Comparison of the macro and microstructure of sleep in a sample of sleep clinic hypersomnia cases

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 1 st oscillation (like N-1 and N-2), 2 nd 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.

Recognizing the Symptom Spectrum of Narcolepsy to Improve Timely Diagnosis: A Narrative Review

“…The sleep pattern at polysomnography (PSG) shows an increased frequency of sleep stage shifts besides multiple, often short awakenings. 15,[51][52][53] Importantly, sleep fragmentation does not seem to account for daytime symptoms. 54,55 Given the frequent occurrence, the presentation of nocturnal sleep fragmentation in combination with daytime sleepiness should prompt suspicion of narcolepsy, even though insomnia is often considered first.…”

Idiopathic Hypersomnia: Historical Account, Critical Review of Current Tests and Criteria, Diagnostic Evaluation in the Absence of Biological Markers and Robust Electrophysiological Diagnostic Criteria

“…23 In addition, in-depth analyses of nocturnal sleep may have a supportive value. [44][45][46][47][48] Circadian control tests, melatonin and cortisol, have value supporting the diagnosis of IHwLSD. 49,50 Currently, neuroimaging, [51][52][53] expression of key circadian proteins in dermal fibroblasts [54][55][56] and measure of an endogenous positive allosteric modulator of GABA-A in the CSF 57 cannot yet be considered as helpful in the diagnosis of IH (Table 2).…”

“…MSLT following night polysomnography Well-standardized procedure, but low validity of the test and low test-retest reliability 24-hour polysomnographic protocols 15,19,40 Inequally standardized procedures; total sleep time cut-off of 11 hours discriminating the best IH patients and controls (sensitivity 72%, specificity 97%) 19 32-hour polysomnographic protocol 41 Standardized and validated procedure; total slee time cut-off of 19 hours discriminating the best IH patients and controls (sensitivity 92%, specificity 85%) 41 Limited feasability in clinical practice Actigraphic monitoring 42 Low sleep-wake activity threshold (SWAT) + 25 epochs of sleep immobility onset and offset duration displayed the least divergent from polysomnography 42 In-depth investigations of nocturnal sleep and MSLT [44][45][46][47][48] Neither sensitive nor specific but supportive…”

“…Comparison of the macro and microstructure of sleep in a sample of NT1 (n=24), NT2 (n=3 and IH (n=25) patients and a snoring reference group of 24 subjects showed a higher sleep efficiency (p < 0.05) and a lower wake after sleep onset (p < 0.01) in patients with IH, but similar arousal indices in comparison with patients with NT1. 47 Maski et al checked if patients with NT1 (n=46), NT2 (n=12) and IH (n= 18) had distinct nocturnal sleep stability measures (number of wake and sleep stage bouts) in comparison with subjectively sleepy controls (n=48). 48 They found out that patients with IH had a similar number of bouts but better survival of stage N2 bouts (p=0.001) and shorter stage N3 bouts in the first 8 hours of sleep (p=0.003).…”