A common but significant change associated with aging is a profound disruption to the daily sleep-wake cycle. It has been estimated that as many as 50% of older adults complain about difficulty initiating or maintaining sleep. Poor sleep results in increased risk of significant morbidity and mortality. Moreover, in younger adults, compromised sleep has been shown to have a consistent effect on cognitive function, which may suggest that sleep problems contribute to the cognitive changes that accompany older age. The multifactorial nature of variables affecting sleep in old age cannot be overstated. Changes in sleep have been thought to reflect normal developmental processes, which can be further compromised by sleep disturbances secondary to medical or psychiatric diseases (e.g., chronic pain, dementia, depression), a primary sleep disorder that can itself be age-related (e.g., Sleep Disordered Breathing and Periodic Limb Movements During Sleep), or some combination of any of these factors. Given that changes in sleep quality and quantity in later life have implications for quality of life and level of functioning, it is imperative to distinguish the normal age-related sleep changes from those originating from pathological processes.

The NOGO P3 event-related potential is a sensitive marker of alcoholism, relates to EEG oscillation in the δ and θ frequency ranges, and reflects activation of an inhibitory processing network. Degradation of white matter tracts related to age or alcoholism should negatively affect the oscillatory activity within the network.

Aging is associated with many changes in sleep, with one of the most prominent being a reduction in slow wave sleep. Traditional measures of this phenomenon rely on spontaneous activity and typically confound the incidence and amplitude of delta waves. The measurement of evoked K-complexes during sleep, enable separate assessment of incidence and amplitude taken from the averaged K-complex waveform. The present study describes data from 70 normal healthy men and women aged between 19 and 78 years. K-Complexes were evoked using short auditory tones and recorded from a midline array of scalp sites. Significant reductions with age were seen in the amplitude of the N550 component of the averaged waveform, which represents the amplitude of the K-complex, with linear regression analysis indicating approximately 50% of the variance was due to age. Smaller, yet still significant reductions were seen in the ability to elicit K-complexes. The data highlight the utility of evoked K-complexes as a sensitive marker of brain aging in men and women.

Background: K-complexes (KCs) are evoked delta frequency electroencephalogram (EEG) responses during sleep that occur when large numbers of healthy cortical cells burst fire in a synchronized manner. The KC amplitude and incidence are sensitive measures of normal healthy brain aging. Given the known neurodegenerative consequences of alcohol abuse it was hypothesized that alcoholism would be associated with further KC amplitude and incidence reductions.Methods: Eighty-four subjects (42 alcoholics) screened for medical, psychiatric, and sleep problems participated. The protocol involved the presentation of auditory stimuli during stage 2 sleep throughout a night in the laboratory. The KCs were identified and averaged, to enable measurement of the P2, N550, and P900 peaks.Results: Compared with control subjects, alcoholic men and women had lower KC incidence (p < .001) and P2 (p < .001), N550 (p < .05), and P900 (p < .05) amplitudes. There was a significant diagnosis X site interaction (p < .001), indicating the group difference was largest at frontal sites. Longer sobriety correlated with increased N550 amplitude (p < .01).Conclusions: The KC incidence and amplitude were negatively impacted in alcoholic men and women with exacerbation of the normal aging effects, particularly over frontal scalp regions. The observed relationship between improvements in KC measures and increased time of abstinence suggests that these measures might provide a useful marker of brain recovery with continued abstinence from alcohol.

This chapter discusses how both auditory- and respiratory-evoked potentials change with non-REM sleep, with particular focus on two components: the N350 and N550. Very early in the history of sleep research, it became apparent that evoked Electroencephalography (EEG) responses could be elicited during non-rapid eye movement (REM) sleep. The first evoked response observed was the K-complex. This was seen in response to a tone played during an afternoon nap when the subject was in what we now call “stage-2 sleep.” Reasons to evaluate event-related potentials (ERPs) during sleep are many and varied. A substantial body of work has focused on the sleep onset period, with the goal of characterizing the loss of wakeful consciousness. Yet other studies have used ERPs during sleep as a way to evaluate the impact of aging or of different pathologies on the sleeping brain. Regardless of the motivation, the use of averaged ERP methods to evaluate sleep EEG is a departure from the standard observational mode of sleep research and provides the opportunity to probe the sleeping nervous system and evaluate the responses under a high level of experimental control.

Following the loss of wakeful consciousness, the averaging of responses to stimuli produce evoked potential waveforms with prominent components either unique to or greatly enhanced by non-REM sleep. In the sleep onset periods (stage 1) these are the P2 and N350. Following the establishment of stable sleep (stage 2 and SWS), the N550 and P900 are also prominent. Investigation of the EEG associated with individual responses indicates that a good proportion of stimuli elicit, K-complexes or vertex sharp waves (VSWs) and occasionally will elicit both. Recent work has indicated that the N550 in the averaged response is due to the presence of K-complexes and that the N350 is at least largely due to the presence of VSWs. The large size of these grapho-elements indicates that they are probably produced by a synchronized discharge of multiple neural units. Both are readily observed in the absence of external stimulation and occur as normal components of sleep, indeed the K-complex is used as one of the identifying features of the onset of stable non-REM sleep. The present review details the investigation of these features and their associated evoked potential components, in terms of stimulus features, brain states associated with their production, their scalp topography, and changes as a function of age.

Journal of Sleep ResearchVolume 9, Issue 1 p. 97-98 Letter to the Editor Self-reported sleep patterns and daytime sleepiness in the neurologically healthy aged Kate Crowley, Kate Crowley Department of Psychology, University of MelbourneSearch for more papers by this authorIan M. Colrain, Ian M. Colrain Department of Psychology, University of Melbourne Sleep Disorders Research Center, Stanford UniversitySearch for more papers by this author Kate Crowley, Kate Crowley Department of Psychology, University of MelbourneSearch for more papers by this authorIan M. Colrain, Ian M. Colrain Department of Psychology, University of Melbourne Sleep Disorders Research Center, Stanford UniversitySearch for more papers by this author First published: 24 December 2001 https://doi.org/10.1046/j.1365-2869.2000.00174.xCitations: 13 Ian M. Colrain, Sleep Disorders Research Center, Stanford University, 401 Quarry Rd, Suite 3301, Stanford, CA 94305, USA. E-mail: icolrain@leland.stanford.edu Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat No abstract is available for this article.Citing Literature Volume9, Issue1March 2000Pages 97-98 RelatedInformation