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1 related sleep disorder, and circadian rhythm sleep disorder.
2 : Narcolepsy is a chronic rapid eye movement sleep disorder.
3 ipants reported having been diagnosed with a sleep disorder.
4 psy, obstructive sleep apnea, and shift-work sleep disorder.
5 and without cognitive impairment or primary sleep disorder.
6 nxiety, learning disability, depression, and sleep disorder.
7 anxiety, depression and any other associated sleep disorder.
8 mpaired D3 activity could contribute to this sleep disorder.
9 this cohort had underlying mental health and sleep disorders.
10 al vulnerability to altered communication in sleep disorders.
11 s to identify genetic underpinnings of human sleep disorders.
12 lex relationship between epilepsy, sleep and sleep disorders.
13 onist under development for the treatment of sleep disorders.
14 nsure optimal treatment of both epilepsy and sleep disorders.
15 herapy for the treatment of circadian rhythm sleep disorders.
16 sfunction in these circuits can give rise to sleep disorders.
17 ers three areas: (a) Genetic determinants of sleep disorders.
18 l for transient insomnia in circadian rhythm sleep disorders.
19 toms include hyperexcitability, anxiety, and sleep disorders.
20 to exclude obstructive sleep apnea or other sleep disorders.
21 lar, pulmonary, and hematologic diseases and sleep disorders.
22 ment of rational treatments for a variety of sleep disorders.
23 tentially contribute to the genesis of these sleep disorders.
24 genes influencing risk for some neurological sleep disorders.
25 eep and wake signals, potentially preventing sleep disorders.
26 nificant differences in Parkinson disease or sleep disorders.
27 ight be effective in treating certain modern sleep disorders.
28 vents were primarily nausea and vomiting and sleep disorders.
29 ns in PD, the PPN could be involved in these sleep disorders.
30 ts and anxiety phenotype, without detectable sleeping disorders.
31 95% confidence interval [CI], 22.4 to 32.3), sleep disorders (11.6 excess cases per 1000; 95% CI, 8.3
32 (95% CI, 33.2 to 45.4), 23.5 excess cases of sleep disorders (95% CI, 19.4 to 27.6), 18.7 excess case
33 roactively identifying signs and symptoms of sleep disorders, a better understanding of their adverse
36 Furthermore, QOL for many symptoms such as sleep disorder and malaise/feebleness was also significa
37 that we observed in patients with shift-work sleep disorder and resulted in a small but significant i
38 licated in an exceedingly common and complex sleep disorder and the development of an RLS animal mode
39 Lewy body dementia, rapid eye movement (REM) sleep disorder and/or multiple system atrophy, following
42 erences in the progression of, for instance, sleep disorders and congestive heart failure in diabetic
44 se (PD) is highly comorbid for a spectrum of sleep disorders and deep brain stimulation (DBS) of the
46 ported in the setting of movement disorders, sleep disorders and even internal medicine disorders, su
47 ng as a new potential therapeutic target for sleep disorders and for neuropsychiatric diseases accomp
48 MOD) is used clinically for the treatment of sleep disorders and has been investigated as a potential
49 epresents a potential therapeutic target for sleep disorders and migraine-associated photophobia.
53 general medical condition, breathing-related sleep disorder, and circadian rhythm sleep disorder.
54 d phase, headache, pyrexia, nasopharyngitis, sleep disorder, and tremor were the most frequent advers
55 ing indications, such as insomnia, circadian sleep disorders, and depression, new potential therapeut
58 suggesting a role of vitamin A, adipokines, sleep disorders, and venous sinus stenosis in the pathog
59 investigated the associations of sleepiness, sleep disorders, and work environment (including truck c
60 fined by the International Classification of Sleep Disorders, and/or a large number of false-positive
61 are," "critical care," "earplugs," "sleep," "sleep disorders," and "delirium." STUDY SELECTION: Inter
62 estigate whether l-dopa treatment alleviates sleep disorders; and (3) to determine whether a choliner
67 Accurate identification and diagnosis of sleep disorders as well as epilepsy is clinically import
69 rder presenting with pharyngitis followed by sleep disorder, basal ganglia signs (particularly parkin
70 tent hypoxia during sleep (IH), as occurs in sleep disordered breathing (SDB), induces spatial learni
71 implicated, including apnoea of prematurity, sleep disordered breathing and congestive heart failure.
