Abstract
The purpose of this study was to elucidate the differentiating or grouping EEG characteristics in various hypersomnias (type 1 and type 2 narcolepsy (N-1 and N-2) and idiopathic hypersomnia (IH) compared to an age-matched snoring reference group (SR). Polysomnogram sleep EEG was decomposed into a 4-frequency state model. The IH group had higher sleep efficiency (SE; 92.3% vs. 85.8%; sp < 0.05), lower WASO (IH = 35.4 vs. N-1 = 65.5 min; p < 0.01), but similar (i.e. high) arousal indices as N-1 (~33/h). N-1 and N-2 had earlier REM latency than IH and SR (N-1 = 64.8, N-2 = 76.3 vs. IH/SR = 118 min, p < 0.05). N-1 and N-2 showed an increase in MF1 segments (characteristic of stage 1 and REM) across the night as well as distinct oscillations every 2 h, but MF1 segment timing was advanced by 30 min compared to the SR group (p < 0.05). This suggests the presence of circadian organization to sleep that is timed earlier or of increased pressure and/or lability. MF1 demonstrated a mixed phenotype in IH, with an early 1st oscillation (like N-1 and N-2), 2nd oscillation that overlapped with the SR group, and a surge prior to wake (higher than all groups). This phenotype may reflect a heterogeneous group of individuals, with some having more narcolepsy-like characteristics (i.e. REM) than others. LF domain (delta surrogate) was enhanced in IH and N-1 and more rapidly dissipated compared to N-2 and SR (p < 0.05). This suggests an intact homeostatic sleep pattern that is of higher need/reduced efficiency whereas rapid dissipation may be an underlying mechanism for sleep disruption.
Highlights
Central nervous system (CNS) hypersomnias are characterized by profound sleepiness in the absence of other explanatory factors, such as behavioral sleep restriction, circadian rhythm misalignment, or other medical/psychological disorders (AASM, 2014)
Narcolepsy is diagnostically partitioned into type 1 (N-1) and type 2 (N-2), with N-1 characterized by the presence of cataplexy or low CSF hypocretin and N-2 being characterized by the absence of cataplexy and/or normal hypocretin levels
Several studies have shown that, compared to controls, N-1 is associated with reduced sleep efficiency, increased wake after sleep onset (WASO), high arousal indices, frequent sleep stage transitions, increased time in “light” sleep (Sorensen et al, 2013; Pizza et al, 2015; Mukai et al, 2003; Khatami et al 2008; Jiménez-Correa et al, 2009; Frauscher et al, 2011; Roth et al, 2013) and abnormal rapid eye movement (REM) sequencing (Liu et al, 2015; Drakatos et al, 2016)
Summary
Central nervous system (CNS) hypersomnias are characterized by profound sleepiness in the absence of other explanatory factors, such as behavioral sleep restriction, circadian rhythm misalignment, or other medical/psychological disorders (AASM, 2014). Several studies have shown that, compared to controls, N-1 is associated with reduced sleep efficiency, increased wake after sleep onset (WASO), high arousal indices, frequent sleep stage transitions, increased time in “light” sleep (Sorensen et al, 2013; Pizza et al, 2015; Mukai et al, 2003; Khatami et al 2008; Jiménez-Correa et al, 2009; Frauscher et al, 2011; Roth et al, 2013) and abnormal REM sequencing (Liu et al, 2015; Drakatos et al, 2016) It is well-documented that N-1 patients have a shortened latency to nocturnal REM, known to be statistically specific for low or absent hypocretin (Andlauer et al, 2013; Reiter et al, 2015; Cairns and Bogan, 2015)
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