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Background and Purpose — Patent foramen ovale (PFO) has been identified as a potential risk factor for stroke, but the mechanisms of PFO-associated stroke remain unsettled. The aim of our study was to evaluate possible differences in stroke risk factors and stroke patterns between patients with and without PFO that may give clues to the mechanism of PFO-associated stroke. Methods — This prospective, multicentric study involved 581 young cryptogenic stroke patients. The presence of PFO and atrial septal aneurysm was assessed by transesophageal echocardiography and reviewed independently by 2 experienced sonographers. Clinical, brain, and vascular imaging findings were reviewed by 2 neurologists and 2 neuroradiologists. Results — Of the 581 stroke patients, 267 (45.9%) had PFO. Patients with PFO were younger (OR, 0.95; 95% CI, 0.93 to 0.97) and less likely to have traditional risk factors such as hypertension (OR, 0.49; 95% CI, 0.28 to 0.85), hypercholesterolemia (OR, 0.56; 95% CI, 0.34 to 0.93), or current smoking (OR, 0.67; 95% CI, 0.47 to 0.97). Features suggestive of paradoxical embolism, such as Valsalva-provoking activities or deep vein thrombosis, were not more frequent in patients with PFO. Migraine was more common in patients with PFO (27.3%) than in those without PFO (14.0%). PFO (OR, 1.75; 95% CI, 1.08 to 2.82), particularly when associated with atrial septal aneurysm (OR, 2.71; 95% CI, 1.36 to 5.41), was significantly associated with migraine after adjustment for age and sex. Conclusions — Differences in stroke risk factors and stroke patterns suggest that different stroke mechanisms occur in patients with and without PFO. PFO is significantly and independently associated with migraine, and this association is even stronger in patients with PFO and atrial septal aneurysm.

Background and Purpose— Unstable clinical course characterizes the first 24 hours after thrombolysis for anterior circulation stroke, including early neurological deterioration (END), a secondary complication consistently predictive of poor outcome. Apart from straightforward causes, such as intracerebral hemorrhage and malignant edema, the mechanism of END remains unclear in the majority of cases (END unexplained ). Based on the core/penumbra model, we tested the hypothesis that END unexplained is caused by infarct growth beyond the initial penumbra and assessed the associated vascular patterns. Methods— From our database of consecutive thrombolyzed patients (n=309), we identified 10 END unexplained cases who had undergone both admission and 24-hour MRI. Diffusion-weighted imaging lesion growth both within and beyond the acute penumbra (T max >6 seconds) was mapped voxelwise. These 10 cases were compared with 30 no-END controls extracted from the database blinded to 24-hour diffusion-weighted imaging to individually match cases (3/case) according to 4 previously identified clinical and imaging variables. Results— As predicted, lesion growth beyond initial penumbra was present in 9 of 10 END unexplained patients (substantial in 8) and its volume was significantly larger in cases than controls (2 P =0.047). All END unexplained cases had proximal arterial occlusion initially, of which only 2 had recanalized at 24 hours. Conclusions— In this exploratory study, most instances of END unexplained were related to diffusion-weighted imaging growth beyond acute penumbra. Consistent presence of proximal occlusion at admission and lack of recanalization at 24 hours in most cases suggest that hemodynamic factors played a key role, via for instance systemic instability/collateral failure or secondary thromboembolic processes. Preventing END after tissue-type plasminogen activator using, eg, early antithrombotics may therefore be feasible.

The typical magnetic resonance imaging picture of arterial dissection, namely, a narrowed eccentric signal void surrounded by a semilunar signal hyper-intensity (corresponding to the mural hematoma) on T1- and T2-weighted images, has been repeatedly reported, but the sensitivity of magnetic resonance imaging for the diagnosis of cervical dissection is poorly known. Another technique, dynamic computed tomography, may provide evidence of mural hematoma, but there has been no systematic evaluation of this technique. The aims of this study were to assess both the sensitivity of routine 0.5-T magnetic resonance imaging for the detection of a typical picture of cervical artery dissection and the value of dynamic computed tomographic scans to provide evidence of dissecting hematoma. Fifteen consecutive patients with angiographically confirmed extracranial internal carotid (n = 9) or vertebral (n = 10) dissections were studied using a standardized 0.5-T spin-echo magnetic resonance imaging protocol with axial slices. Twelve of these patients had dynamic computed tomographic scans at the site of the dissection suggested by angiography. A typical magnetic resonance imaging picture of cervical artery dissection was observed in 12 of 15 (80%) patients and in 13 of 19 (68%) dissected vessels. The sensitivity of magnetic resonance imaging was higher in internal carotid (78%) than in vertebral (60%) dissections and in stenotic-type dissections (85%) than in occlusive or aneurysmal-type dissections. The dynamic computed tomographic scan showed the mural hematoma in 11 of the 12 (92%) patients and in 12 of 15 (80%) dissected vessels. Routine 0.5-T magnetic resonance imaging with axial slices is a sensitive technique for the diagnosis of dissection, but in about 20% of patients with cervical artery dissection magnetic resonance imaging will demonstrate no typical abnormality. Dynamic computed tomographic scans are a sensitive neuroimaging procedure to confirm the presence of the mural hematoma, but it needs to be directed by prior angiography.

Background and Purpose— Hyperintense vessel sign (HVS) on fluid-attenuated inversion recovery (FLAIR) has been described in hyperacute stroke patients with arterial occlusion. We sought to determine whether HVS was more frequent in patients with intracerebral arterial stenoses than in those without stenosis regardless of the presence of a brain infarct. Methods— In this case-control study (19 symptomatic patients with multiple intracerebral arterial stenoses compared with 19 age-matched asymptomatic patients without stenosis), we looked for HVS (ie, focal or tubular hyperintensities in the subarachnoid space) on FLAIR images. We compared the proportion of HVS-positive patients in the 2 groups and evaluated the concordance between the arterial distribution of stenoses on angiogram and that of HVS on FLAIR. Results— HVS was found in 13 of 19 patients (68%) in the study group and 1 of 19 control patients (5.2%) ( P Conclusions— Although their significance remains unclear, multiple HVSs are more frequently observed in symptomatic patients with multiple intracerebral stenoses than in asymptomatic patients without stenosis.