Diffusion tensor histology holds great promise for quantitative characterization of structural connectivity in mouse models of neurological and psychiatric conditions. There has been extensive study in both the clinical and preclinical domains on the complex tradeoffs between the spatial resolution, the number of samples in diffusion q-space, scan time, and the reliability of the resultant data. We describe here a method for accelerating the acquisition of diffusion MRI data to support quantitative connectivity measurements in the whole mouse brain using compressed sensing (CS). The use of CS allows substantial increase in spatial resolution and/or reduction in scan time. Compared to the fully sampled results at the same scan time, the subtle anatomical details of the brain, such as cortical layers, dentate gyrus, and cerebellum, were better visualized using CS due to the higher spatial resolution. Compared to the fully sampled results at the same spatial resolution, the scalar diffusion metrics, including fractional anisotropy (FA) and mean diffusivity (MD), showed consistently low error across the whole brain (< 6.0%) even with 8.0 times acceleration. The node properties of connectivity (strength, cluster coefficient, eigenvector centrality, and local efficiency) demonstrated correlation of better than 95.0% between accelerated and fully sampled connectomes. The acceleration will enable routine application of this technology to a wide range of mouse models of neurologic diseases.
The goal of the present paper is to compare the distributions of α-asarone administered to rats through three different routes: oral, intravenous and intranasal. The concentrations of α-asarone in seven distinct brain regions, the olfactory bulb, cerebellum, hypothalamus, frontal cortex, striatum, hippocampus and medulla/pons as well as in plasma and cerebrospinal fluid (CSF), were determined by HPLC. The quantities of α-asarone accumulated in liver were measured to determine whether α-asarone could generate hepatotoxicity when administered via the three different routes. The results indicated that α-asarone could be absorbed via two different routes into the brain, after intranasal administration of dry powders. In the systemic route, α-asarone immediately entered the brain through the blood-brain barrier (BBB) after uptake into the circulatory system. In the olfactory bulb route, α-asarone traveled from the olfactory epithelium in the nasal cavity straight into brain tissue via the olfactory bulb. Furthermore, intranasal administration of α-asarone as a dry powder can ensure quick absorption and avoid excessive concentrations in the blood and liver, while achieving concentrations in the brain comparable to those attained by intravenous and oral administration routes.
The mechanisms of motor functional recovery after pontine infarction (PI) remain unclear. Here, we assessed longitudinal changes in gray matter volume (GMV) and examined the relationship between GMV and clinical outcome. Fifteen patients with unilateral PI underwent magnetic resonance imaging and neurological exams five times during a period of 6 months. Another 15 healthy participants were enrolled as the normal control (NC) group and were examined with the same protocol. The MR exam included routine protocol and a 3D T1-weighted magnetization-prepared rapid acquisition gradient echo scan. Changes in GMV were assessed using voxel-based morphometry. Furthermore, the correlations between GMV changes in regions of interest and clinical scores were assessed. Compared with NCs, the decreased GMVs in the contralateral uvula of cerebellum and the ipsilateral tuber of cerebellum were detected at third month after stroke onset. At the sixth month after stroke onset, the decreased GMVs were detected in the contralateral culmen of cerebellum, putamen, as well as in the ipsilateral tuber/tonsil of cerebellum. Compared with NC, the PI group exhibited significant increases in GMV at each follow-up time point relative to stroke onset. Specifically, the significant GMV increase was found in the ipsilateral middle frontal gyrus and ventral anterior nucleus of thalamus at second week after stroke onset. At first month after stroke onset, the increased GMVs in the ipsilateral middle temporal gyrus were detected. The significant GMV increase in the ipsilateral mediodorsal thalamus was noted at third month after stroke onset. At the end of sixth month after stroke onset, the GMV increase was found in the ipsilateral mediodorsal thalamus, superior frontal gyrus, and the contralateral precuneus. Across five times during a period of 6-month, a negative correlation was observed between mean GMV in the contralateral uvula, culmen, putamen, and ipsilateral tuber/tonsil and mean Fugl-Meyer (FM) score. However, mean GMV in the ipsilateral mediodorsal thalamus was positively correlated with mean FM score. Our findings suggest that structural reorganization of the ipsilateral mediodorsal thalamus might contribute to motor functional recovery after PI.
In structural Magnetic Resonance Imaging (MRI) of patients with a recent small subcortical infarct (RSSI) and small vessel disease (SVD) imaging markers coexist. However, their spatial distribution and prevalence with respect to the hemisphere of the RSSI remain unknown. From brain MRI in 187 patients with an acute lacunar ischemic stroke clinical syndrome and a relevant diffusion weighted imaging (DWI)-positive lesion, we semiautomatically extracted the RSSI, microbleeds, lacunes, old cortical infarcts, and white matter hyperintensities (WMH) using optimized thresholding in the relevant sequences, and rated the load of perivascular spaces. We registered all images to an age-relevant brain template and calculated the probability distribution of all SVD markers mentioned for patients who had the RSSI in each hemisphere separately. We used the Wilcoxon and chi-squared tests to compare the volumes and frequencies of occurrence, respectively, of the SVD markers between hemispheres throughout the sample. Fifty-two percent patients (= 97) had the RSSI in the left hemisphere, 42% (= 78) in the right, 2.7% (= 5) in both, and 3.7% (= 7) in the cerebellum or brainstem. There was no significant difference in RSSI frequency between left and right hemispheres (= .10) in the sample. The median volume of the RSSI (expressed as a percentage of the total intracranial volume) was 0.05% (IQR = 0.06). There was no difference in median percent volume of the right RSSIs versus left (= .16). Neither was there a significant interhemispheric difference in the volume of any of the SVD markers regardless of the location of the RSSI and they were equally distributed in both hemispheres. Assessment of SVD imaging markers in the contralateral hemisphere could be used as a proxy for the SVD load in the whole brain to avoid contamination by the RSSI of the measurements, especially of WMH.