1 Polysomnographic abnormalities also occurred in unaffect
2 nly suggestive, these findings indicate that
polysomnographic abnormalities may precede the clinical
3 Limited evidence suggests that
polysomnographic alterations may be more prominent early
4 Polysomnographic analysis of TASK-3 mutants reveals incr
5 positive airway pressure (CPAP) treatment on
polysomnographic and neuropsychological testing.
6 xin, tau proteins, and beta-amyloid 1-42 and
polysomnographic assessment of sleep variables.
7 oupling observed patient arousal levels with
polysomnographic characteristics revealed that standard
8 Polysomnographic,
cognitive, behavioral, and health outc
9 This study presents
polysomnographic data and psychiatric history for parent
10 Analysis of
polysomnographic data revealed profound deficiencies in
11 Polysomnographic data were scored manually via this revi
12 after cardioversion than patients without a
polysomnographic diagnosis of sleep apnea.
13 After noting frequent atypical
polysomnographic findings (i.e., lack of stage N2 marker
14 ovements in behavioral, quality-of-life, and
polysomnographic findings and significantly greater redu
15 ng cognition, behavior, quality of life, and
polysomnographic findings has not been rigorously evalua
16 We sought to quantify typical and atypical
polysomnographic findings in critically ill patients and
17 g criteria due to a predominance of atypical
polysomnographic findings in ventilated patients.
18 Normalization of
polysomnographic findings was observed in a larger propo
19 Atypical
polysomnographic findings were characterized and used to
20 y outcomes of behavior, quality of life, and
polysomnographic findings, thus providing evidence of be
21 according to baseline insomnia symptoms and
polysomnographic markers.
22 ep (55% versus 28%), had significantly worse
polysomnographic measures of sleep continuity, and had m
23 Main outcomes included standard
polysomnographic measures of sleep induction, maintenanc
24 Common
polysomnographic measures of sleep-disordered breathing
25 Self-report and
polysomnographic measures of sleep-onset latency, total
26 No other
polysomnographic measures predicted evening-to-morning d
27 crease in wakefulness in rats as measured by
polysomnographic methods.
28 oss five nights in the sleep laboratory with
polysomnographic monitoring (adaptation, baseline, three
29 therapeutic CPAP did not affect any measured
polysomnographic parameter.
30 e relationships between several clinical and
polysomnographic parameters and the degree of hypersomno
31 Additionally, clinical symptoms and
polysomnographic parameters improved similarly with NIV
32 ification in improving clinical symptoms and
polysomnographic parameters, although NIV yielded better
33 meeting study criteria received at least one
polysomnographic recording close to the time of medical/
34 atients with clinical signs of PPS underwent
polysomnographic recording for two consecutive nights.
35 Sleep was monitored using continuous
polysomnographic recording from 3 pm until 10 am.
36 However,
polysomnographic recording in mice exposed to the shifti
37 Male rats were implanted for
polysomnographic recording, and divided into treadmill s
38 t of rats from both groups underwent 48 h of
polysomnographic recording.
39 as in V1 and standard EEG/EMG electrodes for
polysomnographic recording.
40 We analyzed 77 8-h, full
polysomnographic recordings (PSGs) from five healthy sub
41 m of abnormal REM sleep, were assessed using
polysomnographic recordings and the food elicited catapl
42 Participants underwent complete
polysomnographic recordings at home and had extensive ph
43 The aim of the present study was to obtain
polysomnographic recordings during an acute period after
44 and optogenetic manipulations together with
polysomnographic recordings to demonstrate that VTA dopa
45 Polysomnographic recordings were performed in chronicall
46 iring time, cost-intensive sleep studies and
polysomnographic recordings).
47 ond aim of the study was to determine if the
polysomnographic response to the oral mandibular advance
48 The breathing patterns and
polysomnographic responses to air insufflation were stud
49 The results also indicate that
polysomnographic severity of OSA and the site of airway
50 e contributing factors, including changes in
polysomnographic sleep and 24-h hormonal profiles.
51 consumption, respiratory exchange ratio, and
polysomnographic sleep daily.
52 We therefore evaluated
polysomnographic sleep disturbances in PTSD.
53 Prespecified primary efficacy outcomes were
polysomnographic sleep efficiency (phase II study), late
54 as associated with worsening of all measured
polysomnographic sleep outcomes.
55 Participants underwent
polysomnographic sleep recordings on days 1 to 3, 7 to 9
56 Polysomnographic sleep recordings were performed by elec
57 aphic characteristics revealed that standard
polysomnographic staging criteria did not reliably deter
58 Polysomnographic studies conducted in adults with PTSD h
59 Polysomnographic studies conducted on small samples of s
60 Several, though not all,
polysomnographic studies that use conventional visual sc
61 ontrol subjects underwent complete overnight
polysomnographic studies to exclude occult OSA.
62 Multichannel
polysomnographic studies were performed in preterm infan
63 h patient underwent 2 consecutive full-night
polysomnographic studies.
64 eye movement sleep, as illustrated by recent
polysomnographic studies.
65 d subjectively by surveys and objectively by
polysomnographic studies.
66 OSA was further excluded by overnight
polysomnographic studies.
67 We performed a nap
polysomnographic study on 10 normal infants between 2 an
68 nobese children were recruited and underwent
polysomnographic testing (PSG), and fasting endothelial
69 Polysomnographic total recording time and total sleep ti
70 of methodology to characterize the atypical
polysomnographic tracings that confound standard sleep s
71 ion, R-R interval, blood pressure, and other
polysomnographic variables were recorded in eight normal