Peripheral endothelial function and arterial stiffness in patients with chronic migraine: a case–control study

Twenty-one patients with chronic migraine and twenty-one healthy controls matched by sex and gender were recruited. Measurement of the ultrasonographic endothelial function and augmentation index were made according to manufacturer’s protocol.The mean of patient’s peripheral arterial tonometry ratios was 1.93？±？0.39 and for healthy control 2.21？±？0.44 (p？=？0.040). The median of patients’ augmentation index was ？6,0 (IQR: 6.5 to ？15) in healthy controls and 9.0 (IQR: 4 to 12) in chronic migraine, (p？=？0.002).Patients with chronic migraine have ultrasonographic endothelial dysfunction and increase in the arterial stiffness. An improved understanding of the role in the endothelial system of migraine may provide a basis for preventive drugs in migraine and restore the endothelial function.Migraine is a complex and debilitating neurovascular disorder predominantly affecting women. It recurs as attacks of severe headache associated with nausea, vomiting, phonophobia, and photophobia. In some cases, migraine headache is preceded by transient neurologic symptoms that are known as aura. According to the second edition of the International Classification of Headache Disorders (ICHD-II) [1] chronic migraine (CM) is defined as at least 15 days of headache per month over the past months, of which at least eight headache days meet the criteria for migraine without aura or respond to migraine-specific treatment. The prevalence rate of CM is estimated to be 1.4% to 2.2% of the general population [2].Despite its high prevalence, migraine is a disease involving complex pathogenetic mechanisms that remain to be clarified [3]. However, there is strong evidence that nitric oxide (NO) is critically involved in migraine pathophysiology [4]. NO plays an essential role in the control of cerebral blood flow and may be involved in the activation of nociceptors in the trigeminovascular system and release of vasoactive neuropeptides during neurogenic inflammatory response [5]. Endothelial dysfu