Headache and Pain Research

대한두통학회 춘계학술대회 일정표: Published online June 30, 2003

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편두통과 신경성 염증반응: Gyeong-Moon Kim; Korean J Headache. 2003;4(1):1-6. Published online June 30, 2003

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Abstract PDF: Despite considerable research into the pathogenesis of migraine, the pathophysiological mechanisms that underlie migraine headache remain poorly understood. Migraine is thought to be caused by a disten- sion of meningeal blood vessels, the activation of trigeminal sensory neurones and the development of a central sensitization within the trigeminal nucleus caudalis. Neurogenic inflammation within the menin- geal vasculature is elicited by neuropeptide release from trigeminal sensory fibers and characterized by plasma protein extravasation, vasodilation and histamine release from mast cells. Antimigraine agents such as ergots, triptans, opioids, and valproate inhibit neurogenic dural extravasation, suggesting that this activity may be a predictor of potential clinical efficacy of novel agents. Alternatively, it has been sugges- ted that neurogenic vasodilation of meningeal blood vessels could be also a key component of the inflammatory process during migraine headache. This view is supported by the observation that calcitonin gene-related peptide(CGRP), a potent vasodilator, has been detected in increased amounts in external jugular venous blood during migraine attacks and normalized by successful sumatriptan treatment. Nitric oxide donor glyceryl trinitrate provokes delayed migraine attacks when infused into migraineuers and results in NF-kB activation, iNOS expression and subsequent dural inflammation. These findings suggest that CGRP and NO release with associated neurogenic dural inflammation may be important in the generation of migraine headache. Targeting inflammatory response by selectively inhibiting mediators of neurogenic inflammation offers a new approach to the pharmacological treatment of migraine. Korean Journal of Headache 4(1):1-6, 2003

편두통 유전학의 최신지견: Manho Kim; Korean J Headache. 2003;4(1):7-13. Published online June 30, 2003

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Abstract PDF: The genetics of migraine is a fascinating and moving research area. This review focuses on the di- fferent molecular genetic findings in migraine. Familial hemiplegic migraine(FHM) is a rare subtype of migraine with aura, which is inherited as an autosomal dominant. Half the cases of FHM are caused by point mutations in the CACNA1A gene. Other mutation types cause episodic ataxia 2(EA-2) or expan- sions of the CAG in SCA 6. The finding in an ion channel subunit defines migraine as a channelopathy (eg, epilepsy). Mutations in genes on the X chromosome, dopamine receptor genes, ACE gene, genes for nitric oxide synthase, serotonin receptors, MTHFR, and mitochondrial DNA have been investigated. The positive associations have not been reproduced in other studies and therefore they should be interpreted with care. It is to be hoped that in the next few years much more will be known about the molecular genetic mechanisms of migraine Korean Journal of Headache 4(1):7-13, 2003

Migraine Pathogenesis: Stephen D. Silberstein, FACP; Korean J Headache. 2003;4(1):14-21. Published online June 30, 2003

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편두통의 진단: Sun Uck Kwon; Korean J Headache. 2003;4(1):22-29. Published online June 30, 2003

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Abstract PDF: Migraine is characterized by severe unilateral throbbing headache, aura, nausea and vomiting. Inter- national Headache Society has made clear diagnostic criteria for migraine and other headache disorders based on these clinical characteristics. However, differentiation and diagnosis of migraine is not clear when we encounter the patients with chronic recurrent headaches. A lot of patients with migraine have tension-type headache concomitantly. Migraine without aura and episodic tension-type headache share the nature of headache and associated symptoms. Episodic headaches including tension-type headache and migraine have tendency to transform to chronic daily headache. The transformed migraine and chronic tension-type headache have little difference in clinical features. The responsiveness to sumatriptan, which has been developed for migraine specific drug, can not differentiate migraine headache from tension type headache. Given the abundant similarities between clinical features and treatment response, new concepts and hypothesis have been raised such as migraine and tension type headache be considered opposite ends of a clinical spectrum of headache activity, and these headaches as sharing common pathophysiology (convergence hypothesis). Convergence hypothesis for primary headache can also explain the clinical manifestations of sinus headache and temporomandibular headache as well as migraine and tension type headache. Korean Journal of Headache 4(1):22-29, 2003

급성기 편두통 치료의 최근 경향: Jae-Myun Chung; Korean J Headache. 2003;4(1):30-36. Published online June 30, 2003

