At home EEG monitoring technologies for people with epilepsy and intellectual disabilities: A scoping review.

Background: Conducting electroencephalography in people with intellectual disabilities (PwID) can be challenging, but the high proportion of PwID who experience seizures make it an essential part of their care. To reduce hospital-based monitoring, interventions are being developed to enable high-quality EEG data to be collected at home. This scoping review aims to summarise the current state of remote EEG monitoring research, potential benefits and limitations of the interventions, and inclusion of PwID in this research.

Remote Electroencephalography Monitoring of Epilepsy in Adults: Protocol for a Scoping Review.

Background: Electroencephalography (EEG) monitoring is a key tool in diagnosing and determining treatment for people with epilepsy; however, obtaining sufficient high-quality data can be a time-consuming, costly, and inconvenient process for patients and health care providers. Remote EEG monitoring has the potential to improve patient experience, data quality, and accessibility for people with intellectual or developmental disabilities.

Objective: The purpose of this scoping review is to provide an overview of the current research evidence and knowledge gaps regarding the use of remote EEG monitoring interventions for adults with epilepsy.

Hypoglycemia-Induced Changes in the Electroencephalogram: An Overview.

Hypoglycemia is defined by an abnormally low blood glucose level. The condition develops when rates of glucose entry into the systematic circulation are reduced relative to the glucose uptake by the tissues. A cardinal manifestation of hypoglycemia arises from inadequate supply of glucose to the brain, where glucose is the primary metabolic fuel.

CRFR1 activation protects against cytokine-induced β-cell death.

During the development of diabetes β-cells are exposed to elevated concentrations of proinflammatory cytokines, TNFα and IL1β, which in vitro induce β-cell death. The class B G-protein-coupled receptors (GPCRs): corticotropin-releasing factor receptor 1 (CRFR1) and CRFR2 are expressed in pancreatic islets. As downstream signaling by other class B GPCRs can protect against cytokine-induced β-cell apoptosis, we evaluated the protective potential of CRFR activation in β-cells in a pro-inflammatory setting.

Proinflammatory cytokines activate the intrinsic apoptotic pathway in beta-cells.

Objective: Proinflammatory cytokines are cytotoxic to beta-cells and have been implicated in the pathogenesis of type 1 diabetes and islet graft failure. The importance of the intrinsic mitochondrial apoptotic pathway in cytokine-induced beta-cell death is unclear. Here, cytokine activation of the intrinsic apoptotic pathway and the role of the two proapoptotic Bcl-2 proteins, Bad and Bax, were examined in beta-cells.