The mobile sleep medicine model in neurologic practice: Rationale and application

BACKGROUND: Undiagnosed obstructive sleep apnea (OSA) is prevalent in neurological practice and significantly contributes to morbidity and mortality. OSA is prevalent in US adults and causes poor quality sleep and significant neurocognitive, cardiovascular, and cerebrovascular impairments. Timely treatment of OSA reduces cardio-cerebrovascular risks and improves quality of life. However, most of the US population has limited systematic access to sleep medicine care despite its clinical significance. FOCUS: We discuss the importance of systematic screening, testing, and best-practice management of OSA and hypoventilation/hypoxemia syndromes (HHS) in patients with stroke, neurocognitive impairment, and neuromuscular conditions. This review aims to introduce and describe a novel integrated Mobile Sleep Medicine (iMSM) care model and provide the rationale for using an iMSM in general neurological practice to assist with systematic screening, testing and best-practice management of OSA, HHS, and potentially other sleep conditions. KEY POINTS: The iMSM is an innovative, patient-centered, clinical outcome-based program that uses a Mobile Sleep Medicine Unit-a sleep lab on wheels -designed to improve access to OSA management and sleep care at all levels of health care system. The protocol for the iMSM care model includes three levels of operations to provide effective and efficient OSA screening, timely testing/treatment plans, and coordination of further sleep medicine care follow-up. The iMSM care model prioritizes effective, efficient, and patient-centered sleep medicine care; therefore, all parties and segments of care that receive and provide clinical sleep medicine services may benefit from adopting this innovative approach

Cardiorespiratory profiling reveals primary breathing dysfunction in Kcna1-null mice: Implications for sudden unexpected death in epilepsy

Sudden unexpected death in epilepsy (SUDEP) is the leading cause of epilepsy-related mortality, but the relative importance of underlying cardiac and respiratory mechanisms remains unclear. To illuminate the interactions between seizures, respiration, cardiac function, and sleep that contribute to SUDEP risk, here we developed a mouse epilepsy monitoring unit (EMU) to simultaneously record video, electroencephalography (EEG), electromyography (EMG), plethysmography, and electrocardiography (ECG) in a commonly used genetic model of SUDEP, the Kcna1 knockout (Kcna1) mouse. During interictal periods, Kcna1 mice exhibited an abnormal absence of post-sigh apneas and a 3-fold increase in respiratory variability. During spontaneous convulsive seizures, Kcna1 mice displayed an array of aberrant breathing patterns that always preceded cardiac abnormalities. These findings support respiratory dysfunction as a primary risk factor for susceptibility to deleterious cardiorespiratory sequelae in epilepsy and reveal a new role for Kcna1-encoded Kv1.1 channels in the regulation of basal respiratory physiology