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Eus J W Van Someren - One of the best experts on this subject based on the ideXlab platform.
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Resting-State Subjective Experience and EEG Biomarkers Are Associated with Sleep-Onset Latency
Frontiers in psychology, 2016Co-Authors: B. Alexander Diaz, Eus J W Van Someren, Richard Hardstone, Huibert D. Mansvelder, Klaus Linkenkaer-hansenAbstract:Difficulties initiating Sleep are common in several disorders, including insomnia and attention deficit hyperactivity disorder. These disorders are prevalent, bearing significant societal and financial costs which require the consideration of new treatment strategies and a better understanding of the physiological and cognitive processes surrounding the time of preparing for Sleep or falling aSleep. Here, we search for neuro-cognitive associations in the resting state and examine their relevance for predicting Sleep-Onset Latency using multi-level mixed models. Multiple EEG recordings were obtained from healthy male participants (N = 13) during a series of 5 min eyes-closed resting-state trials (in total, n = 223) followed by a period-varying in length up to 30 min-that either allowed subjects to transition into Sleep ("Sleep trials," n Sleep = 144) or was ended while they were still awake ("wake trials," n wake = 79). After both eyes-closed rest, Sleep and wake trials, subjective experience was assessed using the Amsterdam Resting-State Questionnaire (ARSQ). Our data revealed multiple associations between eyes-closed rest alpha and theta oscillations and ARSQ-dimensions Discontinuity of Mind, Self, Theory of Mind, Planning, and Sleepiness. The Sleep trials showed that the transition toward the first Sleep stage exclusively affected subjective experiences related to Theory of Mind, Planning, and Sleepiness. Importantly, Sleep-Onset Latency was negatively associated both with eyes-closed rest ratings on the ARSQ dimension of Sleepiness and with the long-range temporal correlations of parietal theta oscillations derived by detrended fluctuation analysis (DFA). These results could be relevant to the development of personalized tools that help evaluate the success of falling aSleep based on measures of resting-state cognition and EEG biomarkers.
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skin temperature and Sleep Onset Latency changes with age and insomnia
Physiology & Behavior, 2007Co-Authors: Roy J E M Raymann, D F Swaab, Eus J W Van SomerenAbstract:Throughout the 24-hour day, the occurrence of Sleep and wakefulness is closely related to changes in body temperatures. Changes in skin temperature may causally affect the ability to initiate and maintain Sleep. First, we briefly summarize a previously proposed neurobiological mechanism that couples skin temperature to Sleep propensity. Next we review previous findings on the relation between skin temperature and Sleep-Onset Latency, indicating that Sleep propensity can be enhanced by warming the skin to the level that normally occurs prior to and during Sleep. Finally, we present new data indicating age- and insomnia-related changes in the Sleep-Onset Latency response to foot warming, and evaluate whether different methods of foot warming could provide an applicable strategy to address Sleep complaints. Foot temperature manipulations included footbaths before Sleep Onset (1), and heatable bed socks applied either before (2) or after lights-off (3). In adults, Sleep-Onset was accelerated by warm and neutral bed socks after lights-off and correlated to the increase in foot temperature. This increase was attenuated in elderly subjects. In elderly subjects without Sleep difficulties, Sleep Onset could be accelerated with neutral bed socks after lights-off and a warm footbath prior to lights-off. In elderly insomniacs, none of the treatments accelerated Sleep Onset. We illustrate that elderly subjects show an attenuated increase in foot temperature after lights-off and lose the relationship between pre-Sleep heat-loss activation and Sleep Latency. The sensitivity of Sleep propensity to foot warming changes with age and is attenuated in age-related insomnia. Keywords: Sleep electroencephalogram; Core body temperature; Skin temperature; Thermoregulation; Sleep-Onset Latency; Ageing; Insomnia; Foot warming
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Skin temperature and Sleep-Onset Latency: changes with age and insomnia.
