Study Objectives: Mandibular advancement device (MAD) outcome varies between patients. We hypothesized that upper airway collapse sites, patterns, and degrees assessed during baseline drug-induced sleep endoscopy (DISE) affect MAD outcome. Methods: One hundred patients with obstructive sleep apnea (OSA) were included and underwent baseline type 1 polysomnography. MAD was fitted intraorally at fixed 75% maximal protrusion. A total of 72 patients completed 3-month follow-up polysomnography and baseline DISE. Response was defined as apneahypopnea index (AHI) reduction ≥ 50%, deterioration as AHI increases during MAD treatment compared to baseline. Results: Adjusting for baseline AHI and body mass index, patients with tongue base collapse showed 3.69 higher odds (1.27-10.73; P = .0128) for response.Complete concentric collapse at the level of the palate (5.32 [1.21-23.28]; P = .0234) and complete laterolateral oropharyngeal collapse (6.62 [1.14-38.34]; P = .0330) related to deterioration. Results for tongue base collapse and complete concentric collapse at the level of the palate were confirmed in the moderate to severe OSA subgroup. Applying these results to this selected subgroup increased response rate with 54% and decreased deterioration rate with 53%. These results were confirmed using other response and deterioration definitions. Conclusions: Three baseline DISE phenotypes identified during drug-induced sleep were significantly related to MAD treatment outcome: one beneficial, tongue base collapse, and two adverse, complete concentric collapse at the level of the palate and complete laterolateral oropharyngeal collapse. If confirmed in future prospective studies, these results could guide patient selection for MAD outcome. Clinical Trial Registration: This prospective clinical trial (PROMAD) was registered on Clinicaltrials.gov with identifier: NCT01532050.
Misperception of Sleep Onset Latency, often found in Primary Insomnia, has been cited to be influenced by hyperarousal, reflected in EEG- and ECG-related indices. The aim of this retrospective study was to examine the association between Central Nervous System (i.e. EEG) and Autonomic Nervous System activity in the Sleep Onset Period and the first NREM sleep cycle in Primary Insomnia (n=17) and healthy controls (n=11). Furthermore, the study examined the influence of elevated EEG and Autonomic Nervous System activity on Stage2 sleep-protective mechanisms (K-complexes and sleep spindles). Confirming previous findings, the Primary Insomnia-group overestimated Sleep Onset Latency and this overestimation was correlated with elevated EEG activity. A higher amount of beta EEG activity during the Sleep Onset Period was correlated with the appearance of K-complexes immediately followed by a sleep spindle in the Primary Insomnia-group. This can be interpreted as an extra attempt to protect sleep continuity or as a failure of the sleep-protective role of the K-complex by fast EEG frequencies following within one second. The strong association found between K-alpha (K-complex within one second followed by 8-12 Hz EEG activity) in Stage2 sleep and a lower parasympathetic Autonomic Nervous System dominance (less high frequency HR) in Slow-wave sleep, further assumes a state of hyperarousal continuing through sleep in Primary Insomnia.
PurposeThe objective of this randomized controlled trial was to assess the additional effect of a chest-worn sleep position trainer (SPT) in patients with residual supine-dependent obstructive sleep apnea (sdOSA) under mandibular advancement device (MAD) therapy.MethodsBaseline and follow-up polysomnography with MAD were performed. Twenty patients with sdOSA under MAD therapy underwent two consecutive randomized polysomnographies: one with SPT and one with combination of SPT + MAD. Data are presented as median (quartile 1, quartile 3).ResultsThe SPT reduced the time spent in supine sleeping position compared to baseline and MAD therapy. Both MAD and SPT were individually effective in reducing the overall apnea/hypopnea index (AHI) significantly when compared to baseline from 20.8 (15.1; 33.6)/h at baseline to 11.0 (6.7; 13.8)/h and to 11.1 (3.5; 17.7)/h with MAD or SPT, respectively. The combination of SPT + MAD further reduced the overall AHI to 5.7 (3.6; 7.4), which was significantly lower than with MAD alone (p < 0.001) and SPT alone (p < 0.008), respectively.ConclusionsThe results of this study indicate that combination of SPT + MAD leads to a higher therapeutic efficacy in patients with sdOSA under MAD therapy when compared to one of the treatment modalities alone.
Only a limited number of studies dealing with the epidemiology and therapy of central sleep apnea syndrome (CA) are available. The treatment strategies are poorly defined and not well evaluated. The aim of our present study was to treat selected CA patients with low dose acetazolamide (ACET) for a longer time period than has been done before. Previous studies were performed with high dose ACET provoking severe metabolic acidosis, not for more than 1 wk or only in obstructive apnea patients. Referred patients with suspicion of sleep-related breathing disorders (SRBD) were included in the study if, after a first selection night, their central apnea index (CAI) was > 5 or their apnea-hypopnea index (AHI) > 10 and their obstructive apnea index (OAI) < 5. Of 327 screened patients, 14 (4.3%) fulfilled these criteria. Patients were then treated with ACET (250 mg, 1 h before sleep): Polysomnography was repeated once after one single dose (N2) and twice after 1-mo chronic treatment without (N3) and with (N4) additional ACET administration. After each study night, arterial blood gases and chemical drive were measured. CAI (25.5 +/- 6.8 at N1) already decreased during N2 (13.8 +/- 5.2) and further during N3 (6.6 +/- 2.9) and N4 (6.8 +/- 2.8) p < 0.01). OAI remained unchanged. Total sleep time (TST) and sleep efficiency index (SEI) did not change significantly. The number of arousals decreased from 62 +/- 11 at N1 to 40 +/- 5 at N3 (p = 0.019).(ABSTRACT TRUNCATED AT 250 WORDS)
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