and conservative treatment of knee injury patients will be discussed.

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The effects of cryotherapy on delayed onset muscle soreness (지연발생 근육통의 냉치료 효과에 대한 연구)

  • Kim, Sang-Yeob
    • Journal of Korean Physical Therapy Science
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    • v.8 no.2
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    • pp.1065-1071
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    • 2001
  • Delayed onset muscle soreness is a sensation of discomfort that occurs 24 h after exercise, and it is associated with the performance of unfamiliar and high force muscle work, such as eccentric contractions. The injury to the muscle has been well described but the mechanism underlying the injury is not fully understood. Although the pathophysiological processes underlying delayed onset muscle soreness are not completely understood, many researchers have investigated various treatments in a attempt to reduce the soreness. Physical therapy is the most importance techniques to reduce delayed onset muscle soreness. The purpose of this study is to investigate the effect of a cryotherapt on DOMS. Thirty subjects were randomly assigned to experimental group : control, cryotherapy, and placebo group. Elbow flexion range, mechanical pain threshold. and subjective pain were measured 30 min before DOMS was induced and 24, 48, 72 hours after DOMS was induced. The results of this study were as follows: 1. Elbow flexion range showed significant difference each time, especially at 48 and 72 hours 2. Mechanical pain thershold and subjectively pain showed no significant difference between group.

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Opioid-induced Muscle Rigidity with a Delayed Manifestation Misunderstood as a Tension Pneumothorax -A case report- (긴장성 기흉으로 오인된 지연 발현된 아편양 제제 유발 근경축 -증례보고-)

  • Kang, Bong Jin;Kim, Sung Hoon
    • The Korean Journal of Pain
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    • v.21 no.1
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    • pp.66-70
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    • 2008
  • Opioid-induced rigidity is a potentially life-threatening complication that can occur after treatment with large doses of opioids, but with early recognition it can be treated effectively with naloxone or with muscle relaxants. Regarding its onset time, there have been few case reports that have described delayed manifestations of opioid-induced rigidity. The mechanism of this complication is not well understood. In this report we describe a case of incidental overdose injection of sufentanil and subsequently review the confusing clinical features that require immediate diffenrentiation and the possible mechanim of this complication.

What is IMS? (IMS란 무엇인가)

  • Han, Jae-Bok
    • Journal of Acupuncture Research
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    • v.24 no.5
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    • pp.127-136
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    • 2007
  • Objectives : To review the history, the theoretical basis and the technique of Intramuscular Stimulation (IMS), papers and books on IMS were searched. Methods : 15 papers were searched with the keyword 'Gunn CC' at Pubmed(http://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmed). Several full texts of them and other papers were found at the internet homepage of The Institute for the Study and Treatment of Pain (http://www.istop.org/). 16 Korean papers on IMS were searched at KoreaMed(http://www.koreamed.org/SearchBasic.php) and Koreanstudies Infomation Service System(http://kiss.kstudy.com/KsiKiss.asp). Results : Dr. Gunn has made unique model which can explain the pathology of chronic pain and the mechanism of acupuncture treatment. In this model, he postulated that most of chronic pain is radiculopathy due to spondylosis and acupuncture treatment to the hyperalgesic muscle can restore the normal function of involved muscles and nerves. Conclusions : IMS is an acupuncture technique in which the muscles under the Ah-shi or tender points in periphery and intrasegmental paravertebral muscles are stimulated with needles.

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Basic Understanding of Transcutaneous Electrical Nerve Stimulation

  • Jung, Jae-Kwang;Byun, Jin-Seok;Choi, Jae-Kap
    • Journal of Oral Medicine and Pain
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    • v.41 no.4
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    • pp.145-154
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    • 2016
  • Transcutaneous electrical nerve stimulation (TENS) is one of the representative physiotherapical modalities used for the treatment of various musculoskeletal disorders by the application of electrical stimuli. In dental practice, it has long been used in the treatment of acute and chronic orofacial pain conditions including temporomandibular disorders. TENS is the delivery of therapeutic electrical stimuli with a variety of electrical intensity, frequency and duration to stimulate peripheral nerve through surface electrodes with various form and placement. While controversy still remains over the clinical effectiveness and application of TENS, basic understanding of its electrical properties and the expected biological reactions is important to increase the therapeutic effect and decrease the risk of possible side effects. This review, therefore, focuses on basic understanding of TENS including its underlying mechanisms and stimulation parameters.

Sec-O-glucosylhamaudol mitigates inflammatory processes and autophagy via p38/JNK MAPK signaling in a rat neuropathic pain model

  • Oh, Seon Hee;Kim, Suk Whee;Kim, Dong Joon;Kim, Sang Hun;Lim, Kyung Joon;Lee, Kichang;Jung, Ki Tae
    • The Korean Journal of Pain
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    • v.34 no.4
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    • pp.405-416
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    • 2021
  • Background: This study investigated the effect of intrathecal Sec-O-glucosylhamaudol (SOG) on the p38/c-Jun N-terminal kinase (JNK) signaling pathways, nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB)-related inflammatory responses, and autophagy in a spinal nerve ligation (SNL)-induced neuropathic pain model. Methods: The continuous administration of intrathecal SOG via an osmotic pump was performed on male Sprague-Dawley rats (n = 50) with SNL-induced neuropathic pain. Rats were randomized into four groups after the 7th day following SNL and treated for 2 weeks as follows (each n = 10): Group S, sham-operated; Group D, 70% dimethylsulfoxide; Group SOG96, SOG at 96 ㎍/day; and Group SOG192, SOG at 192 ㎍/day. The paw withdrawal threshold (PWT) test was performed to assess neuropathic pain. Western blotting of the spinal cord (L5) was performed to measure changes in the expression of signaling pathway components, cytokines, and autophagy. Additional studies with naloxone challenge (n = 10) and cells were carried out to evaluate the potential mechanisms underlying the effects of SOG. Results: Continuous intrathecal SOG administration increased the PWT with p38/JNK mitogen-activated protein kinase (MAPK) pathway and NF-κB signaling pathway inhibition, which induced a reduction in proinflammatory cytokines with the concomitant downregulation of autophagy. Conclusions: SOG alleviates mechanical allodynia, and its mechanism is thought to be related to the regulation of p38/JNK MAPK and NF-κB signaling pathways, associated with autophagy during neuroinflammatory processes after SNL.

Identification of Differentially Expressed Genes in Murine Hippocampus by Modulation of Nitric Oxide in Kainic Acid-induced Neurotoxic Animal Model

  • Suh, Yo-Ahn;Kwon, O-Min;Yim, So-Young;Lee, Hee-Jae;Kim, Sung-Soo
    • The Korean Journal of Physiology and Pharmacology
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    • v.11 no.4
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    • pp.149-154
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    • 2007
  • Kainic acid (KA) causes neurodegeneration, but no consensus has been reached concerning its mechanism. Nitric oxide may be a regulator of the mechanism. We identified differentially expressed genes in the hippocampus of mice treated with kainic acid, together with or without L-NAME, a nonselective nitric oxide synthase inhibitor, using a new differential display PCR method based on annealing control primers. Eight genes were identified, including clathrin light polypeptide, TATA element modulatory factor 1, neurexin III, ND4, ATPase, $H^+$ transporting, V1 subunit E isoform 1, and N-myc downstream regulated gene 2. Although the functions of these genes and their products remain to be determined, their identification provides insight into the molecular mechanism(s) involved in KA-induced neuronal cell death in the hippocampal CA3 area.