Patient-Provider Communication in Inpatient AAC

This poster provides a definition of effective patient-provider communication and an overview of the barriers to and risks of poor patient-provider communication in an acute setting. The use of augmentative and alternative communication (AAC) supports in inpatient settings to improve patient outcomes and to benefit both patient and provider will be discussed. Strategies to implement AAC tools and the role of the SLP in supporting effective patient-provider communication will be identified.https://griffinshare.fontbonne.edu/slp-posters/1007/thumbnail.jp

Opening an Observation Unit

The definition, benefits, and structure of an observation unit within a hospital.https://digitalcommons.centracare.com/nursing_posters/1068/thumbnail.jp

Average is optimal: An inverted-U relationship between trial-to-trial brain activity and behavioral performance

It is well known that even under identical task conditions, there is a tremendous amount of trial-to-trial variability in both brain activity and behavioral output. Thus far the vast majority of event-related potential (ERP) studies investigating the relationship between trial-to-trial fluctuations in brain activity and behavioral performance have only tested a monotonic relationship between them. However, it was recently found that across-trial variability can correlate with behavioral performance independent of trial-averaged activity. This finding predicts a U- or inverted-U- shaped relationship between trial-to-trial brain activity and behavioral output, depending on whether larger brain variability is associated with better or worse behavior, respectively. Using a visual stimulus detection task, we provide evidence from human electrocorticography (ECoG) for an inverted-U brain-behavior relationship: When the raw fluctuation in broadband ECoG activity is closer to the across-trial mean, hit rate is higher and reaction times faster. Importantly, we show that this relationship is present not only in the post-stimulus task-evoked brain activity, but also in the pre-stimulus spontaneous brain activity, suggesting anticipatory brain dynamics. Our findings are consistent with the presence of stochastic noise in the brain. They further support attractor network theories, which postulate that the brain settles into a more confined state space under task performance, and proximity to the targeted trajectory is associated with better performance

Economies of Plunder: The Case of Rosewood Extraction and Indigenous Rights in Southern Belize

Professional paper for the fulfillment of the Master of Public Policy program.New middle income countries in the Global South are leveraging established neocolonial structures of dependence to extract raw resources from other countries in the Global South. In Belize, China’s demand for tropical hardwoods has come face-to-face with an indigenous land rights movement. Using the extraction of rosewood from Belize as a case, this paper explores the following questions: (1) What do new patterns of neocolonial extraction look like? (2) Who are the actors at both ends of the relationship? (3) What tools have indigenous communities used to protect their economic and self-governing rights? and (4) Have they been successful

A comparison of resting state functional magnetic resonance imaging to invasive electrocortical stimulation for sensorimotor mapping in pediatric patients

Localizing neurologic function within the brain remains a significant challenge in clinical neurosurgery. Invasive mapping with direct electrocortical stimulation currently is the clinical gold standard but is impractical in young or cognitively delayed patients who are unable to reliably perform tasks. Resting state functional magnetic resonance imaging non-invasively identifies resting state networks without the need for task performance, hence, is well suited to pediatric patients. We compared sensorimotor network localization by resting state fMRI to cortical stimulation sensory and motor mapping in 16 pediatric patients aged 3.1 to 18.6 years. All had medically refractory epilepsy that required invasive electrographic monitoring and stimulation mapping. The resting state fMRI data were analyzed using a previously trained machine learning classifier that has previously been evaluated in adults. We report comparable functional localization by resting state fMRI compared to stimulation mapping. These results provide strong evidence for the utility of resting state functional imaging in the localization of sensorimotor cortex across a wide range of pediatric patients

Responsive neurostimulation for people with drug-resistant epilepsy and autism spectrum disorder

