Recent interest in exploring the clinical relevance of cerebral microbleeds (CMBs) has motivated the search for a fast and accurate method to detect them. Visual inspection of CMBs on MR images is a lengthy, arduous task that is highly prone to human error because of their small size and wide distribution throughout the brain. Several computer-aided CMB detection algorithms have recently been proposed in the literature, but their diagnostic accuracy, computation time, and robustness are still in need of improvement. In this study, we developed and tested a semi-automated method for identifying CMBs on minimum intensity projected susceptibility-weighted MR images that are routinely used in clinical practice to visually identify CMBs. The algorithm utilized the 2D fast radial symmetry transform to initially detect putative CMBs. Falsely identified CMBs were then eliminated by examining geometric features measured after performing 3D region growing on the potential CMB candidates. This algorithm was evaluated in 15 patients with brain tumors who exhibited CMBs on susceptibility-weighted images due to prior external beam radiation therapy. Our method achieved heightened sensitivity and acceptable amount of false positives compared to prior methods without compromising computation speed. Its superior performance and simple, accelerated processing make it easily adaptable for detecting CMBs in the clinic and expandable to a wide array of neurological disorders. © 2013 The Authors.

Low-grade gliomas cause considerable morbidity and most will recur after initial therapy. At recurrence, low-grade gliomas can undergo transformation to high-grade gliomas (grade III or grade IV), which are associated with worse prognosis. Temozolomide (TMZ) provides survival benefit in patients with glioblastomas (GBMs) but its value in patients with low-grade gliomas is less clear. A subset of TMZ-treated, IDH-mutant, low-grade astrocytomas recur as more malignant tumors with thousands of de novo, coding mutations bearing a signature of TMZ-induced hypermutation. Preliminary studies raise the hypothesis that TMZ-induced hypermutation may contribute to malignant transformation, although with highly variable latency. On the other hand, hypermutated gliomas have radically altered genomes that present new opportunities for therapeutic intervention. In light of these findings and the immunotherapy clinical trials they inspired, how do patients and providers approach the risks and benefits of TMZ therapy? This review discusses what is known about the mechanisms and consequences of TMZ-induced hypermutation and outstanding questions regarding its clinical significance.

Gliomas are routinely graded according to histopathological criteria established by the World Health Organization. Although this classification can be used to understand some of the variance in the clinical outcome of patients, there is still substantial h

© 2015 Published by Elsevier Inc.Recent technological progress in the multiband echo planer imaging (MB EPI) technique enables accelerated MR diffusion weighted imaging (DWI) and allows whole brain, multi-b-value diffusion imaging to be acquired within a c

Astrocytes, the most abundant cells in the central nervous system, promote synapse formation and help to refine neural connectivity. Although they are allocated to spatially distinct regional domains during development, it is unknown whether region-restric

© 2015 The Authors. Published by Elsevier Inc.PURPOSE: To evaluate the time course and association with survival of anatomic lesion volumes and diffusion imaging parameters for patients with newly diagnosed glioblastoma who were treated with radiation and

We present our initial experience in using single modality fluoromisonidazole (FMISO) PET/MR imaging to noninvasively evaluate the biological effects induced by bevacizumab therapy in a patient treated for recurrent high grade glioma. In this index patient

© 2014 The Author(s) To evaluate metrics that describe changes in apparent diffusion coefficient (ADC) and to examine their association with clinical outcome for patients with newly diagnosed GBM who were participating in a Phase II clinical trial of treat