Is There a Persistent Dysfunction of Neurovascular Coupling in Migraine?

Fabjan, Andrej; Zaletel, Marjan; Žvan, Bojana

doi:10.1155/2015/574186

Cited by 22 publications

(13 citation statements)

References 154 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Migraine without aura is more frequent than migraine aura, 80% versus 20% [3]. Pathophysiology of migraine, at present, involves neurovascular mechanisms regarding cortical spreading depression and activation of trigeminal-vascular system [4,5]. A problem relating to migraine is its chronic course, influencing quality of life of these subjects.…”

Section: Discussionmentioning

confidence: 99%

Preventive Treatment of Migraine: Which Drugs to Choose. Own Experience

Chirchiglia¹,

Torre²,

Stroscio³

et al. 2017

J Headache Pain Manag

View full text Add to dashboard Cite

Migraine prophylaxis is a demonstrated viable therapeutic option, providing positive results through the use of drugs, more and more safe and effective. These drugs are anticonvulsant, antidepressant, calcium channel blockers, beta blockers, making a notable contribution according to studies reported in the literature. But they also have side effects, usually less than their efficacy. In this study we report our series of migraineurs with and without aura, treated with prophylactic drugs. In the study we used the drugs of first choice and we used VAS scale to assess pain intensity, checking patients for 8 months, with good results, in some cases excellent. Data from literature show that these new nutraceutical substances, besides to those already in use, are utilized successfully, opening new therapeutic perspectives. Do not resort to symptomatic drugs, it is very important, being rich in adverse, potentially harmful effects, so migraine prophylaxis remains a useful instrument of defense in these patients.

show abstract

Section: Discussionmentioning

confidence: 99%

Preventive Treatment of Migraine: Which Drugs to Choose. Own Experience

Chirchiglia¹,

Torre²,

Stroscio³

et al. 2017

J Headache Pain Manag

View full text Add to dashboard Cite

show abstract

“…The mechanism for this is unclear; however, one possibility is that flicker is known to increase local metabolic demands and increase local blood flow in the brain (Pastor et al, 2003) and at the retina and optic nerve (Kiryu et al, 1995;Riva et al, 2005). Some authors have therefore posited that disrupted neurovascular coupling is a key pathophysiological mechanism of migraine (reviewed by Fabjan et al, 2015), whereby for a given level of neural activity, the vascular response is disproportionate to that of non-migraine controls (Zaletel et al, 2005). A similar logic may apply to those patients with NTG, whose glaucomatous damage is believed to be associated with retinal vascular dysregulation (Flammer et al, 1999;Grieshaber et al, 2007), thus providing a common aetiology to explain such deficits.…”

Section: Visual Field Testsmentioning

confidence: 99%

Clinical impact of migraine for the management of glaucoma patients

Nguyen

Lek

Vingrys

et al. 2016

Progress in Retinal and Eye Research

View full text Add to dashboard Cite

Migraine is a common and debilitating primary headache disorder that affects 10-15% of the general population, particularly people of working age. Migraine is relevant to providers of clinical eye-care because migraine attacks are associated with a range of visual sensory symptoms, and because of growing evidence that the results of standard tests of visual function necessary for the diagnosis and monitoring of glaucoma (visual fields, electrophysiology, ocular imaging) can be abnormal due to migraine. These abnormalities are measureable in-between migraine events (the interictal period), despite patients being asymptomatic and otherwise healthy. This picture is further complicated by epidemiological data that suggests an increased prevalence of migraine in patients with glaucoma, particularly in patients with normal tension glaucoma. We discuss how migraine, as a co-morbidity, can confound the results and interpretation of clinical tests that form part of contemporary glaucoma evaluation, and provide practical evidence-based recommendations for the clinical testing and management of patients with migraine who attend eye-care settings.

show abstract

“…The extracranial terminal branches of the external carotid artery were suspected to be the reason of pain in the aura [11,12]. Newer data imply that migraine headache is caused by an inappropriate activation of trigeminovascular system, that is, pain sensitive innervation of dural, arachnoid, and pial vessels as well as large intracranial vessels by nociceptive fibers originating in trigeminal ganglion (TG) and travelling mainly through ophthalmic and to a much lesser extent through maxillary and mandibular divisions of trigeminal nerve [10,13,14].…”

Section: Pathophysiology Of Migrainementioning

confidence: 99%