PMC10070273_01
Magnetic resonance imaging pretreatment findings: (a-c) T2WI showed ventricular dilatation of the lateral and the third ventricles but not of the fourth ventricle. Preoperative planning of the endoscopic corridor was shown as red arrow. (d) Heavily T2WI showed an enlarged aqueduct of Sylvius and a membranous structure at its caudal end (yellow arrow). (e) T1WI with gadolinium did not demonstrate any enhanced lesion (blue arrow).
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F1
Narrowing of the subarachnoid space in the parietal region (high cranial area and longitudinal fissure) and heterogeneous enlargement of the basilar and Sylvian fissures indicated idiopathic normal pressure hydrocephalus was not observed [Figures 1a-c]. T2-weighted images showed an enlarged aqueduct of Sylvius and a membranous structure at its caudal end and the bulging of the floor of the third ventricle [Figure 1d]. T1-weighted images with gadolinium showed no enhanced lesion [Figure 1e]. Our endoscopic surgical corridor planned preoperatively from the anterior horn of the right lateral ventricle to the third ventricle floor and the aqueduct of Sylvius was presented [Figures 1a-c].
Magnetic resonance imaging (MRI) posttreatment findings: (a-d) T2WI axial and saggitalimages showed mild ventricular shrinkage and was seen surgical collider at the right frontal lobe (red arrow). (e) Heavily T2WI showed the opening of the aqueduct of Sylvius (yellow arrow). (f) Phase contrast cine MRI showed cerebrospinal fluid flow at the stoma of the third ventricle floor (blue arrow).
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F2
MRI showed a reduction in ventricular size [Figure 2a], the corridor used in the endoscopic surgery is shown in [Figures 2b-d]. Moreover, heavily T2-weighted images showed the opening of the aqueduct of Sylvius [Figure 2e]. Phase-contrast cine MRI showed CSF flow at the floor of the third ventricle [Figure 2f].
Intraoperative findings (a) foramen of Monro was dilated and observed stretched interthalamic adhesion. (b) Membranous structure (yellow arrow) occluded the aqueduct of Sylvius. (c) Membranous structure was removed with forceps. (d) The floor of the third ventricle was thinning (e) A stoma was created at the floor of the third ventricle. (f) The Lilliquist's membrane was thinning and defects in prepontine cistern.
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F3
An enlarged lateral ventricle, foramen of Monro, third ventricle, and stretched interthalamic adhesion were observed, and the septum pellucidum was partially perforated [Figure 3a]. Patency of CSF was observed in the perforated area [Figures 3b-d]. Moreover, ETV was performed on the thinning base of the third ventricle after EPA [Figure 3e]. CSF flow between the third ventricle and prepontine cistern through a stoma was observed [Figure 3e]. The Lilliquist's membrane was thinned out [Figure 3f].
Pathological findings (a and b) island-like cell aggregates with loss of continuity were seen in the neuropil on staining (red dotted circle). (c and d) Cells forming island-like aggregates were glial fibrillary acidic protein (d) positive and epithelial membrane antigen (d) positive. (e) Corpora amylacea were scattered in neuropil on staining.
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F4
Within the cellular matrix, cell aggregates with an island-like distribution and loss of continuity which were observed [Figures 4a and b]. These cells, which formed island-like cell clusters, were positive for glial fibrillary acidic protein: and epithelial membrane antigen: Immunostaining [Figures 4c and d]. Corpora amylacea that stained mild basophilic were also observed in the neuropil [Figure 4e].