2009
DOI: 10.3171/2009.8.focus09161
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The putative role of the venous system in the genesis of vascular malformations

Abstract: Recent clinical and experimental evidence has challenged the traditional concept of the venous system as a “passive” element in the genesis and evolution of intracranial vascular malformations. The authors review the clinical and experimental evidence linking the venous system and its anomalies to the genesis of various intracranial vascular malformations, including dural arteriovenous fistulas, cavernous malformations, parenchymal arteriovenous malformations, and capillary telangiectasia. They also de… Show more

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Cited by 38 publications
(23 citation statements)
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References 70 publications
(53 reference statements)
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“…22 A possible mechanism to explain AVM formation may not be dissimilar to that responsible for dural arteriovenous fistulas-that is, venous thrombosis leading to impaired venous outflow, ischemia, and increased angiogenesis. 1 In the case of brain AVMs, asymptomatic parenchymal venous thrombosis could trigger local venous hypertension and ischemia. 1 The ischemic stimulus triggers vascular proliferation (through increased expression of hypoxia-inducible factor-1), which in normal circumstances is self-limited.…”
mentioning
confidence: 99%
See 1 more Smart Citation
“…22 A possible mechanism to explain AVM formation may not be dissimilar to that responsible for dural arteriovenous fistulas-that is, venous thrombosis leading to impaired venous outflow, ischemia, and increased angiogenesis. 1 In the case of brain AVMs, asymptomatic parenchymal venous thrombosis could trigger local venous hypertension and ischemia. 1 The ischemic stimulus triggers vascular proliferation (through increased expression of hypoxia-inducible factor-1), which in normal circumstances is self-limited.…”
mentioning
confidence: 99%
“…1 In the case of brain AVMs, asymptomatic parenchymal venous thrombosis could trigger local venous hypertension and ischemia. 1 The ischemic stimulus triggers vascular proliferation (through increased expression of hypoxia-inducible factor-1), which in normal circumstances is self-limited. 12 However, in the presence of genetic susceptibility and abnormalities of the angiogenesis and inflammatory cascades, there may be uncontrolled vascular proliferation and arteriovenous shunt forma- tion.…”
mentioning
confidence: 99%
“…12 Growing evidence suggests an ''active'' role of the venous system in the genesis of DAVF. 13 In the presented case, distal sigmoid stenosis caused a preferential retrograde drainage through the transverse sinus, torcula, and even cortical veins, with secondary antegrade drainage through the jugular vein. The stenosis was crossed during the transvenous microcatheterization, and it conferred security to the coil mass, limiting migration and allowing a denser packing.…”
Section: Discussionmentioning
confidence: 95%
“…The high flow inflow from the AVM can be found with duplex. The natural history of the neovasularity in the thrombus in unknown but has been described in the cerebral sinus post thrombosis and in the peripheral veins (Link, Garza et al ;Chikamatsu, Nagashima et al 2001;Aboian, Daniels et al 2009). Many of these patients have been found to be factor V Leiden positive (Link, Garza et al).…”
Section: Arteriovenous Malformations Post Venous Thrombosismentioning
confidence: 99%
“…Many of these patients have been found to be factor V Leiden positive (Link, Garza et al). There is evidence that the veins are not passive and may play a significant and dynamic role in revascularization through angiogenesis (Aboian, Daniels et al 2009). It is unclear whether the AVF/AVM in thrombus is transitory or may remain permanent.…”
Section: Arteriovenous Malformations Post Venous Thrombosismentioning
confidence: 99%