Physiology & Behavior, 2006Co-Authors: Roy J E M Raymann, D F Swaab, Eus J W Van SomerenAbstract:Throughout the 24-hour day, the occurrence of Sleep and wakefulness is closely related to changes in body temperatures. Changes in skin temperature may causally affect the ability to initiate and maintain Sleep. First, we briefly summarize a previously proposed neurobiological mechanism that couples skin temperature to Sleep propensity. Next we review previous findings on the relation between skin temperature and Sleep-Onset Latency, indicating that Sleep propensity can be enhanced by warming the skin to the level that normally occurs prior to – and during – Sleep. Finally, we present new data indicating age- and insomnia-related changes in the Sleep-Onset Latency response to foot warming, and evaluate whether different methods of foot warming could provide an applicable strategy to address Sleep complaints. Foot temperature manipulations included footbaths before Sleep Onset (1), and heatable bed socks applied either before (2) or after lights-off (3). In adults, Sleep-Onset was accelerated by warm and neutral bed socks after lights-off and correlated to the increase in foot temperature. This increase was attenuated in elderly subjects. In elderly subjects without Sleep difficulties, Sleep Onset could be accelerated with neutral bed socks after lights-off and a warm footbath prior to lights-off. In elderly insomniacs, none of the treatments accelerated Sleep Onset. We illustrate that elderly subjects show an attenuated increase in foot temperature after lights-off and lose the relationship between pre-Sleep heat-loss activation and Sleep Latency. The sensitivity of Sleep propensity to foot warming changes with age and is attenuated in age-related insomnia.
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Cutaneous warming promotes Sleep Onset
American Journal of Physiology-regulatory Integrative and Comparative Physiology, 2005Co-Authors: Roy J E M Raymann, D F Swaab, Eus J W Van SomerenAbstract:Sleep occurs in close relation to changes in body temperature. Both the monophasic Sleep period in humans and the polyphasic Sleep periods in rodents tend to be initiated when core body temperature is declining. This decline is mainly due to an increase in skin blood flow and consequently skin warming and heat loss. We have proposed that these intrinsically occurring changes in core and skin temperatures could modulate neuronal activity in Sleep-regulating brain areas (Van Someren EJW, Chronobiol Int 17: 313-54, 2000). We here provide results compatible with this hypothesis. We obtained 144 Sleep-Onset latencies while directly manipulating core and skin temperatures within the comfortable range in eight healthy subjects under controlled conditions. The induction of a proximal skin temperature difference of only 0.78 +/- 0.03 degrees C (mean +/- SE) around a mean of 35.13 +/- 0.11 degrees C changed Sleep-Onset Latency by 26%, i.e., by 3.09 minutes [95% confidence interval (CI), 1.91 to 4.28] around a mean of 11.85 min (CI, 9.74 to 14.41), with faster Sleep Onsets when the proximal skin was warmed. The reduction in Sleep-Onset Latency occurred despite a small but significant decrease in subjective comfort during proximal skin warming. The induction of changes in core temperature (delta = 0.20 +/- 0.02 degrees C) and distal skin temperature (delta = 0.74 +/- 0.05 degrees C) were ineffective. Previous studies have demonstrated correlations between skin temperature and Sleep-Onset Latency. Also, Sleep disruption by ambient temperatures that activate thermoregulatory defense mechanisms has been shown. The present study is the first to experimentally demonstrate a causal contribution to Sleep-Onset Latency of skin temperature manipulations within the normal nocturnal fluctuation range. Circadian and Sleep-appetitive behavior-induced variations in skin temperature might act as an input signal to Sleep-regulating systems.
Martijn Arns - One of the best experts on this subject based on the ideXlab platform.
