Migraine pain associated with middle cerebral artery dilatation: reversal by sumatriptan
References (31)
- et al.
The common migraine attack may not be initiated by cerebral ischaemia
Lancet
(1981) HT1-like receptor agonist, for the treatment of severe migraine
Lancet
(1988)- et al.
Arterial responses during migraine headache
Lancet
(1990) Hemodynamic studies within the brain during migraine
Arch Neurol
(1973)- et al.
Focal hyperemia followed by spreading oligemia and impaired activation of rCBF in classic migraine
Ann Neurol
(1981) - et al.
The changes of regional cerebral blood flow during the course of classical migraine attacks
Ann Neurol
(1983) - et al.
Ischemia may be the primary cause of the neurological deficits in classic migraine
Arch Neurol
(1987) - et al.
Regional cerebral blood flow during migraine attacks by xenon-133 inhalation and emission tomography
Brain
(1984) - et al.
Timing and topography of cerebral blood flow, aura and headache during migraine attacks
Ann Neurol
(1990) - et al.
Focal ischaemia caused by instability of cerebrovascular tone during attacks of hemiplegic migraine: a regional cerebral blood flow study
Brain
(1987)
Delayed hyperemia following hypoperfusion in classic migraine: single photon emission computed tomographic demonstration
Arch Neurol
Regional cerebral blood flow during attacks and when free of symptoms in a large group of migraine patients
Cephalalgia
Early clinical experience with subcutaneous GR43175 in acute migraine: an overview
Cephalalgia
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2022, Comprehensive PharmacologyTargeting the 5-HT<inf>1B/1D</inf> and 5-HT<inf>1F</inf> receptors for acute migraine treatment
2020, Progress in Brain ResearchCitation Excerpt :Triptans are predominantly selective 5-HT1B/1D receptor agonists, and some of them also have affinity for the 5-HT1F receptor (Lanfumey and Hamon, 2004). By binding to 5-HT1B and 5-HT1D receptors, triptans exert antimigraine action through three putative main mechanisms: constricting the cranial vessels, inhibiting the release of nociceptive neurotransmitters from trigeminal sensory afferents, and inhibiting transmission through second-order neurons of the TCC (Feniuk et al., 1989; Friberg et al., 1991; Humphrey and Feniuk, 1991). Regarding intracellular signaling, triptans act at Gi protein-coupled 5-HT1B/1D receptors, leading to a decrease in intracellular cAMP levels, which reduces CGRP release from trigeminal neurons and consequently reduces nociceptive transmission (Gupta et al., 2006; Rubio-Beltrán et al., 2016).
Advanced Imaging in the Evaluation of Migraine Headaches
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