The model describes fast visual information and slow hemodynamics by separate components. We recorded

BOLD signals in occipitotemporal visual cortex of human subjects who watched natural movies and fit the model separately to individual voxels. Visualization of the fit models reveals how early visual areas represent the information in movies. To demonstrate the power of our approach, we also constructed a Bayesian decoder [8] by combining estimated encoding models with a sampled natural movie prior. The decoder provides remarkable reconstructions of the viewed movies. These results demonstrate that dynamic brain activity measured under naturalistic conditions can be decoded using current selleck fMRI technology.”
“Eighty years ago, the Austrian neurologist Josef Gerstmann observed in a few patients a concomitant impairment in discriminating their own fingers, writing by hand, distinguishing

left from right and performing calculations. He claimed that this tetrad of symptoms constituted a syndromal entity, assigned it to a lesion of the dominant parietal lobe and suggested that it was due to damage selleck chemicals of a common functional denominator. Ever since, these claims have been debated and an astute synopsis and sceptical discussion was presented 40 years ago by MacDonald Critchley in this journal. Nonetheless, Gerstmann’s syndrome has continued to intrigue both clinical neurologists and researchers in neuropsychology, and more frequently than not is described in textbooks as an example of parietal lobe damage. In this Wnt inhibition review, we revisit the chequered history of this syndrome, which can be seen as a case study of the dialectic evolution of concepts in neuropsychology. In light of several modern era findings

of pure cases we conclude that it is legitimate to label the conjunction of symptoms first described by Gerstmann as a ‘syndrome’, but that it is very unlikely that damage to the same population of cortical neurons should account for all of the four symptoms. Instead, we propose that a pure form of Gerstmann’s syndrome might arise from disconnection, via a lesion, to separate but co-localized fibre tracts in the subcortical parietal white matter, a hypothesis for which we have recently provided evidence using combined imaging of functional and structural organization in the healthy brain.”
“The lack of fatty aldehyde dehydrogenase function in Sjogren Larsson Syndrome (SLS) patient cells not only impairs the conversion of fatty aldehydes into their corresponding fatty acid but also has an effect on connected pathways. Alteration of the lipid profile in these cells is thought to be responsible for severe symptoms such as ichtyosis, mental retardation, and spasticity.