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Background and Purpose: Susceptibility-weighted magnetic resonance imaging (SWI) yields information regarding tumor biology (e.g., hemorrhage) of growing gliomas. SWI changes can also be observed as a consequence of treatment, for example radiation therapy. The aim of our study was to investigate how susceptibility changes occur during the time course after completion of standard treatment in newly diagnosed glioblastoma (GBM).Methods: Eighteen GBM patients were retrospectively analyzed. After completion of therapy, imaging was performed every 3 months. MRI was analyzed at the following time points: after the third and sixth cycle of adjuvant temozolomide chemotherapy, thereafter in 3 month intervals and at recurrence. The number of SWI positive tumor pixels was quantified and compared with progression as defined by the RANO criteria on T2- and contrast-enhanced T1-weighted MRI sequences (T1-CE).Results: The MRI interval between completion of the sixth chemotherapy cycle and last MRI before progression was 390 ± 292 days. Between the last MRI before progression and at progression a significant increase in SWI positive tumor pixels was observed (P = .012), whereas tumor size remained unchanged (RANO T2: P = .385; RANO T1-CE: P = .165). The number of SWI positive pixels remained unchanged between last MRI before progression until progression (P = .149), whereas RANO T2 and T1-CE showed tumor progression (interval 128 ± 69 days).Conclusions: SWI positive pixel count increases significantly prior to changes in tumor size (RANO). Our findings may be explained by microbleeds compatible with stimulation of angiogenesis and possibly serve as an early biomarker of tumor progression. [ABSTRACT FROM AUTHOR]

Evidence from recent functional magnetic resonance imaging studies suggests that adaptive cortical changes (‘plasticity’) could participate in the maintenance of function in multiple sclerosis (MS). Here, we addressed the impact of brain atrophy on the pattern of cerebral activation in an MS patient with a relapsing-remitting course. This patient showed mildly disabling hemiparesis of the left side (EDSS 2.0), and corresponding brain hemiatrophy (15% volume reduction) of the right hemisphere. The clinical syndrome was considered to result from a lesion in the corona radiata involving corticospinal fibers. Motor-evoked potential recordings confirmed substantial axonal damage to the pyramidal tract arising from that hemisphere. Irrespective of these asymmetries, normal brain activation was found for hand and foot movements for both brain sides. This demonstrates that brain atrophy itself does not necessarily induce cortical adaptive changes, even if mild disability is present. On the other hand, significantly disabling distinct clinical syndromes e.g. arising from spinal cord lesions may evoke cortical changes irrespective of brain atrophy. This issue has to be studied in longitudinal investigations. Copyright © 2004 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Background: The addition of bevacizumab to temozolomide-based chemoradiotherapy (TMZ/RT ! TMZ) did not prolong overall survival (OS) in patients with newly diagnosed glioblastoma in phase III trials. Elderly and frail patients are underrepresented in clinical trials, but early reports suggested preferential benefit in this population. Patients and methods: ARTE was a 2: 1 randomized, multi-center, open-label, non-comparative phase II trial of hypofractionated RT (40 Gy in 15 fractions) with bevacizumab (10 mg/kg×14 days) (arm A, N=50) or without bevacizumab (arm B, N=25) in patients with newly diagnosed glioblastoma aged≤65 years. The primary objective was to obtain evidence for prolongation of median OS by the addition of bevacizumab to RT. Response was assessed by RANO criteria. Quality of life (QoL) was monitored by the EORTC QLQ-C30/BN20 modules. Exploratory studies included molecular subtyping by 450k whole methylome and gene expression analyses. Results: Median PFS was longer in arm A than in arm B (7.6 and 4.8 months, P=0.003), but OS was similar (12.1 and 12.2 months, P=0.77). Clinical deterioration was delayed and more patients came off steroids in arm A. Prolonged PFS in arm A was confined to tumors with the receptor tyrosine kinase (RTK) I methylation subtype (HR 0.25, P=0.014) and proneural gene expression (HR 0.29, P=0.025). In a Cox model of OS controlling for established prognostic factors, associations with more favorable outcome were identified for age<70 years (HR 0.52, P=0.018) and Karnofsky performance score 90%-100% (HR 0.51, P=0.026). Including molecular subtypes into that model identified an association of the RTK II gene methylation subtype with inferior OS (HR 1.73, P=0.076). Conclusion: Efficacy outcomes and exploratory analyses of ARTE do not support the hypothesis that the addition of bevacizumab to RT generally prolongs survival in elderly glioblastoma patients. Molecular biomarkers may identify patients with preferential benefit from bevacizumab. [ABSTRACT FROM AUTHOR]

AbstractThe primary sensorimotor cortex of the adult brain is capable of significant reorganization of topographic maps after deafferentation and de-efferentation. Here we show that patients with spinal cord injury exhibit extensive changes in the activation of cortical and subcortical brain areas during hand movements, irrespective of normal (paraplegic) or impaired (tetraplegic patients) hand function. Positron emission tomography ([15O]-H2O-PET) revealed not only an expansion of the cortical ‘hand area' towards the cortical ‘leg area', but also an enhanced bilateral activation of the thalamus and cerebellum. The areas of the brain which were activated were qualitatively the same in both paraplegic and tetraplegic patients, but differed quantitatively as a function of the level of their spinal cord injury. We postulate that the changes in brain activation following spinal cord injury may reflect an adaptation of hand movement to a new body reference scheme secondary to a reduced and altered spino-thalamic and spino-cerebellar input. [ABSTRACT FROM AUTHOR]

A letter to the editor is presented which discusses a case of a 70-year-old man with recurrent tumour-like intracerebral masses, diagnosed as tumefactive demyelination (TD).