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Are age and sex effects on sleep slow waves only a matter of electroencephalogram amplitude?

ABSTRACT: Aging is associated with reduced slow wave (SW) density (number SW/min in nonrapid-eye movement sleep) and amplitude. It has been proposed that an age-related decrease in SW density may be due to a reduction in electroencephalogram (EEG) amplitude instead of a decline in the capacity to generate SW. Here, we propose a data-driven approach to adapt SW amplitude criteria to age and sex. We predicted that the adapted criteria would reduce age and sex differences in SW density and SW characteristics but would not abolish them. A total of 284 healthy younger and older adults participated in one night of sleep EEG recording. We defined age- and sex-adapted SW criteria in a first cohort of younger (n = 97) and older (n = 110) individuals using a signal-to-noise ratio approach. We then used these age- and sex-specific criteria in an independent second cohort (n = 77, 38 younger and 39 older adults) to evaluate age and sex differences on SW density and SW characteristics. After adapting SW amplitude criteria, we showed maintenance of an age-related difference for SW density whereas the sex-related difference vanished. Indeed, older adults produced less SW compared with younger adults. Specifically, the adapted SW amplitude criteria increased the probability of occurrence of low amplitude SW (<80 µV) for older men especially. Our results thereby confirm an age-related decline in SW generation rather than an artifact in the detection amplitude criteria. As for the SW characteristics, the age- and sex-adapted criteria display reproducible effects across the two independent cohorts suggesting a more reliable inventory of the SW.

SUBMITTER: Rosinvil T

PROVIDER: S-EPMC7953219 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:Epileptic discharges in focal epilepsy are frequently activated during non-rapid eye movement sleep. Sleep slow waves are present during this stage and have been shown to include a deactivated ('down', hyperpolarized) and an activated state ('up', depolarized). The 'up' state enhances physiological rhythms, and we hypothesize that sleep slow waves and particularly the 'up' state are the specific components of non-rapid eye movement sleep that mediate the activation of epileptic activity. We investigated eight patients with pharmaco-resistant focal epilepsies who underwent combined scalp-intracerebral electroencephalography for diagnostic evaluation. We analysed 259 frontal electroencephalographic channels, and manually marked 442 epileptic spikes and 8487 high frequency oscillations during high amplitude widespread slow waves, and during matched control segments with low amplitude widespread slow waves, non-widespread slow waves or no slow waves selected during the same sleep stages (total duration of slow wave and control segments: 49 min each). During the slow waves, spikes and high frequency oscillations were more frequent than during control segments (79% of spikes during slow waves and 65% of high frequency oscillations, both P ∼ 0). The spike and high frequency oscillation density also increased for higher amplitude slow waves. We compared the density of spikes and high frequency oscillations between the 'up' and 'down' states. Spike and high frequency oscillation density was highest during the transition from the 'up' to the 'down' state. Interestingly, high frequency oscillations in channels with normal activity expressed a different peak at the transition from the 'down' to the 'up' state. These results show that the apparent activation of epileptic discharges by non-rapid eye movement sleep is not a state-dependent phenomenon but is predominantly associated with specific events, the high amplitude widespread slow waves that are frequent, but not continuous, during this state of sleep. Both epileptic spikes and high frequency oscillations do not predominate, like physiological activity, during the 'up' state but during the transition from the 'up' to the 'down' state of the slow wave, a period of high synchronization. Epileptic discharges appear therefore more associated with synchronization than with excitability. Furthermore, high frequency oscillations in channels devoid of epileptic activity peak differently during the slow wave cycle from those in channels with epileptic activity. This property may allow differentiating physiological from pathological high frequency oscillations, a problem that is unresolved until now.

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Are age and sex effects on sleep slow waves only a matter of electroencephalogram amplitude?

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