Index by author

Ninety-two consecutive patients with a known (n = 24) or suspected arteriovenous shunting (n = 68) underwent DSA and brain MR imaging, including arterial spin-labeling/SWI and conventional angiographic MR imaging. DSA showed arteriovenous shunting in 63 of the 92 patients. Interobserver agreement was excellent. In 5 patients, arterial spin-labeling/SWI correctly detected arteriovenous shunting, while the conventional angiographic MR imaging did not. The authors conclude that the combined use of arterial spin-labeling and SWI may be an alternative to contrast-enhanced MRA for the detection of intracranial arteriovenous shunting.

The authors investigated the role of emergent endovascular stenting of long-segment carotid dissections in the acute ischemic stroke setting in 15 patients. They specifically evaluated long-segment carotid dissections requiring stent reconstruction with multiple tandem stents (≥ 3 stents) and presenting with acute (<12 hours) ischemic stroke symptoms (NIHSS score, ≥ 4). Carotid stent reconstruction was successful in all patients with no residual stenosis or flow limitation. Nine patients (60%) harbored intracranial occlusions, and 6 patients (40%) required intra-arterial thrombolysis/thrombectomy, achieving 100% TICI 2b–3 reperfusion. They conclude that emergent stent reconstruction of long-segment and flow-limiting carotid dissections in acute ischemic stroke intervention is safe and effective, with favorable clinical outcomes.

Brain dual-echo, 3D T1-weighted, and double inversion recovery scans were acquired at 3T from 62 patients with relapsing-remitting MS and 65 controls. Focal WM and cortical lesions were identified, and volumetric measures from WM, cortical GM, the hippocampus, and deep GM nuclei were obtained. Compared with those with who were cognitively preserved, patients with MS with cognitive impairment had higher T2 and T1 lesion volumes and a trend toward a higher number of cortical lesions. Significant brain, cortical GM, hippocampal, deep GM nuclei, and WM atrophy was found in patients with MS with cognitive impairment versus those who were cognitively preserved. The authors conclude that hippocampal and deep GM nuclei atrophy are key factors associated with cognitive impairment in MS.