Migraine, especially migraine with aura (MA), is an established risk factor for ischemic lesions of the brain. Recent evidence has also linked migraine to a broader range of ischemic vascular disorders including angina, myocardial infarction, coronary revascularization, claudication, and cardiovascular mortality. The mechanisms which link migraine to ischemic vascular disease remain uncertain and are likely to be complex. Cortical spreading depression, the presumed substrate of aura, may directly predispose to brain lesions and that would explain why MA is consistently demonstrated as a risk factor for cerebral ischemia, while for migraine without aura (MO), the evidence is less consistent. Additionally, individuals with migraine have a higher prevalence of risk factors known to be associated with cardiovascular disease (CVD), including hypertension, diabetes, and hyperlipidemia. The increased prevalence of CVD risk factors is also higher for MA than for MO. Since the evidence linking migraine and CVD is getting robust, neurologists should be aware of this association. Individuals with MO seem to be at little increased risk of CVD. MA is associated with an increased risk of ischemic stroke and likely also for other ischemic CVD events. Accordingly, heightened vigilance is recommended for modifiable cardiovascular risk factors in migraineurs, especially with MA. Ultimately, it will be important to determine whether MA is a modifiable risk factor for CVD and if preventive medications for migraine or antiplatelet therapy might reduce the risk of CVD in patients with MA. Neurology ® 2009;72:1864-1871 GLOSSARY BMI ϭ body mass index; CDH ϭ chronic daily headache; CI ϭ confidence interval; CSD ϭ cortical spreading depression; CVD ϭ cardiovascular disease; EPC ϭ endothelial progenitor cells; HR ϭ hazard ratio; MA ϭ migraine with aura; MMP ϭ matrix metalloproteinase; MO ϭ migraine without aura; MTHFR ϭ methyltetrahydrofolate reductase; RR ϭ relative risk.

Background and Purpose: Congenital vertebral artery (VA) hypoplasia is an uncommon embryonic variation of posterior circulation. The frequency of this congenital variation was reported to be 2–6% from autopsy and angiograms. The aim of our study was to elucidate the role of VA hypoplasia in acute ischemic stroke. Method: We examined 191 acute ischemic stroke patients (age 55.8 ± 14.0 years). TOAST subtypes were determined. A cervical magnetic resonance angiogram was performed in every patient. A duplex study of bilateral VA with flow velocities and vessel diameter recording in the intertransverse (V2) segment was performed within 72 h after onset of ischemic stroke. The net VA flow volume was measured in each subject. Result: The overall incidence of a unilateral congenital hypoplastic VA was 11.51%, which was statistically higher especially in cases of brainstem/cerebellar infarction. Of these, subjects with VA hypoplasia had an etiological preponderance of the ‘large-artery atherosclerosis’ subtype and a topographic preponderance of ipsilateral posterior circulation infarction. Conclusions: Based on our results, VA hypoplasia seemed a contributing factor of acute ischemic stroke, especially in posterior circulation territories.

Cough headache is a transient headache upon coughing, bending, stooping, or lifting in the absence of intracranial lesions. Reports show that incompetent jugular venous valve and cerebrospinal fluid hypervolemia are contributing factors. Headache is a common complaint of uremia patients. We conducted a clinical-radiological correlation study on 15 uremia patients with headache and central venous thrombosis. Thirteen patients were diagnosed to have benign cough headache (BCH); the others were diagnosed with chronic tension type headache. Venogram disclosed either internal jugular or vertebral venous regurgitation in the BCH group. Acquired thoracic inlet valvular incompetence might contribute to BCH.

Background and Purpose: Cerebral syncope refers to a loss of consciousness associated with cerebral vasoconstriction in the absence of systemic hypotension. The diagnosis of cerebral syncope could be established by the head-up tilt test (HUT) and transcranial Doppler ultrasonography. Valsalva maneuver (VM) permitted assessment of cerebral autoregulatory function by provoking blood pressure (BP) changes. To develop a path-physiological approach for vasomotor reactivity of cerebral syncope, the authors combined these maneuvers (HUT/transcranial Doppler/VM). Methods: Using transcranial Doppler ultrasonography, we simultaneously recorded systemic arterial BP in the radial artery and flow velocities in both middle cerebral arteries (MCAFV) in 10 cerebral syncope patients (4 males and 6 females, 35.24 ± 4.5 years old) during the Valsalva maneuver. Results: The characteristic changes in BP (phases I–IV) were seen in all subjects, accompanying distinct changes in cerebral blood flow velocity. The BP/heart rate responding to VM was within normal limit in all subjects. There was no orthostatic hypotension. Instead, BP increased during the tilting test in 2 subjects (20.00%). The MCAFV dropped 25.4 ± 2.3% from baseline. Abnormal flattening of MCAFV during late phase II (IIb), the paradoxical drop of flow velocity despite restoration of BP, was noted in 9 subjects (90.00%). Conclusion: During VM there are complex changes in relevant cardiovascular and cerebrovascular variables within a short time span. The paradoxical drop of MCAFV during phase IIb was the result of complex parameters. Among them, a failure in cerebrovascular resistance reduction and even paradoxical vasoconstriction might further compromise cerebral perfusion pressure and lead to syncope.

Atorvastatin effectively reduced plasma concentrations of total cholesterol and LDL-cholesterol, and had beneficial effects on endothelial function, in Chinese patients with carotid arterial stenosis and normal LDL-cholesterol levels.