BACKGROUND AND PURPOSE:Pathological changes in the intracranial aneurysm wall may lead to increases in its permeability; however the clinical significance of such changes has not been explored. The purpose of this pilot study was to quantify intracranial aneurysm wall permeability (K

Background Cognitive impairment affects 40%–68% of relapsing-remitting multiple sclerosis (RRMS) patients. Gray matter (GM) demyelination is complicit in cognitive impairment, yet cortical lesions are challenging to image clinically. We wanted to determine whether cortical cerebral blood flow (CBF), cerebral blood volume (CBV), and mean transit time (MTT) differences exist between cognitively impaired (CI) and unimpaired (NI) RRMS. Methods Prospective study of healthy controls (n = 19), CI (n = 20), and NI (n = 19) undergoing magnetic resonance imaging (MRI) and cognitive testing <1 week apart. White matter (WM) T2 hyperintense lesions and T1 black holes were traced. General linear regression assessed the relationship between lobar WM volume and cortical and WM CBF, CBV, and MTT. Relationship between global and lobar cortical CBF, CBV, and MTT and cognitive impairment was tested using a generalized linear model. Adjusted Bonferroni p < 0.005 was considered significant. Results No significant differences for age, gender, disease duration, and any fractional brain or lesion volume were demonstrated for RRMS subgroups. Expanded Disability Status Scale (EDSS) and Hospital Anxiety and Depression Scale–Depression (HADS-D) were higher in CI. Lobar cortical CBF and CBV were associated with cognitive impairment (p < 0.0001) after controlling for confounders. Cortical CBV accounted for 7.2% of cognitive impairment increasing to 8.7% with cortical CBF (p = 0.06), while WM and cortical CBF accounted for 8.2% of variance (p = 0.04). Conclusion Significant cortical CBF and CBV reduction was present in CI compared to NI in the absence of structural differences.

Purpose This work sought to compare a quantitative T1 bookend dynamic susceptibility contrast MRI based perfusion protocol for absolute cerebral blood flow (qCBF) against CBF measured by the stable‐isotope neutron capture microsphere method, a recognized reference standard for measuring tissue blood flow, at normocapnia, hypercapnia, and in acute stroke. Methods CBF was measured in anesthetized female canines by MRI and microspheres over 2 consecutive days for each case. On day 1, 5 canines were measured before and during a physiological challenge induced by carbogen inhalation; on day 2, 4 canines were measured following permanent occlusion of the middle cerebral artery. CBF and cerebrovascular reactivity measured by MRI and microsphere deposition were compared. Results MRI correlated strongly with microspheres at the hemispheric level for CBF during normo‐ and hypercapnic states (r2 = 0.96), for individual cerebrovascular reactivity (r2 = 0.84), and for postocclusion CBF (r2 = 0.82). Correction for the delay and dispersion of the contrast bolus resulted in a significant improvement in the correlation between MRI and microsphere deposition in the ischemic state (r2 = 0.96). In all comparisons, moderate correlations were found at the regional level. Conclusion In an experimental canine model with and without permanent occlusion of the middle cerebral artery, MRI‐based qCBF yielded moderate to strong correlations for absolute quantitative CBF and cerebrovascular reactivity measurements during normocapnia and hypercapnia. Correction for delay and dispersion greatly improved the quantitation during occlusion of the middle cerebral artery, underscoring the importance for this correction under focal ischemic condition.

Purpose The role of gray matter in Multiple sclerosis (MS) is increasingly evident; however conventional magnetic resonance (MR) images demonstrate limitations in cortical lesion (CL) identification. Perfusion imaging appears sensitive to changes in tissue type and disease severity in MS. We sought to utilize bookend perfusion to quantify parameters in healthy controls (HC), normal appearing and lesional tissue at different RRMS stages. Methods Thirty-nine RRMS patients and 19 age-matched HC were prospectively recruited. MACFIMS battery was used to assess cognitive performance. Perfusion parameters including cerebral blood flow (CBF) and volume (CBV) and mean transit time (MTT) were compared for HC, normal appearing and lesional tissue for all study groups. Dispersion of perfusion measures for white matter lesion (WML) and CLs were assessed. Results Twenty of the 39 RRMS patients were cognitively impaired (RRMS-I). Significant differences were displayed between all RRMS subgroups and HC except for normal appearing gray matter (NAGM) CBV between HC and unimpaired RRMS patients (RRMS-NI) and for all normal appearing white matter (NAWM) perfusion parameters between HC and RRMS-NI. WML but not CL perfusion was significantly reduced in RRMS-I versus RRMS-NI. Perfusion reduction with disease progression was greater in NAGM and NAWM compared to CL and WML. Smaller dispersion was observed for CLs compared to WML for each perfusion parameter. Conclusion Quantitative GM and WM analysis demonstrates significant but disproportionate WML, CL, NAWM and NAGM changes present between healthy controls and RRMS patients with and without cognitive impairment necessitating absolute rather than relative lesion perfusion measurement.

Purpose The purpose of this study was to investigate the diffusional transport of contrast agent and its effects on kinetic modeling of Dynamic Contrast Enhanced (DCE) images. Methods We performed simulations of our diffusion-compensated model and compared these results to human intracranial aneurysms (IAs). We derive an easy to use parameterization of diffusional effects that can provide an accurate estimate of diffusion corrected contrast agent leakage rates (ktrans). Finally, we performed re-analysis of an existing dataset to determine if diffusion-corrected kinetic parameters improve the identification of high-risk IAs, thereby providing a new MRI-based imaging metric of IA stability based on wall integrity. Results Probability distributions of simulated vs. measured data show contrast leakage away from the aneurysm wall. Parameterization of diffusional effects on ktrans showed high correlation with long-chain methods in both surrounding tissue and near the aneurysm wall (r2 = 0.91 and r2=0.90 respectively). Finally, size, ktrans, and (ktrans−ktransDC) showed significant univariate relationships with rupture risk (p<0.05). Conclusions We report the first evidence of diffusion-compensated permeability-modeling in intracranial aneurysms and propose a parameterization of diffusional effects on ktrans. Furthermore, a comparison of measured against simulated data suggests contrast leakage occurs across the aneurysm wall.