Reversible Cortical Hypointensity on T2*‐Weighted MR Image After Embolization for Cerebral Dural Arteriovenous Fistula

Abstract

Cerebral DAVF is one of the vascular malformations with abnormal blood flow via arteriovenous shunts into veins, leading to venous hypertension or the obstruction of venous drainage. It may cause venous infarction and intraparenchymal or subarachnoid hemorrhage. Especially, a subsequent attack is likely to become a serious event for patients with a previous history of cerebral hemorrhage. MRI is a noninvasive tool for diagnosing DAVF. However, conventional MRI usually only shows normal findings in cases without retrograde cortical venous drainage (RCVD). In these patients with DAVF with RCVD, dilated veins can be sometimes observed on the surface of the brain on certain MRI sequences (eg, contrastenhanced T1-weighted images and susceptibility-weighted images [SWI]), and abnormal venous structures are sometimes observed on MR angiography. For those cases with subsequent ictus, various MRI signal changes can often be found, and those include subcortical edema, hemorrhage, calcification, or venous infarction. Thus, the accurate prospective diagnosis of DAVF may not be straightforward in such cases. T2*-weighted imaging (T2*WI) is an MRI sequence that enables detection of hemorrhagic lesions as hypointensity areas. The finding has been generally recognized as being caused by an accumulation of hemosiderin, which tends to last for a long period of time. However, to our knowledge, there has been no report that described the disappearance of a T2*WI finding associated with DAVF. Herein, we present a novel MRI finding, ie, gyriform hypointensity on T2*WI involving the cerebral cortex that completely vanished after successful embolization of the cerebral DAVF. This is potentially a unique sign that contributes to the accurate diagnosis of cerebral DAVF. A 48-year-oldmanwas referred to our hospital with seizures lasting for several seconds and consciousness disturbance. No other neurological deficits were noted. Brain computed tomography (CT) images showed no abnormal findings suggestive of hemorrhage or calcification (Fig. 1). T1-weighted MR images (Discovery MR750w; GE Healthcare, Waukesha, WI) revealed no findings suggestive of hemorrhage (Fig. 2). Fluid attenuation inversion recovery (FLAIR) images revealed hyperintensity at the subcortex of the right superior frontal gyrus. This finding was considered to correspond with subcortical edema. T2*WI showed gyriform hypointensity along the cerebral cortex (Fig. 3). The parameters of T2*WI were as follows: gradient echo, flip angle: 15 degrees, echo time: 20 msec, repetition time: 800 msec, field of view: 230 mm, slice thickness: 5.0 mm, acquisition time: 157 sec, number of slices: 24. Contrast-enhanced T1-weighted images showed a dilated cortical vein in the cerebrospinal fluid space. Selective middle meningeal angiography revealed reflux of the cortical veins at the arterial phase, which is suggestive of DAVF (Borden type III, Cognard type IV) (Fig. 4). Embolization was successfully performed with n-butyl-2-cynaoacrylate (NBCA; Histoacryl, B. Braun, Melsungen, Germany). Postprocedural angiography showed the disappearance of the arteriovenous shunt. The patient’s symptoms, such as seizures, subsequently improved. MRI 3 months after embolization showed that hypointensity on T2*WI along the cortex disappeared (Fig. 5). FLAIR also revealed that the subcortex of the right superior frontal gyrus was normal. The present case report describes a novel MRI finding: hypointensity on T2*WI at the cerebral cortex due to cerebral DAVF that completely disappeared after embolization. The pathogenesis of this finding can be considered an interesting issue to be investigated. In DAVF, hypointensity on T2*WI along the cortex generally suggests the deposition of hemosiderin secondary to hemorrhage or calcification, which are irreversible in most cases. In the present case, hypointensity that matched the cortex completely disappeared after embolization. Therefore, this MRI finding was not considered to be hemorrhage or calcification. Hypointensity on T2*WI at the surface of the cortex in DAVF may be considered superficial siderosis. However, the disappearance of gyriform hypointensity within a few months was apparently inconsistent with the assumption of superficial siderosis. Regarding the similar findings to those of the present case, Hu et al reported gyriform hypointensity along the cortex on SWI in a case of Sturge–Weber syndrome. These findings corresponded to necrosis, gliosis, and cortical calcification that led by venous stasis at the cortex with underlying leptomeningeal angiomatosis. Venous stasis may induce an increase in local deoxyhemoglobin