ObjectiveWe used magnetization transfer imaging to assess white matter tissue integrity in migraine, to explore whether white matter microstructure was more diffusely affected beyond visible white... Show moreObjectiveWe used magnetization transfer imaging to assess white matter tissue integrity in migraine, to explore whether white matter microstructure was more diffusely affected beyond visible white matter hyperintensities (WMHs), and to explore whether focal invisible microstructural changes precede visible focal WMHs in migraineurs.MethodsWe included 137 migraineurs (79 with aura, 58 without aura) and 74 controls from the Cerebral Abnormalities in Migraine, an Epidemiological Risk Analysis (CAMERA) study, a longitudinal population-based study on structural brain lesions in migraine patients, who were scanned at baseline and at a 9-year follow-up. To assess microstructural brain tissue integrity, baseline magnetization transfer ratio (MTR) values were calculated for whole brain white matter. Baseline MTR values were determined for areas of normal-appearing white matter (NAWM) that had progressed into MRI-detectable WMHs at follow-up and compared to MTR values of contralateral NAWM.ResultsMTR values for whole brain white matter did not differ between migraineurs and controls. In migraineurs, but not in controls, NAWM that later progressed to WMHs at follow-up had lower mean MTR (mean [SD] 0.354 [0.009] vs 0.356 [0.008], p = 0.047) at baseline as compared to contralateral white matter.ConclusionsWe did not find evidence for widespread microstructural white matter changes in migraineurs compared to controls. However, our findings suggest that a gradual or stepwise process might be responsible for evolution of focal invisible microstructural changes into focal migraine-related visible WMHs. Show less
The association between migraine and silent ischemic brain lesions was investigated. Also the occurence of right-to-left shunts in different migraine groups and controls. The functional... Show moreThe association between migraine and silent ischemic brain lesions was investigated. Also the occurence of right-to-left shunts in different migraine groups and controls. The functional consequences of silent ischemic brain lesions were investigated. Show less
Decreased cerebral blood flow is frequently observed in patients with heart failure, and this could be the result of impaired cardiac systolic function. Cardiac resynchronization therapy (CRT)... Show moreDecreased cerebral blood flow is frequently observed in patients with heart failure, and this could be the result of impaired cardiac systolic function. Cardiac resynchronization therapy (CRT) improves cardiac function and heart failure symptoms in selected patients. The effects of CRT on cerebral blood flow have not been previously evaluated. In the present study, left ventricular systolic function and cerebral blood flow were assessed in 35 patients with heart failure, before and 6 months after CRT. Additionally, 15 patients with heart failure, who were not candidates for CRT, were included as a control group. The peak systolic velocity, end-diastolic velocity, mean velocity, and pulsatility index ((peak systolic velocity end-diastolic velocity]/mean velocity) were obtained using transcranial Doppler from the right middle cerebral artery from the temporal window in all subjects. Response to CRT was defined as a reduction in the left ventricular end-systolic volume of >= 15%. At 6 months of follow-up, the peak systolic velocity had significantly increased from 83 +/- 20 cm/s to 100 +/- 20 cm/s (p = 0.001), the end-diastolic velocity had increased from 29 +/- 7 cm/s to 37 +/- 8 cm/s (p <0.001), and the mean velocity had increased from 47 +/- 10 cm/s to 58 +/- 11 cm/s (p <0.001) only in the responders to CRT. In contrast, no significant changes in cerebral blood flow were observed in the nonresponders and the controls. In conclusion, CRT induced an increase in cerebral blood flow in patients with heart failure. This increase in cerebral blood flow was related to the improvement in left ventricular systolic function. (C) 2010 Elsevier Inc. All rights reserved. (Am J Cardiol 2010;106:73-77) Show less