PMC7324723_01
Axial T2WI (A), axial FLAIR (B,D,E), axial DWI (C) and sagittal T2WI (F) images at symptom onset: T2WI, FLAIR, and DWI images demonstrated hyperintensity without diffusion restriction in bilateral parieto-occipital region, basal ganglia, and brainstem. FLAIR images demonstrated left frontoparietal sulcus subarachnoid hemorrhage. Axial T2WI images demonstrated mild enlargement of pituitary and dural sinuses.
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F1
Six hours later, brain magnetic resonance imaging revealed vasogenic edema in the bilateral parieto-occipital regions, basal ganglia, and brainstem (Figures 1A-E). Convexity SAH was identified in the left frontal lobes (Figure 1C). In addition, brain MR showed signs of intracranial hypotension including diffuse enhancement of the dura (Figures 2C,D), mild enlargement of pituitary and dural sinuses (Figure 1F), and slightly sagging of brainstem and cerebellum (Figure 1F).
MR angiography (A), MR venography (B), post contrast T1WI (C,D), SWI (E), and ASL (F) MRI images at symptom onset: MR angiography and venography were negative for aneurysms, venous thrombosis, and cerebral vasospasm. SWI images showed lack of the normal hypointensity in deep venous system. Coronal and axial T1WI images with gadolinium-enhancement showed diffuse enhancement of the dura. ASL images showed hyperperfusion areas in bilateral occipitoparietal lobe.
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F2
MR angiography and venography were negative for aneurysms, venous thrombosis, and cerebral vasospasm (Figures 2A,B). The arterial spin labeling perfusion (ASL) imaging showed hyperperfusion areas in the bilateral occipitoparietal lobe (Figure 2F). On susceptibility-weighted imaging (SWI), the commonly marked hypointensity of the cerebral deep venous system was absent, suggestive of blood oxygen level dependent (BOLD) effect probably induced by cerebral hyperperfusion (Figure 2E). In addition, brain MR showed signs of intracranial hypotension including diffuse enhancement of the dura (Figures 2C,D), mild enlargement of pituitary and dural sinuses (Figure 1F), and slightly sagging of brainstem and cerebellum (Figure 1F).
Axial FLAIR (A-C), sagittal T2WI (D), SWI (E), ASL (F) MRI images on follow up: Axial FLAIR imaging demonstrated complete regression of vasogenic edema and convexity SAH. Sagittal T2WI images showed regression of the engorgement of the pituitary and dural sinuses. SWI and ASL images showed the normalization of the signal of the deep venous system and the CBF in bilateral occipitoparietal lobe.
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F3
Follow-up MR imaging showed the complete disappearance of vasogenic edema, venous engorgement and convexity SAH (Figures 3A-D), together with the normalization of the signal of the deep venous system in SWI (Figure 3E) and the cerebral blood flow (CBF) in the bilateral occipitoparietal lobe (Figure 3F).