SUMMARY Electroencephalographic source localization (ESL)by noninvasive means is an area of renewed interest in clinical epileptology. This has been driven by innovations in the computer-assisted modeling of dipolar and distributed sources for the investigation of focal epilepsy; a process fueled by the everincreasing computational power available to researchers for the analysis of scalp EEG recordings. However, demonstration of the validity and clinical utility of these mathematically derived source modeling techniques has struggled to keep pace. This review evaluates the current clinical "fitness" of ESL as applied to the focal epilepsies by examining some of the key studies performed in the field, with emphasis given to clinical work published in the last five years. In doing so, we discuss why ESL techniques have not made an impact on routine epilepsy practice, underlining some of the current problems and controversies in the field. We conclude by examining where ESL currently sits alongside magnetoencephalography and combined EEG-functional magnetic resonance imaging in the investigation of focal epilepsy. KEY WORDS: Source modeling, Dipole, Distributed, Electroencephalography, Magnetoencephalography, Functional magnetic resonance imaging. CONCEPTS AND CONTROVERSIESIn the last five years, research in the field of electroencephalographic source localization (ESL) produced more than 150 scientific papers on computer-assisted mathematical techniques for dipolar and distributed source modeling. By comparison, less than half of this number of publications addressed the clinical validation of such techniques for the investigation of focal epilepsy. Most clinical studies featured less than 20 subjects and few were conducted prospectively. Such an imbalance might be explained away by the relative efficiency with which ESL simulation studies yield publishable results, particularly in the view of the advancing computational power and data storage capacity of the modern PC processor. However, this explanation falls short of addressing the confusion, even cynicism, among neurologists and neurosurgeons as

Background and Purpose-Cerebrovascular disease can complicate head and neck radiotherapy and result in transient ischemic attack and ischemic stroke. Although the incidence of radiation vasculopathy is predicted to rise with improvements in median cancer survival, the pathogenesis, natural history, and management of the disease are ill defined. Methods-We examined studies on the epidemiology, imaging, pathogenesis, and management of medium-and large-artery intra-and extra-cranial disease after head and neck radiotherapy. Controlled prospective trials and larger retrospective trials from the last 30 years were prioritized. Results-The relative risk of transient ischemic attack or ischemic stroke is at least doubled by head and neck radiotherapy.Chronic radiation vasculopathy affecting medium and large intra-and extra-cranial arteries is characterized by increasing rates of hemodynamically significant stenosis with time from radiotherapy. Disease expression is the likely consequence of the combined radiation insult to the intima-media (accelerating atherosclerosis) and to the adventitia (injuring the vasa vasorum). Optimal medical treatment is not established. Carotid endarterectomy is confounded by the need to operate across scarred tissue planes, whereas carotid stenting procedures have resulted in high restenosis rates. Conclusions-Head and neck radiotherapy significantly increases the risk of transient ischemic attack and ischemic stroke.Evidence-based guidelines for the management of asymptomatic and symptomatic (medium-and large-artery) radiation vasculopathy are lacking. Long-term prospective studies remain a priority, as the incidence of the problem is anticipated to rise with improvements in postradiotherapy patient survival. (Stroke. 2011;42:2410-2418.)

This position statement from the Heart Failure Association of the European Society of Cardiology Cardio‐Oncology Study Group in collaboration with the International Cardio‐Oncology Society presents practical, easy‐to‐use and evidence‐based risk stratification tools for oncologists, haemato‐oncologists and cardiologists to use in their clinical practice to risk stratify oncology patients prior to receiving cancer therapies known to cause heart failure or other serious cardiovascular toxicities. Baseline risk stratification proformas are presented for oncology patients prior to receiving the following cancer therapies: anthracycline chemotherapy, HER2‐targeted therapies such as trastuzumab, vascular endothelial growth factor inhibitors, second and third generation multi‐targeted kinase inhibitors for chronic myeloid leukaemia targeting BCR‐ABL, multiple myeloma therapies (proteasome inhibitors and immunomodulatory drugs), RAF and MEK inhibitors or androgen deprivation therapies. Applying these risk stratification proformas will allow clinicians to stratify cancer patients into low, medium, high and very high risk of cardiovascular complications prior to starting treatment, with the aim of improving personalised approaches to minimise the risk of cardiovascular toxicity from cancer therapies.

Accurate identification of seizure-generating brain tissue is challenging, particularly when MRI shows no clear abnormality or extensive abnormality. Plummer et al. achieve this non-invasively by analysing the earliest detectable part of the electromagnetic seizure signal recordable across the head surface. Their findings challenge current practice with its reliance on invasive intracranial monitoring.