# CT ventriculographic identification and neuroendoscopic treatment of acquired hydrocephalus due to cerebral aqueduct lesions: a two-case report

**Authors:** Kai Liu, Yuheng Feng, Shuli Wang, Yubo Zhang, Xiaoxuan Ji, Qiang Li, Xiaodong Luo

PMC · DOI: 10.3389/fonc.2025.1700195 · Frontiers in Oncology · 2026-02-04

## TL;DR

Two pediatric cases of acquired hydrocephalus due to cerebral aqueduct lesions were successfully diagnosed and treated using ventriculography and neuroendoscopic surgery.

## Contribution

Demonstrates the utility of ventriculography and neuroendoscopic resection for diagnosing and treating occult aqueductal lesions.

## Key findings

- Ventriculography identified aqueductal filling defects not visible on MRI.
- Neuroendoscopic resection provided both diagnosis and treatment for mixed germ cell tumors.
- Both patients experienced sustained symptom relief with no complications or recurrence.

## Abstract

Hydrocephalus secondary to cerebral aqueduct lesions poses significant diagnostic and therapeutic challenges, particularly when causative lesions are occult on conventional neuroimaging. We present two pediatric cases of acquired obstructive hydrocephalus, in which routine laboratory tests were unremarkable except for mildly elevated tumor markers. Both patients exhibited acute symptoms of intracranial hypertension. Magnetic resonance imaging (MRI) demonstrated supratentorial hydrocephalus with periventricular edema but failed to visualize a definitive obstructive lesion. Subsequent cerebral ventriculography revealed aqueductal filling defects located at the aqueductal inlet along the floor of the third ventricle. Neuroendoscopic resection of the intraventricular lesions was successfully performed through a right frontal transventricular approach. Histopathological examination played a pivotal role in management: Both cases were postoperatively diagnosed as mixed germ cell tumors. Case 1 received postoperative chemoradiotherapy, whereas Case 2 was treated with postoperative chemotherapy alone. Both patients achieved rapid and sustained symptom relief, with no postoperative complications or recurrence observed during the 12-month follow-up period. These cases underscore the diagnostic value of ventriculography in identifying occult aqueductal lesions and highlight the dual diagnostic and therapeutic utility of neuroendoscopic resection, which provides a definitive histological diagnosis and restores cerebrospinal fluid circulation.

## Linked entities

- **Diseases:** hydrocephalus (MONDO:0001150), intracranial hypertension (MONDO:0006810)

## Full-text entities

- **Genes:** OLIG2 (oligodendrocyte transcription factor 2) [NCBI Gene 10215] {aka BHLHB1, OLIGO2, PRKCBP2, RACK17, bHLHe19}, NCAM1 (neural cell adhesion molecule 1) [NCBI Gene 4684] {aka CD56, MSK39, NCAM}, FLI1 (Fli-1 proto-oncogene, ETS transcription factor) [NCBI Gene 2313] {aka BDPLT21, EWSR2, FLI-1, SIC-1}, VIM (vimentin) [NCBI Gene 7431], CD99 (CD99 molecule (Xg blood group)) [NCBI Gene 4267] {aka HBA71, MIC2, MIC2X, MIC2Y, MSK5X}, PLAA (phospholipase A2 activating protein) [NCBI Gene 9373] {aka DOA1, NDMSBA, PLA2P, PLAP}, CLTA (clathrin light chain A) [NCBI Gene 1211] {aka LCA}, ENO2 (enolase 2) [NCBI Gene 2026] {aka HEL-S-279, NSE}, SYNM (synemin) [NCBI Gene 23336] {aka DMN, SYN}, KIT (KIT proto-oncogene, receptor tyrosine kinase) [NCBI Gene 3815] {aka C-Kit, CD117, MASTC, PBT, SCFR}, AFP (alpha fetoprotein) [NCBI Gene 174] {aka AFPD, FETA, HPAFP}, SALL4 (spalt like transcription factor 4) [NCBI Gene 57167] {aka DRRS, HSAL4, IVIC, ZNF797}, CMPK1 (cytidine/uridine monophosphate kinase 1) [NCBI Gene 51727] {aka CK, CMK, CMPK, UMK, UMP-CMPK, UMPK}, MUC1 (mucin 1, cell surface associated) [NCBI Gene 4582] {aka ADMCKD, ADMCKD1, ADTKD2, CA 15-3, CD227, Ca15-3}
- **Diseases:** Pineal germinoma (MESH:D018237), tumor (MESH:D009369), edema (MESH:D004487), meningeal irritation (MESH:D008580), frontal headache (MESH:D006261), papilledema (MESH:D010211), trauma (MESH:D014947), hereditary disorders (MESH:D009386), space (MESH:D008158), genetic disorders (MESH:D030342), neurological deficits (MESH:D009461), micro-cysts (MESH:C536681), intraventricular (MESH:D006345), germ cell tumors (MESH:D009373), vomiting (MESH:D014839), ventricular dilatation (MESH:C566255), bleeding (MESH:D006470), nausea (MESH:D009325), oculomotor palsies (MESH:D015840), infection (MESH:D007239), and developmental toxicity (MESH:D064420), mature teratoma (MESH:D013724), paroxysmal/episodic hydrocephalus (MESH:D051302), ocular motility restriction (MESH:D015835), disturbances of consciousness (MESH:D003244), brain herniation (MESH:D001927), aqueductal (MESH:D006849), memory disturbances (MESH:D008569), benign cyst (MESH:D003560), intracranial hypertension (MESH:D019586), gait ataxia (MESH:D020234), ventricular enlargement (MESH:D006332), pineal region tumors (MESH:D010871)
- **Chemicals:** VIP (MESH:C056638), Iohexol (MESH:D007472), etoposide (MESH:D005047), cisplatin (MESH:D002945), ifosfamide (MESH:D007069)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

3 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12913108/full.md

## References

32 references — full list in the complete paper: https://tomesphere.com/paper/PMC12913108/full.md

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Source: https://tomesphere.com/paper/PMC12913108