Arterial responses during migraine headache

Iversen, Helle K.; Nielsen, Thue H.; Olesen, Jes; Tfelt-Hansen, P.

doi:10.1016/0140-6736(90)92339-j

Cited by 163 publications

(113 citation statements)

References 9 publications

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“…Dilation or stretching of intracranial arteries can produce a headache. [7][8][9][10][11][12][13][14][15][16] This dilation can be induced by mechanical forces as well as chemicals. It is well known that many patients experience a headache during angioplasty of the intracranial artery, 7,8,13 and a similar mechanism may apply to headache development after coil embolization.…”

Section: Discussionmentioning

confidence: 99%

The Characteristics and Risk Factors of Headache Development after the Coil Embolization of an Unruptured Aneurysm

Hwang

Jeong

Sohn

et al. 2012

AJNR Am J Neuroradiol

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Section: Discussionmentioning

confidence: 99%

The Characteristics and Risk Factors of Headache Development after the Coil Embolization of an Unruptured Aneurysm

Hwang

Jeong

Sohn

et al. 2012

AJNR Am J Neuroradiol

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“…Dilatation of extracranial vessels during attacks (Drummond and Lance, 1983;Iversen, Nielsen, Olesen and Tfelt-Hansen, 1990) may be mediated, at least in part, by release of CGRP from trigeminal nerve terminals as levels were found to be elevated in the external jugular vein (Goadsby, Edvinsson and Ekman, 1990). In animal models of the migraine aura, focal injury or chemicals applied to the cerebral cortex initiate a wave of neural discharge that spreads slowly across the cortex, followed in its wake by depression of neural activity.…”

Section: The Trigeminovascular System In Migrainementioning

confidence: 99%

Migraine and motion sickness: What is the link?

Cuomo-Granston

Drummond

2010

Progress in Neurobiology

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The brainstem is a structurally complex region, containing numerous ascending and descending fibres that converge on centres that regulate bodily functions essential to life. Afferent input from the cranial tissues and the special senses is processed, in part, in brainstem nuclei. In addition, brainstem centres modulate the flow of pain messages and other forms of sensory information to higher regions of the brain, and influence the general excitability of these cortical regions. Thus, disruptions in brainstem processing might evoke a complex range of unpleasant symptoms, vegetative changes and neurovascular disturbances and that, together, form attacks of migraine. Migraine is linked with various co-morbid conditions, the most prominent being motion sickness. Symptoms such as nausea, dizziness and headache are common to motion sickness and migraine; moreover, migraine sufferers have a heightened vulnerability to motion sickness. As both maladies involve reflexes that relay in the brainstem, symptoms may share the same neural circuitry. In consequence, subclinical interictal persistence of disturbances in these brainstem pathways could not only increase vulnerability to recurrent attacks of migraine but also increase susceptibility to motion sickness. Mechanisms that mediate symptoms of motion sickness and migraine are explored in this paper. The physiology of motion sickness and migraine is discussed, and neurotransmitters that may be involved in the manifestation of symptoms are reviewed. Recent findings have shed light on the relationship between migraine and motion sickness, and provide insights into the generation of migraine attacks.

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“…PPE is mediated by sensory neurons that contain potent vasodilator neurotransmitters such as calcitonin generelated peptide (CGRP), substance P (SP), and neurokinin A (NA) (23). As PPE may activate meningeal nociceptors to induce the headache of migraine via neurogenic inflammation (23,24) and dilation of intraand extracranial arteries is related to migraine attacks (25)(26)(27), these effects of SPG stimulation contribute to the pathophysiologic understanding of migraine while introducing the prospect of targeting the ganglion with high-frequency stimulation (100 Hz) for treatment purposes.…”

Section: Anatomo-functional Characteristics Of the Spg And The Trigemmentioning

confidence: 99%

Sphenopalatine ganglion neuromodulation in migraine: What is the rationale?

2013

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Objective: The objective of this article is to review the prospect of treating migraine with sphenopalatine ganglion (SPG) neurostimulation. Background: Fuelled by preliminary studies showing a beneficial effect in cluster headache patients, the potential of treating migraine with neurostimulation has gained increasing interest within recent years, as current treatment strategies often fail to provide adequate relief from this debilitating headache.Common migraine symptoms include lacrimation, nasal congestion, and conjunctival injection, all parasympathetic manifestations. In addition, studies have suggested that parasympathetic activity may also contribute to the pain of migraineurs.The SPG is the largest extracranial parasympathetic ganglion of the head, innervating the meninges, lacrimal gland, nasal mucosa, and conjunctiva, all structures involved in migraine with cephalic autonomic symptoms. Conclusion: We propose two possible mechanisms of action: 1) interrupting the post-ganglionic parasympathetic outflow to inhibit the pain and cephalic autonomic symptoms, and 2) modulating the sensory processing in the trigeminal nucleus caudalis. To further explore SPG stimulation in migraineurs as regards therapeutic potential and mode of action, randomized clinical trials are warranted.

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Arterial responses during migraine headache

Cited by 163 publications

References 9 publications

The Characteristics and Risk Factors of Headache Development after the Coil Embolization of an Unruptured Aneurysm

The Characteristics and Risk Factors of Headache Development after the Coil Embolization of an Unruptured Aneurysm

Migraine and motion sickness: What is the link?

Sphenopalatine ganglion neuromodulation in migraine: What is the rationale?

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