Medication self-management toolkits for adults with multiple sclerosis: A scoping review.

Background: Multiple sclerosis (MS) is an autoimmune disease that is often treated with multiple medications. Managing multiple medications, also known as polypharmacy, can be challenging for persons with MS. Toolkits are instructional resources designed to promote behaviour change. Toolkits may support medication self-management for adults with MS, as they have been useful in other populations with chronic conditions. Objective: The main purpose of this review was to identify and summarize medication self-management toolkits for MS, as related to the design, delivery, components, and measures used to evaluate implementation and/or outcomes. Methods: A scoping review was conducted following guidelines by JBI. Articles were included if they focused on adults (18 years or older) with MS. Results: Six articles reporting on four unique toolkits were included. Most toolkits were technology-based, including mobile or online applications, with only one toolkit being paper-based. The toolkits varied in type, frequency, and duration of medication management support. Varying outcomes were also identified, but there were improvements reported in symptom management, medication adherence, decision-making, and quality of life. The six studies were quantitative in design, with no studies exploring the user experience from a qualitative or mixed-methods design. Conclusions: There is limited research on medication self-management toolkits among adults with MS. Future development, implementation, and evaluation mixed-methods research are needed to explore user experiences and overall design of toolkits.

Secondary thalamic neuroinflammation after focal cortical stroke and traumatic injury mirrors corticothalamic functional connectivity.

While cortical injuries, such as traumatic brain injury (TBI) and neocortical stroke, acutely disrupt the neocortex, most of their consequent disabilities reflect secondary injuries that develop over time. Thalamic neuroinflammation has been proposed to be a biomarker of cortical injury and of the long-term cognitive and neurological deficits that follow. However, the extent to which thalamic neuroinflammation depends on the type of cortical injury or its location remains unknown. Using two mouse models of focal neocortical injury that do not directly damage subcortical structures-controlled cortical impact and photothrombotic ischemic stroke-we found that chronic neuroinflammation in the thalamic region mirrors the functional connections with the injured cortex, and that sensory corticothalamic regions may be more likely to sustain long-term damage than nonsensory circuits. Currently, heterogeneous clinical outcomes complicate treatment. Understanding how thalamic inflammation depends on the injury site can aid in predicting features of subsequent deficits and lead to more effective, customized therapies.

Mapping hepatic blood oxygenation by quantitative BOLD (qBOLD) MRI.

PURPOSE: Abnormalities in hepatic oxygen delivery and oxygen consumption may serve as a significant indicator of hepatic cellular dysfunction and may predict treatment response. However, conventional and oxygen-enhanced hepatic BOLD MRI can only provide semiquantitative assessment of hepatic oxygenation. METHODS: A hepatic quantitative BOLD (qBOLD) model was proposed for noninvasive mapping of hepatic venous blood oxygen saturation (Yv ) and deoxygenated blood volume (DBV) in human subjects. The validity and the estimation bias of the proposed model were evaluated by Monte Carlo simulations. Eight healthy subjects were scanned after written consent with institutional review board approval. RESULTS: Monte Carlo simulations demonstrated that the proposed single-compartment hepatic qBOLD model leads to significant deviation of the predicted T2* decay profile from the simulated signal due to high hepatic blood volume fraction. Small relative estimation bias for hepatic Yv and significant overestimation for hepatic DBV were observed, which can be corrected by applying the calibration curves established from simulations. After correction, the mean hepatic Yv in human subjects was 56.8 ± 6.8%, and the mean hepatic DBV was 0.190 ± 0.035, consistent with measurements from other invasive approaches. Except in regions with significant vascular contamination, the maps for hepatic Yv and DBV were relatively homogenous. CONCLUSIONS: With estimation bias correction, the hepatic qBOLD approach enables noninvasive mapping of hepatic blood volume and oxygenation in human subjects. The established protocol may be used to quantitatively assess hepatic tissue hypoxia in multiple liver diseases.