Background: Aqueduct of Sylvius stenosis/obstruction interferes with cerebrospinal fluid (CSF) flow and leads to the non-communicating hydrocephalus. Acquired non-neoplastic causes of aqueduct of Sylvius stenosis/ obstruction include simple stenosis, gliosis, slit-like stenosis, and septal formation, but the detailed mechanisms are not clear. In the present study, we experienced a case of late-onset aqueductal membranous occlusion (LAMO) successfully treated by neuroendoscopic procedure, which allowed us to examine the pathology of the membranous structures of the aqueduct of Sylvius occlusion. Case Description: A 66-year-old woman presented with gradually progressive gait disturbance, cognitive dysfunction, and urinary incontinenc. Brain magnetic resonance imaging (MRI) showed enlargement of the bilateral lateral ventricles and the third ventricle without dilatation of fourth ventricle, and heavily T2-weighted images showed an enlarged aqueduct of Sylvius and a membranous structure at its caudal end. Gadolinium contrast-enhanced T1-weighted images showed no neoplastic lesions. We diagnosed this case that the hydrocephalus due to late-onset idiopathic aqueductal stenosis or LAMO and the patient underwent endoscopic third ventriculostomy and endoscopic aqueduct oplasty. Membranous tissue specimens were obtained from the occluded aqueduct of Sylvius at the time of treatment. Histopathological examination revealed gliosis, and inside the gliosis, there were cell clusters that appeared to be ependymal cells and were corpora amylacea. We confirmed CSF flow at the site of obstruction of the aqueduct of Sylvius and the stoma of the third ventricle floor by MRI images. Her symptoms were improved immediately. Conclusion: We experienced a case of LAMO successfully treated by neuroendoscopic procedure, which allowed us to examine the pathology of the membranous structure of the aqueduct of Sylvius. The pathological study of LAMO is rare, and we report it, including a review of the literature.

Background: Hemifacial spasm (HFS) is most often caused by blood vessels touching a facial nerve. In particular, responsible vessels compress the root exit zone (REZ) of the facial nerve. Although we recognize these causes of HFS, it is difficult to evaluate the findings of precise lesion in radiological imaging when vessels compress REZ. Hence, we tried to obtain precise images of pre- and postoperative neuroradiological findings of HFS by creating a fusion image of MR angiography and the REZ of facial nerve extracted by magnetic resonance imaging (MRI) diffusion tensor image (DTI). Case Description: A 52-year-old woman had a 2-year history of HFS on the left side of her face. It was confirmed that the left vertebral artery and anterior inferior cerebellar artery were presented near the facial nerve on MRI. REZ of the facial nerve was visualized using DTI and fusion image was created with vascular components, making it possible to recognize the relationship between compression vessels and REZ of the facial nerve in detail. She underwent microvascular decompression and her HFS completely disappeared. We confirmed that the REZ of the facial nerve was decompressed by MRI imaging, in the same way as before surgery. Conclusion: We describe that the REZ of facial nerve and compressive vessels was delineated in detail on MRI and this technique is useful for pre- and postoperative evaluation of HFS.

Objective: We describe a patient treated with transarterial Onyx embolization for a tentorial dural arteriovenous fistula (DAVF) who presented with hemifacial spasm (HFS).Case Presentation: A 56-year-old man suffered from right blepharospasm for 4 years, and the symptom gradually spread to the right side of his face with oculo-oral synkinesis. MRI of the brain revealed abnormal multiple flow voids at the surface of brainstem and cerebellar hemisphere. MRA (time of flight) and spoiled gradient recalled echo-revealed abnormal vessels at the posterior fossa indicated arteriovenous shunting. 3D-MRI fusion images showed that a dilated vein was in contact with the root exit zone (REZ) of the right facial nerve. The right carotid angiography displayed a complex tentorial DAVF on the right side. There were multiple feeding vessels drained to the tentorial sinus at the point where the inferior cerebellar vermian vein met, and severe venous congestion was noted. We diagnosed a tentorial DAVF and thought that this was responsible for the right HFS. We used neuroendovascular treatment for this lesion. After transarterial Onyx embolization, his right HFS diminished. MRI after treatment showed that the vein in contact with the REZ of the right facial nerve had shrank. Conclusion:We experienced a rare case of HFS associated with a DAVF. Our case supports that transarterial Onyx embolization can treat HFS associated with a tentorial DAVF. It is the first description of successful treatment that could be confirmed through postoperative MRI.