Volume 9 Issue 12, December 2013

Chronic cerebrospinal venous insufficiency (CCSVI) has been proposed as a cause of multiple sclerosis (MS). However, two new studies found a very low overall prevalence of definite CCSVI, and no association with MS. The data confirm that the ultrasound findings of CCSVI are extremely variable, subjective, and based on major methodological flaws.

Increasing use of brain monitoring via continuous EEG in intensive care units has revealed that subclinical seizures are common among adults and children with acute brain injury. Subclinical seizures are associated with worse outcomes, but whether their prompt detection and treatment improves outcomes remains a pressing clinical question.

Currently approved multiple sclerosis (MS) treatments mainly target the peripheral immune system, thereby reducing relapse rates and MRI markers of inflammation. A recent phase III trial indicates that laquinimod, a new orally active immunomodulator, has a CNS-intrinsic mode of action that is independent of effects on the peripheral immune response.

Survivors of critical illness can experience substantial morbidity long after the event. Recent findings provide further support that long-term cognitive impairment is frequent in these patients, and that in many cases, delirium due to encephalopathy has a causal role in its development.

Rodent models of nerve injury are frequently used to study peripheral nerve regeneration, but translating the findings to clinical applications has been difficult, in part because in axons in humans generally need to regenerate over much longer distances, leaving the distal nerves and muscle tissue denervated for long periods of time. In this Review, Scheib and Höke discuss the challenges and advances in the study of peripheral nerve regeneration, and suggest that chronic rodent models of nerve injury more closely mimic the chronic denervation condition that is commonly present in human nerve injuries.

Notable failures of amyloid-β-targeted therapies in late-stage clinical trials for Alzheimer disease (AD) suggest the need for a reassessment of the amyloid cascade hypothesis of AD pathology. Here, Giacobini and Gold discuss the limitations of focusing on amyloid-β, and suggest a shift towards tau-directed therapy. They outline the rationale for such an approach and summarize results in animal models that show promise for translation to the clinic.

In addition to difficulties in movement, patients with Parkinson disease (PD) exhibit changes in somatosensory function, which might contribute substantially to disability by interfering with signals that are required for the preparation and execution of voluntary movement. In this article, Conte et al. review the evidence for disrupted tactile, nociceptive, thermal and proprioceptive sensations in PD, and the effects of dopaminergic therapy and deep brain stimulation on these sensations.

Current approaches to rehabiliation of motor and language function after stroke focus on compensation rather than repair of the underlying damage, often with limited clinical benefit. Here, Steven Small and colleagues propose a new model for poststroke therapy that aims to rebuild brain circuits underlying the impaired functional domains. They describe experience with action observation therapy, which harnesses the putative mirror neuron system in humans to improve motor performance and language skills.

Prion-like propagation of pathogenic proteins has been suggested to underlie several neurodegenerative diseases. In this Perspectives article, Braak et al. posit that progressive lesions in amyotrophic lateral sclerosis (ALS) spread through cell-to-cell transfer of 43-kDA transactive response DNA-binding protein, mainly through cortical neuronal projections to other brain areas and the spinal cord. This model could have important implications for our understanding of ALS and approach to treatment.