Polysomnography

About: Polysomnography is a research topic. Over the lifetime, 19527 publications have been published within this topic receiving 858718 citations. The topic is also known as: PSG & polysomnogram.

Distribution of partial seizures during the sleep--wake cycle: differences by seizure onset site.

Abstract: Objective: To evaluate the effects of sleep on partial seizures arising from various brain regions. Methods: The authors prospectively studied 133 patients with localization-related epilepsy undergoing video-EEG monitoring over a 2-year period. Seizure type, site of onset, sleep/wake state at onset, duration, and epilepsy syndrome diagnosis were recorded. Periorbital, chin EMG, and scalp/sphenoidal electrodes were used. A subset of 34 patients underwent all-night polysomnography with scoring of sleep stages. Results: The authors analyzed 613 seizures in 133 patients. Forty-three percent (264 of 613) of all partial seizures began during sleep. Sleep seizures began during stages 1 (23%) and 2 (68%) but were rare in slow-wave sleep; no seizures occurred during REM sleep. Temporal lobe complex partial seizures were more likely to secondarily generalize during sleep (31%) than during wakefulness (15%), but frontal lobe seizures were less likely to secondarily generalize during sleep (10% versus 26%; p Conclusions: Partial-onset seizures occur frequently during NREM sleep, especially stage 2 sleep. Frontal lobe seizures are most likely to occur during sleep. Patients with temporal lobe seizures have intermediate sleep seizure rates, and patients with seizures arising from the occipital or parietal lobes have rare sleep-onset seizures. Sleep, particularly stage 2 sleep, promotes secondary generalization of temporal and occipitoparietal, but not frontal, seizures. These findings suggest that the hypersynchrony of sleep facilitates both initiation and propagation of partial seizures, and that effects of sleep depend in part on the location of the epileptic focus.

Issues of validity in actigraphic sleep assessment.

Abstract: Objectives The Standards of Practice Committee of the American Sleep Disorders Association has supported the use of actigraphy in the assessment of sleep disorders Pollak et al disagree The objective of this paper is to identify and critically evaluate several theoretic and methodologic issues that are central to these divergent views regarding the valid use of actigraphy for sleep assessment Design Critical review, analysis, and comment Setting N/A Patients/participants N/A Interventions N/A Measurements and results N/A Conclusions (1) Coefficients of the validity of actigraphy exceed those associated with common medical tests and the best psychological tests (2) Reasons why actigraphy should be held to a substantially higher empirical standard than common medical tests and the best psychological tests have yet to be advanced (3) Differences between actigraphy and polysomnography are not random and can be reduced (3a) Sleep onset is a gradual rather than a discrete process Actigraphy keys on an earlier phase of the sleep-onset process than does polysomnography, resulting in systematic rather than random differences (3b) A sleep switch device can be used to substantially increase the accuracy of sleep-onset times (3c) The residual unreliability of polysomnographic data explains a portion of the differences between actigraphy and polysomnography Actigraphy cannot be expected to agree more completely with polysomnography than polysomnography does with itself (4) Complete agreement between actigraphy and polysomnography has been presumed, but achieving such a limit is theoretically impossible Some lower maximum agreement limit should be identified (5) Conclusions that actigraphy is not an accurate sleep-wake indicator and that it is inappropriate to infer sleep from actigraphy data are not supported by the findings Conclusions reached, including caveats, by the Standards of Practice Committee remain supported

NREM sleep EEG frequency spectral correlates of sleep complaints in primary insomnia subtypes.

Abstract: Design: We compared EEG frequency spectra from REM and NREM sleep in PPI subjects subtyped as subjective insomnia sufferers (those with relatively long total sleep time and relative underestimation of sleep time compared with PSG), and objective insomnia sufferers (those with relatively short PSG total sleep time) with EEG frequency spectra in normals. We also studied the correlation between these indices and the degree of underestimation of sleep. Further, we determined the degree to which sleep EEG indexes related to sleep complaints. Setting: Duke University Medical Center Sleep Laboratory. Participants: Normal (N=20), subjective insomnia (N=12), and objective insomnia (N=18) subjects. Interventions: N/A Measurements and Results: Lower delta and greater alpha, sigma, and beta NREM EEG activity were found in the patients with subjective insomnia but not those with objective insomnia, compared with the normal subjects. These results were robust to changes in the subtyping criteria. No effects were found for REM spectral indexes. Less delta non- REM EEG activity predicted greater deviation between subjective and PSG estimates of sleep time across all subjects. For the subjective insomnia subjects, diminished low-frequency and elevated higher frequency non- REM EEG activity was associated with their sleep complaints. Conclusions: NREM EEG frequency spectral indexes appear to be physiologic correlates of sleep complaints in patients with subjective insomnia and may reflect heightened arousal during sleep.

Effect of 1 night of total sleep deprivation on cerebrospinal fluid β-amyloid 42 in healthy middle-aged men: a randomized clinical trial

Abstract: IMPORTANCE: Increasing evidence suggests a relationship between poor sleep and the risk of developing Alzheimer disease. A previous study found an effect of sleep on beta-amyloid (Abeta), which is a key protein in Alzheimer disease pathology. OBJECTIVE: To determine the effect of 1 night of total sleep deprivation on cerebrospinal fluid Abeta42 protein levels in healthy middle-aged men. DESIGN, SETTING, AND PARTICIPANTS: The Alzheimer, Wakefulness, and Amyloid Kinetics (AWAKE) study at the Radboud Alzheimer Center, a randomized clinical trial that took place between June 1, 2012, and October 1, 2012. Participants were cognitively normal middle-aged men (40-60 years of age) with normal sleep (n = 26) recruited from the local population. INTERVENTIONS: Participants were randomized to 1 night with unrestricted sleep (n = 13) or 1 night of total sleep deprivation (24 hours of wakefulness) (n = 13). MAIN OUTCOMES AND MEASURES: Sleep was monitored using continuous polysomnographic recording from 3 pm until 10 am. Cerebrospinal fluid samples were collected using an intrathecal catheter at defined times to compare cerebral Abeta42 concentrations between evening and morning. RESULTS: A night of unrestricted sleep led to a 6% decrease in Abeta42 levels of 25.3 pg/mL (95% CI [0.94, 49.6], P = .04), whereas sleep deprivation counteracted this decrease. When accounting for the individual trajectories of Abeta42 over time, a difference of 75.8 pg/mL of Abeta42 was shown between the unrestricted sleep and sleep deprivation group (95% CI [3.4, 148.4], P = .04). The individual trajectories of evening and morning Abeta42 concentrations differed between the unrestricted sleep and sleep deprivation groups (P = .04) in contrast to stable Abeta40, tau, and total protein levels. CONCLUSIONS AND RELEVANCE: Sleep deprivation, or prolonged wakefulness, interferes with a physiological morning decrease in Abeta42. We hypothesize that chronic sleep deprivation increases cerebral Abeta42 levels, which elevates the risk of Alzheimer disease. TRIAL REGISTRATION: clinicaltrials.gov Identifier: NCT01194713.