This measure includes Wolpaw’s information transfer rate as a special case, but addresses the latter’s limitations including its restriction to item-selection tasks. To validate our approach and address challenge (III), we compared four healthy subjects’ performance using an EEG-based BCI, a ‘Direct Controller’ (a high-performance hardware input device), and a ‘Pseudo-BCI Controller’ (the same input device, but with control signals processed by the BCI signal processing pipeline). Main results. Our results confirm the repeatability

and validity of our measures, and indicate that our BCI signal processing pipeline reduced attainable performance by about GSK2126458 33% (21 bits min(-1)). Significance. Our approach provides a flexible basis for evaluating BCI performance and its limitations, across a wide range of tasks and task difficulties.”
“We present the first recorded case of a remote extradural haematoma following extended transsphenoidal surgery (eTSS) for craniopharyngioma. We believe that this is a unique complication related to rapid and excessive intracranial hypotension caused by acute overdrainage of cerebrospinal fluid (CSF) during the eTSS procedure.”
“Heterozygous missense mutations of transient receptor potential

vanilloid 4 channel (TRPV4) cause a spectrum of skeletal disorders, including brachyolmia, spondylometaphyseal dysplasia Kozlowski type, metatropic dysplasia, parastremmatic dysplasia, and spondyloepimetaphyseal dysplasia Maroteaux type. Similarly, heterozygous missense mutations Quizartinib datasheet of TRPV4 cause a spectrum of

peripheral neuropathy, including hereditary motor and sensory neuropathy type IIC, congenital spinal muscular atrophy, LDK378 price and scapuloperoneal spinal muscular atrophy. There are no apparent differences in the amino acid positions affected or type of change predicted by the TRPV4 mutations responsible for the two disease spectrums; nevertheless, no fundamental phenotypic overlap has been shown between the two spectrums. Here, we report on three patients who had both skeletal dysplasia and peripheral neuropathy caused by heterozygous TRPV4 missense mutations. The skeletal and neurologic phenotypes of these patients covered the wide spectrum of reported TRPV4-pathies (disease caused by TRPV4 mutations). The molecular data are complementary, proving that “neuropathic” mutations can cause skeletal dysplasia but also the “skeletopathic” mutations can lead to neuropathies. Our findings suggest that pathogenic mechanisms of TRPV4-pathies in skeletal and nervous systems are not always mutually exclusive and provide further evidence that there is no clear genotype-phenotype correlation for either spectrum.