Asim K. Bag

Imaging manifestations of progressive multifocal leukoencephalopathy.

Progressive multifocal leukoencephalopathy (PML) is a demyelinating disease caused by reactivation of JC virus in immunosuppressed patients. The diagnosis is usually suggested on imaging and confirmed by cerebrospinal fluid polymerase chain reaction (PCR) for JC virus DNA. In this article, we review the imaging manifestations of PML on computed tomography (CT), magnetic resonance imaging (MRI), diffusion-weighted imaging (DWI), diffusion tensor imaging (DTI), MR spectroscopy, single photon-emission computed tomography (SPECT) and positron-emission tomography (PET), and outline the role of imaging in follow-up and prognostication.

JC Virus Infection of the Brain

SUMMARY: Since its initial description, there have been significant changes in the epidemiology, pathogenesis, and clinical and imaging manifestations of JCV infection of brain. The most common clinical manifestation is PML. Other recently described CNS manifestations are JCE, JCVGCN, and JCM. Although AIDS is the most common predisposing factor for JCV reactivation, there is increasing incidence of brain manifestations of JCV reactivation in non-HIV settings, including different rheumatologic, hematologic, and oncologic conditions; monoclonal antibody therapy; transplant recipients; primary immunodeficiency syndromes; and even in patients without any recognizable immune deficiency. IRIS may develop secondary to restoration of immunity in HIV-positive patients with PML receiving antiretroviral therapy. This is of profound clinical significance and needs to be diagnosed promptly. Imaging plays a crucial role in the diagnosis of the disease, monitoring of treatment response, identifying disease progression, and predicting prognosis. In this article, current understanding of the epidemiology, pathogenesis, clinical presentations, and all aspects of imaging of JCV infection of the brain have been comprehensively reviewed.

Intravesical wire as foreign body in urinary bladder

Foreign bodies in the urinary bladder are frequently the objects of jokes among doctors, but they may sometimes cause serious implications to the patients. Here we present our experiences in 3 such cases where long segments of wire were introduced into the urinary bladder through the urethra.

Petrous Apex Lesions: Pictorial Review

Received January 19, 2010; accepted after revision August 4, 2010. 1Department of Radiology, Division of Neuroradiology, University of Alabama at Birmingham Medical Center, 619 19th St S, WP-150, Birmingham, AL 35249-6830. Address correspondence to A. K. Bag (abag@uabmc.edu). 2Present address: Department of Radiology, Edward Hines Jr VA Hospital, Hines, IL. AJR 2011; 196:WS26–WS37 0361–803X/11/1963–WS1

Effects of anti-angiogenesis on glioblastoma growth and migration: model to clinical predictions.

Glioblastoma multiforme (GBM) causes significant neurological morbidity and short survival times. Brain invasion by GBM is associated with poor prognosis. Recent clinical trials of bevacizumab in newly-diagnosed GBM found no beneficial effects on overall survival times; however, the baseline health-related quality of life and performance status were maintained longer in the bevacizumab group and the glucocorticoid requirement was lower. Here, we construct a clinical-scale model of GBM whose predictions uncover a new pattern of recurrence in 11/70 bevacizumab-treated patients. The findings support an exception to the Folkman hypothesis: GBM grows in the absence of angiogenesis by a cycle of proliferation and brain invasion that expands necrosis. Furthermore, necrosis is positively correlated with brain invasion in 26 newly-diagnosed GBM. The unintuitive results explain the unusual clinical effects of bevacizumab and suggest new hypotheses on the dynamic clinical effects of migration by active transport, a mechanism of hypoxia-driven brain invasion.

Diffusion Tensor Imaging in Hypertrophic Olivary Degeneration

SUMMARY: We report DTI and fiber tractography findings in a case of hypertrophic olivary degeneration. A 51-year-old man presented with an abnormal gait and visual difficulties. MR imaging showed enlargement of the right medullary olive and a vascular lesion in the right pontine tegmentum. Fiber tractography showed decreased volume of the right central tegmental tract, supporting a diagnosis of HOD.

Neurodegeneration with Brain Iron Accumulation: Clinicoradiological Approach to Diagnosis

Discovery of genetic abnormalities associated with neurodegeneration with brain iron accumulation (NBIA) has led to use of a genetic‐based NBIA classification schema. Most NBIA subtypes demonstrate characteristic imaging abnormalities. While clinical diagnosis of NBIA is difficult, analysis of both clinical findings and characteristic imaging abnormalities allows accurate diagnosis of most of the NBIA subtypes. This article reviews recent updates in the genetic, clinical, and imaging findings of NBIA subtypes and provides a practical step‐by‐step clinicoradiological algorithm toward clinical diagnosis of different NBIA subtypes.

Neuroimaging: Intrinsic Lesions of the Central Skull Base Region

The sphenoid bone is the osseous foundation of the central skull base. The body of the sphenoid is cuboid in shape and its posterior margin is joined to the basilar occipital bone (basiocciput) via a synchondrosis to form the complete clivus. Traditionally, radiologic discussions of intrinsic disease of the central skull base emphasize marrow space-occupying lesions including metastatic disease, myeloma, and chordoma. Based on our practical experience and the anatomical boundaries of the central skull-based region put forth, we include lesions of the sphenoid sinus and petrous apex in our discussion. We describe lesions that might originate within, be confined to, or principally involve the skeletal foundation of the central skull base, including the pneumatized regions contained within. Intrinsic lesions affecting the central skull base are emphasized and the most important computed tomography and magnetic resonance imaging findings that allow for effective diagnosis, planning, and treatment are highlighted.

