Sleep Medicine 8 Suppl. 1(2007) S3–S4 www.elsevier.com/locate/sleep
Plenary Keynote Lectures PKL.01 Details not available at time of printing. PKL.02 Sleep disorders and public health M. Partinen. President of WASM; Skogby Sleep Clinic, Rinnekoti Research Centre, Espoo, Finland All sleep researchers know that humans must sleep to survive and that 1/3 of life consists of sleep. Sleep medicine is, however, not yet considered as an important field in health and social care. I am not aware of any University in the world where sleep medicine is part of obligatory curriculum during medical studies. This is very interesting if compared with time given in education of many other diseases, of much smaller public health importance. We all should look at mirrors. Have we been too shy, too diplomatic? For more than 20 years sleep clinicians and epidemiologists we have been talking that we need cheaper methods to study and treat sleep disorders such as sleep apnea because we have limited resources in health care. Not many other people in clinical medicine or surgery are talking that they should limit to develop methods because resources are limited. I am afraid that our strategy has not given us more resources. There are some exceptions with professor William (Bill) Dement in the frontline. He has never been shy and his efforts have given resources so that USA is without any question leading the way in sleep medicine. Other brave people to fight for more resources are found e.g. in Germany, which is the leading country in Europe in developing sleep medicine. I will discuss some of the most important areas where we should focus more and more if we think about importance of sleep and sleep disorders in the perspective of public health. Some of there areas are (not necessarily in order of importance): • Sleep loss and traffic/working accidents; cumulative effects of sleep loss • Occupational health, legislation, working times, benefits of screening of sleep apnea • Sleep medicine and health economical issues; treating sleep disorders save money? • Teenager’s sleep; starting times of schools; afternoon programs • Womens’ sleep, menopause and sleep • Sleep disorders and disturbed sleep–wake cycle among elderly people – Intervention studies by long-term monitoring of sleep–wake cycle • Clinical significance of quality of sleep and maintaining sleep • Lack of (good quality) sleep deprivation and insulin resistance/obesity • Sleep apnea in relation to visceral obesity and metabolic syndrome – Interventional studies to prevent/treat visceral obesity • Sleep disorders related to cardiovascular and cerebrovascular disease – Disordered endothelial function, inflammatory processes, prevention • Weight loss in treatment of sleep apnea • Psychiatric disorders and sleep • Restless legs syndrome and other sleep related movement disorders • Development of modern diagnostic methods and methods of evaluating risks of sleep disorders; HRV, autonomic function, biological blood markers, genetics PKL.03 Fatal familial insomnia: sleep and limbic system E. Lugaresi. Sleep Lab, Neurological Clinic, Department of Neurological Sciences, University of Bologna, Italy Fatal familial insomnia (FFI) is a human prion disease linked to the haplotype D172N-129M of the prion protein gene. The disease arises at around age 50 years and has a course of 8 + 32 months. Apathy and drowsiness are the heralding symptoms. Loss of sleep, motor signs and generalized sympathetic activation are the cardinal symptoms and 1389-9457/ $ – see front matter © 2007 Elsevier B.V. All rights reserved.
signs of the disease whose pathological correlate is selective thalamic degeneration predominantly involving the anteroventral and mediodorsal nuclei. Atrophy of the anteroventral and mediodorsal thalamic nuclei severs the connection between limbic cortex and hypothalamus and brain stem reticular formation leading to a state of generalized overactivity. Morvan’s chorea and delirium tremens share the same cardinal features as FFI: the disconnection within the limbic system is again the factor responsible for generalized overactivation resulting in organic insomnia, i.e. agrypnia (from the Greek, to chase sleep) excitata. Sleep is controlled by a neuronal network running from the limbic cortex to the brain stem. This extensive network is embedded in the limbic system and operates in an integrated fashion following a caudo-rostral Jacksonian scheme. PKL.04 Sleep phylogeny: clues and challenges for theories of sleep function J. Siegel. Professor of Psychiatry, UCLA, and Chief of Neurobiology Research VA GLAHS Sepulveda, CA, USA The functions of mammalian sleep remain unclear. Most theories suggest a role for non-REM sleep in energy conservation and in nervous system recuperation from waking activities. Theories of REM sleep function have suggested a role for this state in periodic brain activation during sleep, in localized recuperative processes and in emotional regulation. Across species, the amount and nature of sleep is correlated with age, body size and ecological variables, including life in the terrestrial vs. aquatic environment, diet and the safety of the sleeping site. Sleep may be an efficient time for the completion of a number of neurological and physiological functions, but variations in sleep expression indicate that these functions may differ across species. PKL.05 Narcolepsy: Are we making a difference? M. Thorpy. Director, Sleep–Wake Disorders Center, Montefiore Medical Center, and Professor of Neurology, Albert Einstein College of Medicine, Bronx, New York, USA Narcolepsy treatment has changed dramatically over the last century. For the treatment of sleepiness in narcolepsy we have progressed from the early use of caffeine. We now have available a variety of different stimulants, and a new wake-promoting agent, modafinil, which is widely regarded as the firstline medication for narcolepsy. Cataplexy is now managed by medications whereas behavioral treatment, such as avoidance of emotion, was the only treatment available in the past. From the widespread use of antidepressant medications for cataplexy we now have a medication, sodium oxybate, which is the only FDA approved medication for narcolepsy, yet works by an unknown mechanism. We also recognize that other sleep disorders can occur in narcolepsy, such as obstructive sleep apnea syndrome or REM sleep behavior disorder, and new treatments do allow these comorbid conditions to be effectively treated. However, we cannot cure narcolepsy but are the new treatments for excessive sleepiness and cataplexy effective? Are we improving the quality of life for our patients? Can we do so without harm such as that which occurs due to the adverse effect of medications? Why is it that some of our patients choose not to undergo pharmacotherapy for narcolepsy?