Bench to bedside understanding of migraine pathophysiology

2021 ◽  
Vol 429 ◽  
pp. 118000
Author(s):  
Peter Goadsby
2006 ◽  
Vol 46 (s1) ◽  
pp. S32-S38 ◽  
Author(s):  
David Borsook ◽  
Rami Burstein ◽  
Eric Moulton ◽  
Lino Becerra

Author(s):  
Mark C. Kruit ◽  
Arne May

This chapter focuses on diagnostic clinical neuroimaging in migraine. In most migraine cases, patient history, details of symptoms, and careful clinical neurological examination are together the most important tools in diagnosing and treating migraine, and, consequently, there is mostly no need for further laboratory tests or neuroimaging. In selected non-acute headache cases, neuroimaging is warranted, and recommendations are provided. Good understanding of the migraine pathophysiology allows better interpretation of neuroimaging findings, notably when patients present acutely, in or outside an attack. The neuroradiological findings relevant in understanding the complex relationship between migraine and stroke will therefore be discussed. Similarly, knowledge of the epidemiological findings that have set migraine as a risk factor for (progressive) subclinical brain lesions is relevant in everyday neuroradiological practice.


Cephalalgia ◽  
2020 ◽  
Vol 40 (10) ◽  
pp. 1138-1139
Author(s):  
Kuan-Lin Lai ◽  
David M Niddam ◽  
Jong-Ling Fuh ◽  
Wei-Ta Chen ◽  
Jaw-Ching Wu ◽  
...  

2009 ◽  
Vol 1 ◽  
pp. CMT.S2056
Author(s):  
A.A. Kalanuria ◽  
B.L. Peterlin

Migraine is a common and often disabling neurovascular disorder. Changes in the metabolism and the central processing of serotonin, as well as abnormalities in the modulation of the central and peripheral trigeminal nociceptive pathways, have been shown to play significant roles in migraine pathophysiology. Recent evidence suggests that a low serotonin state facilitates activation of the trigeminal nociceptive pathways. In addition, several pharmacological agents that modulate serotonin are used in the treatment of migraine. Specifically there are seven FDA approved, 5-hydroxytryptamine (5-HT) 1B/1D receptor agonists, used for the acute abortive therapy of migraine. Zolmitriptan is one such triptan. Zolmitriptan is available as a tablet, orally disintegrating tablet and as a nasal spray. It is rapidly absorbed and detectable within the plasma, within 2 to 5 minutes for the nasal spray and within 15 minutes for the tablet. Zolmitriptan reaches peak plasma levels in 2-4 hours, with good levels maintained for up to 6 hours. Although the metabolism of zolmitriptan is predominantly hepatic, only 25% of zolmitriptan is bound to plasma proteins. Thus it is unlikely for drug interactions involving the displacement of highly protein-bound drugs. Zolmitriptan is very well tolerated with less than half of participants in clinical trials reporting adverse events, most of which were mild and transient. Although rare, serious cardiovascular events have been reported with all triptans. However, when patients are appropriately selected, zolmitriptan is both, a safe and effective acute migraine abortive agent. In this article, we will first briefly review the biological role of serotonin and the literature linking serotonin to migraine pathophysiology. This will be followed by a comprehensive review of the pharmacodynamics, pharmacokinetics and efficacy of zolmitriptan. Finally, the clinical application of the use of zolmitriptan in migraine therapy will be discussed.


Pain ◽  
2019 ◽  
Vol 160 (2) ◽  
pp. 385-394 ◽  
Author(s):  
Marta Vila-Pueyo ◽  
Lauren C Strother ◽  
Malak Kefel ◽  
Peter J. Goadsby ◽  
Philip R. Holland

2004 ◽  
Vol 500 (1-3) ◽  
pp. 315-330 ◽  
Author(s):  
Udayasankar Arulmani ◽  
Antoinette MaassenVanDenBrink ◽  
Carlos M. Villalón ◽  
Pramod R. Saxena

Cephalalgia ◽  
2006 ◽  
Vol 26 (6) ◽  
pp. 642-659 ◽  
Author(s):  
U Arulmani ◽  
S Gupta ◽  
A Maassen VanDenBrink ◽  
D Centurión ◽  
CM Villalón ◽  
...  

Although the understanding of migraine pathophysiology is incomplete, it is now well accepted that this neurovascular syndrome is mainly due to a cranial vasodilation with activation of the trigeminal system. Several experimental migraine models, based on vascular and neuronal involvement, have been developed. Obviously, the migraine models do not entail all facets of this clinically heterogeneous disorder, but their contribution at several levels (molecular, in vitro, in vivo) has been crucial in the development of novel antimigraine drugs and in the understanding of migraine pathophysiology. One important vascular in vivo model, based on an assumption that migraine headache involves cranial vasodilation, determines porcine arteriovenous anastomotic blood flow. Other models utilize electrical stimulation of the trigeminal ganglion/nerve to study neurogenic dural inflammation, while the superior sagittal sinus stimulation model takes into account the transmission of trigeminal nociceptive input in the brainstem. More recently, the introduction of integrated models, namely electrical stimulation of the trigeminal ganglion or systemic administration of capsaicin, allows studying the activation of the trigeminal system and its effect on the cranial vasculature. Studies using in vitro models have contributed enormously during the preclinical stage to characterizing the receptors in cranial blood vessels and to studying the effects of several putative antimigraine agents. The aforementioned migraine models have advantages as well as some limitations. The present review is devoted to discussing various migraine models and their relevance to antimigraine therapy.


Cephalalgia ◽  
1986 ◽  
Vol 6 (5_suppl) ◽  
pp. 41-46 ◽  
Author(s):  
Jes Olesen

Noradrenaline, adrenaline, and isoprenaline were infused intracarotidly and the regional cerebral blood flow measured with the intracarotid injection-stationary detector method in patients undergoing carotid angiography. No effect was seen, and beta blockade with intracarotid propranolol also had no effect. The adrenergic effects on cerebral blood vessels are probably neurogenic, and circulating adrenergic agonists and antagonists are unlikely to play a role. Pertubations of adrenergic substances in blood are therefore unlikely to be important in migraine pathophysiology.


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