Diagnosis: Thrombosis of the vein of Galen

Abstract

Ann Saudi Med 2014 September-October www.annsaudimed.net 1 Symmetric thalamic lesions may appear in various disorders, such as in acute disseminated encephalomyelitis, acute hemorrhagic leukoencephalitis, severe hypoxia or traumatic injury, toxins, inflammation, tumors, metabolic disorders, acute necrotizing encephalopathy, arterial or venous infarct, and so on.1-3 Bilateral thalamic lesions occasionally result from venous occlusion, especially thrombosis of the deep cerebral veins (eg, vein of Galen and straight sinus).4 Additionally, as the management and prognosis were distinct between patients with venous and arterial occlusion, early diagnosis is of great importance.5,6 MRI of the patient showed bilateral thalamic lesions with features of abnormal signal intensity, as follows: the T1-weighted image (T1WI) decreased (Figure 2A); gadolinium-enhanced MRI revealed a mild enhancement effect (Figure 2B); the T2-weighted image (T2WI) increased; and the fluid-attenuated inversion recovery (FLAIR) increased (Figure 2C). Of note, the diffusion-weighted imaging (DWI) showed mixed intensity (Figure 2D), while the apparent diffusion coefficient (ADC) was hyperintense (Figure 2E), which was primarily consistent with vasogenic edema. These features noted upon imaging motivated us to focus on the cerebral vein system. It is well known that the internal cerebral veins that receive venous blood from the medullary thalamic and thalamostriate veins converge with the basal veins of Rosenthal into the vein of Galen, and then with the inferior sagittal sinus from the straight sinus.4 After thrombosis of the vein of Galen and straight sinus develops, the venous drainage becomes blocked and vaDiagnosis: Thrombosis of the vein of Galen