PURPOSE: Individuals with autism spectrum disorder (ASD) have comorbid epilepsy at much higher rates than the general population, and about 30% will be refractory to medication. Patients with drug-resistant epilepsy (DRE) should be referred for surgical evaluation, yet many with ASD and DRE are not resective surgical candidates. The aim of this study was to examine the response of this population to the responsive neurostimulator (RNS) System. METHODS: This multicenter study evaluated patients with ASD and DRE who underwent RNS System placement. Patients were included if they had the RNS System placed for 1 year or more. Seizure reduction and behavioral outcomes were reported. Descriptive statistics were used for analysis. RESULTS: Nineteen patients with ASD and DRE had the RNS System placed at 5 centers. Patients were between the ages of 11 and 29 (median 20) years. Fourteen patients were male, whereas five were female. The device was implanted from 1 to 5 years. Sixty-three percent of all patients experienced a \u3e50% seizure reduction, with 21% of those patients being classified as super responders (seizure reduction \u3e90%). For the super responders, two of the four patients had the device implanted for \u3e2 years. The response rate was 70% for those in whom the device was implanted for \u3e2 years. Improvements in behaviors as measured by the Clinical Global Impression Scale-Improvement scale were noted in 79%. No complications from the surgery were reported. CONCLUSIONS: Based on the authors\u27 experience in this small cohort of patients, the RNS System seems to be a promising surgical option in people with ASD-DRE

Axodendritische Verteilung der Isoformen von Tau in primären neuronalen Zellkulturmodellen der Demenz

