Spontaneous disappearance of cerebral arteriovenous angioma

Conforti, P

doi:10.3171/jns.1971.34.3.0432

Cited by 74 publications

(16 citation statements)

References 4 publications

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“…Seventy ®ve percent of our patients had small AVMs and showed single venous drainage. In [2,3,5,6,7,8,9,10,11,12,13,14,15,16,17,18]. However, in our brain AVM database, the spontaneous regression had occurred in only about 0.6% of small (<3 cm) brain AVMs (3/474), and AVMs with multiple draining veins can also progress to spontaneous regression [6,10,11,20].…”

Section: Discussionmentioning

confidence: 70%

“…They include mass eect on the feeding arteries from an intracranial hematoma or associated edema [3,6,7,9,16,18] or feeding arterial occlusion due to atherosclerosis [2], thromboembolism [17] or systemic coagulation disorders [4]. However, if the feeding arteries are completely occluded by any etiological condition, the AVM can recruit arterial collaterals through a non-sprouting angiogenesis if the shunt remains patent [1].…”

Section: Hypotheses For Spontaneous Regression Of the Cerebral Arterimentioning

confidence: 99%

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Spontaneous regression of cerebral arteriovenous malformations: clinical and angiographic analysis with review of the literature

et al. 2002

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Spontaneous regression of cerebral arteriovenous malformation (AVM) is rare and poorly understood. We reviewed the clinical and angiographic findings in patients who had spontaneous regression of cerebral AVMs to determine whether common features were present. The clinical and angiographic findings of four cases from our series and 29 cases from the literature were retrospectively reviewed. The clinical and angiographic features analyzed were: age at diagnosis, initial presentation, venous drainage pattern, number of draining veins, location of the AVM, number of arterial feeders, clinical events during the interval period to thrombosis, and interval period to spontaneous thrombosis. Common clinical and angiographic features of spontaneous regression of cerebral AVMs are: intracranial hemorrhage as an initial presentation, small AVMs, and a single draining vein. Spontaneous regression of cerebral AVMs can not be predicted by clinical or angiographic features, therefore it should not be considered as an option in cerebral AVM management, despite its proven occurrence.

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Section: Discussionmentioning

confidence: 70%

Section: Hypotheses For Spontaneous Regression Of the Cerebral Arterimentioning

confidence: 99%

Spontaneous regression of cerebral arteriovenous malformations: clinical and angiographic analysis with review of the literature

et al. 2002

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“…Spontaneous thrombosis and regression of AVMs have been recog nized in our own experience and that of others [12] but its incidence remains unknown. This phenomenon may have been favorably influenced by radiation delivery in a few select cases.…”

Section: Discussionmentioning

confidence: 99%

Neuropathology of Intracranial Arteriovenous Malformations following Conventional Radiation Therapy

Elisevich

Redekop

Muñoz

et al. 1994

Stereotact Funct Neurosurg

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Conventional fractionated radiation therapy was used in 15 patients to treat arteriovenous malformations (AVMs) of the brain deemed inoperable or incompletely obliterated using endovascular or surgical techniques. The AVMs measured from 0.8 to 85 cm³ (mean 28.2 cm³; median 24 cm³). Angiography in 12 patients 1–21 years following radiation therapy demonstrated no significant change in 7, slight reduction in 2, near complete obliteration in 1, and complete obliteration in 2. Magnetic resonance imaging further demonstrated apparent obliteration in one other case. Three irradiated AVMs were available for pathological examination following fatal recurrent hemorrhage after 21 years in case 1 and following surgery after 5 years in cases 2 and 3. Doses of 20 and 45 Gy were delivered to the area of the AVM in 10 and 15 fractions with a 6-MV linear accelerator in case 1 and in cases 2 and 3, respectively. A blinded histopathological comparison was made of the latter cases and three AVMs removed at surgery that were not previously irradiated and that were comparable in size, number of arterial feeders, and location within the brain. Segmental hyalinization of some blood vessels was seen in both irradiated and nonirradiated cases. The single postmortem specimen showed extensive thrombosis but a patent nidus. The findings are in keeping with the clinical impression that conventional fractionated radiation therapy fails to alter the natural history of cerebral AVMs. The favorable outcome of radiosurgery on small- to medium-sized AVMs appears attributable to the shorter duration of therapy using relatively high-dose prescriptions to the nidus.

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“…18,24,27,47,64,72,75,76,80,81,85,86,90,112,116,118 One series of 106 patients with AVMs has demonstrated that > 50% of the lesions increased in size, whereas 9% decreased over a mean period of 8 years without intervention. Remodeling within these lesions can lead to changes in their angiographic appearance over time.…”

mentioning

confidence: 99%

Cerebral arteriovenous malformations. Part 1: cellular and molecular biology

Moftakhar

Hauptman

Malkasian

et al. 2009

FOC

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Object The scientific understanding of the nature of arteriovenous malformations (AVMs) in the brain is evolving. It is clear from current work that AVMs can undergo a variety of phenomena, including growth, remodeling, and/or regression—and the responsible processes are both molecular and physiological. A review of these complex processes is critical to directing future therapeutic approaches. The authors performed a comprehensive review of the literature to evaluate current information regarding the genetics, pathophysiology, and behavior of AVMs. Methods A comprehensive literature review was conducted using PubMed to reveal the molecular biology of AVMs as it relates to their complex growth and behavior patterns. Results Growth factors involved in AVMs include vascular endothelial growth factor, fibroblast growth factor, transforming growth factor β, angiopoietins, fibronectin, laminin, integrin, and matrix metalloproteinases. Conclusions Understanding the complicated molecular milieu of developing AVMs is essential for defining their natural history. Growth factors, extracellular matrix proteins, and other molecular markers will be the key to unlocking novel targeted drug treatments for these brain malformations.

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Spontaneous disappearance of cerebral arteriovenous angioma

Cited by 74 publications

References 4 publications

Spontaneous regression of cerebral arteriovenous malformations: clinical and angiographic analysis with review of the literature

Spontaneous regression of cerebral arteriovenous malformations: clinical and angiographic analysis with review of the literature

Neuropathology of Intracranial Arteriovenous Malformations following Conventional Radiation Therapy

Cerebral arteriovenous malformations. Part 1: cellular and molecular biology

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