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Headache
Published in Philip B. Gorelick, Fernando D. Testai, Graeme J. Hankey, Joanna M. Wardlaw, Hankey's Clinical Neurology, 2020
Cluster headache is a neurovascular disorder, which is hypothesized to be generated in the CNS in pacemaker or circadian regions of the hypothalamic gray matter. The trigeminal autonomic reflex is central to the pathogenesis (see section on Migraine). Activation of the trigeminovascular system (i.e. release of CGRP from peripheral terminals of trigeminal nociceptive neurons, which supply cephalic blood vessels) underlies symptoms of cluster headache. Increases in neuropeptide markers of this system rapidly return to normal after treatment with sumatriptan.
Headache associated with vascular disease: migraine and stroke
Published in Stephen D. Silberstein, Richard B. Upton, Peter J. Goadsby, Headache in Clinical Practice, 2018
Stephen D. Silberstein, Richard B. Upton, Peter J. Goadsby
Angiography in migraine sufferers revealed severe narrowing in both the vertebral and basilar arteries and occlusion of the basilar or posterior cerebral arteries. This was interpreted as spasm but is very similar to the characteristic ‘string sign’ of carotid dissection.61,62 In fact, migraine is a risk factor for dissection.63 Another possibility is that migraine produces ‘pseudo-occlusion’ due to vasoconstriction (‘spasm’) severe enough to prevent anterograde flow. Alternatively, prolonged vasoconstriction could also lead to hemostasis and in situ thrombosis. Moskowitz,64 in his model of neurogenic inflammation, showed that platelet aggregation occurs in the lumen of blood vessels. Thus, pathologic activation of the trigeminovascular system could result in structural changes of the cerebral vessels, linking the mechanism for headache pain and the potential for cerebral ischemia.
Posttraumatic Headache
Published in Gary W. Jay, Clinician’s Guide to Chronic Headache and Facial Pain, 2016
The trigeminovascular system is of great import in migraine (38). In some children who develop posttraumatic neurological deterioration without focal lesions after minor head trauma, there may be an association with an “unstable trigeminovascular reflex,” which induces the release of perivascular vasodilatory peptides that can contribute to cerebral hyperemia (27).
Real world considerations for newly approved CGRP receptor antagonists in migraine care
Published in Expert Review of Neurotherapeutics, 2022
Damiana Scuteri, Paolo Tonin, Pierluigi Nicotera, Giacinto Bagetta, Maria Tiziana Corasaniti
Migraine is a neurovascular primary disorder with episodic manifestations [15] due to dural vessels dilation and neural events responsible for headache, further nerve activation, with sensitization and the currently CSD [16] (corresponding to animal Leão’s SD of activity [17] and phenotypically to aura), long considered not caused by a vascular event but by aminergic ion channels dysfunction in the brainstem nuclei modulating sensory stimuli [18]. The crime scene is the trigeminocervical complex within which pain is generated, even though its pathogenesis is not completely clear since it is believed to origin from dural and peri-dural vessel vasodilation that may be triggered by branches of the ophthalmic division of the trigeminal nerve or of the C2 nerve roots [18]. The progresses in this field in the last decade deliver the knowledge that an alteration of brain excitability can activate the trigeminovascular system in susceptible patients. Hypothalamic dysfunction is correlated with premonitory symptoms and it has been involved in migraine, in drugs action [19] and suggested as primary trigger [20] with a possible role of hypocretin/orexin pathway in the posterior hypothalamic area [21] and the loss of hypothalamic control over limbic nuclei [22] (Figure 2) with CSD-like events that need confirmation in asymptomatic prodromal attacks [23].
Unmet needs for migraine
Published in Current Medical Research and Opinion, 2021
Paolo Martelletti, Martina Curto
We have always witnessed the exponential and tumultuous growth of scientific publications in the imminence and during the stages of RCTs registration of new drugs for a specific disease. All this upstream of the identification of new pathophysiological mechanisms that have led to the development of new molecules contrasting the evolution of the disease. All of this is happening in the multidisciplinary clinical area of migraine. After the realization that Calcitonin Gene Related Peptide (CGRP) played a pivotal role in the development of migraine attacks, in the activation of the trigeminovascular system and therefore the generation of migraine pain, and after new pharmacological classes (monoclonal antibodies for CGRP or its receptor (CGRPr) or small molecules such as gepants, antagonists of the same receptor for CGRP or ditans, agonists of the 1 F serotonin receptor (5-HT1F) have progressively appeared on the market, the following question has arisen: are we ready for the transition to novel treatments?
CGRP inhibitors for migraine prophylaxis: a safety review
Published in Expert Opinion on Drug Safety, 2020
Eduardo Rivera-Mancilla, Carlos M. Villalón, Antoinette MaassenVanDenBrink
The exact pathophysiological mechanisms underlying the onset of a migraine attack remain unclear. However, extensive research in the last three decades has demonstrated that calcitonin gene-related peptide (CGRP) plays an important role in the genesis of migraine via the activation of the trigeminovascular system [4–7]. In this respect, as previously reported: (i) activation of the trigeminovascular system (which includes the meninges and intracranial blood vessels) results in cranial vasodilation mainly mediated by CGRP release [6]; (ii) serum levels of CGRP are elevated during migraine attacks [4]; and (iii) intravenous administration of CGRP produces vasodilation of the middle meningeal artery [12] and triggers migraine-like headaches [13,14]. These findings, which further support the key role of CGRP in the pathophysiology of migraine, indicate that CGRP and its receptor may be therapeutic targets for developing new antimigraine drugs [15].