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Steiger, A.

Publications and source records attributed to Steiger, A..

9 recordsLinked to original sources

Electrophysiological correlates of lucid dreaming

Lucid dreaming (LD) is a state of conscious awareness of the current dream state, predominantly associated with REM sleep. Research progress in uncovering the neurobiological basis of LD has been hindered by low sample sizes, diverse EEG setups, and specific artifact issues like saccadic eye movements and signal non-stationarity. To address these matters, we developed a multi-stage preprocessing pipeline that integrates standardized early-stage preprocessing, artifact subspace reconstruction, and signal-space projection. This approach enhanced data quality by precisely removing saccadic potential effects even in setups with minimal channels. To robustly identify the electrophysiological correlates of LD, we applied this methodology to LD data collected across laboratories (pooled N = 44) and explored sensor-and source-level markers hypothesized to underlie LD. Compared to non-lucid REM sleep, we observed few robust differences on the EEG sensor level, which is in line with recent findings. In contrast, on the source level, gamma1 power (30-36 Hz) showed increases during LD in left-hemispheric temporal areas, which might reflect verbal insight processes. Gamma1 power also increased around the onset of LD eye signaling in right temporo-occipital regions including the right precuneus, in line with its involvement in self-referential thinking. Reductions in beta power (12-30 Hz) during LD in right central and parietal areas including the temporo-parietal junction are potentially associated with a conscious reassessment of the veridicality of the currently perceived reality. Notably, functional connectivity in alpha band (8-12 Hz) increased during LD, in contrast to the reductions typically seen in psychedelic states, highlighting enhanced self-awareness. Taken together, these findings illuminate the electrophysiological correlates of LD state, and may serve as a basis to uncover neural mechanisms at the time point of lucid dream insight.

neuroscience↗

Fractal cycles of sleep: a new aperiodic activity-based definition of sleep cycles

Nocturnal human sleep consists of 4 - 6 ninety-minute cycles defined as episodes of non-rapid eye movement (non-REM) sleep followed by an episode of REM sleep. While sleep cycles are considered fundamental components of sleep, their functional significance largely remains unclear. One of the reasons for a lack of research progress in this field is the absence of a data-driven definition of sleep cycles. Here, we proposed to base such a definition on fractal (aperiodic) neural activity, a well-established marker of arousal and sleep stages. We explored temporal dynamics of fractal activity during nocturnal sleep using electroencephalography. Based on the observed pattern of fractal fluctuations, we introduced a new concept of fractal activity-based cycles of sleep or "fractal cycles" for short, defined as a time interval during which fractal activity descends from its local maximum to its local minimum and then leads back to the next local maximum. Next, we assessed correlations between fractal and classical (i.e., non-REM - REM) sleep cycle durations. We also studied cycles with skipped REM sleep, i.e., the cycles where the REM phase is expected to appear except that it does not, being replaced by lightening of sleep. Regarding the sample, we examined fractal cycles in healthy adults (age range: 18 - 75 years, n = 205) as well as in children and adolescents (range: 8 - 17 years, n = 21), the group characterized by deeper sleep and a higher frequency of cycles with skipped REM sleep. Further, we studied fractal cycles in major depressive disorder (n = 111), the condition characterized by altered REM sleep (in addition to its clinical symptoms). We found that fractal and classical cycle durations (89 {+/-} 34 min vs 90 {+/-} 25 min) correlated positively (r = 0.5, p < 0.001). Cycle-to-cycle overnight dynamics showed an inverted U-shape of both fractal and classical cycle durations and a gradual decrease in absolute amplitudes of the fractal descents and ascents from early to late cycles. In adults, the fractal cycle duration and participants age correlated negatively (r = -0.2, p = 0.006). Children and adolescents had shorter fractal cycles compared to young adults (76 {+/-} 34 vs 94 {+/-} 32 min, p < 0.001). The fractal cycle algorithm detected cycles with skipped REM sleep in 91 - 98% of cases. Medicated patients with depression showed longer fractal cycles compared to their own unmedicated state (107 {+/-} 51 min vs 92 {+/-} 38 min, p < 0.001) and age-matched controls (104 {+/-} 49 vs 88 {+/-} 31 min, p < 0.001). In conclusion, fractal cycles are an objective, quantifiable, continuous and biologically plausible way to display sleep neural activity and its cycles. They are useful in healthy adult and pediatric populations as well as in patients with major depressive disorder. Fractal cycles should be extensively studied to advance theoretical research on sleep structure. Highlights- Fractal activity-based cycles of sleep or "fractal cycles" for short is a new concept based on cyclic changes in fractal (aperiodic) neural activity during sleep. - Durations of fractal and classical cycles correlate, and both show an inverted U-shape when seen from early to late cycles. - The fractal cycle algorithm is effective in detecting cycles with skipped REM sleep. - Older healthy adults shower shorter fractal - but not classical - cycle durations. - Fractal cycle duration is shorter in children and adolescents compared to young adults. - In major depressive disorder, antidepressant medication is associated with longer fractal cycles.