Are There Differences between Macrocyclic Gadolinium Contrast Agents for Brain Tumor Imaging? Results of a Multicenter Intraindividual Crossover Comparison of Gadobutrol with Gadoteridol (the TRUTH Study)

BACKGROUND AND PURPOSE: Gadobutrol (Gadavist) and gadoteridol (ProHance) have similar macrocyclic molecular structures, but gadobutrol is formulated at a 2-fold higher (1 mol/L versus 0.5 mol/L) concentration. We sought to determine whether this difference impacts morphologic contrast-enhanced MR imaging. MATERIALS AND METHODS: Two hundred twenty-nine adult patients with suspected or known brain tumors underwent two 1.5T MR imaging examinations with gadoteridol or gadobutrol administered in randomized order at a dose of 0.1 mmol/kg of body weight. Imaging sequences and T1 postinjection timing were identical for both examinations. Three blinded readers evaluated images qualitatively and quantitatively for lesion detection and for accuracy in characterization of histologically confirmed brain tumors. Data were analyzed by using the Wilcoxon signed rank test, the McNemar test, and a mixed model. RESULTS: Two hundred nine patients successfully completed both examinations. No reader noted a significant qualitative or quantitative difference in lesion enhancement, extent, delineation, or internal morphology (P values = .69–1.00). One hundred thirty-nine patients had at least 1 histologically confirmed brain lesion. Two readers found no difference in the detection of patients with lesions (133/139 versus 135/139, P = .317; 137/139 versus 136/139, P = .564), while 1 reader found minimal differences in favor of gadoteridol (136/139 versus 132/139, P = .046). Similar findings were noted for the number of lesions detected and characterization of tumors (malignant/benign). Three-reader agreement for characterization was similar for gadobutrol (66.4% [κ = 0.43]) versus gadoteridol (70.3% [κ = 0.45]). There were no significant differences in the incidence of adverse events (P = .199). CONCLUSIONS: Gadoteridol and gadobutrol at 0.1 mmol/kg of body weight provide similar information for visualization and diagnosis of brain lesions. The 2-fold higher gadolinium concentration of gadobutrol provides no benefit for routine morphologic imaging.

Central variant of posterior reversible encephalopathy syndrome in systemic lupus erythematosus: new associations?

Sir, There are only a few reported cases of isolated deep or central (including brain stem) brain involvement in posterior reversible encephalopathy syndrome (PRES) without involving other more commonly involved areas of brain. This central involvement secondary to connective tissue disorders is not unknown. Isolated central brain involvement in uncomplicated systemic lupus erythematosus (SLE) has never been reported before in peer-reviewed English literature. Also, central brain involvement secondary to mercaptopurine and hydroxychloroquine therapy has never been described before. We are reporting a 23-year-old white female, who had a 9-year history of SLE that was controlled with oral low-dose steroids, hydroxychloroquine and mercaptopurine, was admitted to the Rheumatology Service with worsening skin rash. Biochemical markers for lupus were not elevated. She was consistently normotensive. Her renal function was also normal. Intravenous steroid therapy (methylprednisolone 40mg q8h) was initiated. Over the next few days, she developed altered sensorium and showed markedly diminished verbal responses. Over 24 h, she became responsive only to painful stimuli. Her blood pressure and renal function remained normal. A magnetic resonance imaging (MRI) scan of the brain revealed bilateral thalamic and cerebral peduncle T2 hyperintensity with facilitated diffusion on diffusionweighted imaging (DWI). There was patchy enhancement of the thalamic lesions (Figure 1). Extensive laboratory investigations did not reveal any metabolic causes for the altered mental status and abnormal MRI findings. Even higher doses of intravenous steroid (methylprednisolone 500mg daily) and cyclophosphamide were administered at this time. There was subsequent gradual improvement of her alertness over next 6 days. The highest blood pressure, recorded 2 days after the ictus, was 141/91. MRI after 8months of this event was completely normal. Although first described in 1996, the exact pathophysiological mechanism of PRES remains unclear. As was originally described, the most common underlying condition continues to be hypertension. The pathophysiological mechanism for hypertension-related PRES is believed to be due either to arterial pressure exceeding the limits of cerebral vascular autoregulation and producing hydrostatic brain edema or to hypertension-induced cerebral autoregulatory vasoconstriction leading to ischemia and subsequent brain edema. The pathophysiology of PRES in the connective tissue disorders is less well understood. In most of the reported cases of SLE-related PRES, the immunomodulators used to treat the SLE were suggested as causative factors. However, SLE itself or SLE-related hypertension, antiphospholipid antibodies or renal failure may also be causative. Enhanced endothelial activation and leukocyte trafficking problems have recently been cited to cause brain and systemic hypoperfusion, which may be causative factors for PRES in SLE. Our patient was normotensive before the onset of the ictus. She had only one recording of high blood pressure, that recording too was after the ictus. On MRI, there was hyperintensity on T2, facilitated diffusion on DWI and subtle enhancement of both thalami. Facilitated diffusion suggested vasogenic rather than cytotoxic edema. Contrast enhancement suggests blood–brainbarrier breakdown. The cause of this blood– brain-barrier breakdown is most likely due to local endothelial injury by the antigen–antibody complexes. Obviously, development of PRES in this case was not due to hypertension. There was also no SLE-associated complication known to be associated with PRES. The most likely underlying mechanism of PRES in this patent is altered immune homeostasis due to SLE itself, confirming the view of Ishimoril et al. Alternatively, PRES in this case is secondary to mercaptopurine or hydroxychloroquine therapy: a new association. Correspondence to: Dr Asim K. Bag, Division of Neuroradiology, Department of Radiology, University of Alabama at Birmingham, 619 19TH ST SO, WP 150, AL-35249–6830, USA. Email: abag@uabmc.edu Received 19 July 2008; accepted 30 June 2009