Perfusion MR imaging and proton MR spectroscopic imaging in differentiating necrotizing cerebritis from glioblastoma multiforme

Abstract

We describe a lesion with the magnetic resonance imaging (MRI) characteristics of a glioblastoma mutiforme and demonstrate how perfusion MRI and proton MR spectroscopic imaging can be used to differentiate necrotizing cerebritis from what appeared to be a high-grade glioma. A 43-year-old woman presented to her physician complaining of progressive visual disturbance and headache for several weeks. Conventional MRI demonstrated a parietal peripherally enhancing mass with central necrosis and moderate to severe surrounding T2 hyperintensity, suggesting an infiltrating high-grade glioma. However, advanced imaging, including dynamic susceptibility contrast MRI (DSC MRI) and magnetic resonance spectroscopic imaging (MRSI), suggested a nonneoplastic lesion. The DSC MRI data demonstrated no hyperperfusion within the lesion and surrounding T2 signal abnormality, and the MRSI data showed overall decrease in metabolites in this region, except for lactate. Because of the aggressive appearance to the lesion and the patients' worsening symptoms, a biopsy was performed. The pathologic diagnosis was necrotizing cerebritis. After the commencement of steroid therapy, imaging findings and patient symptoms improved. This report will review the utility of advanced imaging for differentiating inflammatory from neoplastic appearing lesions on conventional imaging.

Primary Central Nervous System Angiitis

“…In an adult case of PCNSA, Pivawer reported that MRSI did not show any rise in choline (Cho) but, rather, an overall decrease in metabolites (Pivawer et al 2007). In pseudotumor PCNSA cases, Panchal and Beppu reported that MRSI was less useful for diagnosis because it displayed a non-specific pattern similar to that of a malignant neoplasm with a significant elevation of choline (Cho) and creatinine (Cr) peaks suggesting respectively an increased cell turnover and an energy-dependent system.…”

“…The wide spectrum of protean clinical signs is related to ischemia which affects any part of the brain and can be micro-or macroscopic, focal, multifocal or diffuse. It contrasts with the paucity of extraneurologic signs and the preserved general state, at least at the beginning of the disease's evolution (Younger 2004;Rosenbaum et al 1998;Soloman et al 2000;Hajj-Ali et al 2002;Zuber 2005;Noskin et al 2006;Calabrese et al 2007;Pivawer et al 2007). All the combinations between the various following manifestations are possible, but the triad of headache, organic brain syndrome, and multifocal neurologic deficits is most suggestive (Salvarani et al 2007(Salvarani et al , 2008a: -Headache (63%), typically persistent, insidious and progressive, sometimes accompanied by other signs of intracranial hypertension with nausea and vomiting; -Diffuse encephalopathy signs including altered cognitive function (50%) and amnestic syndrome (9%); -Focal neurological signs including:…”

“…Anatomically, the angiitic process has a focal and segmental distribution which explains the possibility of false-negative biopsy results. Within the wall, inflammation affects primarily the intimal layer, but may spread to all layers causing a transmural vasculitis, and preservation of the media is commonly observed (Zuber et al 1999;Moritani et al 2004;Pivawer et al 2007). …”

“…Through the determination of the relative cerebral blood volume (rCBV), cerebral blood flow (CBF), mean transit time (MTT), and time to peak, PWI can currently directly assess hypoperfusion at the microcirculatory level and identify the hypoperfused territories not detected by conventional MRI and CCA (Pivawer et al 2007). For these reason, PWI is particularly helpful, when the MRI study is normal, to initiate the therapy without a brain biopsy (Wasserman et al 2001).…”

“…Sometimes, abnormalities are only observed at the time of a second CCA, because of progression of the inflammatory infiltration towards larger arteries, whereas the initial examination was normal (Zuber 2005). The other less typical findings include micro-aneurysms induced by vascular wall fragility, single or multiple arterial cut-offs related to vascular occlusion, vessel walls irregularities, delayed vessel emptying, and development of new anastomotic collateral branches (Moore 1998;Zuber et al 1999;Hajj-Ali et al 2002;Moritani et al 2004;Aviv et al 2006;Pivawer et al 2007). CCA could also help to monitor any changes.…”