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Keywords

vein of Galen malformation
transvenous embolization
venous hypertension
endovascular complications
thalamic infarction

How to Cite

Freire-Figueroa, I. A., Zapata-Castro, J. C., Patiño-Aristizabal, M., Uribe-Torrado, J. P., Vargas-Ardila, P. A., Bonilla-Lersundy, M. C., Montoya- Molina, F. A., & Caballero-Restrepo, A. F. (2026). Delayed thalamic infarction following transvenous vein of Galen malformation embolization: Balancing complete occlusion and risk. Romanian Neurosurgery, 40(1), 15–21. Retrieved from https://journals.lapub.co.uk/index.php/roneurosurgery/article/view/3182

Abstract

Background: Vein of Galen malformation embolisation achieves favourable outcomes in most patients through staged endovascular approaches. However, severe neurological complications occur in up to 30% of cases, with mechanisms of delayed ischemic events following near-complete occlusion remaining incompletely understood. This is particularly concerning in asymptomatic patients with favourable preoperative profiles, where the risk-benefit balance of pursuing complete angiographic cure versus accepting substantial flow reduction remains unclear.

Case Presentation: A 15-month-old asymptomatic boy with mural-type Vein of Galen malformation and high Bicêtre score (15 points) underwent three staged transarterial embolisations, achieving progressive flow reduction. The first two sessions successfully reduced flow by approximately 70% without complications. Given small-calibre residual arterial feeders in the third session, a combined transarterial and transvenous approach was employed, achieving near-complete occlusion. Eighteen hours post-procedure, the patient developed acute left hemiparesis. Imaging revealed right thalamic infarction with intraventricular haemorrhage. Conservative management with intensive rehabilitation resulted in complete functional recovery within one month. Follow-up angiography demonstrated persistent occlusion without recanalisation and development of superficial venous collateral drainage.

Conclusion: This case demonstrates that severe neurological complications can occur even in optimal candidates undergoing staged embolisation. The delayed thalamic infarction with hemorrhagic component following transvenous occlusion suggests acute venous hypertension as the primary mechanism, compromising deep venous drainage before adequate collaterals developed. In asymptomatic patients achieving substantial flow reduction through transarterial approaches, accepting incomplete occlusion may be safer than pursuing complete angiographic cure via transvenous techniques when collateral venous pathways appear limited. Extended neurological monitoring for 48-72 hours after high-grade occlusion procedures is essential. Despite severe complications, excellent functional recovery is achievable through aggressive early rehabilitation.

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