[EEG diagnosticsof non-convulsive status epilepticus in critically ill patients].

Critically ill patients are at high risk of non-convulsive status epilepticus (NCSE). As clinical signs of NCSE are subtle and unspecific, EEG is necessary to make the diagnosis. This is a review of the terminology for EEG reporting and the criteria for NCSE in critically ill patients. We discuss the newly proposed ictal-interictal continuum, and how caution is needed when assessing EEG criteria in order to avoid both over- and undertreatment. Finally, we discuss how specific EEG findings, in combination with clinical information, can help infer treatment decision and need for continuous EEG monitoring.

Better Diffusion Segmentation in Acute Ischemic Stroke Through Automatic Tree Learning Anomaly Segmentation.

Stroke is the second most common cause of death worldwide, responsible for 6.24 million deaths in 2015 (about 11% of all deaths). Three out of four stroke survivors suffer long term disability, as many cannot return to their prior employment or live independently. Eighty-seven percent of strokes are ischemic. As an increasing volume of ischemic brain tissue proceeds to permanent infarction in the hours following the onset, immediate treatment is pivotal to increase the likelihood of good clinical outcome for the patient. Triaging stroke patients for active therapy requires assessment of the volume of salvageable and irreversible damaged tissue, respectively. With Magnetic Resonance Imaging (MRI), diffusion-weighted imaging is commonly used to assess the extent of permanently damaged tissue, the core lesion. To speed up and standardize decision-making in acute stroke management we present a fully automated algorithm, ATLAS, for delineating the core lesion. We compare performance to widely used threshold based methodology, as well as a recently proposed state-of-the-art algorithm: COMBAT Stroke. ATLAS is a machine learning algorithm trained to match the lesion delineation by human experts. The algorithm utilizes decision trees along with spatial pre- and post-regularization to outline the lesion. As input data the algorithm takes images from 108 patients with acute anterior circulation stroke from the I-Know multicenter study. We divided the data into training and test data using leave-one-out cross validation to assess performance in independent patients. Performance was quantified by the Dice index. The median Dice coefficient of ATLAS algorithm was 0.6122, which was significantly higher than COMBAT Stroke, with a median Dice coefficient of 0.5636 (p < 0.0001) and the best possible performing methods based on thresholding of the diffusion weighted images (median Dice coefficient: 0.3951) or the apparent diffusion coefficient (median Dice coefficeint: 0.2839). Furthermore, the volume of the ATLAS segmentation was compared to the volume of the expert segmentation, yielding a standard deviation of the residuals of 10.25 ml compared to 17.53 ml for COMBAT Stroke. Since accurate quantification of the volume of permanently damaged tissue is essential in acute stroke patients, ATLAS may contribute to more optimal patient triaging for active or supportive therapy.

Transit time homogenization in ischemic stroke - A novel biomarker of penumbral microvascular failure?

Cerebral ischemia causes widespread capillary no-flow in animal studies. The extent of microvascular impairment in human stroke, however, is unclear. We examined how acute intra-voxel transit time characteristics and subsequent recanalization affect tissue outcome on follow-up MRI in a historic cohort of 126 acute ischemic stroke patients. Based on perfusion-weighted MRI data, we characterized voxel-wise transit times in terms of their mean transit time (MTT), standard deviation (capillary transit time heterogeneity - CTH), and the CTH:MTT ratio (relative transit time heterogeneity), which is expected to remain constant during changes in perfusion pressure in a microvasculature consisting of passive, compliant vessels. To aid data interpretation, we also developed a computational model that relates graded microvascular failure to changes in these parameters. In perfusion-diffusion mismatch tissue, prolonged mean transit time (>5 seconds) and very low cerebral blood flow (≤6 mL/100 mL/min) was associated with high risk of infarction, largely independent of recanalization status. In the remaining mismatch region, low relative transit time heterogeneity predicted subsequent infarction if recanalization was not achieved. Our model suggested that transit time homogenization represents capillary no-flow. Consistent with this notion, low relative transit time heterogeneity values were associated with lower cerebral blood volume. We speculate that low RTH may represent a novel biomarker of penumbral microvascular failure.

