case_images: PMC9671071_01
case_images: Radiological evaluation of the parenchymal lesion preoperatively. An initial CT scan showed a hypodense irregular mass located in the right frontal cortex (A, B), which enlarged in size in the second scan performed 4 days later (C, D). The lesion was hyper-intense on T2WI (E). Post-contrast (gadolinium-enhanced) axial (F) and coronal MRI (G) showed prominent heterogeneous enhancement. MRS showed that there was no obvious change in the ratios of NAA/Cr (1.65) and Cho/Cr (0.83) in the lesion (H) compared with its counterpart (NAA/Cr: 1.50; Cho/Cr: 0.82) on the contralateral side (I). Each region of interest in the MR images showed the location where the spectrum was obtained.
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case_images: PMC9671071_01_fonc-12-977038-g001.jpg
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case_images: An initial computed tomography (CT) revealed a cortical based right frontoparietal hypodense lesion ( Figures 1A, B ), which prompted her presentation to our facility three days later. A repeated CT scan showed the expansion of the lesions of hypodensity in the right frontoparietal cortex ( Figures 1C, D ). On magnetic resonance (MR) images, the lesion presented high signal intensity on T2-weighted images ( Figure 1E ), and a mixture of hypointensity and isointensity on T1-weighted images. Focal enhancement was observed in the contrast-enhanced MRI ( Figures 1F, G ). Proton MR spectra (MRS) revealed no obvious change in N-acetylaspartate (NAA)/creatine (Cr) ratio or choline/Cr ratio within the lesion compared with contralateral frontal lobe ( Figures 1H, I ). At a five-year follow-up, the patient denied any symptom recurrence ( Supplemental Figure 1 ).
case_images: Radiological images indicating the ICVT. Preoperative MRV revealed an absence of flow (arrowheads) in the left central sulcus vein (A). Preoperative contrast MRI showed an intraluminal filling defect at the site where the deep branch of the right central sulcus vein enters the main trunk (arrow), likely indicative of ICVT (B). Follow-up MRV showed the recanalization (arrowheads) of the right central sulcus vein after surgical thrombectomy (C).
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case_images: There seemed to be no obvious abnormity in the MR venography (MRV) when assessed pre-operatively ( Figure 2A ). Upon revisiting the imaging data, we identified filling defect in the central sulcus vein ( Figure 2A ) and a suspected site of thrombosis in the deep branch of the central sulcus vein ( Figure 2B ). Follow-up MRV obtained 3 months after discharge showed cortical vein recanalization ( Figure 2C ).
case_images: Surgical thrombectomy and pathological confirmation of ICVT. An intraoperative image showing that the cortical vein (indicated by yellow arrowheads) as well as its deep branch (the yellow arrow) became darkened and stiff. The arrowheads denoted the starting and ending points of the thrombosis (A). After surgical thrombectomy, both the occluded vein and an adjacent cortical vein (the white arrow) returned to normal color (B). The framed area in (B) was magnified in (C), indicating suture of the vein after thrombus removal. Bars = 1 cm in (A, B), and 200 mm in (C) The operation approach (D) and surgical thrombectomy (E) were further illustrated by cartoon images. Hematoxylin-eosin staining under light microscopy showed thrombosis in some venules (blue arterisks), vascular malformation (the purple arterisk) and proliferation (green arrows), and gliosis (the red arrow) (F-H). The framed area in (F) was magnified in (G). Bars = 50 mum in (F-H).
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case_images: This thrombus started approximately 3 centimeters away from the superior sagittal sinus, terminated before the bifurcation of the vein, and spread into the lumen of a deep branch ( Figure 3A ). Next, the lumen of the vein was perfused with heparin in order for preventing thrombosis, and the incision was continuously sutured with 7-0 threads ( Figures 3B, C ). Finally, cortical tissue around the occluded deep branch were harvested for pathological examination, and then the branch was sacrificed ( Figures 3B-E ). Pathological analysis revealed proliferation of small vessels and reactive gliocytes, vascular malformation, and thrombosis in some vessels, with no characteristics of tumour-like lesions observed ( Figures 3F-H ).