Representative illustration of three-dimensional lesion reconstruction.

<p>Stroke caused by arterial dissection of the left internal carotid artery, representations of the acute lesion are shown in red as two-dimensional overlay on diffusion weighted images (A) and as three-dimensional reconstructions (B). Bounding box of the lesion is illustrated in C.</p

Group comparison of morphological lesion shape measures for patients with embolic strokes of either cardiac or non-cardiac origin.

<p>Cardioembolic stroke was defined in patients classified by ASCOD as cardioembolism (C1 and C2; n = 37), a non-cardioembolic origin (n = 54) defined for strokes caused by atherothrombosis (A1, A2), arterial dissection (D1) and other known causes (O1); Multiple arterial pattern is defended as lesions located in at least two of the main arterial territories of the brain (left or right internal carotid artery or posterior circulation territory).</p

Two- and three-dimensional representations of acute stroke lesions analyzed in this study.

<p>Acute stroke lesions are shown in red overlayed on diffusion-weighted images in the first column. Three-dimensional reconstructions are illustrated in the second column. The third column shows application of morphological shape measures for lesions caused by cardioembolism (A), atherothrombosis (B) and small-vessel disease (C).</p

Table_2_Clinical Outcome of Isolated Cerebellar Stroke—A Prospective Observational Study.DOCX

<p>Background: The aim of this prospective study was to investigate clinical deficits of patients with isolated cerebellar stroke applying a dedicated clinical score, the modified International Cooperative Ataxia Rating Scale (MICARS) and identifying factors that influence recovery.</p><p>Methods: Fifteen patients with acute isolated cerebellar stroke received a standard stroke MRI on the day of admission and were clinically assessed using the mRS, NIHSS and the modified International Cooperative Ataxia Rating Scale (MICARS) on day 1, 3, 7, 30, and 90. A generalized linear model for repeated measures was employed to analyze the effect of stroke lesion location, volume, days after stroke, patient age, and MICARS score at admission on the total MICARS score.</p><p>Results: Median patient age was 54 years, lesion location in most cases was right (87%) and in the PICA territory (11/15). Median lesion volume was 3.2 ml. Median NIHSS was 1. The median MICARS decreased from on day 1 with 23–4 at day 90. The generalized linear model identified MICARS score at day 1, lesion location, days after admission and the interaction of the last two on the total MICARS score, whereas there was no significant effect of stroke volume or patient age.</p><p>Conclusions: Isolated cerebellar stroke can present with low NIHSS while more specific scales like the MICARS indicate a severe deficit. Patient age at onset of stroke and lesion volume had no significant effect on recovery from cerebellar symptoms as opposed to severity of symptoms at admission and lesion location.</p

Deficiency in Serine Protease Inhibitor Neuroserpin Exacerbates Ischemic Brain Injury by Increased Postischemic Inflammation

<div><p>The only approved pharmacological treatment for ischemic stroke is intravenous administration of plasminogen activator (tPA) to re-canalize the occluded cerebral vessel. Not only reperfusion but also tPA itself can induce an inflammatory response. Microglia are the innate immune cells of the central nervous system and the first immune cells to become activated in stroke. Neuroserpin, an endogenous inhibitor of tPA, is up-regulated following cerebral ischemia. To examine neuroserpin-dependent mechanisms of neuroprotection in stroke, we studied neuroserpin deficient (<i>Ns^−/−</i>) mice in an animal model of temporal focal ischemic stroke. Infarct size and neurological outcome were worse in neuroserpin deficient mice even though the fibrinolytic activity in the ischemic brain was increased. The increased infarct size was paralleled by a selective increase in proinflammatory microglia activation in <i>Ns^−/−</i> mice. Our results show excessive microglial activation in <i>Ns^−/−</i> mice mediated by an increased activity of tPA. This activation results in a worse outcome further underscoring the potential detrimental proinflammatory effects of tPA.</p></div

Table_1_Clinical Outcome of Isolated Cerebellar Stroke—A Prospective Observational Study.DOCX

<p>Background: The aim of this prospective study was to investigate clinical deficits of patients with isolated cerebellar stroke applying a dedicated clinical score, the modified International Cooperative Ataxia Rating Scale (MICARS) and identifying factors that influence recovery.</p><p>Methods: Fifteen patients with acute isolated cerebellar stroke received a standard stroke MRI on the day of admission and were clinically assessed using the mRS, NIHSS and the modified International Cooperative Ataxia Rating Scale (MICARS) on day 1, 3, 7, 30, and 90. A generalized linear model for repeated measures was employed to analyze the effect of stroke lesion location, volume, days after stroke, patient age, and MICARS score at admission on the total MICARS score.</p><p>Results: Median patient age was 54 years, lesion location in most cases was right (87%) and in the PICA territory (11/15). Median lesion volume was 3.2 ml. Median NIHSS was 1. The median MICARS decreased from on day 1 with 23–4 at day 90. The generalized linear model identified MICARS score at day 1, lesion location, days after admission and the interaction of the last two on the total MICARS score, whereas there was no significant effect of stroke volume or patient age.</p><p>Conclusions: Isolated cerebellar stroke can present with low NIHSS while more specific scales like the MICARS indicate a severe deficit. Patient age at onset of stroke and lesion volume had no significant effect on recovery from cerebellar symptoms as opposed to severity of symptoms at admission and lesion location.</p

Modeling of Large-Scale Functional Brain Networks Based on Structural Connectivity from DTI: Comparison with EEG Derived Phase Coupling Networks and Evaluation of Alternative Methods along the Modeling Path

<div><p>In this study, we investigate if phase-locking of fast oscillatory activity relies on the anatomical skeleton and if simple computational models informed by structural connectivity can help further to explain missing links in the structure-function relationship. We use diffusion tensor imaging data and alpha band-limited EEG signal recorded in a group of healthy individuals. Our results show that about 23.4% of the variance in empirical networks of resting-state functional connectivity is explained by the underlying white matter architecture. Simulating functional connectivity using a simple computational model based on the structural connectivity can increase the match to 45.4%. In a second step, we use our modeling framework to explore several technical alternatives along the modeling path. First, we find that an augmentation of homotopic connections in the structural connectivity matrix improves the link to functional connectivity while a correction for fiber distance slightly decreases the performance of the model. Second, a more complex computational model based on Kuramoto oscillators leads to a slight improvement of the model fit. Third, we show that the comparison of modeled and empirical functional connectivity at source level is much more specific for the underlying structural connectivity. However, different source reconstruction algorithms gave comparable results. Of note, as the fourth finding, the model fit was much better if zero-phase lag components were preserved in the empirical functional connectome, indicating a considerable amount of functionally relevant synchrony taking place with near zero or zero-phase lag. The combination of the best performing alternatives at each stage in the pipeline results in a model that explains 54.4% of the variance in the empirical EEG functional connectivity. Our study shows that large-scale brain circuits of fast neural network synchrony strongly rely upon the structural connectome and simple computational models of neural activity can explain missing links in the structure-function relationship.</p></div

Functional Connectivity Metrics.

<p>Functional Connectivity Metrics.</p

Both genotype groups show similar learning success during associative vocabulary learning.

<p>Both genotype groups show similar learning success during associative vocabulary learning.</p

Translation rate after training does not differ between BDNF genotypes (total and for Object words (OW) and Action words (AW)).

<p>Translation rate after training does not differ between BDNF genotypes (total and for Object words (OW) and Action words (AW)).</p