Developmental venous anomalies (DVAs), previously called venous angiomas, are the most frequently encountered cerebral vascular malformations. However, DVA is considered to be rather an extreme developmental anatomical variation of medullary veins than true malformation. DVAs are composed of dilated medullary veins converging centripetally into a large collecting venous system that drains into the superficial or deep venous system. Their etiology and mechanism are generally accepted that DVAs result from the focal arrest of the normal parenchymal vein development or occlusion of the medullary veins as a compensatory venous system. DVAs per se are benign and asymptomatic except for under certain unusual conditions. The pathomechanisms of symptomatic DVAs are divided into mechanical, flow-related causes, and idiopathic. However, in cases of DVAs associated with hemorrhage, cavernous malformations (CMs) are most often the cause rather than DVAs themselves. The coexistence of CM and DVA is common. There are some possibilities that DVA affects the formation and clinical course of CM because CM related to DVA is generally located within the drainage territory of DVA and is more aggressive than isolated CM in the literature. Brain parenchymal abnormalities surrounding DVA and cerebral varix have also been reported. These phenomena are considered to be the result of venous hypertension associated with DVAs. With the advance of diagnostic imagings, perfusion study supports this hypothesis demonstrating that some DVAs have venous congestion pattern. Although DVAs should be considered benign and clinically silent, they can have potential venous hypertension and can be vulnerable to hemodynamic changes.

obJective The middle meningeal artery (MMA) is suspected to play an important role in the development of chronic subdural hematoma (CSDH). The aim of this study was to clarify whether the MMA was enlarged in patients with CSDHs. Methods The authors retrospectively assessed 55 patients in whom CSDH was diagnosed between 2010 and 2014 and who underwent MR angiography (MRA) after the onset of CSDH. The authors compared MMA diameters between hemispheres with and without CSDHs on MR angiograms. A case-control study was also performed with 55 sex- and age-matched patients with incidental unruptured aneurysms as controls. results In 55 patients with CSDHs, the diameters of the 79 MMAs on the CSDH side were significantly larger than the diameters of the 31 MMAs on the non-CSDH side (p < 0.05). In 24 patients with bilateral CSDHs, no significant difference was found between the MMA diameters on the larger hematoma side and those on the smaller hematoma side. In 13 patients who underwent MRA before the onset of the CSDH, the MMAs on MR angiograms acquired after onset of the CSDH were significantly larger than those on MR angiograms acquired before the CSDH onset (p < 0.05). The diameters of the MMAs in 55 patients with CSDHs were significantly larger than those of the MMAs in the 55 control patients (p < 0.05). coNclusioNs The MMA is enlarged with development of a CSDH. Information about the MMA observed on MRA in patients with CSDHs may be useful in developing a strategy for future treatment of CSDHs.

Object The purpose of this study is to analyze the clinical presentation, morphological characteristics, angio-architecture, and outcome of vertebrobasilar dissection (VBD) in the pediatric population. Methods The authors retrospectively reviewed 29 consecutive cases involving children younger than 16 years of age who were diagnosed with symptomatic VBDs. Data were gathered with respect to the patient's age, sex, clinical history, associated underlying disease, and symptoms (headache, vertigo) as well as the location of the dissection and the imaging appearance. Results The patients' mean age was 8.24 years (range 2 months–15 years). There was an overall 3:1 male predominance, although among children older than 8 years, girls and boys were similarly affected. Hemorrhagic dissections occurred in 10 of 29 cases. In nonhemorrhagic dissections, stroke occurred in 16 cases, with the most common presenting symptoms being headaches and vertigo; in the other 3 cases, mass effect due to a chronic dissecting aneurysm was present. In 7 children an underlying vessel wall disease was found. The location of the dissection was extradural in 11 cases and intradural in the remainder. There was no preference with respect to side. The basilar artery was affected in 9 patients. Conclusions The imaging appearance and clinical presentation of symptomatic VBDs in the pediatric population differs from that in adults. Boys are more often affected, especially at younger ages, and hemorrhagic presentation is more common, presumably owing to the fact that the basilar artery is more commonly involved. Depending on the pathogenetic mechanism underlying the dissection, different clinical symptoms will evolve, necessitating individually tailored treatment.

Spontaneous resolution of intradural dissecting aneurysm with or without parent artery occlusion is not uncommon even in the pediatric population. Aneurysm repair is a dynamic and multifaceted entity. Mural hematoma appears to be the most important factor promoting thrombosis and healing of the dissecting intracranial aneurysms.