Tau ist ein neuronales Protein, welches in kausalen Zusammenhang mit der Alzheimer Demenzerkrankung (AD), der Frontotemporalen Demenz (FTD), und anderen Tauopathien gebracht wird. Als Mikrotubuli-Assoziertes Protein (MAP) ist Tau vorwiegend in axonalen Fortsätzen von Neuronen lokalisiert. Im pathologischen Verlauf der AD wird Tau aber auch in die dendritischen Fortsätze von Neuronen umverteilt. Die polare Verteilung von Tau wird somit aufgehoben. Tau kommt im Zentralen Nervensystem von Erwachsenen in 6 Isoformen vor, die sich durch die An- oder Abwesenheit von 2 N-terminalen Einschüben (N) oder der 2. (von insgesamt 4) Repeat-Einheit (R) unterscheiden. Der Einfluss dieser 6 Isoformen von Tau auf den Prozess der pathologischen Fehlverteilung ist nicht bekannt. In dieser Arbeit wurde daher die physiologische und die pathologische Verteilung der unterschiedlichen Tau-Isoformen untersucht. Als Modell wurde ein definiertes Modell der neuronalen Zellpolarität, primäre Nagetiervorderhirnneurone, verwendet. Primäre Neurone sind ein etabliertes Modellsystem für die Untersuchung von Tau im Kontext der neuronalen Entwicklung, sowie für die Untersuchung neuronaler Krankheitsprozesse. Primäre Neuronen zu kultivieren ist jedoch aufwendig und erfordert meist die Verwendung von kostenintensiven und patent-geschützten Zellkulturmedien unbekannter Zusammensetzung. Im ersten Kapitel wird daher eine kostengünstige und simplifizierte Prozedur zum Kultivieren von primären Neuronen beschrieben, basierend auf einer mittlerweile kommerziell erhältlichen Variante eines neuronalen Zellkultursupplement (NS21) mit bekannter Zusammensetzung. Weiterhin werden Techniken für die Fixierung und Immunfluoreszenzfärbung beschrieben, die für die Untersuchung der Verteilung von Tau in primären Neuronen notwendig sind. Primäre Neurone sind mit nicht-viralen Vektoren schwierig zu transfizieren und empfind-lich gegenüber zytoskelettalen Manipulationen und Lebend-Zell-Beobachtung, insbeson-dere nach mehrwöchiger Kultivierung. In einem zweiten Kapitel wird daher eine einfache nicht-virale Transfektionsmethode beschrieben, die es ermöglicht Tau in allen neuronalen Entwicklungsstufen in ähnlich niedrigen Mengen wie endogenes Tau zu exprimieren. Mithilfe der o. g. Methoden, insbesondere Transfektion der unterschiedlichen Tau-Isoformen des Menschen und der Maus in primären Neuronen, wurde schließlich in einem dritten Kapitel das axodendritische Verteilungsmuster von Tau untersucht. Es zeigte sich, dass die Tau Diffusionsbarriere (TDB), lokalisiert inmitten des Axon-Initialen-Segments (AIS), sowohl die retrograde als auch die anterograde Ausbreitung von Tau kontrolliert. Während die Tau-Isoformen ohne N-terminale Inserts effizient in das Axon geleitet werden, verbleibt die längste Tau-Isoform (2N4R-Tau) teilweise im Zellsoma und Dendriten, wo sie das Wachstum von Dendriten und dendritischen Dornen beschleunigt. Die TDB (lokalisiert im AIS) wurde durch Knockdown von AIS-Komponenten (ankyrin G, EB1), oder Überexpression einer AD-assozierten Kinase, Glykogen-Synthase-Kinase-3-beta (GSK3beta), gestört. Mithilfe von hochauflösender Nanoskopie und Lebendzellbeobachtung konnte gezeigt werden, dass die Mikrotubuli im AIS sehr dynamisch sind, eine axonale Besonderheit essentiell für die Funktion der TDB. Pathomechanistische Veränderungen im AIS nach Exposition mit Amyloid-beta (der AD-auslösende Faktor) waren Aktivierung von Cofilin und f-Aktin Umstrukturierung (beides wichtige Regulatoren des Aktin basierten Zytoskeletts), sowie eine reduzierte Dynamik des Mikrotubuli-Zellskelettsystems. Gleichzeitig brach die AIS/TDB Verteilungsfunktion zusammen, was zu AD-ähnlicher Fehlverteilung von Tau führte. Insgesamt wurden in der vorliegenden Arbeit Methoden für die Kultivierung und Transfektion von primären Neuronen entwickelt, mittels welcher dann gezeigt wurde, dass die unterschiedlichen Tau Isoformen von Mensch und Maus sich sowohl untereinander, als auch in AD-ähnlichem Stress im axodendritischen Verteilungsmuster unterscheiden. Die Tau-Isoformen beschleunigen in unterschiedlichem Ausmaß das Dendriten- und dendritisches Dornenwachstum. Weiterhin hängt die differenzielle axodendritische Verteilung der Tau Isoformen von der Integrität der TDB und des AIS ab. Zukünftige Forschung wird die spezielle Verteilung und die dendritischen Effekte insbesondere von 2N4R-Tau, welches derzeit bevorzugt für Mausmodelle eingesetzt wird, in Betracht ziehen müssen.Tau isoforms show differential axodendritic distributions in primary neuronal cell culture models of dementia The protein Tau is a neuronal protein associated with Alzheimer Disease (AD), Frontotemporal Dementia (FTD) and many other neurological diseases summarized as Tauopathies. Tau is a Microtubule Associated Protein (MAP) present predominantly in axons, but becomes mislocalized in pathological settings. In the human central nervous system (CNS), Tau exists in 6 splice variants, differentiated by the presence or absence of the second of four repeats or of 2 N-terminal inserts. The contribution of these Tau isoforms to axodendritic mislocalization in neuropsychiatric disease is understudied. Here we investigate the physiological sorting and pathological missorting of the different isoforms of Tau in primary rodent forebrain neurons. This cell model is an established model of neuronal cell polarity. Primary neurons have proven to be an invaluable tool for the investigation of Tau and neuronal cell polarity in the context of neuronal development and neurodegeneration. Culturing neurons, however, is time consuming and requires multiple feeding steps and media exchanges, and either the use of proprietary media supplements or tedious preparation of complex media. In a first step we describe and define a relatively cheap and easy cell culture procedure based on a commercially available neuronal culture supplement with 21 ingredents (NS21) of known composition, as well as basic fixation techniques. Also, mature primary neurons are notoriously difficult to transfect with nonviral vectors and are very sensitive both to cytoskeletal manipulation and to imaging. Thus, in a second step, we developed and described a simple nonviral transfection method enabling transfection of Tau to achieve expression levels comparable to endogenous Tau. Finally, using the above described methods such as expression of different isoforms of human and mouse Tau in primary neurons, we investigated the sorting behavior of Tau. We found that the Tau diffusion barrier (TDB), located within the axon initial segment (AIS), controls not only retrograde but also anterograde traffic of Tau. Tau isoforms without the N-terminal inserts were sorted efficiently into the axon. However, the longest isoform (2N4R-Tau) was partially retained in cell bodies and dendrites, where it accelerated spine and dendrite growth. The TDB was impaired when AIS components (ankyrin G, EB1) were knocked down or when glycogen synthase kinase-3-beta (GSK3beta; an AD-associated kinase tethered to the AIS) was overexpressed. Using superresolution nanoscopy and live-cell imaging, we observed that microtubules within the AIS appeared highly dynamic, a feature essential for the TDB. Pathomechanistically, amyloid-beta insult caused cofilin activation, f-actin remodeling and subsequent impaired microtubule dynamics in the AIS. Concomitantly, the AIS/TDB sorting function failed, causing AD-like Tau missorting. In summary, we provide evidence that the Tau isoforms differ in physiological and pathological axodendritic sorting, and that the axodendritic distribution of Tau depends on AIS integrity and maintenance of microtubule dynamics. Current mouse models mainly expressing only human 2N4R-Tau isoform will have to be reevaluated due to the particular distribution and function of this usually very little expressed isoform

