Intracranial dural arteriovenous fistulas (DAVFs) are lesions with a heterogeneous clinical course, related to the varying patterns of venous drainage. Dural arteriovenous fistulas without cortical venous involvement tend to be relatively benign in course, while lesions with cortical venous drainage (whether direct or via reflux from dural venous sinuses) are more aggressive, having a higher rate of clinical presentation with aggressive neurological symptoms and intracranial haemorr-ABSTRACT: Purpose: To present our experience with the endovascular management of intracranial dural arteriovenous fistulas with direct cortical venous drainage by trans-arterial embolisation using Onyx. Materials & Methods: Between January 2004 and April 2008, 12 consecutive high grade intracranial dural arteriovenous fistulas (Cognard type III (eight patients) or IV (three patients)) were treated by trans-arterial embolisation with Onyx. The majority of cases were treated by Onyx embolisation alone. One case had additional embolisation with n-butyl-2-cyanoacrylate at the same session. Imaging follow-up was obtained in all but one patient (mean 3.6 months). Results: Nine patients had a technical success at the end of the embolisation procedure with complete angiographic exclusion of the fistula. Two patients had a small residual fistula at the end of embolisation, one of which had residual mild cortical venous drainage. Both were stable at follow-up angiography. One patient had a residual fistula supplied by the ophthalmic artery, which was thought to be unsafe to embolise and was sent for surgery, which was curative. In one patient the microcatheter ruptured, with a fragment of the distal microcatheter left in the occipital artery. No clinical complications were observed in this series at clinical follow-up (mean 3.3 months). Two patients were noted to have significant radiation dose. Conclusion: Endovascular management of intracranial dural arteriovenous fistulas with direct venous cortical drainage by trans-arterial Onyx embolisation is a safe and effective treatment according to our experience. Fluoroscopy times and radiation dose may be a concern. Chez un patient une embolisation additionnelle de n-butyl-2-cyanoacrylate (nBCA) a été effectuée au cours de la même session. Une imagerie a été obtenue chez tous les patients sauf un au cours du suivi (moyenne de 3,6 mois). Résultats : Nous avons obtenu un succès technique chez neuf patients à la fin de l'embolisation, avec exclusion angiographique complète de la fistule. Deux patients avaient une petite fistule résiduelle à la fin de l'embolisation, dont un présentait un léger drainage veineux cortical résiduel. Ces deux patients étaient stables à l'angiographie de suivi. Un patient avait une fistule résiduelle nourrie par l'artère ophtalmique dont l'embolisation a été jugée trop risquée. Il a été référé en chirurgie et l'intervention a été un succès. Chez un patient, le microcathéter s'est rompu et un fragment distal du microcathéter s'est logé dans l'artère occipitale. Il a été lai...

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We report a case of optic nerve involvement by multiple myeloma in which progressive visual loss heralded leukemic transformation and intracranial involvement. Imaging showed enhancing nodules in the intracranial segments of both optic nerves posterior to the optic canals and in the anterior optic tract, optic chiasm, and basal leptomeninges. Postmortem histopathologic examination disclosed malignant plasma cells in the subarachnoid spaces around the optic nerves and in the optic nerves. Infarctions were present in both optic nerves near their junction with the globes. Microscopic examination also showed malignant plasma cell infiltration of the leptomeninges of the cerebrum, brain stem, optic chiasm, pituitary gland, cranial bone marrow, and subarachnoid blood vessels. This is the first reported histopathologic examination in conjunction with MRI of multiple myeloma involving the anterior visual pathway. The mechanism of optic neuropathy in this case is probably related to infiltration of the optic nerve meninges by malignant plasma cells and impaired vascular supply caused by aggregated intraluminal plasma cells and monoclonal hypergammaglobulinemia.