Elsevier

Clinical Radiology

Volume 58, Issue 3, March 2003, Pages 251-256
Clinical Radiology

De Novo Formation of a Cavernous Malformation of the Brain in the Presence of a Developmental Venous Anomaly

https://doi.org/10.1016/S0009-9260(02)00470-1Get rights and content

Introduction

Cavernous malformations and developmental venous anomalies (DVA) have been detected with increasing frequency in the brain using computed tomography (CT) and magnetic resonance imaging (MRI). Although reports have been published describing the association between these two vascular malformations of the brain, there is still continuing debate about the reason for this association 1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11. Some theories have been proposed for the de novo formation of non-familial form of cavernous malformations in the patients with a known DVA, based on a few cases reported in the literature 1, 2, 4, 10, 12, 13, 14, 15, 16.

We present serial medical imaging studies including CT, MRI, and angiography of a patient with an incidentally detected cerebral DVA, in whom formation of an adjacent cavernous malformation has been observed over a period of 3 years.

Section snippets

Case Report

A 35-year-old man patient presented with a throbbing headache, that had been gradually increasing over a period of 2 years. CT of the brain was performed (Siemens Somatom Plus 4, Erlangen, Germany) with 5 mm-slice thickness. Unenhanced studies revealed a linear hyperdense structure along the right thalamus, internal capsule, and head of caudate nucleus. There were minute calcifications within this. After intravenous administration of iodinated contrast material, the linear structure showed

Discussion

Cavernous malformations or cavernomas are the most common angiographically detected occult vascular malformations. They are angiogenically immature lesions with endothelial proliferation and increased neoangiogenesis. Their prevalence is thought to be around 0.5%. Almost 75% of cavernomas are solitary sporadic lesions, whereas 10–30% are part of the multiple familial form 2, 4, 6, 10, 13. They are discrete, lobulated, and bluish-purple nodules with pseudocapsule consisting of gliotic,

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    There is an equal prevalence in women and men.11-15 Although initially thought to be congenital lesions, CMs are now known to be acquired, as confirmed by many reports of patients with normal MRI findings who later developed a CM.16-24 Data demonstrating an increasing prevalence of CM with age also support an acquired etiology.25

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    Many authors favor the hypothesis, proposing that venous congestion associated with a DVA could cause ischemia or repeated microhemorrhage, leading to reactive angiogenesis and formation of cavernoma (6,32–34). This hypothesis is strengthened by reports of de novo cavernomas and cavernoma-like lesions developing in the drainage territories of DVAs (35–39). Additional support derives from the natural history of concurrent lesions; cavernomas associated with DVA are more likely to have symptomatic and repeated hemorrhage than cavernomas without DVA, which may be related to venous congestion in the associated DVA (40).

  • Long-Term Outcome of Gamma Knife Radiosurgery for Brain Cavernoma: Factors Associated with Subsequent De Novo Cavernoma Formation

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    To our knowledge, the nonfamilial type of de novo cavernoma was first described in 1997.12 De novo cavernoma formations can develop because of multiple factors, such as intracerebral hemorrhage, developmental venous anomaly (DVA), radiation, mesial temporal sclerosis, surgery, and traumatic injury.13-23 Chiu and Phatouros20 proposed that brain cavernoma could be formed by angiogenic proliferation secondary to microhemorrhage.

  • Pathology of cavernous malformations

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    One theory is that sporadic CMs may develop from a pre-existing DVA as a result of diapedesis of red blood cells (Dillon, 1997). There are reported cases and small case series that support this hypothesis (Pozzati et al., 1989; Maeder et al., 1998; Cakirer, 2003; Campeau and Lane, 2005; Wurm et al., 2005); however, this does not account for sporadic CMs that develop without DVAs. Familial CMs have been reported to have a more aggressive course (Maiuri et al., 2006; Petersen et al., 2010).

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    Selection bias may exist. But one consistent finding is that brainstem hemorrhage from DVA is rare [4–28]. Theoretically, after to a “negative” digital subtraction angiography study, coexistent CM should be excluded before the hemorrhage is attributed to the DVA.

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