Return to Play After Athletic Concussion
The management of sport-related concussion, especially involving return-to-play decisions, is one of the most important challenges confronting sports medicine physicians and neurologists. Mayers (SEE ARTICLE) points out that current guidelines for return to play are too lenient and that a postconcussion return-to-play interval of at least 4 weeks is imperative.
Monoclonal Therapies and Neurologic Disorders
Novak et al (SEE ARTICLE) report that monoclonal antibody therapy for treating medical conditions has expanded greatly in the past 30 years, and monoclonal antibody treatments are currently being tested for conditions such as neuromuscular disorders and demyelinating diseases. The authors provide a well-focused and comprehensive review of this important clinical subject, highlighting the use of monoclonal antibodies in treating neurologic conditions and their neurologic adverse effects.
Bridging Anticoagulation After Cardioembolic Stroke
Hallevi and colleagues (SEE ARTICLE) provide new data supporting the position that anticoagulation in patients with cardioembolic stroke can be safely started with warfarin shortly after stroke. However, they point out that heparin bridging (intravenous heparin in the acute phase followed by warfarin) and enoxaparin bridging (full-dose enoxaparin combined with warfarin) increase the risk of serious bleeding. Editorial perspective is provided by Robert J. Wityk, MD. (SEE ARTICLE)
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The timing of hemorrhagic transformation (HT). PH2 indicates parenchymal hematoma, grade 2.
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Aggressive Blood Pressure Lowering Before Intravenous Tissue Plasminogen Activator Treatment for Acute Stroke
Martin-Schild et al (SEE ARTICLE) find that blood pressure reduction before intravenous tissue plasminogen activator (tPA) treatment may not be associated with a higher rate of hemorrhage or poor outcome. Their data indicate that patients with acute ischemic stroke who require aggressive blood pressure treatment should not be excluded from tPA therapy.
Diffusion Tensor Imaging and Functional Brain Injury
Fox and colleagues (SEE ARTICLE) identified diffusion tensor imaging (DTI) evidence of pathological disruption of a small brainstem fiber pathway that is crucial for accurate horizontal eye movements. They noted important correlations between DTI changes and oculomotor dysfunction.
Transactivation Response DNA-Binding Protein 43 Mutations and Familial Amyotrophic Lateral Sclerosis
Mutations in transactivation response DNA-binding protein 43 (TDP-43) are a rare cause of familial non-SOD1 amyotrophic lateral sclerosis (ALS). Kühnlein and colleagues (SEE ARTICLE), in providing an identification of TDP-43 mutations, provide strong evidence for a direct link between TDP-43 dysfunction and neurodegeneration in ALS.
Pain as a Nonmotor Symptom of Parkinson Disease
Defazio et al (SEE ARTICLE) have found that the overall frequency of pain was significantly greater in patients with Parkinson disease than in control subjects. They establish that pain may be a nonmotor feature of Parkinson disease.
Cardiac Involvement With Limb-Girdle Type 2 and Becker Muscular Dystrophies
This study by Sveen et al (SEE ARTICLE) demonstrates a high prevalence of cardiac involvement in patients with limb-girdle type 2 and Becker muscular dystrophies.
Prediction of Rate of Cognitive Decline by Cerebral Atrophy and White Matter Changes in Alzheimer Disease
Brickman et al (SEE ARTICLE) show that the degree of cerebral atrophy and the severity of white matter hyperintensities (WMH) are associated with the rapidity of cognitive decline in Alzheimer disease (AD). They believe that atrophy and WMH may interact to have a synergistic effect on future decline. Patients with AD with both of these features have a particularly rapid degree of cognitive decline.
Inability of Alzheimer Disease Neuropathology to Explain Dementia in the Oldest-Old
Neuropathological features of dementia in oldest-old persons are not the same as those of cognitively impaired younger-old persons, as reported in this provocative and highly interesting report by Haroutunian and colleagues (SEE ARTICLE).
Optical Coherence Tomography in Multiple Sclerosis
Cettomai et al (SEE ARTICLE) demonstrate that mean retinal nerve fiber layer (RNFL) thickness can be reproducibly measured by experienced personnel using optical coherence tomography–3 (OCT-3). Measures of RNFL thickness from cohorts of age-matched controls and patients with multiple sclerosis from 3 research centers were highly similar. This shows that OCT-3 is a reliable means to follow up patients with ocular nerve lesions due to multiple sclerosis.
Gray Matter Atrophy and Benign Multiple Sclerosis
Mesaros et al (SEE ARTICLE) report that cerebellar gray matter atrophy is a major determinant of irreversible locomotor disability in patients with multiple sclerosis. The absence of cognitive impairment and a longer disease duration and lower Expanded Disability Status Scale score may identify those patients with benign multiple sclerosis with the potential for a favorable disease evolution.
Cerebral Hypometabolism With Future Memory Decline
Caselli and colleagues (SEE ARTICLE) find that patients with amnestic pre–mild cognitive impairment showed significantly greater correlations between cerebral hypometabolism and subsequent long-term memory decline than nondecliners in Alzheimer disease–affected brain regions.
