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. 2017 Jan 16;37(11):3599–3614. doi: 10.1177/0271678X16685573

Figure 2.

Figure 2.

MRI signals associated with evolution of microinfarct pathology. (a) Longitudinal imaging of two microinfarcts using IR, T2 and DKI (MK) sequences. Lower green circle shows location of a penetrating arteriole occlusion. Upper green circle shows location of penetrating venule occlusion. Yellow circle is the location of a control off-target irradiation. (b) Area of microinfarcts plotted as function of post-occlusion time. We detected a statistically significant difference between imaging sequences (p = 0.01 main effect F(2,38) = 5.2; two-way ANOVA with repeated measures). Tukey post hoc analysis revealed differences between T2 versus IR at three days (p = 0.003) and five days (p < 0.001), MK versus T2 at seven days (p = 0.003), and MK and IR at five days (p < 0.001) and seven days (p < 0.001). Data are mean ± SEM. Panels b and c comprise data from n = 12 penetrating arteriole and n = 8 penetrating venule occlusions over seven mice. (c) Larger microinfarcts exhibit longer durations of visibility with DKI (p = 0.002, R2 = 0.43, Pearson’s correlation). (d) Post-mortem histology of mouse shown in panel (a). NeuN immunostaining shows the extent of the microinfarct core (yellow dotted line). GFP-labeled microglia intrinsic to the transgenic mouse used (CX3CR1-GFP+/−) and GFAP immunostain show the extent of neuroinflammation in surrounding tissues.