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片頭痛の病態はどのように理解されているのか |
論文抄録 |
Current theories propose that the primary dysfunction in migraine occurs within the CNS and that this evokes changes in blood vessels within pain-producing intracranial meningeal structures that give rise to headache pain. Migraine is now thought of as a neurovascular disorder. It has been proposed that genetic abnormalities may be responsible for altering the response threshold to migraine specific trigger factors in the brain of a migraineur compared to a normal individual. The exact nature of the central dysfunction that is produced in migraineurs is still not clear and may involve spreading depression-like phenomena and activation of brain stem monoaminergic nuclei that are part of the central autonomic, vascular and pain control centers. It is generally thought that local vasodilatation of intracranial extracerebral blood vessels and a consequent stimulation of surrounding trigeminal sensory nervous pain pathways is a key mechanism underlying the generation of headache pain associated with migraine. This activation of the 'trigeminovascular system' is thought to cause the release of vasoactive sensory neuropeptides, especially CGRP, that increase the pain response. The activated trigeminal nerves convey nociceptive information to central neurons in the brain stem trigeminal sensory nuclei that in turn relay the pain signals to higher centers where headache pain is perceived. It has been hypothesized that these central neurons may become sensitized as a migraine attack progresses. The 'triptan' anti-migraine agents (e.g. sumatriptan, rizatriptan, zolmitriptan naratriptan) are serotonergic agonists that have been shown to act selectively by causing vasoconstriction through 5-HT1B receptors that are expressed in human intracranial arteries and by inhibiting nociceptive transmission through an action at 5-HT1D receptors on peripheral trigeminal sensory nerve terminals in the meninges and central terminals in brain stem sensory nuclei. These three complementary sites of action underlie the clinical effectiveness of the 5-HT1B/1D agonists against migraine headache pain and its associated symptoms. |
文献 PubMed−ID |
PMID: 10563228 |
エビデンスレベル |
N/A |
文献タイトル (日本語) |
片頭痛の病態生理—新たな知見より |
目的 |
現在の片頭痛の病態生理についてまとめたもの． |
研究デザイン |
N/A |
研究施設 |
Merck Research Laboratories, West Point PA 9486, USA . |
研究期間 |
N/A |
対象患者 |
N/A |
介入 |
N/A |
主要評価項目とそれに用いた 統計学的手法 |
N/A |
備考 |
Publication Types: |
作成者 |
濱田潤一，永田栄一郎 |
2) Edvinsson L. Pathophysiology of primary headaches. Curr Pain Headache Rep. 2001 Feb;5(1):71-8. |
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論文抄録 |
The cerebral circulation is innervated by sympathetic, parasympathetic, and sensory nerves, which store a considerable number of neurotransmitters. The role of these has been evaluated in primary headaches. A clear association between head pain and the release of calcitonin gene-related peptide was demonstrated. In cluster headache and in a case of chronic paroxysmal headache there was in addition the release of vasoactive intestinal peptide, which was associated with the facial symptoms (nasal congestion, rhinorrhea). In parallel with sumatriptan treatment, head pain subsided and neuropeptide release normalized. These data show the involvement of sensory and parasympathetic mechanisms in the pathophysiology of primary headaches. |
文献 PubMed−ID |
PMID: 11252141 |
文献タイトル (日本語) |
一次性頭痛の病態生理 |
目的 |
一次性頭痛の病態生理を現在の仮説で解説． |
研究施設 |
Department of Internal Medicine, Lund University Hospital , Lund S-221 85, Sweden . |
コメント |
体系的に頭痛の病態生理をまとめている． |
備考 |
Publication Types: l Substances: |
作成者 |
濱田潤一，永田栄一郎 |