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Abstract PDF: Migraine is becoming to be recognized as one of the most significant health burden to people as well as one of the most challenging clinical problem to clinicians. Since the role of serotonin in the patho- genesis of migraine was established, there have been leaping advances in migraine therapy which were in conjunction with the advent of sumatriptan followed by various second generation triptans. Nowadays what agent clinicians should select in acute treatment of various migraines is changing in relation to such advances. In this review, the author described recent trends in acute migraine therapy with stress on evidence-based guideline for migraine headache published by the Quality Standards Subcommittee of the American Academy of Neurology in company with some remarks on the various triptans. Korean Journal of Headache 4(1):30-36, 2003

편두통 발작 예방 요법의 근거: Chin-Sang Chung; Korean J Headache. 2003;4(1):37-40. Published online June 30, 2003

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Abstract PDF: Currently a migraine attack is considered as originating in the brain. Triggers initiate depolarizing neu- roelectric and metabolic events resulting in spreading depression of Leao. This activates the headache and associated features of the attack by mechanisms involving either peripheral trigeminovascular or brains- tem pathways, or both. Interictal excitability of cell membranes that is in part genetically determined is the brain's susceptibility to attacks. Factors that increase or decrease neuronal excitability constitute the threshold for triggering attacks. Susceptibility to migraine attacks appears related to brain hyperexcitabi- lity. Recent functional neuroimaging techniques have shown the primary neural basis of migraine attack with secondary vascular changes(neuro-vascular mechanism). On this basis the prophylaxis for migraine should reduce the hyperexcitability and enhance the inhibitory activity of the sensitive migraine brain, thereby reducing the frequency, intensity, and duration of migraine attacks and enhancing the quality of life of migraine patients. Korean Journal of Headache 4(1):37-40, 2003

바이오피드백 소개: Sang-Wook Kim; Korean J Headache. 2003;4(1):41-47. Published online June 30, 2003

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Abstract PDF: Biofeedback can be defined as the technique of using electronic equipment to reveal to human beings some of their internal physiological events, normal and abnormal, in the form of visual and auditory signals in order to teach them to manipulate these otherwise involuntary or unfelt events by manipulating the displayed signals. The use of electromyograph(EMG) and peripheral skin temperature are the prin- ciple modalities used today in clinical practice. Tension headaches or muscle contraction headaches in which the muscle groups or the head, neck and shoulders are involved to a great extent can be treated effectively with EMG biofeedback. Some migraine patients can be treated effectively with thermal biofeedback training. Biofeedback is a powerful therapeutic tool which teaches persons to take responsi- bility to learn self-regulation of themselves and their bodies. Korean Journal of Headache 4(1):41-47, 2003

Antiepileptic Drugs in Migraine Prevention: Stephen D. Silberstein, FACE; Korean J Headache. 2003;4(1):48-59. Published online June 30, 2003

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보톡스 사용의 개요: Tae-Kyu Lee; Korean J Headache. 2003;4(1):60-62. Published online June 30, 2003

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Abstract PDF: Although controversial, Botulinum toxin type A(Botox) can be effectively used for migraine preven- tion. Injection of 25U Botox was reported to be effective for migraine prevention, but 75U without statistically significant effect. Furthermore, the way how to use Botox for each patients has not been evaluated. It may not be appropriate to inject Botox into scalp area far from migraine pain site. The author suggests for injecting Botox into and around migraine pain areas which vary from patient to patient. Korean Journal of Headache 4(1):60-62, 2003

측두하악장애와 편두통: Seong Taek Kim, Youn Joong Kim, Chong-Youl Kim; Korean J Headache. 2003;4(1):62-69. Published online June 30, 2003

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Abstract PDF: Temporomandibular disorders is a collective term embracing a number of clinical problems that in- volve the temporomandibular joint(TMJ), the masticatory muscles, and associated structures. Myofascial pain, one of the most common diagnosis in the TMD classification, is characterized by a regional, dull, aching muscle pain and the presence of localized trigger points in muscle, tendon, or fascia and it has been known as a pathogenetic factor in tension-type headache and migraine. According to the previous studies, the central sensitization following continuous nociceptive input of myofascial pain may play a important role in the pathogenesis of migraine and the mechanisms probably involves activation of N-Methyl-D-Aspartate(NMDA) receptors and production of Nitric Oxide(NO). Therefore the therapy for myofascial pain enhancing central inhibition through pharmacological mana- gement or behavioral interventions and simultaneously reducing peripheral inputs through physical therapies, orthopedic appliances and trigger point injections, can be considered as an effective treatment in migraine patients with myofascial pain. Korean Journal of Headache 4(1):62-69, 2003

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