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Differential effects of theta/beta and SMR neurofeedback in ADHD on Sleep Onset Latency
Frontiers in human neuroscience, 2014Co-Authors: Martijn Arns, Ilse Feddema, J. Leon KenemansAbstract:Recent studies suggest a role for Sleep and Sleep problems in the etiology of attention deficit hyperactivity disorder (ADHD) and a recent model about the working mechanism of sensori-motor rhythm (SMR) neurofeedback, proposed that this intervention normalizes Sleep and thus improves ADHD symptoms such as inattention and hyperactivity/impulsivity. In this study we compared adult ADHD patients (N = 19) to a control group (N = 28) and investigated if differences existed in Sleep parameters such as Sleep Onset Latency (SOL), Sleep Duration (DUR) and overall reported Sleep problems (PSQI) and if there is an association between Sleep-parameters and ADHD symptoms. Secondly, in 37 ADHD patients we investigated the effects of SMR and Theta/Beta (TBR) neurofeedback on ADHD symptoms and Sleep parameters and if these Sleep parameters may mediate treatment outcome to SMR and TBR neurofeedback. In this study we found a clear continuous relationship between self-reported Sleep problems (PSQI) and inattention in adults with- and without-ADHD. TBR neurofeedback resulted in a small reduction of SOL, this change in SOL did not correlate with the change in ADHD symptoms and the reduction in SOL only happened in the last half of treatment, suggesting this is an effect of symptom improvement not specifically related to TBR neurofeedback. SMR neurofeedback specifically reduced the SOL and PSQI score, and the change in SOL and change in PSQI correlated strongly with the change in inattention, and the reduction in SOL was achieved in the first half of treatment, suggesting the reduction in SOL mediated treatment response to SMR neurofeedback. Clinically, TBR and SMR neurofeedback had similar effects on symptom reduction in ADHD (inattention and hyperactivity/impulsivity). These results suggest differential effects and different working mechanisms for TBR and SMR neurofeedback in the treatment of ADHD.
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differential effects of theta beta and smr neurofeedback in adhd on Sleep Onset Latency
Frontiers in Human Neuroscience, 2014Co-Authors: Martijn Arns, Ilse Feddema, Leon J KenemansAbstract:Recent studies suggest a role for Sleep and Sleep problems in the etiology of attention deficit hyperactivity disorder (ADHD) and a recent model about the working mechanism of sensori-motor rhythm (SMR) neurofeedback, proposed that this intervention normalizes Sleep and thus improves ADHD symptoms such as inattention and hyperactivity/impulsivity. In this study we compared adult ADHD patients (N = 19) to a control group (N = 28) and investigated if differences existed in Sleep parameters such as Sleep Onset Latency (SOL), Sleep Duration (DUR) and overall reported Sleep problems (PSQI) and if there is an association between Sleep-parameters and ADHD symptoms. Secondly, in 37 ADHD patients we investigated the effects of SMR and Theta/Beta (TBR) neurofeedback on ADHD symptoms and Sleep parameters and if these Sleep parameters may mediate treatment outcome to SMR and TBR neurofeedback. In this study we found a clear continuous relationship between self-reported Sleep problems (PSQI) and inattention in adults with- and without-ADHD. TBR neurofeedback resulted in a small reduction of SOL, this change in SOL did not correlate with the change in ADHD symptoms and the reduction in SOL only happened in the last half of treatment, suggesting this is an effect of symptom improvement not specifically related to TBR neurofeedback. SMR neurofeedback specifically reduced the SOL and PSQI score, and the change in SOL and change in PSQI correlated strongly with the change in inattention, and the reduction in SOL was achieved in the first half of treatment, suggesting the reduction in SOL mediated treatment response to SMR neurofeedback. Clinically, TBR and SMR neurofeedback had similar effects on symptom reduction in ADHD (inattention and hyperactivity/impulsivity). These results suggest differential effects and different working mechanisms for TBR and SMR neurofeedback in the treatment of ADHD.
Leon J Kenemans - One of the best experts on this subject based on the ideXlab platform.
