Sleep evoked delta frequency responses show a linear decline in amplitude across the adult lifespan

Colrain, Ian M.; Crowley, Kate; Nicholas, Christian L.; Afifi, Lamia; Baker, Fiona C.; Padilla, Mayra; Turlington, Sharon R.; Trinder, John

doi:10.1016/j.neurobiolaging.2008.06.003

Cited by 53 publications

(50 citation statements)

References 56 publications

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“…Evoked K-complexes, provide a unique opportunity to test and probe the sleeping nervous system and extract a delta frequency 'signal' from pathological 'delta' noise. Results revealed reduced delta generation in AD patients compared to elderly controls (Crowley et al 2005) with a significant divergence from the normal aging linear relationship that we have established (Colrain et al 2010) which can be interpreted as reflecting accelerated deterioration over and above normal aging.…”

Section: Alzheimer's Diseasementioning

confidence: 60%

“…K-Complexes can thus be used to test the ability of the brain to produce large amplitude synchronized waveforms. Aging has been shown to impact delta generation during sleep with a decrease in the incidence of spontaneous K-complexes (Crowley et al 2002b;Kubicki et al 1989) as well as the incidence and amplitude of the evoked K-complex (Colrain et al 2010;Crowley et al 2004;Crowley et al 2002a). A linear regression analysis ( Fig.…”

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confidence: 99%

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Sleep and Sleep Disorders in Older Adults

2011

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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.

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Section: Alzheimer's Diseasementioning

confidence: 60%

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confidence: 99%

Sleep and Sleep Disorders in Older Adults

2011

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“…These neurons need to be simultaneously active and the synchronization of their firing is contingent on healthy white matter tracts. It is therefore not surprising that the amplitude of the prominent negative component of the averaged evoked K-complex (N550) declines with normal aging in healthy men and women (Crowley, Trinder, and Colrain 2002; Crowley, Trinder, and Colrain 2004; Colrain et al 2010). This decrease parallels age-related decreases in gray matter volume (Pfefferbaum et al 1994).…”

Section: 0 Evoked Potentials During Sleepmentioning

confidence: 99%

“…This decrease parallels age-related decreases in gray matter volume (Pfefferbaum et al 1994). We have thus hypothesized that the K-complex may also be a sensitive marker of the brain degradation seen in chronic alcoholism (Colrain et al 2010). …”

Section: 0 Evoked Potentials During Sleepmentioning

confidence: 99%

Alcohol and the sleeping brain

Colrain

Nicholas

Baker

2014

Handbook of Clinical Neurology

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132

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Alcohol acts as a sedative that interacts with several neurotransmitter systems important in the regulation of sleep. Acute administration of large amounts of alcohol prior to sleep leads to decreased sleep onset latency and changes in sleep architecture early in the night, when blood alcohol levels are high, with subsequent disrupted, poor quality sleep later in the night. Alcohol abuse and dependence are associated with chronic sleep disturbance, lower slow wave sleep, and more rapid eye movement sleep than normal, that last long into periods of abstinence and may play a role in relapse. The chapter outlines the evidence for acute and chronic alcohol effects on sleep architecture and sleep EEG, evidence for tolerance with repeated administration, and possible underlying neurochemical mechanisms for alcohol’s effects on sleep. Also discussed are sex differences as well as effects of alcohol on sleep homeostasis and circadian regulation. Evidence for the role of sleep disruption as a risk factor for developing alcohol dependence is discussed in the context of research conducted in adolescents. The utility of sleep evoked potentials in the assessment of the effects of alcoholism on sleep and the brain and in abstinence-mediated recovery is also outlined. The chapter concludes with a series of questions that need to be answered to determine the role of sleep and sleep disturbance in the development and maintenance of problem drinking and the potential beneficial effects of the treatment of sleep disorders for maintenance of abstinence in alcoholism.

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“…Aging and AUD appear to have parallel effects on both the KC and brain structural integrity, leading to the hypothesis that N550 amplitude is related to quality of brain integrity (Colrain et al 2010). Both KC incidence and N550 amplitude are reduced with age (Crowley et al 2002; Colrain et al 2010) and in abstinent AUD (Nicholas et al 2002; Colrain et al 2009).…”

Section: Introductionmentioning

confidence: 99%

Partial K-Complex Recovery Following Short-Term Abstinence in Individuals with Alcohol Use Disorder

Willoughby

Zambotti

Baker

et al. 2015

Alcohol Clin Exp Res

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Background The K-complex (KC) is a brain potential characteristic of non-rapid eye movement (NREM) sleep resulting from the synchronous activity of a large population of neurons and hypothesized to reflect brain integrity. KC amplitude is lower in individuals with Alcohol Use Disorder (AUD) compared with age-matched controls but its recovery with short-term abstinence has not been studied. Therefore, we investigated whether the KC shows significant recovery over the first four months of abstinence in individuals with AUD. Methods 16 recently abstinent AUD (46.6 ± 9.3 years) and 13 gender and age-matched healthy controls (41.6 ± 8.3 years) were studied on three occasions: the Initial session was within 1 month of the AUD last drink, then 1 month and 3 months later. Overnight electroencephalogram (EEG) was recorded while participants were presented with tones during stage 2 NREM sleep to elicit KCs. Results At the Initial session, AUD showed significantly lower KC amplitude and incidence compared with controls. In the AUD individuals, KC amplitude increased significantly from the Initial to the 1 month session. KC incidence showed a marginally significant increase. Neither KC amplitude nor incidence changed from the 1 month to the 3 month session. No changes in KC amplitude or incidence across sessions were observed in the control group. Conclusions Our results demonstrate partial KC recovery during the first two months of abstinence. This recovery is consistent with the time course of structural brain recovery in abstinent AUD demonstrated by recent neuroimaging results.

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Sleep evoked delta frequency responses show a linear decline in amplitude across the adult lifespan

Cited by 53 publications

References 56 publications

Sleep and Sleep Disorders in Older Adults

Sleep and Sleep Disorders in Older Adults

Alcohol and the sleeping brain

Partial K-Complex Recovery Following Short-Term Abstinence in Individuals with Alcohol Use Disorder

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