Perinidal Dilated Capillary Networks in Cerebral Arteriovenous Malformations

Sato, Sonomi; Kodama, Namio; Sasaki, Tatsuya; Matsumoto, Masato; Ishikawa, Toshihito

doi:10.1227/01.neu.0000097518.57741.be

Cited by 60 publications

(34 citation statements)

References 23 publications

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“…7 The inhomogeneous distribution of discrete perfusion abnormalities can be better explained by local differences in the arteriolar angioarchitecture than by the hemispheric asymmetry and the arterioarterial redistribution on a macrovascular level that we observed. Both levels of perfusion impairment are visible in Fig 3. The local CBF decrease is compatible with recent histologic reports of a perinidal dilated capillary network in 85%-100% of patients with AVM 24,25 and may be due to an exhausted compensatory mechanism. These capillaries are connected not only to the nidus, feeding arteries, and draining veins via arterioles and venules but also to normal capillaries, arterioles, and venules.…”

Section: Discussionsupporting

confidence: 90%

“…These capillaries are connected not only to the nidus, feeding arteries, and draining veins via arterioles and venules but also to normal capillaries, arterioles, and venules. The perinidal brain parenchyma has been reported to show significant ischemic changes, 24,25 though a previous diffusion-weighted imaging study did not reveal perinidal ischemia in unselected patients with AVM. 14 The conclusions that can be drawn from our study are limited by the low number of patients and high variability of brain AVMs.…”

Section: Discussionmentioning

confidence: 95%

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Territorial and Microvascular Perfusion Impairment in Brain Arteriovenous Malformations

Fiehler¹,

Illies²,

Piening³

et al. 2008

AJNR Am J Neuroradiol

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Section: Discussionsupporting

confidence: 90%

Section: Discussionmentioning

confidence: 95%

Territorial and Microvascular Perfusion Impairment in Brain Arteriovenous Malformations

Fiehler¹,

Illies²,

Piening³

et al. 2008

AJNR Am J Neuroradiol

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“…These factors cause the reactivation of quiescent endothelium, breakdown of vessel walls, and the fusion of perinidal capillaries with the nidus, enlarging the AVM. 60 On the cellular level, AVMs are dynamic lesions, expanding or shrinking depending on the concentration of inflammatory cytokines and the expression of angiogenic factors and receptors on ECs. AVM ECs express elevated amounts of VEGF-A, -B, -C, -D, and VEGF receptor-1.…”

Section: Angiogenesis In Avms and The Link To Inflammationmentioning

confidence: 99%

Biology of Cerebral Arteriovenous Malformations with a Focus on Inflammation

Mouchtouris

Jabbour

Starke

et al. 2014

J Cereb Blood Flow Metab

124

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Cerebral arteriovenous malformations (AVMs) entail a significant risk of intracerebral hemorrhage owing to the direct shunting of arterial blood into the venous vasculature without the dissipation of the arterial blood pressure. The mechanisms involved in the growth, progression and rupture of AVMs are not clearly understood, but a number of studies point to inflammation as a major contributor to their pathogenesis. The upregulation of proinflammatory cytokines induces the overexpression of cell adhesion molecules in AVM endothelial cells, resulting in enhanced recruitment of leukocytes. The increased leukocyte-derived release of metalloproteinase-9 is known to damage AVM walls and lead to rupture. Inflammation is also involved in altering the AVM angioarchitecture via the upregulation of angiogenic factors that affect endothelial cell proliferation, migration and apoptosis. The effects of inflammation on AVM pathogenesis are potentiated by certain single-nucleotide polymorphisms in the genes of proinflammatory cytokines, increasing their protein levels in the AVM tissue. Furthermore, studies on metalloproteinase-9 inhibitors and on the involvement of Notch signaling in AVMs provide promising data for a potential basis for pharmacological treatment of AVMs. Potential therapeutic targets and areas requiring further investigation are highlighted.

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“…Dysplastic capillaries appear tortuous and enlarged. 31 Thus, to create an objective measurement of vessel dysplasia, we used capillary diameter (Ͼ10 m) as a variable. The Dysplasia Index was calculated as the number of dysplastic capillaries per 200 capillaries examined.…”

Section: Quantitative Assessment Of Vessel Morphologymentioning

confidence: 99%

Reduced Expression of Integrin αvβ8 Is Associated with Brain Arteriovenous Malformation Pathogenesis

Kim

Pawlikowska

et al. 2010

The American Journal of Pathology

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Brain arteriovenous malformations (BAVMs) are a rare but potentially devastating hemorrhagic disease. Transforming growth factor-␤ signaling is required for proper vessel development, and defective transforming growth factor-␤ superfamily signaling has been implicated in BAVM pathogenesis. We hypothesized that expression of the transforming growth factor-␤ activating integrin, ␣v␤8, is reduced in BAVMs and that decreased ␤8 expression leads to defective neoangiogenesis. We determined that ␤8 protein expression in perivascular astrocytes was reduced in human BAVM lesional tissue compared with controls and that the angiogenic response to focal vascular endothelial growth factor stimulation in adult mouse brains with local Cre-mediated deletion of itgb8 and smad4 led to vascular dysplasia in newly formed blood vessels. In addition, common genetic variants in ITGB8 were associated with BAVM susceptibility, and ITGB8 genotypes associated with increased risk of BAVMs correlated with decreased ␤8 immunostaining in BAVM tissue. These three lines of evidence from human studies and a mouse model suggest that reduced expression of integrin ␤8 may be involved in the pathogenesis of sporadic BAVMs. (Am J Pathol

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Perinidal Dilated Capillary Networks in Cerebral Arteriovenous Malformations

Cited by 60 publications

References 23 publications

Territorial and Microvascular Perfusion Impairment in Brain Arteriovenous Malformations

Territorial and Microvascular Perfusion Impairment in Brain Arteriovenous Malformations

Biology of Cerebral Arteriovenous Malformations with a Focus on Inflammation

Reduced Expression of Integrin αvβ8 Is Associated with Brain Arteriovenous Malformation Pathogenesis

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