Characterization of Scale-Free Properties of Human Electrocorticography in Awake and Slow Wave Sleep States

Like many complex dynamic systems, the brain exhibits scale-free dynamics that follow power-law scaling. Broadband power spectral density (PSD) of brain electrical activity exhibits state-dependent power-law scaling with a log frequency exponent that varies across frequency ranges. Widely divergent naturally occurring neural states, awake and slow wave sleep (SWS), were used to evaluate the nature of changes in scale-free indices of brain electrical activity. We demonstrate two analytic approaches to characterizing electrocorticographic (ECoG) data obtained during awake and SWS states. A data-driven approach was used, characterizing all available frequency ranges. Using an equal error state discriminator (EESD), a single frequency range did not best characterize state across data from all six subjects, though the ability to distinguish awake and SWS ECoG data in individual subjects was excellent. Multi-segment piecewise linear fits were used to characterize scale-free slopes across the entire frequency range (0.2–200 Hz). These scale-free slopes differed between awake and SWS states across subjects, particularly at frequencies below 10 Hz and showed little difference at frequencies above 70 Hz. A multivariate maximum likelihood analysis (MMLA) method using the multi-segment slope indices successfully categorized ECoG data in most subjects, though individual variation was seen. In exploring the differences between awake and SWS ECoG data, these analytic techniques show that no change in a single frequency range best characterizes differences between these two divergent biological states. With increasing computational tractability, the use of scale-free slope values to characterize ECoG and EEG data will have practical value in clinical and research studies

A Pilot Study of Continuous Limited-Channel aEEG in Term Infants with Encephalopathy

ObjectiveTo evaluate the accuracy, feasibility, and impact of limited-channel amplitude integrated electroencephalogram (aEEG) monitoring in encephalopathic infants. Study design Encephalopathic infants were placed on limited-channel aEEG with a software-based seizure event detector for 72 hours. A 12-hour epoch of conventional EEG-video (cEEG) was simultaneously collected. Infants were randomly assigned to monitoring that was blinded or visible to the clinical team. If a seizure detection event occurred in the visible group, the clinical team interpreted whether the event was a seizure, based on review of the limited-channel aEEG. EEG data were reviewed independently offline. Results In more than 68 hours per infant of limited-channel aEEG monitoring, 1116 seizures occurred (>90% clinically silent), with 615 detected by the seizure event detector (55%). Detection improved with increasing duration of seizures (73% >30 seconds, 87% >60 seconds). Bedside physicians were able to accurately use this algorithm to differentiate true seizures from false-positives. The visible group had a 52% reduction in seizure burden (P = .114) compared with the blinded group. Conclusions Monitoring for seizures with limited-channel aEEG can be accurately interpreted, compares favorably with cEEG, and is associated with a trend toward reduced seizure burden