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Sustained polyphasic sleep restriction abolishes human growth hormone release

Voluntary sleep restriction is a common phenomenon in industrialized societies aiming to increase time spent awake and thus productivity. We explored how restricting sleep to a radically polyphasic schedule affects neural, cognitive, and endocrine characteristics. Ten young healthy participants were restricted to one 30-min nap opportunity at the end of every 4 hours (i.e., 6 sleep episodes per 24 hours) without any extended core sleep window, which resulted in a cumulative sleep amount of just 2 hours per day (i.e., [~]20 min per bout). All but one participant terminated this schedule during the first three weeks. The remaining participant (a 25-year-old male) succeeded to adhere to a polyphasic schedule for 5 weeks with no apparent impairments in cognitive and psychiatric measures except for psychomotor vigilance. While in-blood cortisol or melatonin release pattern and amounts were unaltered by the polyphasic as compared to monophasic sleep, growth hormone seemed almost entirely abolished (>95% decrease), with the residual release showing a considerably changed polyphasic secretional pattern. While coarse sleep structure appeared intact during polyphasic sleep, REM sleep showed decreased oscillatory and increased aperiodic EEG activity compared to monophasic sleep. Considering the decreased vigilance, abolished growth hormone release, and neurophysiological changes observed, it is doubtful that radically polyphasic sleep schedules can subserve the different functions of sleep to a sufficient degree.

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Divergent associations of slow-wave sleep vs. REM sleep with plasma amyloid-beta

BackgroundRecent evidence shows that during slow-wave sleep (SWS), the brain is cleared from potentially toxic metabolites, such as the amyloid-beta protein. Poor sleep or elevated cortisol levels can worsen amyloid-beta clearance, potentially leading to the formation of amyloid plaques, a neuropathological hallmark of Alzheimers disease. Here, we explore how nocturnal neural and endocrine activity affects amyloid-beta fluctuations in the peripheral blood as a reflection of cerebral clearance. MethodsSimultaneous polysomnography and all-night blood sampling were acquired in 60 healthy volunteers aged 20-68 years old. Nocturnal plasma concentrations of two amyloid-beta species (amyloid-beta-40 and amyloid-beta-42), cortisol, and growth hormone were assessed every 20 minutes from 23:00-7:00. Amyloid-beta fluctuations were modeled with sleep stages, (non)-oscillatory power, and hormones as predictors while controlling for age and multiple comparisons. Time lags between the predictors and amyloid-beta ranged from 20 to 120min. FindingsThe amyloid-beta-40 and amyloid-beta-42 levels correlated positively with growth hormone concentrations, SWS proportion, slow-wave (0.3-4Hz) oscillatory and high-band (30-48Hz) non-oscillatory power, but negatively with cortisol concentrations and rapid eye movement sleep (REM) proportion measured 40-100min before (all t-values>|3|, p-values<0.003). Older participants showed higher amyloid-beta-40 levels. InterpretationSlow-wave oscillations are associated with higher plasma amyloid-beta levels, reflecting their contribution to cerebral amyloid-beta clearance across the blood-brain barrier. REM sleep is related to decreased amyloid-beta plasma levels; however, this link may reflect passive aftereffects of SWS and not REMs effects per se. Strong associations between cortisol, growth hormone, and amyloid-beta presumably reflect the sleep-regulating role of the corresponding releasing hormones. A positive association between age and amyloid-beta-40 may indicate that peripheral clearance becomes less efficient with age. Our study provides important insights into the specificity of different sleep features effects on brain clearance and suggests that cortisol nocturnal fluctuations may serve as a new marker of clearance efficiency.

