Katsuhiro Mizutani, Arturo Consoli, Federico Di Maria, Stéphanie Condette Auliac, Anne Boulin, Oguzhan Coskun, Julie Gratieux, and Georges Rodesch
Few classifications of intradural spinal arteriovenous shunts (ID-SAVSs) have considered their anatomical localization in relation to their phenotype and angioarchitectonics. The authors propose another vision of ID-SAVSs allowing a reappraised classification based on analysis of the anatomical disposition, angioarchitecture, and histogenetic location of these vascular malformations.
The radiological and clinical records of 210 patients with ID-SAVSs were retrospectively reviewed, considering their localization, vascular architectonics, and correlation with the 5 histogenetic units of the spinal cord. Among these, 183 files with complete data allowed precise analysis of the ID-SAVSs.
Among these 183 files (162 and 21 cases with single and multiple lesions, respectively), different entities were identified: 13 pial macro arteriovenous fistulas (MAVFs), 92 pial micro arteriovenous fistulas (mAVFs), 33 superficial pial niduses, and 69 intramedullary niduses. Thirteen sulcal shunts (either fistulas or niduses) were considered subtypes of pial lesions. Among the 21 multiple cases, 11 were monomyelomeric while 10 were multimyelomeric. Pial lesions, either fistulas or niduses, were dominantly vascularized by pial arteries (anterior or posterior depending on the localization of the shunt) and occasionally (except for MAVFs) by transmedullary arteries. Pial niduses occasionally extended into the funiculus by recruiting intrinsic veins or by extension of the nidus itself inside the white matter. Intramedullary niduses were always vascularized by both centrifugal and centripetal feeders, respectively, from sulcal arteries (SAs) and pial arteries. Sulcal lesions are pial lesions located within the ventral median sulcus and vascularized by SAs and veins. Single or multiple ID-SAVSs can be part of various syndromes such as hereditary hemorrhagic telangiectasia, Parkes-Weber, RASA1, CLOVES, and spinal arteriovenous metameric syndromes. Histogenetic analyses revealed a specific distribution of each ID-SAVS in the 5 histogenetic units of the spinal cord: intramedullary niduses were found almost equally from cervical to thoracic units, while MAVFs and mAVFs were mostly found from thoracic to postcrural ones. Pial niduses showed intermediate features between intramedullary and fistulous lesions and were mostly distributed from brachial to crural segments.
Precise analysis of the anatomical disposition of ID-SAVSs in relation to functional histogenetic units allows a better understanding of these lesions and improved therapeutic management.
Pierre Guedin, Stephan Gaillard, Anne Boulin, Stephanie Condette–Auliac, Frederic Bourdain, Stephanie Guieu, Michel Dupuy, and Georges Rodesch
There is a strong correlation between the venous drainage pattern of intracranial dural arteriovenous shunts (ICDAVSs) and the affected patients' clinical presentation. The ICDAVSs that have cortical venous reflux (CVR) (retrograde leptomeningeal drainage: Borden Type 2 and 3 lesions) are very aggressive and have a poor natural history. Although the necessity of treatment remains debatable in ICDAVSs that drain exclusively into a sinus (Borden Type 1), lesions with CVR must be treated because of the negative effects of the retrograde venous drainage. Surgery, radiosurgery, and embolization have been proposed for management of these lesions, but endovascular therapy is considered the most appropriate therapeutic strategy in ICDAVSs. New embolic materials, such as Onyx, have been recently developed and are considered to represent a kind of “gold standard” for embolization of these lesions. The purpose of this study is to emphasize the importance of transarterial embolization using acrylic glue in the therapeutic management of ICDAVSs with CVR, and to compare the results the authors obtained using this treatment with those reported in the literature for Onyx treatment of the same type of dural shunts.
The clinical and radiological records of 53 consecutive patients suffering from ICDAVSs with CVR (Borden Types 2 or 3) were reviewed. All cases were managed with the same angiographic and therapeutic protocol. Localization of the lesions, their clinical symptoms, their angioarchitecture, their therapeutic management, and the results were analyzed.
Fourteen ICDAVSs were located at the superior sagittal sinus and/or convexity veins, 13 at the transverse and sigmoid sinuses, 10 at the tentorium, 5 in the anterior cranial fossa, 4 at the foramen magnum, 3 at the torcula, 2 at the straight sinus, and 1 at the vein of Galen. One patient presented with an infantile form of ICDAVS with multiple shunts. Hemorrhage had occurred in 36% of cases. Forty-three patients underwent transarterial embolization (42 with acrylic glue). Complete closure of the fistula was obtained in 34 patients. Suppression of the CVR with partial occlusion of the main shunt was achieved in all other cases. No mortality or permanent morbidity was observed in this series.
Intracranial dural arteriovenous shunts can be safely managed by transarterial embolization, which can be considered in most instances as an effective first-intention treatment. Acrylic glue still allows a cheap, fast, and effective treatment with high rates of cures that compare favorably to those obtained with new embolic materials.