Table 3.

Imaging findings in patients with reversible cerebral vasoconstriction syndrome and coronavirus disease 2019.

Patient	Imaging
Patient 1	MRI: Hyperintense T2 and T2 FLAIR signal in the frontal, temporal, parietal, and occipital subcortical white matter and pons without restricted diffusion or enhancement. MRA: Long segment irregularity and narrowing of distal left MCA) with most pronounced involvement of the ACA and left MCA branches. Long segment irregularity and narrowing of distal right PCA branches with lesser involvement of the distal left PCA branches
	MRI/MRA (3 month follow up): Interval resolution of previously seen predominantly white matter T2 FLAIR hyperintensity in the parietal and occipital lobes involving subcortical and deep white matter. Central pontine T2 FLAIR hyperintensity persists and is not substantially changed in the interval. There also has been interval resolution of the previously seen irregularity involving the distal left MCA, left ACA, right PCA, and left PCA
Patient 2	CT: Acute parenchymal hemorrhage centered in the left frontal lobe measuring 2.8 × 2.4 × 2.3cm with adjacent vasogenic edema. There is a large volume subarachnoid hemorrhage that emanates from this position and is likely a direct extension from the parenchymal hemorrhage. It is also present in the interpeduncular cistern, ambient cistern, and extends to the left sylvian fissure. There is additional subarachnoid hemorrhage present in the left frontoparietal convexity and right temporal sulci. CTA: Left MCA M2 distribution multivessel long segment high-grade stenosis affecting essentially all of the M2 segment branches. High-grade stenosis extends into the M3 segment and M4 segment of multiple of these branches as well. This is in the region of the large subarachnoid hemorrhage. Low-attenuation in the left thalamus and medial left basal ganglia is nonspecific but suspicious for acute ischemic change.
	DSA: Multifocal caliber irregularities in the left MCA, affecting the larger proximal branches as well as the smaller distal vessels.
	CTA (3 month follow up): Interval significant improvement of previously seen stenosis involving the left M2, M3, and M4 segments
Patient 3	CTA (1): Approximately 50% stenosis of the proximal portion of the left internal carotid artery. Multifocal areas of moderate to marked stenosis of nearly all intracranial vessels. Vertebrobasilar junction and the basilar artery demonstrate multifocal areas of stenosis and luminal irregularity but is patent throughout its course. There is an luminal irregularity near the tip of the basal artery at the takeoff of the bilateral posterior cerebral arteries.
	CTA (2): Moderate irregular stenosis of the distal left internal carotid artery and proximal portions of the left MCA and ACA. Severe stenosis of the terminal right ICA and of the proximal right ACA and MCA. The more distal right MCA and its branches are partially patent, improved from prior.
	MRI: Large areas of restricted diffusion involving the R MCA, L parietal; also with FLAIR gyral swelling in the R posterior cerebral cortex with minimal convexal SAH of the right parietal lobe
Patient 4	CTA: Diminutive L MCA (M1) branch with only minimal reconstitution of a few distal cortical branches. Paucity of opacified intracranial arteries with focal narrowing. Occlusion of mid to distal right ACA A2 segment.
Patient 5	CTA: Unremarkable
	MRI/MRA: Unremarkable
	DSA: Unremarkable
Patient 6	CTA: Convexal SAH left superior parietal lobe, subtle multifocal stenosis of the bilateral ACA and MCA
	MRI: Convexal SAH of left superior parietal lobe, small SDH of left parietal lobe
	DSA: Mild left cervical ICA irregularity
	CT/MRI/MRA (3 week follow up): CT head with residual left parietal SAH; MRI/MRA with residual SAH, small SDH
Patient 7	CTA: L inferior M2 occlusion
	DSA: L inferior division M2 occlusion s/p mechanical thrombectomy with TICI3 reperfusion. Diffuse vasculopathy of the M2 and M3 divisions of bilateral MCA, left pericallosal artery
	MRI: Mixed signal intensity areas corresponding to the region of hypodensity and sulcal effacement in the L frontal lobe and insula are consistent with recent infarction. Areas of restricted diffusion in other portions of L frontal, parietal, and occipital lobes, L posterior limb of internal capsule extending to brainstem and punctate area in the R frontal lobe. Moderate bilateral confluent FLAIR hyperintensities are typical of small vessel disease.
Patient 8	CTA (1): Progressive moderate/severe narrowing involving the proximal/mid M1 segment of the L MCA and distal M1 of R MCA. Multifocal severe luminal narrowing of M2 branches of bilateral MCA. Moderate stenosis of R A1 and R P1
	MRI/MRA: 3cm hemorrhage in the L occipital lobe. Narrowing of the precavernous L ICA. Slightly decreased caliber of the M1 segment of the L MCA is seen, however no significant focal stenosis is seen. The M1 segment of the R MCA is unremarkable. ACA and PCA are unremarkable.
	CTA (2): Stable IPH in the L occipital lobe, more extensive than better demarcated hypodensities in the bilateral parietal and occipital lobes representing recent ischemic infarcts; multifocal mod/severe involving bilateral M1/M2 segments, bilateral A1 segments, R>L, bilateral A2, bilateral PCA worsened from prior
	DSA: Diffuse multifocal narrowings of the intracranial circulation involving the MCA, ACA, and PCA as well as the PICA/AICA. There was moderate improvement after injection of small dose milrinone and verapamil.
Patient 9	CTA: Diffuse vasospasm
	MRI/MRA: Acute ischemic bilateral occipital strokes; Diffuse vasospasm
	DSA: Subtle diffuse irregularity of the distal MCA territories bilaterally. Attenuated posterior cerebral artery parietal occipital territories.
Patient 10	CTA: Diffuse intracranial vascular abnormalities concerning for vasospasm or vasculitis. No large territory infarct on CT perfusion.