Cerebral small vessel disease: Capillary pathways to stroke and cognitive decline.

Cerebral small vessel disease (SVD) gives rise to one in five strokes worldwide and constitutes a major source of cognitive decline in the elderly. SVD is known to occur in relation to hypertension, diabetes, smoking, radiation therapy and in a range of inherited and genetic disorders, autoimmune disorders, connective tissue disorders, and infections. Until recently, changes in capillary patency and blood viscosity have received little attention in the aetiopathogenesis of SVD and the high risk of subsequent stroke and cognitive decline. Capillary flow patterns were, however, recently shown to limit the extraction efficacy of oxygen in tissue and capillary dysfunction therefore proposed as a source of stroke-like symptoms and neurodegeneration, even in the absence of physical flow-limiting vascular pathology. In this review, we examine whether capillary flow disturbances may be a shared feature of conditions that represent risk factors for SVD. We then discuss aspects of capillary dysfunction that could be prevented or alleviated and therefore might be of general benefit to patients at risk of SVD, stroke or cognitive decline.

Changing the needle for lumbar punctures: results from a prospective study.

OBJECTIVE: Post-dural puncture headache (PDPH) is a common complication of diagnostic lumbar punctures. Both a non-cutting needle design and the use of smaller size needles have been shown to greatly reduce the risk of PDPH. Nevertheless, larger cutting needles are still widely used. This study describes the process of changing the needle in an outpatient clinic of a Danish neurology department. METHODS: Prospective interventional trial. Phase 1: 22G cutting needle. Phase 2: 25G non-cutting needle. Practical usability of each needle was recorded during the procedure, while the rate of PDPH and the occurrence of socioeconomic complications were acquired from a standardized questionnaire. RESULTS: 651 patients scheduled for diagnostic lumbar punctures were screened for participation and 501 patients were included. The response rate was 80% in both phases. In phase 2, significant reductions were observed in occurrence of PDPH (21 vs. 50, p=0.001), number of days spent away from work (55 vs. 175, p<0.001), hospitalizations (2 vs. 17, p<0.001), and number of bloodpatch treatments (2 vs. 10, p=0.019). Furthermore, during the procedure, both the need for multiple attempts (30% vs. 44%, p=0.001), and the failure-rate of the first operator (17% vs. 29%, p=0.005) were reduced. CONCLUSIONS: Our study showed that smaller, non-cutting needles reduce the incidence of PDPH and are easily implemented in an outpatient clinic. Changing the needle resulted in fewer socioeconomic complications and fewer overall costs, while also reducing procedural difficulty.

Capillary transit time heterogeneity and flow-metabolism coupling after traumatic brain injury.

Most patients who die after traumatic brain injury (TBI) show evidence of ischemic brain damage. Nevertheless, it has proven difficult to demonstrate cerebral ischemia in TBI patients. After TBI, both global and localized changes in cerebral blood flow (CBF) are observed, depending on the extent of diffuse brain swelling and the size and location of contusions and hematoma. These changes vary considerably over time, with most TBI patients showing reduced CBF during the first 12 hours after injury, then hyperperfusion, and in some patients vasospasms before CBF eventually normalizes. This apparent neurovascular uncoupling has been ascribed to mitochondrial dysfunction, hindered oxygen diffusion into tissue, or microthrombosis. Capillary compression by astrocytic endfeet swelling is observed in biopsies acquired from TBI patients. In animal models, elevated intracranial pressure compresses capillaries, causing redistribution of capillary flows into patterns argued to cause functional shunting of oxygenated blood through the capillary bed. We used a biophysical model of oxygen transport in tissue to examine how capillary flow disturbances may contribute to the profound changes in CBF after TBI. The analysis suggests that elevated capillary transit time heterogeneity can cause critical reductions in oxygen availability in the absence of 'classic' ischemia. We discuss diagnostic and therapeutic consequences of these predictions.