Background: The etiology of ischemic strokes remains cryptogenic in about one third of patients, even after extensive workup in specialized centers. Atherosclerotic plaques in the aorta can cause thromboembolic events but are often overlooked. They can elude standard identification by transesophageal echocardiography (TEE), which is invasive or at best uncomfortable for many patients. CT angiography (CTA) can be used as an alternative or in addition to TEE if this technique fails to visualize every part of the aorta and in particular the aortic arch. Methods: We prospectively studied 64 patients (47 men, age 60 ± 13 years) classified as having cryptogenic stroke after standard and full workup [including brain MRI and 24-hour electrocardiogram (ECG)] with ECG-triggered CTA of the aorta in search of plaques and compared the results with those of TEE. Investigators were blinded to the results of both techniques. Plaques were graded on CTA according to their presence (0 = not present; 1 = mild; 2 = severe) and degree of calcification (1a or 2a = noncalcified; 1b or 2b = calcified). Associations with risk factors and infarct localization were also assessed. Results: Only 21 of 64 patients (32.8%) had aortic plaques identified by TEE, compared to 43 of 64 (67.2%) with CTA (p < 0.05). The plaque localization was as follows (TEE vs. CTA): ascending aorta, 10 vs. 20 (p < 0.05); aortic arch, 10 vs. 40 (p < 0.05), and descending aorta, 20 vs. 34 (p < 0.05). Grade 1 plaques were most commonly found in the aortic arch (25; 39%), while grade 2 plaques were most often detected in the aortic arch (15; 23.4%) and the descending aorta (14; 21.9%). There was no significant correlation between plaque location, infarct territory or vascular risk profile, except for hypertension (p = 0.003), which was significantly associated with the presence of plaques. Conclusions: CTA identifies more plaques throughout the aortic arch and around the origins of the major cerebral arteries in particular compared to TEE. These may represent potential embolic sources of acute ischemic stroke. Better plaque detection may have an impact on the best available secondary prevention regimen in individual patients if proximal embolic sources are suspected.

Marchiafava-Bignami disease (MBD) is a neurological disorder that has been found to be associated with chronic alcoholism and malnutrition. MBD classically results in acute edema and demyelination of the corpus callosum. Edema of the complete corpus callosum has been described to be an unfavorable prognostic factor. We present an acute onset of MBD with diffusion restriction of the complete corpus callosum and symmetric bilateral extension into the semioval center, that almost completely resolved clinically as well as in MRI only 3 days later. With early detection and treatment, the prognosis of MBD may be good even in cases with severe diffusion restriction of the complete corpus callosum.

Background and Purpose. Cerebral white matter hyperintensities (WMHs) are regarded as typical MRI expressions of small-vessel disease (SVD) and are common in hypertensive patients. Hypertension induces pathologic changes in macrocirculation and in microcirculation. Changes in microcirculation may lead to SVD of brain and consequently to hypertensive end-organ damage. This damage is regarded the result of interactions between the macrovascular and microvascular levels. We sought to investigate the association of cerebral WMHs with ultrasonographic parameters of cerebral macrocirculation evaluated by carotid duplex ultrasound (CDU) and transcranial doppler (TCD). Subjects and Methods. The study was prospective, cross-sectional and consecutive and included hypertensive patients with brain MRI with WMHs. Patients underwent CDU and TCD. The clinical variables recorded were demographic characteristics (age, gender, race) and vascular risk factors (hypertension, diabetic mellitus, hypercholesterolemia, current smoking, and body mass index). Excluded from the study were patients with history of clinical stroke (including lacunar stroke and hemorrhagic) or transient ischemic attack (either hemispheric or ocular), hemodynamically significant (>50%) extra- or intracranial stenosis, potential sources of cardioembolism, and absent transtemporal windows. WMHs were quantified with the use of a semiquantitative visual rating method. Ultrasound parameters investigated were (1) common carotid artery (CCA) diameter and intima-media thickness, (2) blood flow velocity in the CCA and internal carotid artery (ICA), and (3) blood flow velocity and pulsatility index of middle cerebral artery (MCA). Results. A total of 52 patients fulfilled the study inclusion criteria (mean age 71.4 ± 4.5 years, 54% men, median WMH-score: 20). The only two ultrasound parameters that were independently associated with WMH score in multivariate linear regression models adjusting for demographic characteristics and vascular risk factors were increased mean common carotid artery (CCA) diameter (beta = 0.784, SE = 0.272, P = 0.006, R 2 = 23.9%) and increased middle cerebral artery pulsatility index (MCA-PI; beta = 0.262, SE = 0.110, P = 0.025, R 2 = 9.0%). Among all ultrasound parameters the highest AUC (areas under the receiver operating characteristic curve) were documented for MCA-PI (AUC = 0.82, 95% CI = 0.68−0.95, P < 0.001) and mean CCA diameter (AUC = 0.80, 95% CI = 0.67−0.92, P < 0.001). Conclusions. Our study showed that in hypertensive individuals with brain SVD the extent of structural changes in cerebral microcirculation as reflected by WMHs burden is associated with the following ultrasound parameters of cerebral macrocirculation: CCA diameter and MCA-PI.