e212
Abstracts / Clinical Neurophysiology 128 (2017) e178–e303
O386 Prevalence and impact of subclinical epileptiform activity } cs, Gábor in Alzheimer’s-disease—András Horváth, Anna Szu Barcs, Anita Kamondi (Institute of Clinical Neurosciences, Budapest, Hungary) Introduction: Alzheimer’s-disease (AD) is the most common type of neurodegenerative disorders leading to a significant social and medical burden on the society. Evidence suggests that epileptiform activity might have a prominent role in the pathophysiology of AD. While numerous studies investigated the prevalence of epileptic seizures in AD, we lack of observations on the incidence and importance of subclinical epileptiform activity. The aim of our study was to examine AD patients using long-term EEG recording to identify the prevalence of epileptiform activity and to measure its impact on the progression of AD. Methods: We selected 42 patients meeting the criteria for probable AD. The patients underwent rigorous clinical investigation including long-term (24 h) EEG monitoring. We followed them in a 3 years long period and applied serial neuropsychological examination. Results: We identified subclinical epileptiform activity in 47% of AD patients. Activity was visible mostly on the frontotemporal electrodes (95%) with significant left side predominance (65%). Epileptiform potentials occurred prominently in sleep (82%), especially in slow wave sleep (45%). We were able to follow 21 patients (8 with-, 13 without epileptiform activity) through 3 years. Patients with epileptiform discharges showed 2-times faster cognitive decline. Conclusion: Epileptiform activity is frequent in AD, predominantly occurring in slow-wave sleep with left frontotemporal origin. Since epileptiform discharges are important contributors in the progression, antiepileptic treatment might represent a promising future target in AD. doi:10.1016/j.clinph.2017.07.113
Symposium XV. – Registering sleep objectively S103 Polysomnographic features of narcolepsy types 1 and 2, and of idiopathic hypersomnia: Strengths and limitations—Michel Billiard (Gui de Chauliac Hospital, Department of Neurology, Montpellier, France) Objectives: Current diagnostic criteria of narcolepsy types 1 (NT1), type 2 (NT2) and idiopathic hypersomnia (IH), including clinical, electrophysiological and biologic criteria are listed in the International classification of sleep disorders, 3rd edition (ICSD-3). Electrophysiological criteria have been recently weakened with the demonstration that the multiple sleep latency test (MSLT) has poor test/retest reliability. Thus the search for additional electrophysiological criteria for these central disorders of hypersomnolence. Methods: To review recent electrophysiological strategies. aiming at reinforcing current electrophysiological criteria of NT1, NT2 and IH, namely analysis of sleep stage sequence organization and complexity, sleep stage sequence analysis of sleep onser REM periods, daytime continuous polysomnography and analysis of sleep onset criteria at the MSLT. Results: Patients with NT1 differed significantly from the two other patient groups. The latter, in turn, were not different between each other. Discussion: These results show the limits of polysomnography and MSLT in accurate phenotyping of NT2 and IH, hence calling for further clinical and biologic markers of these sleep disorders.
Conclusion: Recent additional electrophysiological strategies reinforce the identity of NT1, not these of either NT2 or IH. Significance: In spite of sustained efforts, NT2 and IH lack sufficient electrophysiological diagnostic criteria. Further research is urgently needed.
doi:10.1016/j.clinph.2017.07.114
S104 Polysomnography: From the basis to the information content—Béla Faludi (University of Pécs, Neurology Department, Pécs, Hungary) Objectives and methods: Polysomnography (PSG) is the widely used diagnostic method of sleep medicine. The recorded parameters are the EEG, eye movements, muscle tone, different cardiorespiratory parameters (nasal air flow, breathing effort, ECG, oxygen saturation, etc.), body position, snoring and limb movements. On the base of the recorded parameters the alteration of the sleep architecture and background pathology can be determined. The polysomnographic abnormalities are described in the guidelines. The main challenge of PSG is the interpretation of these result. Here we present the basic principles and interpretation aspects of polysomnography. Results: The two most important background pathologies - affecting the sleep architecture - are the breathing abnormalities and movement events. The patterns of respiratorical abnormalities can define different clinical pictures. The same movement event can be the consequence of many different background pathologies (from breathing related events to periodic limb movement disorder or narcolepsy). Discussion: Interpretation of different polysomnographic abnormalities and patterns are more than a simple count of the pathological events. Different pathological backgrounds can lead to the same basic abnormalities. The clinical information about the sleep disorders will help to improve the interpretation of the polysomnographic abnormalities. Beside the clinical information, the interpretation of the polysomnographic recording depends on the reliability of the scoring and staging of the pathological events. Conclusions: Clinical information is essential for the appropriate interpretation of the polysomnographic results. Significance: Clinical information based interpretation of the PSG. Keywords: Polysomnography, Interpretation, Reliability doi:10.1016/j.clinph.2017.07.115
S105 Changes in sleep-related abnormal EEG oscillations may predict the therapeutic efficacy of drugs in mouse models of Huntington’s disease—Sandor Kantor, Janos Varga, Jennifer Morton (University of Cambridge, Department of Physiology, Anatomy and Neuroscience, Cambridge, United Kingdom) Objectives: Sleep and EEG abnormalities typically appear in Huntington’s disease (HD) before the onset of overt motor symptoms. Since drugs used for the symptomatic treatment of HD also affect sleep, we tested whether they might correct the sleep and EEG abnormalities seen in HD. Methods: We treated wild-type (WT) mice and a transgenic mouse model of HD (R6/2) acutely with zolpidem, amitriptyline, or paroxetine (0, 5, 10 and 20 mg/kg for each drug). A subgroup of R6/2 mice