PMC5897547_01
(A) Three-dimensional time-of-flight magnetic resonance angiography (MRA): severe stenosis in the right middle cerebral artery (red arrow). (B) Brain T1-weighted 3D spoiled gradient echo sequence MRI in June 2007 after initial presentation and (C) after the development of a lacunar infarct in the right centrum semiovale (red arrow) during a follow-up in September 2007.
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F1
The MR sequences include a T1-weighted 3D spoiled gradient echo (FAST-SPGR) anatomical sequence, a T2*-weighted echoplanar gradient BOLD sequence for measurement of CVR, a T2-weighted fluid-attenuated inversion recovery (FLAIR), and a time-of-flight MR angiography (MRA). The scan was normal except for a few 1-2 mm non-specific foci of high FLAIR signal within the white matter. The MRA showed a proximal right M1 stenosis (Figure 1A). During a 4-month follow-up visit, structural MRI revealed the evolution of a 1 cm lacunar infarct in the right centrum semiovale where prior CVR imaging showed intracerebral steal (Figures 1B,C).
Cerebrovascular reactivity (CVR) maps and regions of interest overlaid on cortical surfaces. (A,C) Right and left CVR maps overlaid on inflated cortical surface from the February 2008 time point (A) and December 2016 time point (C). (B) The same CVR maps as in panel (A) that also include the region of interest (ROI) traced around the blue region of steal physiology in the right hemisphere and around the same region with normal CVR in the left hemisphere. These ROI masks were applied to subsequent time points for cortical thickness measurements as exemplified in panel (D).
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F2
CVR in the index case revealed a large area of impaired CVR with a paradoxical decrease in BOLD signal with hypercapnia involving the right MCA territory, indicating steal physiology (blue color) (Figures 2A and 3A). For longitudinal assessment (2008-2016), each ROI was copied to subsequent anatomical volumes, and CT measures were derived from these confined ROIs (Figure 2).
(A) Cerebrovascular reactivity maps overlaid on anatomical 3D T1-weighted acquisitions for registration to MNI space for displaying matching coordinates for region analysis. (B) 3D time-of-flight magnetic resonance angiography (MRA) of the circle of Willis that were re-registered to one another and slice corrected to include only the identical slices within the brain slab for each acquisition. Blue arrows denote the new collateralized vessels compared with previous scans.
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F3
CVR in the index case revealed a large area of impaired CVR with a paradoxical decrease in BOLD signal with hypercapnia involving the right MCA territory, indicating steal physiology (blue color) (Figures 2A and 3A). The CVR maps showed persistent steal; however, there was a trend toward improvement (Figure 3A). In the recent follow-up (December 2016), the MRI showed no new changes; there continued to be a high-grade stenosis of the proximal right MCA (Figure 3B). CVR study revealed decreased steal physiology in the right hemisphere compared with the previous study (depicted in blue on CVR maps in Figure 3A). Clinically, the patient had no new symptoms since 2008 except for minor left arm and hand tingling, and from a neurological standpoint, it appeared that the patient had clearly developed adequate collateral supply and hence became a candidate for reduced risk for recurring stroke.