Figure 8.

Core versus peri-lesional changes and relation to MRI signal. (a) Two arteriole microinfarcts imaged with DKI over a span of 14 days post-occlusion. (b) MK was quantified in core and peri-lesional regions. The regions of interest were selected from a time-point of peak microinfarct visibility (typically one day post-occlusion) and applied to all other time-points. See Materials and Methods for additional details. (c) MK of the microinfarct core plotted as a function of post-occlusion time (p = 0.0001 main effect, F(4, 20) = 15.86, one-way ANOVA with repeated-measures; Tukey post hoc yields *p < 0.05, compared to 0.1, 7, and 14 days; n = 6 arteriole microinfarcts over three mice). Data = mean ± SEM. (d) Mean kurtosis of peri-lesional tissues for the same microinfarcts plotted as a function of post-occlusion time. (*p = 0.02 main effect, F(4, 20) = 3.59, one-way ANOVA with repeated-measures; Tukey post hoc yields *p < 0.05, compared to 0.1 day). Data = mean ± SEM. (e) Evolution of acute microinfarct pathology. At 1–3 days post-occlusion, the non-viable core is visible to both structural (T2/IR) and diffusion MRI. Peri-lesional tissues remain viable, but are functionally impaired and insufficiently detected by MRI. At 7–9 days, the core is detectable only to diffusion MRI. The peri-lesional tissues begin to recover in function, and show a modest increase in MK relative to earlier time-points. At 14–21 days, the core is no longer visible to MRI, and peri-lesional tissues exhibit only partial responsiveness to sensory input.