BackgroundThe plaques at the dorsal or lateral wall of basilar artery (BA) are associated with pontine infarcts. We sought to explore the correlations between vertebrobasilar artery geometry and BA plaque locations.MethodsWe retrospectively analyzed the imaging and clinical data of 84 patients with BA atherosclerosis. On three-dimensional time-of-flight images, a side to side diameter difference of bilateral vertebral artery (VA) and BA bending were assessed. The vertebrobasilar artery geometry was qualitatively classified into four basic configurations: Walking, Tuning Fork, Dominant-Lambda, and Hypoplasia-Lambda. On high-resolution magnetic resonance imaging, the plaques were categorized based on the involvement of the ventral, dorsal, or lateral sides of BA wall. The relationships between vertebrobasilar artery geometry parameters and plaque locations were analyzed.ResultsLeft VA dominance was identified in 28(33%) patients, and right VA dominance in 22(26%) patients. BA bending were detected in 49 patients. There were no significant correlations between the diameter difference/ratio of VA diameters and plaque locations, or between BA bending and plaque locations. BA plaques were evenly distributed in the vertebrobasilar arteries with Tuning Fork and Dominant-Lambda configurations. In Hypoplasia-Lambda group, however, plaques were more frequently located at the dorsal wall (58.57%) than at the ventral (14.43%) and lateral wall (26.71%; P = 0.001). In Walking group, the plaques more likely occurred at the lateral (49.79%) and dorsal (35.07%) wall than at the ventral wall (14.86%, P = 0.02).ConclusionsThe geometric configurations of vertebrobasilar artery strongly influence the BA plaque locations. Further prospective studies are warranted to testify whether Hypoplasia-Lambda and Walking configurations are independent risk factors for pontine infarcts.Electronic supplementary materialThe online version of this article (10.1186/s12883-018-1084-6) contains supplementary material, which is available to authorized users.

Purpose:To optimize the free-breathing whole-body diffusion-weighted imaging (WB-DWI) protocol by using the short TI inversion-recovery diffusion-weighted echo-planar imaging (STIR-DWEPI) sequence and the built-in body coil. Additionally, to evaluate the feasibility of tumor screening using high-resolution three-dimensional (3D) maximum intensity projection (MIP) images. Materials and Methods:The prescan procedure of STIR-DWEPI was modified using the data from 30 volunteers. During each exam, an optimized center frequency (CF) was used to minimize the slice offsets in consecutive scan stations. Prescan time was reduced from 50 seconds to 20 seconds with improved station profile. Total scan time was 30 minutes for five stations and 1.2 m coverage. A total of 30 patients with histologically-proven malignant disease were scanned under the final protocol using a built-in body coil. The image quality and the degree of background body signal suppression were assessed.Results: Free-breathing WB-DWI was 100% successfully performed in all patients, without slice misregistration, fat contamination, significant distortion, or nonuniformity. The reconstructed 3D-MIP images were adequate to depict malignant lesions in all 30 patients. The results of WB-DWI were found to be comparable to those of single-photon emission computed tomography (SPECT) and positron emission tomography (PET). Conclusion:Stable and high-resolution WB-DWI is feasible using the technical improvements described in this study. WB-DWI might have important clinical value for the detection of primary and metastatic malignancies within the whole body. The potential for diagnosis and therapeutic assessment of tumors should be further assessed in a larger patient cohort.

BackgroundThe underlying pathophysiology of BA distribution is unclear and intriguing. Using high-resolution magnetic resonance imaging (HR-MRI), we sought to explore the plaque distribution of low-grade basilar artery (BA) atherosclerosis and its clinical relevance.MethodsWe retrospectively analyzed the imaging and clinical data of 61 patients with low-grade atherosclerotic BA stenosis (<50%). On HR-MRI, the plaques were categorized based on the involvement of the ventral, dorsal, or lateral sides of BA wall. A culprit plaque was defined if it was on the same slice or neighboring slices of symptomatic pontine infarcts and played a probable causal role (dorsal plaques with median pontine infarcts or lateral plaques with ipsilateral pontine infarcts). The relationships between plaque distribution and clinical presentations were analyzed.ResultsTwenty-five symptomatic and thirty-six asymptomatic BAs with 752 HR-MRI image slices were studied. The average length of BA atherosclerosis plaques was 12.16 ± 5.61mm (10.30 ± 6.44mm in symptomatic and 13.46 ± 7.03mm in asymptomatic patients, p = 0.079). The plaque distribution was similar at ventral (29.0%), dorsal (37.6%) and lateral walls (33.1%). The BA plaques in symptomatic patients were more frequently located at the dorsal (42.5%) and lateral (41.2%) walls than at the ventral walls (16.1%; P < 0.05). Compared with symptomatic patients, asymptomatic patients more likely had their plaques distributed at the ventral walls (P = 0.022). Culprit plaques were observed in 85.0% (17/20) pontine infarcts in symptomatic patients and only 14.3% (2/14) silent pontine infarcts in asymptomatic patients (p < 0.001).ConclusionsLow-grade BA atherosclerosis has a long distribution and evenly involves ventral, dorsal and lateral walls. The plaques at dorsal and lateral walls are associated with symptomatic pontine infarcts but not with silent infarcts.Electronic supplementary materialThe online version of this article (doi:10.1186/s12883-016-0785-y) contains supplementary material, which is available to authorized users.

Middle cerebral artery superior-wall plaques are associated with acute DBIs, while MCA lumen dilation is associated with WMLs.

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Our aim is to investigate the association of cerebral deep medullary veins (DMVs) with white matter microstructural integrity and regional brain atrophy in MRI. In a community-based cohort of 979 participants (mean age 55.4 years), DMVs were identified on susceptibility-weighted imaging. Brain structural measurements including gray matter and hippocampus volumes, as well as diffusion tensor metrics, were evaluated. The mean (SD)number of DMVs was 19.0 (1.7). A fewer number of DMVs was related to lower fractional anisotropy and higher mean diffusivity in multiple voxels on the white matter skeleton (threshold-free cluster enhancement corrected p < 0.05, adjusted for age and sex). Also, fewer DMVs were significantly related to a lower gray matter fraction and a hippocampal fraction (0.10 and 0.11 per DMV, respectively; SE, 0.03 for both; p < 0.001 for both). A significant correlation between DMVs’ reduction and cortical atrophy was observed in the bilateral occipital lobes, temporal lobes, hippocampus, and frontal lobes (p < 0.001, adjusted for age, sex, and total intracranial volume). Our results provided evidence that cerebral small venules disease play a role in brain parenchymal lesions and neurodegenerative processes.