Several behavioral, physiological, and subjective variables were examined in subjects reporting chronic insomnia (IN group) and subjects with no complaint of insomnia (NC group) to determine factors predictive of poor sleep as measured by electroencephalography (EEG sleep).
A total of 177 subjects (121 in the IN group and 56 in the NC group) were evaluated on the basis of EEG sleep, subjective sleep, sleepiness, performance, mood, personality, and metabolic parameters during a 36-hour laboratory stay.
Equal percentages of subjects in each group had 0, 1, or 2 nights of poor EEG sleep, indicating that the IN group was not more likely to have impaired sleep in the laboratory. Results of the Minnesota Multiphasic Personality Inventory showed that subjects in the IN group had more pathological personality profiles, and results of laboratory studies showed that these subjects had worse mood ratings, less subjective sleepiness, poorer memory performance, and longer midafternoon sleep latencies. Subjects in the IN group also rated their laboratory sleep as poorer in quality with more time awake after sleep onset and longer sleep latencies, but no differences in EEG sleep were observed. Poor nights of EEG sleep were associated with being male, increasing age, and a history of more time awake after sleep onset; among the laboratory tests, poor EEG sleep was associated with worse mood ratings, poorer memory performance, longer sleep latencies (as indicated by higher scores on the Multiple Sleep Latency Test), higher sleep/wake ratios for metabolic parameters, lower ratings of sleep quality, and longer perceived sleep latencies.
A history of chronic insomnia does not predict poor EEG sleep. Both chronic insomnia and poor EEG sleep are associated independently with dysphoria, hyperarousal, diminished waking function, and negative subjective sleep quality. Separate arousal and sleep systems are posited to account for these results.
"However, both informants' subjective sleep reports were found to be internally consistent and differentiated the anxious and control groups. Moreover, the low correspondence estimates observed between subjective and objective sleep measures is consistent with the mental health field in general (De Los Reyes and Aldao 2015; De Los Reyes et al. 2015; De Los Reyes and Kazdin 2005; De Los Reyes et al. 2013b) and sleep research in general (Edinger et al. 2000; Rosa and Bonnet 2000). "
[Show abstract][Hide abstract] ABSTRACT: We compared subjective and objective sleep patterns and problems, and examined cross-method correspondence across parent reports, child reports, and actigraphy-derived sleep variables in clinically-anxious children and healthy controls. In a multi-site, cross-sectional study, 75 pre-adolescent children (6 to 11 years; M=8.7 years; SD=1.4; 39/52% female) were examined including 39 with a diagnosis of primary generalized anxiety disorder (GAD) and 36 controls recruited from university-based clinics in Houston, TX and Washington, DC. Structured interviews, validated sleep questionnaires, and 1-week of actigraphy data were utilized. Despite subjective reports of significantly greater sleep problems among anxious children, actigraphy data revealed no significant differences between the groups. All parents estimated earlier bedtimes and greater total sleep duration relative to actigraphy, and all children endorsed more sleep problems than parents. With few exceptions, subjective reports exhibited low and non-significant correspondence with actigraphy-based sleep patterns and problems. Our findings suggest that high rates of sleep complaints found among children with GAD (and their parents) are not corroborated by objective sleep abnormalities, with the exception of marginally prolonged sleep onset latency compared to controls. Objective-subjective sleep discrepancies were observed in both groups but more apparent overall in the GAD group. Frequent complaints of sleep problems and daytime tiredness among anxious youth might more accurately reflect difficulties prior to the actual sleep period, cognitive-affective biases associated with sleep, and/or an increased sleep need. Findings highlight the importance of considering sleep from multiple perspectives.
[Show abstract][Hide abstract] ABSTRACT: 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 8-12Hz 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.
International journal of psychophysiology: official journal of the International Organization of Psychophysiology 10/2013; 91(3). DOI:10.1016/j.ijpsycho.2013.10.012 · 2.88 Impact Factor
"However, in contrast to these clear differences in subjective symptoms the differences in objective sleep diary variables, daytime hypersomnia scales, and PSG sleep parameters between migraineurs and controls were smaller. A similar discrepancy has previously been found among chronic insomniacs . Insomnia is also a risk factor for migraine . "
[Show abstract][Hide abstract] ABSTRACT: Our aim was to compare subjective and objective sleep quality and arousal in migraine and to evaluate the relationship between sleep quality and pain thresholds (PT) in controls, interictal, preictal and postictal migraine.
Polysomnography and PT (to pressure, heat and cold) measurements were done in 34 healthy controls and 50 migraineurs. Subjective sleep quality was assessed by sleep diaries, Epworth sleepiness scale, Karolinska sleep questionnaire and Pittsburgh sleep quality index. Migraineurs who had their sleep registration more than 48 h from an attack were classified as interictal while those who were less than 48 h from an attack were classified as either preictal or postictal.
Migraineurs reported more insomnia and other sleep-related symptoms than controls, but the objective sleep differences were smaller and we found no differences in daytime sleepiness. Interictal migraineurs had more awakenings (p=0.048), a strong tendency for more slow-wave sleep (p=0.050), lower thermal pain thresholds (TPT) (heat pain thresholds p=0.043 and cold pain thresholds p=0.031) than controls. Migraineurs in the preictal phase had shorter latency to sleep onset than controls (p=0.003). Slow-wave sleep correlated negatively with pressure PT and slow bursts correlated negatively with TPT.
Lower PT in interictal migraineurs seems related to increased sleep pressure. We hypothesize that migraineurs on the average suffer from a relative sleep deprivation and need more sleep than healthy controls. Lack of adequate rest might be an attack-precipitating- and hyperalgesia-inducing factor.
The Journal of Headache and Pain 02/2013; 14(1):12. DOI:10.1186/1129-2377-14-12 · 2.80 Impact Factor
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