Spontaneous K-complexes in chronic psychophysiological insomnia

Bastien, Célyne; St-Jean, Geneviève; Turcotte, Isabelle; Morin, Charles M.; Lavallée, Mélanie; Carrier, Julie; Forget, Daniel

doi:10.1016/j.jpsychores.2009.01.014

Cited by 23 publications

(10 citation statements)

References 39 publications

(67 reference statements)

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“…Similar to previous reports (Bastien et al. , 2009b), the groups did not differ in the number of spontaneous KCs, although INS participants did not show an increase in the number of KCs during stimulus presentation.…”

Section: Discussionsupporting

confidence: 90%

Sensory gating in primary insomnia

Hairston

Talbot

Eidelman

et al. 2010

Eur J of Neuroscience

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Although previous research indicates that sleep architecture is largely intact in primary insomnia (PI), the spectral content of the sleeping electroencephalographic trace and measures of brain metabolism suggest that individuals with PI are physiologically more aroused than good sleepers. Such observations imply that individuals with PI may not experience the full deactivation of sensory and cognitive processing, resulting in reduced filtering of external sensory information during sleep. To test this hypothesis, gating of sensory information during sleep was tested in participants with primary insomnia (n = 18) and good sleepers (n = 20). Sensory gating was operationally defined as (i) the difference in magnitude of evoked response potentials elicited by pairs of clicks presented during Wake and Stage II sleep, and (ii) the number of K complexes evoked by the same auditory stimulus. During wake the groups did not differ in magnitude of sensory gating. During sleep, sensory gating of the N350 component was attenuated and completely diminished in participants with insomnia. P450, which occurred only during sleep, was strongly gated in good sleepers, and less so in participants with insomnia. Additionally, participants with insomnia showed no stimulus-related increase in K complexes. Thus, PI is potentially associated with impaired capacity to filter out external sensory information, especially during sleep. The potential of using stimulus-evoked K complexes as a biomarker for primary insomnia is discussed.

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Section: Discussionsupporting

confidence: 90%

Sensory gating in primary insomnia

Hairston

Talbot

Eidelman

et al. 2010

Eur J of Neuroscience

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“…To score a KC, the following criteria were applied: a nonstationary event with (a) a marked and well-delineated sharp wave initially negative in polarity, immediately followed by a positive polarity component; (b) maximum amplitude at frontocentral derivations; (c) a minimum duration of 0.5 s and a maximum duration of 3 s. According to Crowley and coworkers28, no amplitude criterion was applied in the present study, since the previously observed amplitude decrease in older subjects29. If multiple KCs appeared in sequence, only the first one was considered64. KC density was calculated as the number of KCs divided by NREM stage 2 sleep minutes.…”

Section: Discussionmentioning

confidence: 98%

The Fall of Sleep K-Complex in Alzheimer Disease

Gennaro

Gorgoni

Reda

et al. 2017

Sci Rep

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Although a slowing of electroencephalographic (EEG) activity during wakefulness and –to some extent- sleep of Alzheimer disease (AD) patients (i.e., increased slow-frequency activity) was documented, recent findings in healthy elderly show a decreased 0.6–1 Hz slow wave activity (SWA) during NREM, which was associated to β-amyloid deposition and impaired hippocampal memory consolidation. We hypothesize that the apparent contradiction may be explained by the partial overlap between 0.6–1 Hz EEG activity and K-Complex (KC). According to this view, we studied both frontal KCs and SWA in 20 AD patients and 20 healthy age-matched controls (HC) during nightly sleep, under the hypothesis that KCs better discriminate patients from healthy elderly than ≤1 Hz SWA. A drastic decrease of KC density during stage 2 NREM was found in AD compared to HC. Patients show more than 40% reduction of the KC density, allowing a correct classification of 80%. On the other hand, ≤1 Hz SWA of AD patients is slightly (not significantly) higher in most cortical areas compared to HC. Although no significant changes of ≤1 Hz SWA are detectable over frontal areas in AD, KC density decreases over the same location, and its decrease is related to the cognitive decline.

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“…To score a KC, the same criteria of the previous study [43] were applied: a non-stationary event with (a) a marked and well-delineated initial negative sharp wave, immediately followed by a positive component; (b) a maximum amplitude at frontocentral derivations; (c) a minimum duration of 0.5 s and a maximum duration of 3 s. In accordance with Crowley et al [38], no amplitude criterion was applied in the present study, due to the previously observed amplitude decrease in older subjects [37]. If multiple KCs appeared in sequence, only the first one was considered [65]. KC density was calculated as the number of KCs divided by NREM stage 2 sleep minutes.…”

Section: Methodsmentioning

confidence: 95%

In Search of Sleep Biomarkers of Alzheimer’s Disease: K-Complexes Do Not Discriminate between Patients with Mild Cognitive Impairment and Healthy Controls

et al. 2017

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The K-complex (KC) is one of the hallmarks of Non-Rapid Eye Movement (NREM) sleep. Recent observations point to a drastic decrease of spontaneous KCs in Alzheimer’s disease (AD). However, no study has investigated when, in the development of AD, this phenomenon starts. The assessment of KC density in mild cognitive impairment (MCI), a clinical condition considered a possible transitional stage between normal cognitive function and probable AD, is still lacking. The aim of the present study was to compare KC density in AD/MCI patients and healthy controls (HCs), also assessing the relationship between KC density and cognitive decline. Twenty amnesic MCI patients underwent a polysomnographic recording of a nocturnal sleep. Their data were compared to those of previously recorded 20 HCs and 20 AD patients. KCs during stage 2 NREM sleep were visually identified and KC densities of the three groups were compared. AD patients showed a significant KC density decrease compared with MCI patients and HCs, while no differences were observed between MCI patients and HCs. KC density was positively correlated with Mini-Mental State Examination (MMSE) scores. Our results point to the existence of an alteration of KC density only in a full-blown phase of AD, which was not observable in the early stage of the pathology (MCI), but linked with cognitive deterioration.

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Spontaneous K-complexes in chronic psychophysiological insomnia

Cited by 23 publications

References 39 publications

Sensory gating in primary insomnia

Sensory gating in primary insomnia

The Fall of Sleep K-Complex in Alzheimer Disease

In Search of Sleep Biomarkers of Alzheimer’s Disease: K-Complexes Do Not Discriminate between Patients with Mild Cognitive Impairment and Healthy Controls

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