Page 61 - Migraine, the heart and the brain

to a Doppler system (Multi Dop T2 [DWL, Sipplingen, Germany], Pioneer TC
8080 [Nicolet, Kleinostheim, Germany], or PMD 100 or ST3 [Spencer Technologies,
Seattle, WA]). Signal recording was commenced 10 seconds before application of the
contrast medium and halted after 60 seconds recording time. The procedure was
carried out 3 times in a standardized and xed order: in the rst measurement, to
detect spontaneous RLS, contrast medium was injected during normal breathing.
In the second and third measurement, to detect RLS after provocation, contrast 3 medium was injected and followed after 5 seconds by a 5-second Valsalva maneuver.
Participants were instructed and coached in a standardized way to press rmly with their mouth closed to produce a Valsalva maneuver. The procedure was performed by 2 experienced investigators (H.K. and I.H.P.-M.) blinded for MRI ndings and migraine diagnosis; participants were instructed not to talk about their medical history. TCD-c investigation was performed immediately after MRI on the same day.
Offline reading started after completion of the study. Two experienced observers (R.W.K. and W.H.M.) rated presence and size category of RLS, blinded to participant characteristics. Passing MBs were unequivocally characterized acoustically by the typical chirping sound and visually by the spike-like appearance in the frequency spectrum. RLS were rated according to number of MBs detected during 60 seconds of each TCD-c investigation: no RLS (0 MB), small (1–9 MB), or large ( > 9 MB). The interrater agreement for presence of RLS was excellent ( = 0.95; p < 0.001).
MRI.
As suggested recently,24 we replaced the previously used term infarct-like lesions2,3 with silent infarcts. Silent infarcts were de ned as non-mass parenchymal defects with a vascular distribution, isointense to CSF signal on all sequences, and when supratentorial, surrounded by a hyperintense rim on fluidattenuated inversion recovery images.2 Virchow-Robin spaces were excluded based on typical location, shape, and absence of a hyperintense rim.2 In the basal ganglia, in order to exclude nonspeci c lesions, only parenchymal defects larger than 3 mm in diameter were considered.2 Location and vascular territory of new and preexisting infarcts were read by 2 experienced neuroradiologists (M.C.K. and Junya Konishi), who were blinded to diagnosis. The interrater agreement was excellent (k =0.87; p<0.001).2
White matter lesions were segmented automatically. Deep white matter hyperintensities were located supratentorial and not attached to the lateral ventricle.2 High volume of deep white matter lesions (upper 20th percentile) was used as variable. For infratentorial hyperintensities, presence vs absence was used.
Right-to-left shunts and migraine
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