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Saul F. Morales-Valero, Carlo Bortolotti, Carmelo Sturiale, and Giuseppe Lanzino

A long-held dogma in neurosurgery is that parenchymal arteriovenous malformations (AVMs) are congenital lesions. This dogma is based on the observation that these lesions can occur in children and adults alike, but there is little convincing evidence as to its scientific truth. Over the past 2 decades, our understanding of parenchymal AVMs has improved and more information has been gained about their molecular and genetic basis. An increasing number of convincing observations of de novo AVM formation have put into question the long-held dogma that these

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transverse—sigmoid dural arteriovenous malformations (AVMs). The reason for their more aggressive natural history is that, as discussed by the authors, they seem to have a peculiar tendency to drain into the pial venous system as opposed to draining into dural sinuses or dural veins. This pial venous drainage system results in a propensity for hemorrhage because the pial veins are not protected by a dural envelope. In addition, the pial drainage can result, as discussed by the authors, in protean symptomatology related to venous hypertension, particularly in the posterior

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Neurosurgical Forum: Letters to the Editor To The Editor Masaaki Yamamoto , M.D. Tokyo Women's Medical College Dai-ni Hospital Tokyo, Japan 979 980 I read with great interest the article by Kihlström, et al. (Kihlström L, Guo WY, Karlsson B, et al: Magnetic resonance imaging of obliterated arteriovenous malformations up to 23 years after radiosurgery. J Neurosurg 86: 589–593, April, 1997). The authors reported that among 18 patients with arteriovenous malformations (AVMs) in whom postradiosurgical

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Siyu Shi, Raghav Gupta, Justin M. Moore, Christoph J. Griessenauer, Nimer Adeeb, Rouzbeh Motiei-Langroudi, Ajith J. Thomas, and Christopher S. Ogilvy

B rain arteriovenous malformations (AVMs) are direct, abnormal connections between arteries and veins without intervening capillary beds. 15 Parenchymal AVMs have traditionally been considered congenital lesions, arising from aberrant vascular development during the intrauterine period. 20 However, individual case reports published over the past 2 decades have suggested that other mechanisms may also play a role in de novo AVM development and that these lesions are both dynamic and reactive. 2 , 4–8 , 11–14 , 17–19 , 22 , 23 , 25–27 De novo AVM formation has

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Robert F. Spetzler, Joseph M. Zabramski, and Richard A. Flom

S pinal cord arteriovenous malformations (AVM's) are most commonly classified into one of four categories: Type I, long dorsal or dural spinal AVM's; Type II, compact or glomus lesions, usually intramedullary with multiple feeders; Type III, large juvenile malformations; and Type IV, direct arteriovenous fistulas without an intervening network of small vessels. Type III or juvenile malformations are characterized by their large size, high flow, and frequent extension to paraspinal structures including bone ( Fig. 1 ). Management of these formidable lesions

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Karl-Fredrik Lindegaard, Peter Grolimund, Rune Aaslid, and Helge Nornes

A cerebral arteriovenous malformation (AVM) can be considered in two parts: the arteriovenous shunt itself and the primarily normal arteries and veins involved in conveying blood to and from the AVM. 10 The arteries feeding and veins draining the AVM also have branches responsible for nutritional perfusion of adjacent normal brain areas. Angiography provides the essential mapping of the AVM complex; however, it is difficult to assess hemodynamic information from an angiographic series. Methods to investigate individual hemodynamic states would therefore

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George A. C. Mendes, Eduardo Pedrolo Silveira, Suzana Saleme, Christina Iosif, Sanita Ponomarjova, François Caire, and Charbel Mounayer

E ndovascular management of brain arteriovenous malformations (AVMs) has been revolutionized since the introduction of Onyx (Covidien Neurovascular) liquid embolic agent 8 , 11 , 16 Contemporary technology has afforded better catheter flexibility, facilitating a closer approach to the nidus. 8 However, unfavorable anatomical configuration of the feeders may preclude a successful approach to the nidus. Excessive attempts to gain distal access may increase the risk of hemorrhagic complications 2 and lead to unsuccessful endovascular management. First

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Keith L. Black, Jonathan M. Rubin, William F. Chandler, and John E. McGillicuddy

T echnical improvements and innovations continue to reduce the morbidity and mortality associated with resection of arteriovenous malformations (AVM's) and giant aneurysms. 8 In this paper, the use of intraoperative color-flow Doppler sonography of AVM's and aneurysms is described. With a color-flow Doppler ultrasound unit, a two-dimensional color-encoded intraoperative image of a vascular lesion can be obtained in which an ultrasonic shift is measured in every pixel in the image. Flow is encoded in color, with red being assigned to flows in one direction and

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Eduardo Lamas, Ramiro D. Lobato, Javier Esparza, and Luis Escudero

A rteriovenous malformations (AVM's) have been angiographically classified into pial, dural, and mixed pial-dural types. 15, 30 Although AVM's are more frequently found in the supratentorial compartment than in the posterior fossa, 35 the dural types, representing only 10% to 15% of AVM's, are preferentially located at the skull base, especially in the posterior fossa. 15 The majority of dural AVM's are congenital in origin. Their location along the base of the skull and tentorium may be accounted for by the late embryological development of the external

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Roberto C. Heros, Gerard M. Debrun, Robert G. Ojemann, Pierre L. Lasjaunias, and Pierre J. Naessens

S pinal cord arteriovenous malformations (AVM's) can be classified into one of three categories: Type I, the dorsal extramedullary AVM; Type II, the compact, usually intramedullary AVM with multiple feeders; and Type III, the extensive juvenile malformation. 8, 17, 26, 30 This report describes a patient with a direct arteriovenous fistula involving the anterior spinal artery, which cannot be classified under any of these categories. The literature is reviewed and it is proposed that a new category — Type IV, a direct arteriovenous fistula involving the normal