Migraine is a neurovascular disorder characterized by autonomic nervous system dysfunction and severe headache attacks. Studies have shown that changes in the intracranial vessels during migraine have an important role in the pathophysiology. Many studies have been conducted on the increased risk of stroke in patients with migraine, but insufficient data are available on the mechanism underlying the increase. This study aimed to evaluate basal cerebral blood flow velocity and vasomotor reactivity in patients with chronic migraine. We evaluated 38 patients with chronic migraine. Three of them were excluded because they had auras and four of them were excluded because of their use of medication that can affect cerebral blood flow velocity and breath holding index (beta or calcium channel blockers). Our study population consisted of 31 patients with chronic migraine without aura and 29 age- and gender-matched healthy individuals who were not taking any medication. The mean blood flow velocity and breath holding index were measured on both sides from the middle cerebral artery and posterior cerebral artery, with temporal window insonation. The breath holding index for middle cerebral artery and posterior cerebral artery was significantly lower in the migraine group compared to that of the control group (p < 0.05).The vasomotor reactivity indicates the dilatation potential of a vessel, and it is closely related to autoregulation. According to our results, the vasodilator response of cerebral arterioles to hypercapnia was lower in patients with chronic migraine. These findings showed the existence of impairments in the harmonic cerebral hemodynamic mechanisms in patients with chronic migraine. This finding also supports the existing idea of an increased risk of stroke in patients with chronic migraine due to impaired vasomotor reactivity.

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Myasthenia gravis is an important indication for the long-term prescription of corticosteroids. We present a patient with myasthenia gravis who had worsening of symptoms associated with the use of alendronate. A 24-year-old patient with myasthenia gravis had been administered oral systemic corticosteroid (deflazacort 40 mg/day) for 3 years in order to control his myasthenic symptoms. One year earlier, his lumbar spine bone mineral density was decreased. He was started on oral calcium/vitamin D3 and alendronate (70-mg tablets once a week) for osteoporosis. He reported an exacerbation of muscle weakness and extreme fatigue on days when he took alendronate. He could not work on these days and has to be on leave. Alendronate was stopped, and he was started on intravenous ibandronate injections given every 3 months. He did not experience muscle weakness and fatigue with ibandronate therapy. Alendronate should be used with caution in patients with myasthenia gravis who have corticosteroid-induced osteoporosis.

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