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differential effects of theta beta and smr neurofeedback in adhd on Sleep Onset Latency
Frontiers in Human Neuroscience, 2014Co-Authors: Martijn Arns, Ilse Feddema, Leon J KenemansAbstract:Recent studies suggest a role for Sleep and Sleep problems in the etiology of attention deficit hyperactivity disorder (ADHD) and a recent model about the working mechanism of sensori-motor rhythm (SMR) neurofeedback, proposed that this intervention normalizes Sleep and thus improves ADHD symptoms such as inattention and hyperactivity/impulsivity. In this study we compared adult ADHD patients (N = 19) to a control group (N = 28) and investigated if differences existed in Sleep parameters such as Sleep Onset Latency (SOL), Sleep Duration (DUR) and overall reported Sleep problems (PSQI) and if there is an association between Sleep-parameters and ADHD symptoms. Secondly, in 37 ADHD patients we investigated the effects of SMR and Theta/Beta (TBR) neurofeedback on ADHD symptoms and Sleep parameters and if these Sleep parameters may mediate treatment outcome to SMR and TBR neurofeedback. In this study we found a clear continuous relationship between self-reported Sleep problems (PSQI) and inattention in adults with- and without-ADHD. TBR neurofeedback resulted in a small reduction of SOL, this change in SOL did not correlate with the change in ADHD symptoms and the reduction in SOL only happened in the last half of treatment, suggesting this is an effect of symptom improvement not specifically related to TBR neurofeedback. SMR neurofeedback specifically reduced the SOL and PSQI score, and the change in SOL and change in PSQI correlated strongly with the change in inattention, and the reduction in SOL was achieved in the first half of treatment, suggesting the reduction in SOL mediated treatment response to SMR neurofeedback. Clinically, TBR and SMR neurofeedback had similar effects on symptom reduction in ADHD (inattention and hyperactivity/impulsivity). These results suggest differential effects and different working mechanisms for TBR and SMR neurofeedback in the treatment of ADHD.
J. Leon Kenemans - One of the best experts on this subject based on the ideXlab platform.
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Differential effects of theta/beta and SMR neurofeedback in ADHD on Sleep Onset Latency
Frontiers in human neuroscience, 2014Co-Authors: Martijn Arns, Ilse Feddema, J. Leon KenemansAbstract:Recent studies suggest a role for Sleep and Sleep problems in the etiology of attention deficit hyperactivity disorder (ADHD) and a recent model about the working mechanism of sensori-motor rhythm (SMR) neurofeedback, proposed that this intervention normalizes Sleep and thus improves ADHD symptoms such as inattention and hyperactivity/impulsivity. In this study we compared adult ADHD patients (N = 19) to a control group (N = 28) and investigated if differences existed in Sleep parameters such as Sleep Onset Latency (SOL), Sleep Duration (DUR) and overall reported Sleep problems (PSQI) and if there is an association between Sleep-parameters and ADHD symptoms. Secondly, in 37 ADHD patients we investigated the effects of SMR and Theta/Beta (TBR) neurofeedback on ADHD symptoms and Sleep parameters and if these Sleep parameters may mediate treatment outcome to SMR and TBR neurofeedback. In this study we found a clear continuous relationship between self-reported Sleep problems (PSQI) and inattention in adults with- and without-ADHD. TBR neurofeedback resulted in a small reduction of SOL, this change in SOL did not correlate with the change in ADHD symptoms and the reduction in SOL only happened in the last half of treatment, suggesting this is an effect of symptom improvement not specifically related to TBR neurofeedback. SMR neurofeedback specifically reduced the SOL and PSQI score, and the change in SOL and change in PSQI correlated strongly with the change in inattention, and the reduction in SOL was achieved in the first half of treatment, suggesting the reduction in SOL mediated treatment response to SMR neurofeedback. Clinically, TBR and SMR neurofeedback had similar effects on symptom reduction in ADHD (inattention and hyperactivity/impulsivity). These results suggest differential effects and different working mechanisms for TBR and SMR neurofeedback in the treatment of ADHD.
Ilse Feddema - One of the best experts on this subject based on the ideXlab platform.
