BACKGROUND AND PURPOSE: The pathophysiology of wall contrast enhancement in thrombosed intracranial aneurysms is incompletely understood. This in vivo study aimed to investigate wall microstructures with gadolinium-enhanced 7T MR imaging. MATERIALS AND METHODS: Thirteen patients with 14 thrombosed intracranial aneurysms were evaluated using a 7T whole-body MR imaging system with nonenhanced and gadolinium-enhanced high-resolution MPRAGE. Tissue samples were available in 5 cases, and histopathologic findings were correlated with 7T MR imaging to identify the gadolinium-enhancing microstructures. RESULTS: Partial or complete inner wall enhancement correlated with neovascularization of the inner wall layer and the adjacent thrombus. Additional partial or complete outer wall enhancement can be explained by formation of vasa vasorum in the outer aneurysm wall layer. The double-rim enhancement correlated with perifocal edema and wall histologic findings suggestive of instability. CONCLUSIONS: Two distinct aneurysm wall microstructures responsible for gadolinium enhancement not depictable at lower spatial resolutions can be visualized in vivo using high-resolution gadolinium-enhanced 7T MR imaging.

Histological evaluation of dissecting aneurysms of the cerebral arteries has suggested that defects in the internal elastic lamina (IEL) induce dissection of the arterial wall. Dissecting aneurysms occur most frequently in the vertebral artery (VA). The present study examined sections of the normal VA to elucidate the mechanisms of arterial dissection. Bilateral VAs (20 vessels) were obtained from 10 patients who died of causes other than intracranial lesions. The VAs were detached from the VA union to the site 10 mm proximal from the point penetrating the dura mater. The VAs were cut at 5-mm intervals, and each segment was observed using modified Masson's trichrome staining for elastic fibers. The thickness of the media and adventitia significantly thinned after the origin of the posterior inferior cerebellar artery (PICA). IEL defects were observed at 35 sites in 11 vessels from six subjects. There was a high incidence of IEL defects in the extradural portion and near the origin of the PICA, areas frequently involved in arterial dissection. There was a high incidence of intimal thinning at areas of IEL defects (19 of 35), and thinning was particularly marked distal to the origin of the PICA. In the absence of intimal thickening, the vascular strength at the site of IEL defects may be reduced, which would promote the occurrence and progression of arterial dissection.

BACKGROUND AND PURPOSE: Collateral networks in Moyamoya angiopathy have a complex angioarchitecture difficult to comprehend on conventional examinations. This study aimed to evaluate morphologic patterns and the delineation of deeply seated collateral networks using ultra-high-field MRA in comparison with conventional DSA. MATERIALS AND METHODS: Fifteen white patients with Moyamoya angiopathy were investigated in this prospective trial. Sequences acquired at 7T were TOF-MRA with 0.22 × 0.22 × 0.41 mm³ resolution and MPRAGE with 0.7 × 0.7 × 0.7 mm³ resolution. Four raters evaluated the presence of deeply seated collateral networks and image quality in a consensus reading of DSA, TOF-MRA, and MPRAGE using a 5-point scale in axial source images and maximum intensity projections. Delineation of deeply seated collateral networks by different imaging modalities was compared by means of the McNemar test, whereas image quality was compared using the Wilcoxon signed-rank test. RESULTS: The relevant deeply seated collateral networks were classified into 2 categories and 6 pathways. A total of 100 collateral networks were detected on DSA; 106, on TOF-MRA; and 73, on MPRAGE. Delineation of deeply seated collateral networks was comparable between TOF-MRA and DSA (P = .25); however, both were better than MPRAGE (P < .001). CONCLUSIONS: This study demonstrates excellent delineation of 6 distinct deeply seated collateral network pathways in Moyamoya angiopathy in white adults using 7T TOF-MRA, comparable to DSA.

Neurofibromatosis type 2 (NF2) causes bilateral vestibular schwannomas (VSs), leading to deafness. VS is treated by surgery or radiation, but neither treatments prevent hearing loss. Bevacizumab was found to be effective in suppressing the tumor’s growth and may help to improve hearing. We are conducting a randomized, double-blind, multicenter clinical trial to verify the efficacy and safety of bevacizumab in NF2-related VS. The primary objective is to evaluate the efficacy of bevacizumab in improving hearing in the affected ear. One of the secondary objectives is to evaluate bevacizumab’s efficacy in rechallenge treatment in relapsed cases. Sixty patients will randomly receive either bevacizumab or a placebo and will be clinically observed for 48 weeks in the initial intervention phase. In the first half (24 weeks), they will receive either 5 mg/kg of bevacizumab or a placebo drug. In the second half, all patients will receive 5 mg/kg of bevacizumab. If hearing function deteriorated in a patient who had shown improvement during the first phase, a rechallenge dose with bevacizumab would be offered.