TY - ABST
T1 - Evaluation of micro-sleep stability in patients with neurodegeneration using an automated algorithm
AU - Muntean, Maria-Lucia
AU - Cesari, Matteo
AU - Sixel-Döring, F
AU - Mollenhauer, Brit
AU - Christensen, Julie Anja Engelhard
AU - Bjarup Dissing Sørensen, Helge
AU - Jennum, Poul Jørgen
AU - Trenkwalder, C
PY - 2019
Y1 - 2019
N2 - Background and aims: Neurodegeneration is expected to alter sleep architecture and stability. We aimed to analyze micro-sleep stability in patients with Parkinson’s Disease (PD) compared to healthy controls (HC) and patients with isolated rapid eye movement (REM) sleep behavior disorder (iRBD), using an automated algorithm. Methods: Video-polysomnography data from 57 de novo PD patients without RBD(PD-RBD), 31 patients with iRBD, 30 de novo PD with RBD patients (PD+RBD) and 41 HC were analyzed. For micro-sleep staging, a validated algorithm (Cesari et al., IEEE 2019) classified each 5-s sleep mini-epoch as either wakefulness(W), REM or NREM sleep. To reduce the algorithm bias, we removed from analysis 5-s mini-epochs where the stage was estimated with low confidence . To quantify micro-sleep stability we used the following indices: wake-sleep(W-S) transition index (the number of transitions from wake to sleep, or vice-versa, per total sleep time), and the REM and NREM fragmentation indices(the number of transitions from REM or NREM to another stage per hour of REM or NREM sleep respectively). Results: After removing the uncertain mini-epochs, we analysed: 90.05±4.15% mini-epochs in HC, 88.87±7.86% in PD-RBD, 81.61±7.38% in iRBD and 81.10±8.00% in PD+RBD. The micro-sleep fragmentation indices were significantly higher in iRBD and PD+RBD patients compared to HC and PD-RBD(Table 1). Conclusion: Our data show a higher micro-sleep fragmentation in presence of RBD, compared to PD-RBD and HC, suggesting that the networks responsible for maintaining stable sleep may be compromised in RBD. Further research is needed to investigate the pathophysiology of micro-sleep instability. Disclosure: The patients in this study are part of the DeNoPa Cohort. The DeNoPa Study was supported by unrestricted grants from the University Medical Center Goettingen, the Paracelsus-Elena-Klinik, Kassel, Germany, the Michael J Fox Foundation for Parkinson’s Research (MJFF), ParkinsonFonds Deutschland and from TEVA Pharma.
AB - Background and aims: Neurodegeneration is expected to alter sleep architecture and stability. We aimed to analyze micro-sleep stability in patients with Parkinson’s Disease (PD) compared to healthy controls (HC) and patients with isolated rapid eye movement (REM) sleep behavior disorder (iRBD), using an automated algorithm. Methods: Video-polysomnography data from 57 de novo PD patients without RBD(PD-RBD), 31 patients with iRBD, 30 de novo PD with RBD patients (PD+RBD) and 41 HC were analyzed. For micro-sleep staging, a validated algorithm (Cesari et al., IEEE 2019) classified each 5-s sleep mini-epoch as either wakefulness(W), REM or NREM sleep. To reduce the algorithm bias, we removed from analysis 5-s mini-epochs where the stage was estimated with low confidence . To quantify micro-sleep stability we used the following indices: wake-sleep(W-S) transition index (the number of transitions from wake to sleep, or vice-versa, per total sleep time), and the REM and NREM fragmentation indices(the number of transitions from REM or NREM to another stage per hour of REM or NREM sleep respectively). Results: After removing the uncertain mini-epochs, we analysed: 90.05±4.15% mini-epochs in HC, 88.87±7.86% in PD-RBD, 81.61±7.38% in iRBD and 81.10±8.00% in PD+RBD. The micro-sleep fragmentation indices were significantly higher in iRBD and PD+RBD patients compared to HC and PD-RBD(Table 1). Conclusion: Our data show a higher micro-sleep fragmentation in presence of RBD, compared to PD-RBD and HC, suggesting that the networks responsible for maintaining stable sleep may be compromised in RBD. Further research is needed to investigate the pathophysiology of micro-sleep instability. Disclosure: The patients in this study are part of the DeNoPa Cohort. The DeNoPa Study was supported by unrestricted grants from the University Medical Center Goettingen, the Paracelsus-Elena-Klinik, Kassel, Germany, the Michael J Fox Foundation for Parkinson’s Research (MJFF), ParkinsonFonds Deutschland and from TEVA Pharma.
M3 - Conference abstract in journal
SN - 1351-5101
VL - 26
SP - 77
JO - European Journal of Neurology
JF - European Journal of Neurology
IS - Suppl. 1
M1 - O2223
ER -