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Non-REM sleep in major depressive disorder

Disturbed sleep is a key symptom in major depressive disorder (MDD). REM sleep alterations are well described in the current fliterature, but little is known about non-REM sleep alterations. Additionally, sleep disturbances relate to a variety of cognitive symptoms in MDD, but which features of non-REM sleep EEG contribute to this, remains unknown. We comprehensively analyzed non-REM sleep EEG features in three independently collected datasets (N=284). These included MDD patients with a broad age range, varying duration and severity of depression, unmedicated or medicated, age- and gender-matched to healthy controls. We explored changes in sleep architecture including sleep stages and cycles, spectral power, sleep spindles, slow waves (SW), and SW-spindle coupling. Next, we analyzed the association of these sleep features with acute measures of depression severity and overnight consolidation of procedural memory. Overall, no major systematic alterations in non-REM sleep architecture were found in patients compared to controls. For the microstructure of non-REM sleep, we observed a higher spindle amplitude in unmedicated patients compared to controls, and after the start of antidepressant medication longer SWs with lower amplitude and a more dispersed SW-spindle coupling. In addition, long-term, but not short-term medication seemed to lower spindle density. Overnight procedural memory consolidation was impaired in medicated patients and associated with lower sleep spindle density. Our results suggest that alterations in non-REM sleep EEG might be more subtle than previously reported. We discuss these findings in the context of antidepressant medication intake and age. Statement of SignificanceDepression affects large and diverse populations worldwide, including their sleep. Most sleep is non-REM sleep, which is vital to cognitive function, including memory. How non-REM is affected during a depression or medical treatment remains poorly investigated. We classified non-REM sleep of depressive patients against healthy controls in unprecedented analysis detail and confidence using the largest dataset published so far while also test sleep alterations associations with impaired memory. Surprisingly, severe depression alone did not alter sleep. We observed severe non-REM sleep alterations only worsening under patient medication, which ultimately coincided with 24-hour memory impairments. Though causal influences of medication on sleep in depressive patients remains to be investigated, this cautions common clinical practice in long-term treatment with antidepressants.

neuroscience↗

Durable memories and efficient neural coding through mnemonic training using the method of loci

Mnemonic techniques, such as the method of loci, can powerfully boost memory. Here, we compared memory athletes ranked among the worlds top 50 in memory sports to mnemonics-naive controls. In a second study, participants completed a six-weeks memory training, working memory training, or no intervention. Behaviorally, memory training enhanced durable, longer-lasting memories. fMRI during encoding and recognition revealed task-based activation decreases in lateral prefrontal, as well as in parahippocampal and retrosplenial cortices in both memory athletes and participants after memory training, partly associated with better performance after four months. This was complemented by hippocampal-neocortical coupling during consolidation, which was stronger the more durable memories participants formed. Our findings are the first to demonstrate that mnemonic training boosts durable memory formation via decreased task-based activation and increased consolidation thereafter. This is in line with conceptual accounts of neural efficiency and highlights a complex interplay of neural processes critical for extraordinary memory.

