The Future of Sleep in Neurology Is Here Now

In this issue of the Journal of Clinical Neurophysiology, we present papers that summarize and expand on symposia and debates on “The Future of Sleep in Neurology,” which we presented in September 2004 at the annual meeting of the American Clinical Neurophysiology Society (ACNS) in Montreal. Our goal then was to show how sleep and its disorders crucially affect some of our most common neurologic disorders. Then and now, we want to tempt clinical neurophysiologists and neurologists to expand their areas of interest and expertise to include sleep medicine. We believe the practice of sleep medicine and polysomnography has a natural home within the clinical neurophysiology laboratory: that clinical neurophysiologists are well suited to expand their knowledge base by learning sleep medicine. We also strive to show how “Sleep is that golden chaine that ties health and our bodies together” (Thomas Dekker, 1609). In the first article, I review rapidly burgeoning medical evidence that suggests that obstructive sleep apnea (OSA) is an independent risk factor for hypertension, stroke, and transient ischemic attack and severe untreated OSA (a mean of 30 or 40 apneas and hypopneas per hour of sleep) as a risk for sudden death during sleep. A dose-response association between OSA severity and hypertension has been convincingly shown, and untreated OSA alone can induce hypertension, especially in younger men (Nieto et al., 2000; Peppard et al., 2000; Sjostrum et al., 2002). Patients with untreated OSA have more strokes, stroke morbidity, and mortality than those treated. Treating patients with OSA with continuous positive airway pressure can prevent or improve hypertension, reduce abnormal elevations of inflammatory cytokines and adhesion molecules, reduce excessive sympathetic tone, avoid increased vascular oxidative stress, reverse coagulation abnormalities, and reduce leptin levels. Additionally, growing evidence shows that sleep deprivation and untreated apnea alter carbohydrate metabolism can make one fat, rather than vice versa. I argue that if OSA is so common in patients with strokes or transient ischemic attack, with the condition and its pathologies potentially reversible and diagnosis and initiation of treatment done by performing a polysomnogram, then a polysomnogram should be considered for each patient who presents with a transient ischemic attack or stroke. When I first said that, my colleagues looked at me askance, but more recently others have suggested the same (Dziewas et al., 2005). Dr. Foldvary-Schaefer and I then review the literature on sleep and epilepsy, what we know, don’t know, and need to know. Long-term video-EEG and, more recently, video-polysomnogram, have provided the means to confirm and expand on the interconnections between sleep and epilepsy. When Dr. Foldvary-Schaefer first presented part of this paper at the ACNS, she summarized some of the more firmly established relationships between sleep and epilepsy and identified intriguing associations that require further study. I think you will find this paper a critical and timely review of this growing literature on the effects of the newer antiepileptics on sleep and sleepiness, the circadian differences between temporal and extratemporal epilepsies, sleep appearing to be more independently disturbed in those with temporal lobe epilepsy, the high prevalence of sleep/wake