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Differential effects of theta/beta and SMR neurofeedback in ADHD on Sleep Onset Latency
Frontiers in human neuroscience, 2014Co-Authors: Martijn Arns, Ilse Feddema, J. Leon KenemansAbstract:Recent studies suggest a role for Sleep and Sleep problems in the etiology of attention deficit hyperactivity disorder (ADHD) and a recent model about the working mechanism of sensori-motor rhythm (SMR) neurofeedback, proposed that this intervention normalizes Sleep and thus improves ADHD symptoms such as inattention and hyperactivity/impulsivity. In this study we compared adult ADHD patients (N = 19) to a control group (N = 28) and investigated if differences existed in Sleep parameters such as Sleep Onset Latency (SOL), Sleep Duration (DUR) and overall reported Sleep problems (PSQI) and if there is an association between Sleep-parameters and ADHD symptoms. Secondly, in 37 ADHD patients we investigated the effects of SMR and Theta/Beta (TBR) neurofeedback on ADHD symptoms and Sleep parameters and if these Sleep parameters may mediate treatment outcome to SMR and TBR neurofeedback. In this study we found a clear continuous relationship between self-reported Sleep problems (PSQI) and inattention in adults with- and without-ADHD. TBR neurofeedback resulted in a small reduction of SOL, this change in SOL did not correlate with the change in ADHD symptoms and the reduction in SOL only happened in the last half of treatment, suggesting this is an effect of symptom improvement not specifically related to TBR neurofeedback. SMR neurofeedback specifically reduced the SOL and PSQI score, and the change in SOL and change in PSQI correlated strongly with the change in inattention, and the reduction in SOL was achieved in the first half of treatment, suggesting the reduction in SOL mediated treatment response to SMR neurofeedback. Clinically, TBR and SMR neurofeedback had similar effects on symptom reduction in ADHD (inattention and hyperactivity/impulsivity). These results suggest differential effects and different working mechanisms for TBR and SMR neurofeedback in the treatment of ADHD.
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differential effects of theta beta and smr neurofeedback in adhd on Sleep Onset Latency
Frontiers in Human Neuroscience, 2014Co-Authors: Martijn Arns, Ilse Feddema, Leon J KenemansAbstract:Recent studies suggest a role for Sleep and Sleep problems in the etiology of attention deficit hyperactivity disorder (ADHD) and a recent model about the working mechanism of sensori-motor rhythm (SMR) neurofeedback, proposed that this intervention normalizes Sleep and thus improves ADHD symptoms such as inattention and hyperactivity/impulsivity. In this study we compared adult ADHD patients (N = 19) to a control group (N = 28) and investigated if differences existed in Sleep parameters such as Sleep Onset Latency (SOL), Sleep Duration (DUR) and overall reported Sleep problems (PSQI) and if there is an association between Sleep-parameters and ADHD symptoms. Secondly, in 37 ADHD patients we investigated the effects of SMR and Theta/Beta (TBR) neurofeedback on ADHD symptoms and Sleep parameters and if these Sleep parameters may mediate treatment outcome to SMR and TBR neurofeedback. In this study we found a clear continuous relationship between self-reported Sleep problems (PSQI) and inattention in adults with- and without-ADHD. TBR neurofeedback resulted in a small reduction of SOL, this change in SOL did not correlate with the change in ADHD symptoms and the reduction in SOL only happened in the last half of treatment, suggesting this is an effect of symptom improvement not specifically related to TBR neurofeedback. SMR neurofeedback specifically reduced the SOL and PSQI score, and the change in SOL and change in PSQI correlated strongly with the change in inattention, and the reduction in SOL was achieved in the first half of treatment, suggesting the reduction in SOL mediated treatment response to SMR neurofeedback. Clinically, TBR and SMR neurofeedback had similar effects on symptom reduction in ADHD (inattention and hyperactivity/impulsivity). These results suggest differential effects and different working mechanisms for TBR and SMR neurofeedback in the treatment of ADHD.