In summary, although actigraphy is not as accurate as PSG for determining some sleep measurements, studies are in general agreement that actigraphy, with its ability to record continuously for long time periods, is more reliable than sleep logs which rely on the patients' recall of how many times they woke up or how long they slept during the night and is more reliable than observations which only capture short time periods. Actigraphy can provide information obtainable in no other practical way. It can also have a role in the medical care of patients with sleep disorders. However, it should not be held to the same expectations as polysomnography. Actigraphy is one-dimensional, whereas polysomnography comprises at least 3 distinct types of data (EEG, EOG, EMG), which jointly determine whether a person is asleep or awake. It is therefore doubtful whether actigraphic data will ever be informationally equivalent to the PSG, although progress on hardware and data processing software is continuously being made. Although the 1995 practice parameters paper determined that actigraphy was not appropriate for the diagnosis of sleep disorders, more recent studies suggest that for some disorders, actigraphy may be more practical than PSG. While actigraphy is still not appropriate for the diagnosis of sleep disordered breathing or of periodic limb movements in sleep, it is highly appropriate for examining the sleep variability (i.e., night-to-night variability) in patients with insomnia. Actigraphy is also appropriate for the assessment of and stability of treatment effects of anything from hypnotic drugs to light treatment to CPAP, particularly if assessments are done before and after the start of treatment. A recent independent review of the actigraphy literature by Sadeh and Acebo reached many of these same conclusions. Some of the research studies failed to find relationships between sleep measures and health-related symptoms. The interpretation of these data is also not clear-cut. Is it that the actigraph is not reliable enough to the access the relationship between sleep changes and quality of life measures, or, is it that, in fact, there is no relationship between sleep in that population and quality of life measures? Other studies of sleep disordered breathing, where actigraphy was not used and was not an outcome measure also failed to find any relationship with quality of life. Is it then the actigraph that is not reliable or that the associations just do not exist? The one area where actigraphy can be used for clinical diagnosis is in the evaluation of circadian rhythm disorders. Actigraphy has been shown to be very good for identifying rhythms. Results of actigraphic recordings correlate well with measurements of melatonin and of core body temperature rhythms. Activity records also show sleep disturbance when sleep is attempted at an unfavorable phase of the circadian cycle. Actigraphy therefore would be particularly good for aiding in the diagnosis of delayed or advanced sleep phase syndrome, non-24-hour-sleep syn...

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The Consensus Sleep Diary was the result of collaborations with insomnia experts and potential users. The adoption of a standard sleep diary for insomnia will facilitate comparisons across studies and advance the field. The proposed diary is intended as a living document which still needs to be tested, refined, and validated.

Adoption of a standard research assessment of insomnia disorders will facilitate comparisons among different studies and advance the state of knowledge. These recommendations are not intended to be static but must be periodically revised to accommodate further developments and evidence in the field.

Context Sleep-disordered breathing (SDB), characterized by recurrent arousals from sleep and intermittent hypoxemia, is common among older adults. Cross-sectional studies have linked SDB to poor cognition; however, it remains unclear whether sleep disordered breathing precedes cognitive impairment in older adults. Objectives To determine the prospective relationship between sleep disordered breathing and cognitive impairment and to investigate potential mechanisms of this association. Design, Setting, and Participants Prospective sleep and cognition study of 298 women without dementia (mean [SD] age: 82.3 [3.2] years) who had overnight polysomnography (PSG) measured between January 2002 and April 2004 in a substudy of the Study of Osteoporotic Fractures. Sleep disordered breathing was defined as an apnea-hypopnea index of 15 or more events per hour of sleep. Multivariate logistic regression was used to determine the independent association of sleep disordered breathing with risk of mild cognitive impairment or dementia and adjustments were made for age, race, body mass index, education, smoking status, presence of diabetes, presence of hypertension, medication use (antidepressants, benzodiazepines, or non-benzodiazepine anxiolytics), and baseline cognitive scores. Measures of hypoxia, sleep fragmentation, and sleep duration were investigated as underlying mechanisms for this relationship. Main Outcome Measures Adjudicated cognitive status (normal, dementia, or mild cognitive impairment [MCI]) based on data collected between November 2006 and September 2008 Results Compared with the 193 women without sleep disordered breathing, the 105 women (35.2%) with SDB were more likely to develop MCI/dementia (n=60 (31.1%) vs n=47 (44.8%)) even after multivariate adjustment (adjusted OR=1.85, 95% CI 1.11-3.08). Elevated oxygen desaturation index (≥15 events/hour) and high percentage (>7%) of sleep time in apnea or hypopnea, both measures of disordered breathing, were associated with risk of developing MCI/dementia (adjusted OR=1.71, 95% CI 1.04 − 2.83 and adjusted OR=2.04, 95% CI 1.10 − 3.78, respectively). Measures of sleep fragmentation (arousal index and wake after sleep onset) or sleep duration (total sleep time) were not associated with risk of cognitive impairment. Conclusions Among older women, those with sleep disordered breathing, compared with those without SDB, were associated with an increased risk of developing cognitive impairment.

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The 1968 Rechtschaffen and Kales (R & K) sleep scoring manual was published 15 years after REM sleep was discovered. Advances in the ensuing 28 years warranted a re-look at visual scoring of sleep stages. This paper describes the work of the AASM Visual Scoring Task Force, including methodology, a literature review and the rationale behind the new rules. Reliability studies of R & K scoring were reviewed; reliability was low for stage one and moderate for slow wave sleep. Evidence indicated that K complexes and slow waves are expressed maximal frontally, spindles centrally and alpha rhythm over the occipital region. Three derivations of EEG, two of electro-oculography, and one of chin EMG were recommended. Scoring by 30-second epochs was retained. New terminology for sleep stages was proposed. Attenuation of alpha rhythm was determined to be the most valid electrophysiological marker of sleep onset. Alternative measures were proposed for non-alpha generating subjects. K complexes associated with arousals were determined to be insufficient alone to define the new stage N2. No evidence was found to justify dividing slow wave sleep into two stages. No reasons were found to alter the current slow wave amplitude criteria at any age. The phenomena of REM sleep were defined. The rules for defining onset and termination of REM sleep periods were simplified. Movement time was eliminated and major body movements defined. Studies are needed to test the reliability of the new rules. Future advances in technology may require modification of these rules with time.

Independent evidence associates β-amyloid pathology with both NREM sleep disruption and memory impairment in older adults. However, whether the influence of β-amyloid pathology on hippocampus-dependent memory is, in part, driven by impairments of NREM slow wave activity (SWA) and associated overnight memory consolidation is unknown. Here, we show that β-amyloid burden within medial prefrontal cortex (mPFC) is significantly correlated with the severity of impairment in NREM SWA generation. Moreover, reduced NREM SWA generation was further associated with impaired overnight memory consolidation and impoverished hippocampal-neocortical memory transformation. Furthermore, structural equation models revealed that the association between mPFC β-amyloid pathology and impaired hippocampus-dependent memory consolidation is not direct, but instead, statistically depends on the intermediary factor of diminished NREM SWA. By linking β-amyloid pathology with impaired NREM SWA, these data implicate sleep disruption as a novel mechanistic pathway through which β-amyloid pathology may contribute to hippocampus-dependent cognitive decline in the elderly.