73 have also highlighted the manifestations of sleep disordered breathing in children with sickle cell
79 isk factors for excessive sleepiness: severe sleep-disordered breathing (apnea-hypopnea index, >30 ep
80 t prevalence estimates of moderate to severe sleep-disordered breathing (apnea-hypopnea index, measur
82 sis was limited to those 27 patients who had sleep-disordered breathing (more than 5 apneas or hypopn
83 , and body mass index: (1) 228 subjects with sleep-disordered breathing (respiratory disturbance inde
84 ce index>or=30) and (2) 338 subjects without sleep-disordered breathing (respiratory disturbance inde
85 ing evidence suggests an association between sleep-disordered breathing (SDB) and cognitive decline i
86 of the insertion/deletion polymorphism with sleep-disordered breathing (SDB) and hypertension in 1,1
87 tional association has been reported between sleep-disordered breathing (SDB) and insulin resistance,
99 ng of intrinsic information in children with sleep-disordered breathing (SDB) is different from healt
103 sibility (UAC) is increased in children with sleep-disordered breathing (SDB), but during wakefulness
108 ongest in older participants in whom overall sleep-disordered breathing also increased atrial fibrill
110 events, we aimed to assess the prevalence of sleep-disordered breathing and associated clinical featu
112 ights the complex interrelationships between sleep-disordered breathing and cardiovascular disease, p
113 e directionality of the relationship between sleep-disordered breathing and heart failure is controve
114 born preterm exhibit increased incidence of sleep-disordered breathing and hypertension, suggesting
115 more in-depth discussion of indications for sleep-disordered breathing and recurrent throat infectio
116 gnificant relation was also observed between sleep-disordered breathing and ventricular ectopic beats
120 drigeminy) were more common in subjects with sleep-disordered breathing compared with those without s
122 articipants who had objective assessments of sleep-disordered breathing during pregnancy were asked t
124 ds of complex arrhythmias than those without sleep-disordered breathing even after adjustment for pot
125 dered breathing, can itself trigger specific sleep-disordered breathing events including air leaks, p
127 rdered breathing compared with those without sleep-disordered breathing had an increased risk of deve
128 ent coronary heart disease, individuals with sleep-disordered breathing had four times the odds of at
133 between the use of replacement hormones and sleep-disordered breathing in a sample of 2,852 noninsti
135 e in addressing pitfalls in the diagnosis of sleep-disordered breathing in neuromuscular diseases, id
137 m the brain, and hypoxemia characteristic of sleep-disordered breathing increases Abeta production.
144 reathing, the current evidence suggests that sleep-disordered breathing may function as a risk factor
146 lectively studied in populations at risk for sleep-disordered breathing or cardiovascular diseases.
147 ent studies show either absence of change in sleep-disordered breathing or improved sleep cardiovascu
149 gnition; however, it remains unclear whether sleep-disordered breathing precedes cognitive impairment
150 tion association, prospective data examining sleep-disordered breathing predicting incident atrial fi
151 oing obesity epidemic, previous estimates of sleep-disordered breathing prevalence require updating.
157 thing in neuromuscular diseases, identifying sleep-disordered breathing triggered by noninvasive vent
161 inverse association between hormone use and sleep-disordered breathing was evident in various subgro
163 pause, perimenopause, and postmenopause with sleep-disordered breathing was investigated with a popul
166 rdered breathing, the 105 women (35.2%) with sleep-disordered breathing were more likely to develop m
167 ted with cardiorespiratory diseases, such as sleep-disordered breathing with apnoea, congestive heart
168 to determine the independent association of sleep-disordered breathing with risk of mild cognitive i
169 for sleep duration, sleep fragmentation, and sleep-disordered breathing) in the development of cognit
171 trategies for management of hypoventilation, sleep-disordered breathing, and cough insufficiency are
173 re, specific exercise, opioids, treatment of sleep-disordered breathing, and interventions to address
175 opause is considered to be a risk factor for sleep-disordered breathing, but this hypothesis has not
176 on, a standard-of-care management option for sleep-disordered breathing, can itself trigger specific
177 s, dyslipidemia, obstructive sleep apnea and sleep-disordered breathing, certain cancers, and major c
178 ry artery disease, congestive heart failure, sleep-disordered breathing, gastro-oesophageal reflux di
179 iated with an increased likelihood of having sleep-disordered breathing, independent of known confoun
180 intermittent hypoxia (IH), such as occurs in sleep-disordered breathing, is associated with neurobeha
181 owever, its indication for all patients with sleep-disordered breathing, regardless of daytime sympto
183 though stroke can lead to the development of sleep-disordered breathing, the current evidence suggest
184 entral apnea, Cheyne-Stokes respiration, and sleep-disordered breathing-age interaction terms were si
199 rdered breathing compared with those without sleep-disordered breathing: 4.8 versus 0.9% (p=0.003) fo
201 a may worsen epilepsy and treatment of these sleep disorders can lead to improved seizure control.
