|Results 1-1||<< Back|
Mentions: The anatomical and dynamic characteristics of vein of Galen malformation are studied by transcranial Doppler ultrasonography and cross-sectional imaging including computed tomography and magnetic resonance imaging. Color Doppler imaging demonstrates hemodynamic disturbances of the malformation and 2D imaging shows parenchymal changes such as atrophy and encephalomalacia [Figure 3]. Parenchymal calcifications due to chronic venous hypertension and ventricomegaly may be demonstrated.[33–35] Plain and contrast enhanced CT scan reveals abnormally “dilated vein of Galen” in the midline and hydrocephalus. Thrombus and calcification in its wall may be seen [Figure 4]. Brain atrophy, parenchymal calcification or hemorrhage, and brain stem compression can be appreciated. Of interest is to note curvilinear peripheral rim calcification in the midline in the region of pineal gland on the plain X rays [Figure 5]. Magnetic resonance imaging supplemented by MR angiography and MR venography reveal the venous anomalies in greater detail [Figure 6]. Hemorrhagic components are better shown by MR evaluation. Digital subtraction angiography including both vertebral and both carotid arterial examinations identifies the precise type of the malformation delineating both the arterial feeders and venous drainage. Angiographically four types are identified. Type I is an enlarged and tortuous midline venous varix having multiple feeding arteries into its wall. Generally the feeding arteries are the branches of anterior and posterior choroidal arteries, pericallosal arteries, and superior cerebellar arteries. Transmesencephalic and transdiencephalic perforators establish fistulous connection within the wall of the midline persistent vein in type II. Type III is a combination of types I and II. Secondary dilatation of the vein of Galen due to hemodynamic overload through the venous outflow by a mesencephalic, diencephalic, or cerebellar arteriovenous malformation is classified as type IV. Collateral venous pathways, reflux into dural sinuses and cortical venous rerouting are best revealed by angiography which have significant strategic implications during endovascular therapy. Stenosis or occlusion of the outflow at the straight sinus, torcula, dural sinuses, or internal jugular vein is well seen in the venous phase of angiograpy. Anomalies of dural sinuses, duplications, fenestrations, falcine sinus, falcine loop, and suboccipital sinuses are apparent on careful examination of the delayed venous images [Figure 7]. These structures may appear very early in the arterial phase itself because of high flow across the arteriovenous communications.
Pediatric aneurysms and vein of Galen malformations
Bottom Line: Based on the degree of AV shunting they may present with failure to thrive, with hydrocephalus or in severe cases with heart failure.Rarely transtorcular approach is needed.These cases should be managed by an experienced neurointerventionist.
Affiliation: Department of Radiodiagnosis and Imaging, Kasturba Hospital, Manipal, India.
Pediatric aneurysms are different from adult aneurysms - they are more rare, are giant and in the posterior circulation more frequently than in adults and may be associated with congenital disorders. Infectious and traumatic aneursyms are also seen more frequently. Vein of Galen malformations are even rarer entities. They may be of choroidal or mural type. Based on the degree of AV shunting they may present with failure to thrive, with hydrocephalus or in severe cases with heart failure. The only possible treatment is by endovascular techniques - both transarterial and transvenous routes are employed. Rarely transtorcular approach is needed. These cases should be managed by an experienced neurointerventionist.