The central theme of my research is integration of data obtained from diverse physiological measurement tools to better understand sleep and sleepiness. Functional neuroimaging has demonstrated the neurocircuitry vulnerable in sleep apnea, narcolepsy, and following sleep deprivation and fragmentation. Assessment of hypoxia effects relatively free from sleep fragmentation is ongoing. There are strong suggestions that residual symptoms in highly treatment compliant patients with sleep apnea are due to ongoing sleep fragmentation from "complex disease" - chemoreflex mediated or modulated upper airway obstruction. We are developing methods to modulate CO2 to improve management of chemoreflex-driven sleep apnea syndromes.
The development of a ECG-based sleep spectrographic technique has provided profound insights into the nature of sleep that challenges the conventional characterization of sleep (staging, utility of delta power as an assay of sleep homeostatic drive, arousal scoring, respiratory event scoring). Sleep spectrograms are now being applied to rodent models of heart failure to between understand the temporal relationships between sleep fragmentation and heart failure. The hereditability of spectrographic phenotyping characteristics is being evaluated.