Shinya Haryu1, Hidenori Endo2, Toshiki Endo3, Kenichi Sato4, Miki Fujimura3, Teiji Tominaga5. 1. Department of Neurosurgery, Tohoku University Graduate School of Medicine, Sendai, Japan; Department of Neurosurgery, Kohnan Hospital, Sendai, Japan. 2. Department of Neurosurgery, Tohoku University Graduate School of Medicine, Sendai, Japan. Electronic address: hideendo@gmail.com. 3. Department of Neurosurgery, Kohnan Hospital, Sendai, Japan. 4. Department of Neuroendovascular Therapy, Kohnan Hospital, Sendai, Japan. 5. Department of Neurosurgery, Tohoku University Graduate School of Medicine, Sendai, Japan.
Abstract
BACKGROUND: Varix of the drainage route can spontaneously develop thrombosis and disappear after the treatment of the associated cerebral arteriovenous malformation (AVM). We report a rare case in which a thrombosed cerebral venous varix of the drainage route exhibited growth despite complete resection of the associated cerebral AVM. CASE DESCRIPTION: A 46-year-old man was diagnosed with an AVM in the left temporal lobe. The AVM was accompanied by a large venous varix in the superficial venous drainage route. Transarterial embolization was performed followed by resection of the nidus. The venous varix in the drainage route was not resected, as it was buried in the temporal lobe of the dominant hemisphere. The venous varix was ligated using a titanium clip and nylon thread. Postoperative angiography confirmed the disappearance of the AVM, and magnetic resonance imaging showed thrombosis of the venous varix. However, follow-up magnetic resonance imaging performed 5 months after surgery showed the enlargement of the thrombosed venous varix and emergence of perilesional cerebral edema. The venous varix was excised by reoperation to prevent further growth. Histopathologic evaluation showed infiltration of macrophages and multinucleated giant cells and proliferation of capillaries vessels within the walls of the varix, particularly around the embolic and ligation materials. CONCLUSIONS: To the best of our knowledge, this is the first report of the growth of a thrombosed cerebral venous varix after the resection of a cerebral AVM. The possible cause of this rare phenomenon is excessive inflammation with neovascularization within the wall of the venous varix during thrombogenesis, enhanced by reaction against embolic and ligation materials.
BACKGROUND: Varix of the drainage route can spontaneously develop thrombosis and disappear after the treatment of the associated cerebral arteriovenous malformation (AVM). We report a rare case in which a thrombosed cerebral venous varix of the drainage route exhibited growth despite complete resection of the associated cerebral AVM. CASE DESCRIPTION: A 46-year-old man was diagnosed with an AVM in the left temporal lobe. The AVM was accompanied by a large venous varix in the superficial venous drainage route. Transarterial embolization was performed followed by resection of the nidus. The venous varix in the drainage route was not resected, as it was buried in the temporal lobe of the dominant hemisphere. The venous varix was ligated using a titanium clip and nylon thread. Postoperative angiography confirmed the disappearance of the AVM, and magnetic resonance imaging showed thrombosis of the venous varix. However, follow-up magnetic resonance imaging performed 5 months after surgery showed the enlargement of the thrombosed venous varix and emergence of perilesional cerebral edema. The venous varix was excised by reoperation to prevent further growth. Histopathologic evaluation showed infiltration of macrophages and multinucleated giant cells and proliferation of capillaries vessels within the walls of the varix, particularly around the embolic and ligation materials. CONCLUSIONS: To the best of our knowledge, this is the first report of the growth of a thrombosed cerebral venous varix after the resection of a cerebral AVM. The possible cause of this rare phenomenon is excessive inflammation with neovascularization within the wall of the venous varix during thrombogenesis, enhanced by reaction against embolic and ligation materials.