Open AccessCase Report
Occipital Pial AVM Rupture in a Young Adult: Dual Intranidal Aneurysms, Solitary Parasagittal SSS Drainage, and Hematoma-Corridor Microsurgical Cure
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Alexandru Breazu, Stefan Oprea, Nicolaie Dobrin, Ionut Bogdan Diaconescu, Octavian Munteanu, Matei Șerban, Răzvan-Adrian Covache-Busuioc, Corneliu Toader, Mugurel Petrinel Rădoi and Cosmin Pantu
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Abstract
Background and Clinical Significance: Focal hemorrhagic severity associated with posterior convexity pial brain arteriovenous malformation (AVM) cases can be exacerbated by hemodynamic stress focusing on focal areas of architectural weakness and by superficial venous outflow being restricted by non-redundant superficial venous drainage. This
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Background and Clinical Significance: Focal hemorrhagic severity associated with posterior convexity pial brain arteriovenous malformation (AVM) cases can be exacerbated by hemodynamic stress focusing on focal areas of architectural weakness and by superficial venous outflow being restricted by non-redundant superficial venous drainage. This clinical case report exemplifies how bedside neurologic localization and angioarchitectural characteristics can inform the selection of microsurgical approaches for the treatment of ruptured AVMs that are directed at reducing hemorrhage recurrence risk through corridors based on rupture location.
Case Presentation: An otherwise healthy young adult male (modified Rankin scale [mRS] pre-morbid = 0) initially presented with a thunderclap headache, emesis, photophobia, decreased level of consciousness (admitted Glasgow Coma Score [GCS] = 11; E3V3M5), and subsequent deficits including left-sided pyramidal weakness, visual field loss, and visuo-spatial neglect. A non-contrast computed tomogram (CT) confirmed an intraparenchymal hemorrhage (ICH) located within the right hemisphere’s posterior lobe. Angiographic evaluation of this AVM with catheter injection and three-dimensional reconstruction revealed a compact right occipital posterior convexity pial AVM (nidus 8 × 3 mm) supplied by distal cortical branches of the right middle cerebral artery (MCA); all blood draining from the nidus was directed to a single cortical vein which then drained into the superior sagittal sinus; there were two additional intranidal saccular aneurysms (approximately 3 × 2 mm and 3 × 3 mm). Because of the acute worsening secondary to ICH and because all venous drainage was superficial-only, a single-stage approach was selected given the urgency: decompressive evacuation of the hematoma via a corridor to the site of the AVM, followed by microsurgical removal of the AVM. The removal of the AVM was accomplished in a feeder-first, vein-last sequence, and en-passage arteries and parasagittal bridging veins were preserved throughout the procedure. Additionally, the two intranidal aneurysms identified as potential weak points during progressive devascularization of the AVM were specifically treated during the removal procedure. Following the successful removal of the AVM, the patient experienced a rapid recovery and returned to a nearly premorbid state of functioning, excepting a persistent small area of quadrantanopia.
Conclusions: Rupture of posterior convexity AVMs may result in increased hemorrhagic severity due to localized architectural weaknesses in addition to the overall size of the AVM nidus. By correlating neurological findings, the topography of the hemorrhage, and angioarchitectural features early after rupture, emergency decisions regarding management can be better informed. The application of a hematoma-corridor, feeder-first/vein-last microsurgical approach for the treatment of such AVMs can achieve definitive curative results while minimizing damage to posterior cortical regions.
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