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ARTICLES: R. Napoli, V. Guardasole, E. Zarra, M. Matarazzo, C. D'Anna, F. Saccà, F. Affuso, A. Cittadini, P. B. Carrieri, and L. Saccà Vascular smooth muscle cell dysfunction in patients with migraine Neurology 2009; 72: 2111-2114 [Abstract] [Full text] [PDF]

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Vascular smooth muscle cell dysfunction in patients with migraine

William N. Devor, MD   (2 September 2009)

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Raffaele Napoli, L. Saccà   (2 September 2009)

Vascular smooth muscle cell dysfunction in patients with migraine 2 September 2009
William N. Devor, MD, Kaiser Permanente San Diego, UCSD Neurosciences Department Neurology Department, 4405 Vandever Avenue, San Diego, CA 92120 Send Correspondence to journal: Re: Vascular smooth muscle cell dysfunction in patients with migraine wdevor{at}san.rr.com William N. Devor, MD	The article by Napoli et al. describing experimental techniques to quantify vascular endothelial reactivity illuminates the presence of arterial endothelial acetylcholine receptors which are known to be coupled to the NO vasodilatory pathway. [1] The endothelial cholinergic receptors are presumably associated with vascular cholinergic nerve terminals arising from nervi vasorum present in the arterial tunica adventia. Such cholinergic vascular nerve terminals have been demonstrated in skin biopsy specimens using stains for acetylcholinesterase. Cholinergic nerve terminals are the target of botulinum toxin raising the possibility that cholinergic denervation of the scalp arteries may underlie the benefit of botulinum toxin injections in the treatment of migraine. Typical injection sites used for treatment of migraine in the areas of the temporalis, frontalis and occipitalis muscles are close to the temporal, supraorbital and occiptal arteries. Abundant data exist describing the role of vasodilation of the extracranial scalp arteries in a subset of migraine patients. Does cholinergic denervation of the scalp arteries reduce vasodilation and thereby ameliorate migraine? The findings of Napoli et al. suggest that this may not be the case as responsiveness to intravascular acetylcholine is reduced in migraine patients. The hypothesis that cholinergic denervation of the scalp arteries may underlie the benefit of cranial botulinum toxin injections in the treatment of migraine should be explored. Reference 1. Napoli R, Guardasole V, Zarra E et al. Vascular smooth muscle cell dysfunction in patients with migraine. Neurology 2009;72:2111-2114. Dr. Devor received an honorarium from Plaza Research; and administers botulinum toxin for treatment of headache in a non-profit setting.
Reply from the author 2 September 2009
Raffaele Napoli, Dept. of Internal Medicine, University Federico II Via pansini, 5 - 80131 ,Naples, Italy, L. Saccà Send Correspondence to journal: Re: Reply from the author napoli{at}unina.it Raffaele Napoli, et al.	We thank Dr. Devor for his interest in our article on vascular reactivity in patients with migraine. [1] Endothelial dysfunction and abnormal vascular reactivity are involved in the onset and progression of atherosclerosis and subsequently the increased risk of cardiovascular diseases. Given the increased risk of cardiovascular events associated with migraine, we aimed to explore the reactivity of both endothelial and vascular smooth muscle cells (VSMCs) in patients with migraine in the headache-free state. We found that in migraine patients studied in the interictal period, endothelial function is normal and a clear defect in the VSMCs response emerges. In human vessels, acetylcholine vasodilatory response is due to the stimulation of specific receptors located on the surface of the endothelial cells which in turn activate nitric oxide synthase in order to produce nitric oxide (NO). Once released, NO triggers vasodilation by stimulating cGMP production in the VSMCs. In our data, the response to the intra-arterial infusion of acetylcholine is reduced in patients with migraine. However, this reduction is not due to a defect in the ability of acetylcholine to induce NO production and release by the endothelial cells, but rather to a severe impairment of VSMCs to respond to NO stimulation. This is demonstrated because we detected a normal release of NO during acetylcholine infusion by the endothelial cells. In addition, there was an impaired vasodilation during the infusion of sodium nitroprusside (a NO donors) in patients with migraine due to the insufficient response to NO by the VSMCs. Therefore, acetylcholine response by the endothelial cells in patients with migraine during the interictal period is normal. Since we were interested in the mechanisms of cardiovascular risk, we also studied vascular reactivity in the brachial artery as a well established model of coronary vascular reactivity. However, the relationship between peripheral vascular reactivity and cerebral circulation is still unclear. Since we studied vascular reactivity in the headache-free period, the vascular mechanisms underlying the migraine attack in both peripheral and cerebral circulation cannot be clarified by our study. The possibility arises that vascular reactivity can be different during the migraine attack. Disclosure: Drs. Napoli and Saccà received compensation for a study from Pfizer Italia.