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Transcranial Direct Current Stimulation in Stroke Recovery
Schlaug and colleaguesArticle review transcranial direct current stimulation (TDCS) as a facilitator of stroke recovery, the different modes of TDCS, and potential mechanisms underlying the neural effects of TDCS.
Parkinson Disease and the Central Role of α-Synuclein Oligomers
Kazantsev and KolchinskyArticle support the concept that the selective death of nigrostriatal neurons leading to Parkinson disease is explained by misfolding of brain α-synuclein. They offer the possibility of protein deacetylase sirtuins as new potential therapeutic targets involved in this process.
Clinical Trial of Ethyl-Eicosapentaenoic Acid in Huntington Disease
Dorsey and colleaguesArticle studied ethyl-eicosapentaenoic acid (ethyl-EPA), an ω-3 fatty acid, to see if it improved the motor features of Huntington disease. A multicenter, randomized, double-blind, placebo-controlled trial was conducted. Ethyl-EPA was found to be safe and well tolerated, but after 6 months it was not an effective treatment for Huntington disease. Its potentially beneficial effects observed at 12 months require confirmation in longer-term placebo-controlled studies.
Communicating Clinical Trials Results to Research Participants
Dorsey and colleaguesArticle evaluated the effectiveness of a plan to communicate results in an industry-sponsored, randomized, controlled trial for Huntington disease (the TREND-HD study). Surveyed research participants learned of TREND-HD study results soon after public release and highly valued the personalized and accurate communication efforts by study investigators.
Natalizumab Decreases the Numbers of Dendritic Cells and CD4+ T Cells in Cerebral Perivascular Spaces
Del Pilar Martin and colleaguesArticle found that the absolute number of cerebral perivascular spaces (CPVS) in a patient with multiple sclerosis treated with natalizumab was significantly lower than in control groups. The numbers of dendritic cells were decreased in the CPVS of a patient with multiple sclerosis treated with natalizumab. No CD4+ T cells were detectable. These important observations may explain the differential and prolonged effects of natalizumab therapy on leukocyte numbers in the cerebrospinal fluid. Editorial perspective is provided by Burkhard Becher, MD.Article
Gambling in Parkinson Disease
Cilia et alArticle found that patients with Parkinson disease and pathological gambling have abnormal resting state dysfunction of the mesocorticolimbic network, possibly associated with a drug-induced overstimulation of relatively preserved reward-related neuronal systems. These data support the concept that pathological gambling is a behavioral addictive disorder.
Continuous Electroencephalogram Monitoring in Critically Ill Patients With Central Nervous System Infections
Carrera and colleaguesArticle report that in patients with central nervous system infection who are undergoing continuous electroencephalographic monitoring, electrographic seizures and/or periodic epileptiform discharges were frequent, occurring in 48% of the cohort. Electrographic seizures and periodic epileptiform discharges were each independently associated with poor outcome.
Difference in prevalence of electrographic seizures among patients with and without the corresponding periodic epileptiform discharges (PEDs). P values are in comparison with the group with no PEDs. PLEDs indicates periodic lateralized epileptiform discharges; GPEDs, generalized PEDs; BIPLEDs, bilateral independent PLEDs; and EEG, electroencephalographic.
Hippocampal Volumes, Proton Magnetic Resonance Spectroscopy Metabolites, and Cerebrovascular Disease in Mild Cognitive Impairment Subtypes
Kantarci and colleaguesArticle show that magnetic resonance imaging and proton magnetic resonance spectroscopy findings in single-domain amnestic mild cognitive impairment (MCI) are consistent with an Alzheimer disease–like pattern. Absence of this pattern on average in patients with nonamnestic MCI suggests that cerebrovascular disease and other neurodegenerative diseases may be contributing to cognitive impairment in many nonamnestic MCI subjects.
Intracranial Hemorrhage in Children
Lo and colleaguesArticle find that brain tumors and congenital heart disease accounted for a greater proportion of intracranial hemorrhages in their series of patients than in previous studies. The mortality rate of intracranial hemorrhage remains high but may be related as much to the severity of the underlying illnesses as to the hemorrhage itself. There is significant long-term morbidity, but more than half of the survivors for whom follow-up data are available have no detectable deficits.
Clincial Features in Alzheimer Disease and Dementia With Lewy Bodies
Nervi et alArticle report that, compared with persons with Alzheimer disease, persons with dementia with Lewy bodies are more severely impaired in various cognitive domains, particularly in orientation and visuospatial function. Whether this divergence in cognitive functions is caused by gene-gene or gene-environment interactions remains unclear.
Variants in SORL1 Are Associated With Cerebrovascular and Neurodegenerative Changes Related to Alzheimer Disease
Cuenco et alArticle show that SORL1 variants previously associated with Alzheimer disease are also associated with magnetic resonance imaging and neuropathological measures of neurodegenerative and cerebrovascular disease. These data raise the possibility that multiple SORL1 variants influence amyloid precursor protein, endothelial lipoprotein processing, or both in different regions of the brain.
Quantitative Brain Measures in Community-Dwelling Elderly Persons With Mild Parkinson Disease
Louis and colleaguesArticle find in this magnetic resonance imaging study of community-dwelling elderly persons that white matter hyperintensity volume was associated with mild Parkinson disease while total relative hippocampal volume was not. These data raise the possibility that vascular disease plays a role in the development of mild Parkinson disease.
This Month in Archives of Neurology. Arch Neurol. 2008;65(12):1564–1565. doi:10.1001/archneurol.2008.518
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