Greater insights into the mechanisms and consequences of sleep and sleep disorders have been achieved through advances in brain imaging methods that describe various aspects of neural function. These are collectively referred to as functional neuroimaging. These include techniques such as PET, fMRI, single-photon emission computed tomography (SPECT), transcranial sonography, magnetoencephalography (MEG), low-resolution brain electromagnetic tomography (LORETA), and combined methods such as combined EEG and fMRI. Extensive applications of brain imaging have been made to help clarify the changes in regional brain function that result from perturbations in either homeostatic or circadian processes, and also have clarified the relationship between these brain changes and the behavioral consequences of these disruptions. The earliest applications of neuroimaging to the study of sleep disorders were those of functional neuroimaging methods to study the global brain states of waking, NREM, and REM sleep. Brain imaging studies have been utilized in narcolepsy and the hypersomnias.

This chapter addresses the prevalence of sleepiness in obstructive sleep apnea syndrome (OSA) and the potential confusion with fatigue, depression and attentional deficits. In clinical practice, sleepiness is in most cases evaluated by the Epworth Sleepiness Scale (ESS). Sleep fragmentation and other sleep structure disturbances are classically considered the main causes of daytime sleepiness in OSA patients. Sleepiness, regardless of its cause, affects driving ability through increased reaction time, inattentiveness or microsleep episodes. Obstructive sleep apnea syndrome (OSAS) and hypertension are linked in a dose-response fashion. This is true even when taking into account confounding factors such as age, alcohol, tobacco consumption, and body mass index (BMI). The beneficial continuous positive airway pressure (CPAP) effect is obtained after only a few weeks of treatment, with quality of life returning to normal. CPAP treatment restores normal alertness except in some patients with residual excessive sleepiness.

This chapter reviews the clinical and polysomnographic features of elderly narcoleptic subjects, and considers co-morbidity and therapeutic issues. A number of narcoleptic patients are older than 40 at diagnosis, this being due either to mild disease severity or misdiagnosis, or diagnosis delayed until late-life expression of cataplexy, or narcolepsy lacking cataplexy. Knowledge about the co-morbid disorders in narcolepsy is important inasmuch as it may sometimes contribute to diagnosis and it may also bring some insights into the pathophysiology of narcolepsy. Among the most frequently associated diseases were parasomnias, sleep-related breathing disorders, sleep-related movement disorders, internistic diseases, neurological disorders, and psychiatric disorders. Moreover, various drugs, such as stimulants, antidepressants, and sodium oxybate used in narcolepsy have been tested in adult patients over a range of ages, but not specifically in elderly subjects.