1 Polysomnographic abnormalities also occurred in unaffect
2 nly suggestive, these findings indicate that
polysomnographic abnormalities may precede the clinical
3 e derived using a validated model fit to the
polysomnographic airflow signal.
4 Limited evidence suggests that
polysomnographic alterations may be more prominent early
5 Polysomnographic analysis of TASK-3 mutants reveals incr
6 this, we conducted a retrospective study of
polysomnographic and clinical records of patients presen
7 positive airway pressure (CPAP) treatment on
polysomnographic and neuropsychological testing.
8 Combining
polysomnographic and photometric recordings in mice, we
9 Polysomnographic and quality of life outcomes were asses
10 Electroencephalographic and
polysomnographic assessment of sleep and postmortem immu
11 xin, tau proteins, and beta-amyloid 1-42 and
polysomnographic assessment of sleep variables.
12 oupling observed patient arousal levels with
polysomnographic characteristics revealed that standard
13 Polysomnographic,
cognitive, behavioral, and health outc
14 n of cerebral blood flow in the cortex of 20
polysomnographic-
confirmed patients with isolated REM sl
15 This study presents
polysomnographic data and psychiatric history for parent
16 Raw baseline
polysomnographic data from 91/126 patients were availabl
17 Analysis of
polysomnographic data revealed profound deficiencies in
18 Polysomnographic data were scored manually via this revi
19 after cardioversion than patients without a
polysomnographic diagnosis of sleep apnea.
20 uced sleep endoscopy.Objectives: Here we use
polysomnographic endotyping to assess the pathophysiolog
21 After noting frequent atypical
polysomnographic findings (i.e., lack of stage N2 marker
22 ovements in behavioral, quality-of-life, and
polysomnographic findings and significantly greater redu
23 ng cognition, behavior, quality of life, and
polysomnographic findings has not been rigorously evalua
24 We sought to quantify typical and atypical
polysomnographic findings in critically ill patients and
25 g criteria due to a predominance of atypical
polysomnographic findings in ventilated patients.
26 Untreated OSA can show
polysomnographic findings that are similar to narcolepsy
27 Normalization of
polysomnographic findings was observed in a larger propo
28 Atypical
polysomnographic findings were characterized and used to
29 y outcomes of behavior, quality of life, and
polysomnographic findings, thus providing evidence of be
30 nical Ventilation]), we aimed to investigate
polysomnographic indexes as well as a continuous index f
31 nsider how the link between ANS activity and
polysomnographic markers of sleep may help elucidate bot
32 according to baseline insomnia symptoms and
polysomnographic markers.
33 ep (55% versus 28%), had significantly worse
polysomnographic measures of sleep continuity, and had m
34 Main outcomes included standard
polysomnographic measures of sleep induction, maintenanc
35 Common
polysomnographic measures of sleep-disordered breathing
36 Self-report and
polysomnographic measures of sleep-onset latency, total
37 No other
polysomnographic measures predicted evening-to-morning d
38 crease in wakefulness in rats as measured by
polysomnographic methods.
39 oss five nights in the sleep laboratory with
polysomnographic monitoring (adaptation, baseline, three
40 Fragmented sleep was the only
polysomnographic parameter associated with a worse Eyesi
41 therapeutic CPAP did not affect any measured
polysomnographic parameter.
42 e relationships between several clinical and
polysomnographic parameters and the degree of hypersomno
43 Additionally, clinical symptoms and
polysomnographic parameters improved similarly with NIV
44 ciations between most treatment outcomes and
polysomnographic parameters were weak.
45 ification in improving clinical symptoms and
polysomnographic parameters, although NIV yielded better
46 meeting study criteria received at least one
polysomnographic recording close to the time of medical/
47 atients with clinical signs of PPS underwent
polysomnographic recording for two consecutive nights.
48 Sleep was monitored using continuous
polysomnographic recording from 3 pm until 10 am.
49 However,
polysomnographic recording in mice exposed to the shifti
50 ral 13C-labeled glucose tolerance test and a
polysomnographic recording were performed.
51 Male rats were implanted for
polysomnographic recording, and divided into treadmill s
52 t of rats from both groups underwent 48 h of
polysomnographic recording.
53 as in V1 and standard EEG/EMG electrodes for
polysomnographic recording.
54 We analyzed 77 8-h, full
polysomnographic recordings (PSGs) from five healthy sub
55 m of abnormal REM sleep, were assessed using
polysomnographic recordings and the food elicited catapl
56 Participants underwent complete
polysomnographic recordings at home and had extensive ph
57 sonance imaging, cued fear conditioning, and
polysomnographic recordings combined with in vivo photom
58 The aim of the present study was to obtain
polysomnographic recordings during an acute period after
59 Long-term
polysomnographic recordings from mice were used to asses
60 and optogenetic manipulations together with
polysomnographic recordings to demonstrate that VTA dopa
61 Polysomnographic recordings were performed in chronicall
62 iring time, cost-intensive sleep studies and
polysomnographic recordings).
63 ung and 29 older adults underwent a night of
polysomnographic recordings.
64 Further clinical and
polysomnographic research is warranted to better underst
65 ond aim of the study was to determine if the
polysomnographic response to the oral mandibular advance
66 The breathing patterns and
polysomnographic responses to air insufflation were stud
67 and certain medications can also affect the
polysomnographic results.
68 Observers were blinded to
polysomnographic results.
69 The results also indicate that
polysomnographic severity of OSA and the site of airway
70 e contributing factors, including changes in
polysomnographic sleep and 24-h hormonal profiles.
71 cipants received electroencephalographic and
polysomnographic sleep assessments.
72 consumption, respiratory exchange ratio, and
polysomnographic sleep daily.
73 We therefore evaluated
polysomnographic sleep disturbances in PTSD.
74 Prespecified primary efficacy outcomes were
polysomnographic sleep efficiency (phase II study), late
75 as associated with worsening of all measured
polysomnographic sleep outcomes.
76 rithm trained and validated on +30,000 hr of
polysomnographic sleep recordings across heterogeneous p
77 Participants underwent
polysomnographic sleep recordings on days 1 to 3, 7 to 9
78 Polysomnographic sleep recordings were performed by elec
79 aphic characteristics revealed that standard
polysomnographic staging criteria did not reliably deter
80 Polysomnographic studies conducted in adults with PTSD h
81 Polysomnographic studies conducted on small samples of s
82 Several, though not all,
polysomnographic studies that use conventional visual sc
83 ontrol subjects underwent complete overnight
polysomnographic studies to exclude occult OSA.
84 Multichannel
polysomnographic studies were performed in preterm infan
85 h patient underwent 2 consecutive full-night
polysomnographic studies.
86 eye movement sleep, as illustrated by recent
polysomnographic studies.
87 d subjectively by surveys and objectively by
polysomnographic studies.
88 OSA was further excluded by overnight
polysomnographic studies.
89 This
polysomnographic study in male rats showed that the firs
90 We performed a nap
polysomnographic study on 10 normal infants between 2 an
91 A registered
polysomnographic technologist live-scored sleep stage an
92 nobese children were recruited and underwent
polysomnographic testing (PSG), and fasting endothelial
93 Polysomnographic total recording time and total sleep ti
94 of methodology to characterize the atypical
polysomnographic tracings that confound standard sleep s
95 ion, R-R interval, blood pressure, and other
polysomnographic variables were recorded in eight normal