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A new set of composite, non-redundant electroencephalogram measures of non-rapid eye movement sleep based on the power law scaling of the Fourier spectrum

A novel method for deriving composite, non-redundant measures of non-rapid eye movement (NREM) sleep electroencephalogram (EEG) is developed on the basis of the power law scaling of the Fourier spectra. Measures derived are the spectral intercept, the slope (spectral exponent), as well as the maximal whitened spectral peak amplitude and frequency in the sleep spindle range. As a proof of concept, we apply these measures on a large sleep EEG dataset (N = 175; 81 females; age range: 17-60 years) with previously demonstrated effects of age, sex and intelligence. As predicted, aging is associated with decreased overall spectral slopes (increased exponents) and whitened spectral peak amplitudes in the spindle frequency range. In addition, age associates with decreased sleep spindle spectral peak frequencies in the frontal region. Women were characterized by higher spectral intercepts and higher spectral peak frequencies in the sleep spindle range. No sex differences in whitened spectral peak amplitudes of the sleep spindle range were found. Intelligence correlated positively with whitened spectral peak amplitudes of the spindle frequency range in women, but not in men. Last, age-related increases in spectral exponents did not differ in subjects with average and high intelligence. Our findings replicate and complete previous reports in the literature, indicating that the number of variables describing NREM sleep EEG can be effectively reduced in order to overcome redundancy and Type I statistical errors in future electrophysiological studies of sleep. Author summaryGiven the tight reciprocal relationship between sleep and wakefulness, the objective description of the complex neural activity patterns characterizing human sleep is of utmost importance in understanding the several facets of brain function, like sex differences, aging and cognitive abilities. Current approaches are either exclusively based on visual impressions expressed in graded levels of sleep depth (W, N1, N2, N3, REM), whereas computerized quantitative methods provide an almost infinite number of potential metrics, suffering from significant redundancy and arbitrariness. Our current approach relies on the assumptions that the spontaneous human brain activity as reflected by the scalp-derived electroencephalogram (EEG) are characterized by coloured noise-like properties. That is, the contribution of different frequencies to the power spectrum of the signal are best described by power law functions with negative exponents. In addition, we assume, that stages N2-N3 are further characterized by additional non-random (non-noise like, sinusoidal) activity patterns, which are emerging at specific frequencies, called sleep spindles (9-18 Hz). By relying on these assumptions we were able to effectively reduce 191 spectral measures to 4: (1) the spectral intercept reflecting the overall amplitude of the signal, (2) the spectral slope reflecting the constant ratio of low over high frequency power, (3) the frequency of the maximal sleep spindle activity and (4) the amplitude of the sleep spindle spectral peak. These 4 measures were efficient in characterizing known age-effects, sex-differences and cognitive correlates of sleep EEG. Future clinical and basic studies are supposed to be significantly empowered by the efficient data reduction provided by our approach.

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Individual slow wave morphology is a marker of ageing

Slow wave activity is a hallmark of deep NREM sleep. Scalp slow wave morphology is stereotypical, it is highly correlated with the synchronized onset and cessation of cortical neuronal firing measured from the surface or depth of the cortex, strongly affected by ageing, and these changes are causally associated with age-related cognitive decline. We investigated how normal ageing affects the individual morphology of the slow wave, and whether these changes are captured by the summary slow wave parameters generally used in the literature. We recorded full-night polysomnography in 159 subjects (age 17-69 years) and automatically detected slow waves using six different detection methods to ensure methodological robustness. We established individual slow morphologies at 501 data points for each subject and also calculated the individual average slow wave amplitude, average ascending and descending slope steepness and the total number of slow waves (gross parameters). Using LASSO penalized regression we found that fine-grained slow wave morphology is associated with age beyond gross parameters, with young subjects having faster slow wave polarity reversals, suggesting a more efficient initiation and termination of slow wave down- and upstates. Our results demonstrate the superiority of the high-resolution slow wave morphology as a biomarker of ageing, and highlights state transitions as promising targets of restorative stimulation-based interventions.

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2D:4D and spatial abilities: From rats to humans

Variance in spatial abilities are thought to be determined by in utero levels of testosterone and oestrogen, measurable in adults by the length ratio of the 2nd and 4th digit (2D:4D). We confirmed the relationship between 2D:4D and spatial performance using rats in two different tasks (paired-associate task and watermaze) and replicated this in humans. We further clarified anatomical and functional brain correlates of the association between 2D:4D and spatial performance in humans.

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