Quantification (mean±standard deviation) of initial MRI defects in Experiment 1 (n = 15): diffusion (ADC map), perfusion (MPC map) and perfusion-diffusion mismatch volumes, expressed as % of ipsilateral hemisphere.

<p>Mice were grouped according to presence/absence of ischemic lesion on baseline DWI and final histology. Group A (white bars, n = 6) = initial and final lesion; group B (gray bars, n = 5) = initial without final lesion; group C (black bars, n = 4) = neither initial nor final lesion (i.e., lesion <5% of ipsilateral hemisphere, confined to the surgical site).</p

Acute multi-slice, multiparametric MRI of thromboembolic stroke in mice.

<p>(<b>A</b>) MR Angiography (maximum intensity projection). MCA signals were manually overlaid in red for clarity. Note the distally interrupted flow in the right MCA (bars). (<b>B</b>) Perfusion (MPC) map overlaid on corresponding T2-WI. Note the large perfusion defect in the right MCA territory (arrow) (<b>C</b>, <b>D</b>) Diffusion (ADC) maps overlaid on corresponding T2-WI. Note the cortico-striatal decrease in <b>D</b> (same animal as <b>B</b>), in contrast with <b>C</b>.</p

Pooled data from Experiment 1 (n = 13, full circles) and Experiment 2 (n = 4, open circles).

<p>Evolution of lesion volume (expressed as % of ipsilateral hemisphere) between 0 hour (ADC map) and 24 hours (histology in Experiment 1; T2-WI in Experiment 2). Only animals displaying a significant lesion beyond surgical site on ADC (i.e., lesion >5% of ipsilateral hemisphere) were considered. Two animals from Experiment 1 died shortly after MRI completion (no histological staining).</p

Evolution of hypoperfusion areas (expressed as % of ipsilateral hemisphere) between 0 and 3 hours in Experiment 2 (n = 6).

<p>CBF maps were thresholded at the 10^th percentile value of perfusion in the contralateral hemisphere.</p

Single-slice perfusion (PASL) follow-up between 0 and 3 hours of thromboembolic stroke in mice.

<p>(<b>A</b>) CBF at 0 hour and (<b>B</b>) CBF after 3 hours in an animal with spontaneous reperfusion. (<b>C</b>) CBF at 0 hour and (<b>D</b>) CBF after 3 hours in an animal without reperfusion.</p

Comprehensive analysis of early fractional anisotropy changes in acute ischemic stroke

<div><p>Background and purpose</p><p>Cerebral ischemia leads to a rapid decrease of the apparent diffusion coefficient. For fractional anisotropy both increase and decrease have been reported in acute ischemic stroke. Aim of this study was to characterize early water diffusion changes in a homogenous group of acute stroke patients and to clarify the issue of early fractional anisotropy changes and their relation to time from symptom onset.</p><p>Methods</p><p>MRI data of patients with acute ischemic stroke examined by diffusion tensor imaging within 8h after symptom were analyzed. We calculated fractional anisotropy, eigenvalues and the isotropic and anisotropic components of the diffusion tensor. The values were calculated as ratios between the ischemic lesion and a mirror region in the unaffected side and correlated with clinical parameters.</p><p>Results</p><p>We included 63 patients: 49% female, mean age 69 ± 14 years, median NIHSS on admission 9 (IQR 4–14). For the whole sample, mean fractional anisotropy was increased (ratio: 1.083 ± 0.168), while all other diffusion parameters were decreased. Both the isotropic and anisotropic component of the diffusion tensor were decreased with a more pronounced decrease of the isotropic component (ratios: isotropic = 0.730 ± 0.106, anisotropic = 0.788 ± 0.127; p<0.001). There was no correlation of fractional anisotropy with time from symptom onset. Looking at individual patients, fractional anisotropy was increased in 70%. There were no differences in clinical characteristics between patients with increased and decreased fractional anisotropy.</p><p>Conclusion</p><p>Fractional anisotropy increase in acute stroke results from a more pronounced decrease of the isotropic diffusion component and is not related to time from symptom onset. Thus, fractional anisotropy is not helpful as a surrogate marker of lesion age in the very first hours of stroke.</p></div

Mapping of the eigenvalues as ellipsoids, unaffected side and affected side.

<p>Mapping of the eigenvalues as ellipsoids divided into unaffected side (A) with FA = 0.292 and affected side (B) with FA = 0.313.</p

Ratios of isotropic components (p) versus anisotropic components (q) of the diffusion tensor.

<p>The ratios of isotropic components (p) are plotted against the anisotropic components (q) of the diffusion tensor.</p

Ratio of FA versus p and q.

<p>The ratio of FA is plotted against p and q, showing FA is increasing with increasing q.</p

Values of FA, MD, eigenvalues (λ1, λ2 and λ3) and q divided into affected and unaffected side.

<p>Values of FA, MD, eigenvalues (λ1, λ2 and λ3) and q divided into affected and unaffected side.</p