Figure 5.
Infarct density maps in children with overt infarct and in children with SCIs who had overt infarct or recurrent silent infarcts by 3-year follow-up. (A) Infarct density map for children in the SIT Trial with SCIs, but excluded from adjudication as an SCI as a result of having an overt infarct (n = 13). Overt infarcts are predominantly located within the border zone region, however, were larger and extend into the gray matter. (B) Mean cerebral blood flow was measured within regions of low (1%-25%) and high (26%-50%) infarct density. *White matter cerebral blood flow was lower in the region of highest infarct density (Wilcoxon rank sum test, P < .001). Similar to finding low cerebral blood flow in region of high silent infarct density, these data are suggestive that a nadir in resting cerebral blood flow may contribute to the presence of overt infarcts. (C) Infarct density map for the subset of children in the SIT Trial with SCIs who had overt or recurrent silent infarcts by 3-year follow-up (n = 20). Baseline MRI is shown on left, and 3-year follow-up MRI is shown on right. The baseline MRI scan demonstrated significantly larger lesions than baseline lesions from the larger SIT Trial cohort. The influence of baseline infarct volume on infarct recurrence was evaluated using logistic regression models (Table 3). By 3-year follow-up, the infarct pattern demonstrated persistent regional vulnerability within the border zone territory, yet lesions were enlarged and extended into gray matter.

Infarct density maps in children with overt infarct and in children with SCIs who had overt infarct or recurrent silent infarcts by 3-year follow-up. (A) Infarct density map for children in the SIT Trial with SCIs, but excluded from adjudication as an SCI as a result of having an overt infarct (n = 13). Overt infarcts are predominantly located within the border zone region, however, were larger and extend into the gray matter. (B) Mean cerebral blood flow was measured within regions of low (1%-25%) and high (26%-50%) infarct density. *White matter cerebral blood flow was lower in the region of highest infarct density (Wilcoxon rank sum test, P < .001). Similar to finding low cerebral blood flow in region of high silent infarct density, these data are suggestive that a nadir in resting cerebral blood flow may contribute to the presence of overt infarcts. (C) Infarct density map for the subset of children in the SIT Trial with SCIs who had overt or recurrent silent infarcts by 3-year follow-up (n = 20). Baseline MRI is shown on left, and 3-year follow-up MRI is shown on right. The baseline MRI scan demonstrated significantly larger lesions than baseline lesions from the larger SIT Trial cohort. The influence of baseline infarct volume on infarct recurrence was evaluated using logistic regression models (Table 3). By 3-year follow-up, the infarct pattern demonstrated persistent regional vulnerability within the border zone territory, yet lesions were enlarged and extended into gray matter.

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