Journal of Neuroradiology (2015) 42, 126—131

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CORRESPONDENCES Focal herniation of cerebral parenchyma into transverse sinus Parenchymal herniation of the brain into dural venous sinuses is an extremely rare entity, recently demonstrated on magnetic resonance imaging (MRI) in a few reports

according to our best knowledge [1—3]. The etiology and clinical significance are controversial. Most of the cases were incidentally found. Headache or tinnitus can be seen with brain herniations; however, there is no direct relationship or association between these symptoms and brain herniations. Here, we report a case of 9-year-old girl who presented

Figure 1 Axial T2-weighted (A) MRI shows brain herniation into transverse sinus (star) surrounded by CSF (arrow). Axial fluid attenuated inversion recovery (FLAIR) sequence (B) shows signal suppression in CSF around the herniated parenchyma (arrow). Sagittal contrast-enhanced T1-weighted (C) MRI shows the herniated parenchyma (arrow) isointense with the cerebral parenchyma and no enhancement. 0150-9861/© 2014 Elsevier Masson SAS. All rights reserved.

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to emergency department with mild head trauma. Initial head computerized tomography (CT) incidentally showed a mass in the right transverse sinus suspected of being a tumor. Magnetic resonance imaging revealed a temporal lobe herniation into the transverse sinus surrounded with cerebrospinal fluid (CSF) (Fig. 1). Differentiation of brain herniation from other pathologies is important for the management strategy. A schedule of differential diagnosis for similar conditions seen in the dural venous sinuses include dural venous sinus thrombosis, giant arachnoid granulation, calvarial osseous lesions, meningiomas, metastases, arachnoid cysts, dermoids, epidermoids, and extra-axial hemangiomas, including papillary endothelial hyperplasia [4]. Also, lately a report of transverse-sigmoid sinus aneurysm was published as an etiology of pulsatile tinnitus, which is also suggested to be an embryologic remnant of petrosquamous sinus [5]. However, brain herniation has not been listed in this schedule yet. Hence, it can be added into that list and should be kept in mind as a differential diagnosis. Contrast-enhanced MRI is the useful imaging tool that can determine the herniation of brain parenchyma into the dural venous sinus. The herniated part is isointense with the brain parenchyma in all sequences without contrast enhancement and surrounded by CSF.

Disclosure of interest The authors declare that they have no conflicts of interest concerning this article.

References [1] C ¸ oban G, Yıldırım E, Horasanlı B, et al. Unusual cause of dizziness: occult temporal lobe encephalocele into transverse sinus. Clin Neurol Neurosurg 2013;115:1911—3. [2] Battal B, Castillo M. Brain herniations into the dural venous sinuses or calvarium: MRI of a recently recognized entity. Neuroradiol J 2014;27:55—62. [3] Chan WC, Lai V, Wong YC, et al. Focal brain herniation into giant arachnoid granulation: a rare occurrence. Eur J Radiol Extra 2011;78:e111—3. [4] Trimble CR, Harnsberger HR, Castillo M, et al. Giant arachnoid granulations just like CSF? NOT!! Am J Neuroradiol 2010;31:1724—8. [5] Lenck S, Mosimann PJ, Labeyrie MA, et al. Pulsatile tinnitus caused by an aneurysm of the transverse-sigmoid sinus: a new case report and review of literature. J Neuroradiol 2012;39:276—9.

Ali Kocyigit Duygu Herek ∗ Department of Radiology, Faculty of Medicine, Kinikli Kampusu, Pamukkale University, 20100 Denizli, Turkey Yasemin Isik Balci Department of Pediatrics, Faculty of Medicine, Kinikli Kampusu, Pamukkale University, 20100 Denizli, Turkey ∗

Corresponding author. Department of Radiology, Faculty of Medicine, Kinikli Kampusu, Pamukkale University, 20100 Denizli, Turkey. Tel.: +905326583946; fax: +902582134922. E-mail address: [email protected] (D. Herek) Available online 8 November 2014 http://dx.doi.org/10.1016/j.neurad.2014.05.009

Extensive acute toxic leukoencephalopathy induced by Fludarabine: Two months follow-up on brain MRI Introduction Acute toxic leukoencephalopathy (ATL) is a rare but classical complication of Fludarabin with poor prognosis. Here, we report a case of Fludarabin toxicity with four successive MRI during follow-up that reveal new data about its extension and the evolution of diffusion-weighted imaging (DWI) in specific areas.

Case report A 51-year-old man, with a diagnosis of type IV acute myelogenous leukemia, underwent a first chemotherapy (Cytarabine + Daunorubicine) in March. In May and July, he underwent consolidation chemotherapies based on 5-day infusion of Cytarabine and Clofarabine. Remission was obtained and he was conditioned for a blood marrow transplant (BMT) with 5-day of Cyclophosphamide and Fludarabine (40 mg/m2 per day) followed by a single total body irradiation of 2 Gy the day before the BMT. The BMT was done on September the 11th associated with immunosuppressive graft prophylaxis (Cyclosporine + Mycophenolate mofetil). Prior to the BMT, blood analysis only revealed slightly altered renal function (Creatine = 120 ␮mol/L). In October the 10th, about four weeks after the BMT (and its preparation by Cyclophosphamide + Fludarabine + irradiation), he complained of blurred vision. The ophtalmologic examination revealed bilateral and acute decreased visual acuity but without oculomotor palsy. The lumbar puncture, performed three days later, was strictly normal. Polymerase chain reactions for Adenovirus, CMV, HIV, HHV-6, VZV, EBV, JC virus were all negative as well as CSF analysis for Aspergillus, Toxoplasmosis and Cryptococcus. Brain CT scan before and after iodine contrast injection was normal. The day after, the patient developed a complete blindness. A first brain MRI at 1.5 Tesla, initially considered as normal, exposed only equivocal bilateral and symmetric linear T2-FLAIR hypersignal in occipital deep white matter along the optical radiations on axial 2D — T2-FLAIR sequence (Fig. 1). As Cyclosporine ocular toxicity was initially suspected, Cyclosporine was stopped and a 2 mg/kg per day corticotherapy begun on October the 15th, without any efficiency. The clinical status progressively worsened, blindness being associated with confusion and frontal syndrome after few days. A second brain MRI (Fig. 1) at 1.5 Tesla was performed on October the 24th that showed high T2 signal bilaterally and symmetrically, without mass effect, following the optical radiations. These areas showed high signal on diffusion-weighted imaging (DWI, b = 1000 s/mm2 , slice thickness = 5 mm) and ADC restriction. Gadolinium injection did not reveal any enhancement. Finally, the clinical status of the patient further worsened and he developed lethargy, bilateral pyramidal syndrome

Focal herniation of cerebral parenchyma into transverse sinus.

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