A Comparison of the Clinical Profile of Cavernous Malformations with and without Associated Venous Malformations

Abdulrauf, Saleem I.; Kaynar, Mehmet Yaşar; Awad, Issam A.

doi:10.1097/00006123-199901000-00020

Cited by 186 publications

(123 citation statements)

References 30 publications

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“…Cases were classified as sporadic if they harbored a solitary lesion (or cluster of lesions with associated developmental venous anomaly). 5,16 Lesion burden was cataloged including the number of CCM lesions seen on T2-weighted images and on SWI sequences in each case. 16 If the patient had 4100 lesions on SWI images, the number of lesions counted was considered as 100.…”

Section: Extraction Of Clinical Parametersmentioning

confidence: 99%

Vascular Permeability in Cerebral Cavernous Malformations

Mikati

Khanna

Zhang

et al. 2015

J Cereb Blood Flow Metab

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Patients with the familial form of cerebral cavernous malformations (CCMs) are haploinsufficient for the CCM1, CCM2, or CCM3 gene. Loss of corresponding CCM proteins increases RhoA kinase-mediated endothelial permeability in vitro, and in mouse brains in vivo. A prospective case-controlled observational study investigated whether the brains of human subjects with familial CCM show vascular hyperpermeability by dynamic contrast-enhanced quantitative perfusion magnetic resonance imaging, in comparison with CCM cases without familial disease, and whether lesional or brain vascular permeability correlates with CCM disease activity. Permeability in white matter far (WMF) from lesions was significantly greater in familial than in sporadic cases, but was similar in CCM lesions. Permeability in WMF increased with age in sporadic patients, but not in familial cases. Patients with more aggressive familial CCM disease had greater WMF permeability compared to those with milder disease phenotype, but similar lesion permeability. Subjects receiving statin medications for routine cardiovascular indications had a trend of lower WMF, but not lesion, permeability. This is the first demonstration of brain vascular hyperpermeability in humans with an autosomal dominant disease, as predicted mechanistically. Brain permeability, more than lesion permeability, may serve as a biomarker of CCM disease activity, and help calibrate potential drug therapy.

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Section: Extraction Of Clinical Parametersmentioning

confidence: 99%

Vascular Permeability in Cerebral Cavernous Malformations

Mikati

Khanna

Zhang

et al. 2015

J Cereb Blood Flow Metab

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“…1,51,55,76,77 A higher incidence of coinciding lesions (86%) was found when postoperative pathology reports were included in the analysis, or when CT angiograms (60%) were used as a diagnostic tool, 27,51 as opposed to MR imaging alone. 1 The radiological association between DVAs and CMs is much more commonly seen in infratentorial CMs (Fig. 3) than in their supratentorial counterparts (Fig.…”

Section: Parenchymal Dvas Associated With Cmsmentioning

confidence: 99%

The putative role of the venous system in the genesis of vascular malformations

Aboian

Daniels

Rammos

et al. 2009

FOC

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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 describe the potential significance of different associations of these vascular anomalies.

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“…[15] Currently, due to progress in brain investigation, they can be diagnosed with a higher frequency. [16][17][18][19][20] DVAs are the most commonly encountered vascular malformation in the CNS, accounting for up to 60% of them. Their prevalence is about 2.5% to 9%, [21] and they are usually solitary.…”

Section: Discussionmentioning

confidence: 99%

New Trends in Management of Epilepsy in Patients with Cerebral Venous Malformations: Our Experience

Artyukhov¹,

Дмитренко²,

Shnayder³

et al. 2016

Int J Biomed

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Background: Venous vascular malformations, also known as venous angiomas or, more exactly, developmental venous anomalies (DVAs), represent congenital, anatomically variant pathways in the normal venous drainage of the brain area. In general neurological practice, DVAs are not considered epileptogenic, therefore, in conducting neuroimaging as a rule, not taken into account. A positive correlation, however, between the location of DVAs and the electroencephalographic seizure focus is debated. Materials and Methods:The present study provides a complete analysis of clinical and MRI characteristics of symptomatic epilepsies associated with cerebral venous malformations in children and adults. Patients were selected after a retrospective search through the database of the University Clinic into which, since 2016, patients were prospectively entered. To date (February 2016), there is a total of 5,856 patients with epilepsy of which there are 105 patients with congenital malformations of the brain, and 32 of them were found to have principal diagnosis of DVA.Results: Cavernous angiomas prevailed among venous anomalies (53.1%); DVAs were registered in 46.9% of cases. The associated analysis of DVA localization and the epileptic seizure types showed a direct relationship in 60.0% cases.Conclusion: DVAs as a cause of seizures are important to consider when examining patients with epileptic seizures. (Int J Biomed. 2016;6(3):207-212.).

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A Comparison of the Clinical Profile of Cavernous Malformations with and without Associated Venous Malformations

Cited by 186 publications

References 30 publications

Vascular Permeability in Cerebral Cavernous Malformations

Vascular Permeability in Cerebral Cavernous Malformations

The putative role of the venous system in the genesis of vascular malformations

New Trends in Management of Epilepsy in Patients with Cerebral Venous Malformations: Our Experience

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