Volume 6 Issue 12, December 2010

Thromboembolism resulting from complex atheromatous plaque formation at the origin of the internal carotid artery is a common cause of ischemic stroke. In appropriately selected patients, plaque removal by carotid endarterectomy is of substantial net benefit. Endovascular stenting appears less 'invasive' than endarterectomy, but is the former as safe and effective as the latter?

Lesion location might turn out to be an important factor in long-term disability prediction in patients with primary progressive multiple sclerosis (MS). Using a lesion probability mapping approach, researchers have identified brain regions where the presence of MS lesions predicts an early need for bilateral walking support.

Alzheimer disease (AD) biomarkers reflect specific features of AD pathology. These biomarkers may be used in the diagnosis and staging of AD, or may act as surrogate end points in clinical trials. Thus, a thorough understanding of the diagnostic accuracy of and longitudinal change in cerebrospinal fluid and MRI AD biomarkers is important.

Antiepileptic drugs (AEDs) are receiving increasing attention for a possible association with suicidal thoughts and behaviors. Several recent studies examining this association, however, have yielded inconsistent findings, particularly in terms of the risk of suicidal behavior conferred by specific AEDs. In patients with epilepsy, heightened suicide risk is also attributable to comorbid psychiatric conditions.

Two new studies suggest that pediatric medulloblastomas and high-grade gliomas are genetically different from the same tumors in adults. Age-dependent gene expression might affect tumor biology; therefore, therapies for adult medulloblastomas or gliomas might not produce the same clinical outcomes in pediatric patients, and vice versa.

Natural history studies have identified numerous features of disability progression in patients with multiple sclerosis (MS), and have provided valuable insight into the underlying pathology of the disease that could assist the development of new treatment strategies. A new study indicates that disability progression occurs in two stages in patients with MS.

Chemotherapy-induced peripheral neurotoxicity (CIPN) is a frequent consequence of cancer treatment, and can profoundly affect the quality of life of individuals who survive cancer. In this article, Cavaletti and Marmiroli review the mechanistic and clinical aspects of CIPN, as well as assessing the current status of neuroprotective approaches and other treatment options for this condition.

Progressive multifocal leukoencephalopathy (PML) is a demyelinating disease of the brain caused by the JC virus. PML usually only develops in individuals who are immunocompromised, and can be caused by immunomodulatory therapies. In this article, Brew et al. review the literature relating to the diagnosis and management of PML. The authors also suggest practical management guidelines for this condition.

Traditional stroke risk factors do not seem to fully account for the epidemiology of this disease. Here, Grau and colleagues explore the increasing body of evidence indicating that recent acute infection and various chronic infectious diseases might be risk factors for—or triggers of—stroke. In addition to examining the epidemiological evidence supporting these associations, the authors discuss possible mechanisms that might underlie infection-related stroke, and treatment implications.

Diagnosis of low-grade inflitrating gliomas—a class of brain tumors that includes diffuse astrocytoma, oligoastrocytoma and oligodendroglioma—currently relies largely on histological classification, although molecular discoveries are beginning to generate new paradigms for diagnosis and management. Bourne and Schiff highlight the molecular abnormalities that have been identified in low-grade gliomas, and discuss how factors such as chromosome 1p19q codeletion andMGMTpromoter methylation status are facilitating stratification of patients in clinical trials.

Protein misfolding and aggregation occur in most neurodegenerative disorders, but the concept of spreading and infectivity of aggregates in the CNS has, until recently, been confined to prion diseases such as Creutzfeldt–Jakob disease. New evidence suggests that prion-like spreading, involving proteins such as amyloid-β, tau, huntingtin and α-synuclein, can occur in other neurodegenerative disorders. In this article, Lee et al. discuss the underlying molecular mechanisms and consider the therapeutic implications of the new data.