202 stipation, pain, genitourinary problems, and sleep disorders, can be improved with available treatmen
203 arm); physical disorders (cancers, diabetes, sleep disorder, cardiovascular diseases, chronic lower r
204 rcolepsy with cataplexy is a rare and severe sleep disorder caused by the destruction of orexinergic
205 y-two of 538 subjects (5.9%) examined in our sleep disorders center received diagnoses of restless le
208 Variation in chronotype has been linked to sleep disorders, cognitive and physical performance, and
210 resence of psychiatric complications such as sleep disorder, depression, anxiety and somatoform disor
211 xt revision; International Classification of Sleep Disorders: Diagnostic and Coding Manual II, Intern
212 rcadian disorders, or specific physiological sleep disorders--eg, sleep apnoea and periodic limb move
214 positive for obstructive sleep apnea or any sleep disorder had an increased prevalence of reported p
216 Sleep duration, mostly short sleep, and sleep disorders have emerged as being related to adverse
221 nd video polysomnography to identify a novel sleep disorder in three patients referred to the Sleep U
222 s study were as follows: (1) to characterize sleep disorders in a monkey model of PD; (2) to investig
223 we explored the mechanistic basis for these sleep disorders in a mouse model of Angelman syndrome (U
226 e sleep apnea(OSA) is one of the most common sleep disorders in kidney transplant recipients, however
227 ing, and the presence of physician-diagnosed sleep disorders in metropolitan, urban, and rural US Geo
228 of 2911 men in the observational Outcomes of Sleep Disorders in Older Men (MrOS) Sleep Study cohort u
229 llow-up (2009-2012) waves of the Outcomes of Sleep Disorders in Older Men Study (an ancillary study t
230 he efficacy of l-dopa treatment in improving sleep disorders in parkinsonian monkeys, and that adding
232 n promise for the treatment of insomnias and sleep disorders in several recent clinical trials in vol
233 an deficits that we report may contribute to sleep disorders in severe myoclonic epilepsy of infancy
234 s with some of the more commonly encountered sleep disorders in this age group, and to review their d
235 ort the use of melatonin in the treatment of sleep disorders in which the circadian melatonin rhythm
236 ut the prevalence of insomnia, a distressing sleep disorder, in these populations has yet to be deter
237 knowledge on the role of genetic factors in sleep disorders, in particular circadian disorders, narc
238 that occur in PD such as depression, apathy, sleep disorders (including rapid-eye movement sleep beha
239 The management of pediatric and adolescent sleep disorders is in the forefront of the pediatric lit
240 The development of new therapeutics for sleep disorders is increasingly dependent upon understan
241 At the same time, research guided by human sleep disorders is leading to important basic sleep conc
244 patients undergoing sleep evaluation for any sleep disorders (low pretest probability for narcolepsy)
246 ants, 40.4% screened positive for at least 1 sleep disorder, most of whom had not been diagnosed prev
247 d with comorbid medical conditions including sleep disorders, motor hyperactivity, and seizures.
248 determine whether patients with a non-apnea sleep disorder (NA-SD) and comorbidity have an increased
249 tin/orexin (Hcrt), whose loss results in the sleep disorder narcolepsy and that has also been implica
252 he discovery of a single gene underlying the sleep disorder narcolepsy, and identification of loci th
253 neuropeptides that are dysfunctional in the sleep disorder narcolepsy, may be involved in the expres
254 xin neurons in humans is associated with the sleep disorder narcolepsy, which is characterized by exc
259 portant areas for pediatric office practice: sleep disorders, new immunizations, sports injuries, and
260 our important office-based pediatric topics: sleep disorders, new immunizations, sports injuries, and
261 t guidelines pertaining to the management of sleep disorders of children on the autism spectrum.
262 plications of drowsy driving, and the common sleep disorders of obstructive sleep apnea and insomnia.
265 erent samples: controls, patients with other sleep disorders, patients with other hypersomnias, and p
266 toms including anxiety, cognitive defect and sleep disorder precede the onset of motor impairment, an
267 colepsy type 1 is a devastating neurological sleep disorder resulting from the destruction of orexin-
270 orders, or in the context of another primary sleep disorder such as restless legs syndrome, or second
271 n rhythm period and phase, which can lead to sleep disorders such as Familial Advanced Sleep Phase Sy
272 The understanding of the neurophysiology of sleep disorders such as insomnia, parasomnias, and narco
275 More recent studies have shown that primary sleep disorders such as obstructive sleep apnoea may wor
277 f REM sleep mechanisms underlie debilitating sleep disorders such as REM sleep behaviour disorder and
280 wever, a positive MSLT may be found in other sleep disorders, such as behaviourally induced inadequat
281 imately 14 loci increasing susceptibility to sleep disorders, such as narcolepsy and restless leg syn
283 1,2,3,6-tetrahydropyridine treatment induced sleep disorders that comprised sleep episodes during day
284 nsider the pathophysiological basis of major sleep disorders that often are seen by neurologists, inc
285 ature's solutions to heart, lung, blood, and sleep disorders through future research in this area.
286 ndomly assigned 209 patients with shift-work sleep disorder to receive either 200 mg of modafinil or
287 iew the evidence relating sleep duration and sleep disorders to cardiometabolic risk and call for hea
288 ehavior, fueled by evidence directly linking sleep disorders to genetic mutations affecting circadian
289 pulation-based controls or all patients with sleep disorders undergoing a nocturnal sleep study (area
290 een healthy adults (age 35-65 years) without sleep disorders underwent 5-14 days of actigraphy, follo
291 hose respondents who screened positive for a sleep disorder vs those who did not had a higher rate of
292 t visit of 5 years (range 2-12); in four the sleep disorder was the initial and most prominent featur
293 g a group of North American police officers, sleep disorders were common and were significantly assoc
294 ent with NA-SD, two matched controls without sleep disorders were randomly selected for comparison.
296 ng physical disorders, such as cirrhosis and sleep disorders, were also noted as well as the use of m
297 on with broad medical implications including sleep disorders, which can exacerbate metabolic disturba
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