S30
2nd WASM World Congress, Bangkok, 4–8 February 2007 / Sleep Medicine 8 Suppl. 1 (2007) S11–S47
domains, such as executive function, seems to be particularly vulnerable to sleep loss. However, few studies in humans demonstrate that neural systems involved in executive function (i.e., prefrontal cortex) are more susceptible to sleep deprivation in some individuals than others. Sleep deprivation associated with disease-related sleep fragmentation, such as sleep apnea and restless legs syndrome (RLS), also results in neurocognitive deficit similar to those observed in sleep restriction/sleep loss studies [1]. There are several published data on cognitive function in sleep apnea [2], but data on RLS are very few. Recently, we evaluated 10 patients with idiopathic RLS and PLM (mean PLM index = 37.8), 10 patients with PLMD and without RLS (mean PLM index = 39), 10 patients with psychophysiological insomnia (mean PLM index = 4.8) and 20 age-matched controls [3]. A cognitive impairment has been found in the three patient group in comparison to controls by regarding: reaction time test (sustained attention), Corsi supraspan test (learning test), digit span forward (verbal short-memory). The lowest scores have been found in RLS group; in the same group, significantly lower scores in comparison to the others have been found in the Purdue Pegboard test (motor and constructional abilities). The results of Epworth Sleepiness Scale were similar in patients compared to controls, as well as those obtained in the Beck Depression rating scale. Our data suggest that RLS “per se” may determine a cognitive impairment and, moreover, may worse the negative profile caused by PLM-sleep fragmentation. The cognitive deficit in RLS patients seems to be unrelated to excessive daytime sleepiness or depressive symptoms. In another recent study, Pearson et al. [4] evaluated 16 RLS patients compared to age-matched controls by cognitive tests, including those particularly sensitive to pre-frontal cortical (PFC) functioning and sleep loss. RLS patients showed significant (p < 0.05) and sizeable (20−40%) deficits on two of the three PFC tests. Further studies by evaluating the specific treatment for RLS and PLMD may elucidate the possible reversibility of the cognitive impairment.
be presented. The therapy we developed is the first psychologically based treatment for adjunctive treatment in RLS and might provide an important step in the development of an integrated treatment approach in RLS.
Reference(s) [1] Durmer JS, Dinges DF. Neurocognitive consequences of sleep deprivation. Semin Neurol.2005; 25(1): 117−29. [2] Wong KK, Grunstein R, Bartlett D, Gordon E. Brain function in OSA: results from the Brain Resources International Database. J Integr Neurosci 2006; 5: 111−21. [3] Ferini-Strambi L. Cognitive functions in RLS patients with PLM and in PLMD patients without RLS. Sleep Med 2005; 6(Suppl 2): S31. [4] Pearson VE, Allen RP, Dean T et al. Cognitive deficits associated with RLS. Sleep Med 2006; 7: 25−30.
C.H. Schenck. Minnesota Regional Sleep Disorders Center, Hennepin County Medical Center, University of Minnesota Medical School, South Minneapolis, MN, USA
S25.D Quality of life in restless legs syndrome R. Kohnen. IMEREM GmbH, Nuremberg, Germany Changes in disease-specific quality of life (QoL) are a usual outcome measure in clinical trials on medications to treat RLS. Three questionnaires have been developed and validated. Results from clinical trials consistently show statistically significant improvements in clinical trials with dopamine agonists. Obviously, improvement in QoL is strongly associated with relief from symptoms as indicated by severity scales like the International RLS severity scale (IRLS). At the same time, health related QoL studies showed a relationship between impairment of QoL and severity of RLS symptoms: while mild RLS does not differ from the normal population values in the Short-Form 36 method, impairments in QoL increase with increasing severity of RLS. In severe RLS, QoL is as bad or even worse than in other chronic or life-threatining disorders. The relevance of QoL assessments and the relationship between diseasespecific and health-related QoL research in RLS will be discussed. The main message of this contribution will address the central importance of QoL measures in RLS for health-economic decisions which might overweight the treatment-related improvements in RLS symptoms.
S26. REM sleep behavior disorder 20 years later: sleep disorder or syndrome?
S26.1 Symposium summary
S25.B Cognitive functions in RLS S. Fulda *, J. Winkelmann, T.C. Wetter. Max Planck Institute of Psychiatry, Munich, Germany RLS is a burdening disorder with sleep disturbances and impaired quality of life. Comparatively less is known about cognitive functioning in patients with RLS. In the presentation we will review the available evidence and present new data on neuropsychological test performance in patients with RLS. S25.C Better living with RLS: optimizing the patients’coping strategies M. Hornyak. Sleep Disorders Unit, Psychiatry and Psychotherapy, University of Freiburg, Germany Current treatment trials in RLS still focus on drug therapy by assessing the control of motor and sensible symptoms. Comprehensive psycho-biological management strategies have yet to be elaborated for this patient population. Considering the high prevalence of RLS, its chronic course, and the accompanying psychosocial impairment, we developed a psychologicallybased approach to treatment, tailored to the specific aspects of the disorder, with the aim of improving coping strategies and quality of life of RLS patients (The RELEGS, “Restless Legs Skills”, Therapy Program). The therapy integrates cognitive behavioral elements and acceptance-based mindfulness approaches. Results of the proof-of-concept investigation to evaluate the feasibility, patient acceptance and efficacy of the therapy will
A symposium on REM Behavior Disorders is quite timely, given the rapid growth of clinical and research findings on RBD that raise the question of the extent to which RBD is a sleep disorder or a syndrome related to neurodegenerative disorders. Various other updates on RBD would also be timely for sleep clinicians. An international historical perspective can sharpen the focus for appreciating the implications of these new findings, and various clinical, ethical and research considerations need to be addressed and discussed. • Chair: Carlos H. Schenck, MD • Co-Chair: Rosalia Silvestri, MD, Clinica Neurologica I, Policlinico G. Martino, Via Consolare Valeria, Messina, Italy • 1st Speaker: Nana (Naoko) Tachibana, MD, PhD, Department of Brain Pathophysiology Human Brain Research Center, Kyoto University Graduate School of Medicine, Kyoto, Japan, and Director, Sleep Disorders Center, Kansai Electric Power Company Hospital, 2-1−7 Fukushima, Fukushima, Osaka, 553–0003 Japan. Phone: +81−75– 751−3695; fax: +81−75–751−3202.
[email protected] • 2nd Speaker: Jacques Montplaisir, MD, PhD, Professor of Psychiatry and Neuroscience, University of Montreal, Montreal, Canada.
[email protected] • 3rd Speaker: Carlos H. Schenck, MD • 4th Speaker: Alex Iranzo, MD • 5th Speaker: Rosalia Silvestri, MD REM sleep behavior disorder (RBD) is a parasomnia featuring loss of REMatonia, increased phasic muscle activity during REM sleep, and problematic release of dream-enacting behaviors that was formally identified 20 years ago, and subsequently incorporated within the International Classification of Sleep Disorders. During the preceding 10−20 years, however, various polysomnographic and clinical features of RBD had been detected and described by investigators from Japan, Europe and North America. An historical overview is now timely, since research on RBD has been growing and expanding rapidly. RBD typically affects middle-aged and older men, but can affect females and any age group. At the time of RBD diagnosis, affected men are