The European Insomnia Guideline: An update on the diagnosis and treatment of insomnia 2023.

Progress in the field of insomnia since 2017 necessitated this update of the European Insomnia Guideline. Recommendations for the diagnostic procedure for insomnia and its comorbidities are: clinical interview (encompassing sleep and medical history); the use of sleep questionnaires and diaries (and physical examination and additional measures where indicated) (A). Actigraphy is not recommended for the routine evaluation of insomnia (C), but may be useful for differential-diagnostic purposes (A). Polysomnography should be used to evaluate other sleep disorders if suspected (i.e. periodic limb movement disorder, sleep-related breathing disorders, etc.), treatment-resistant insomnia (A) and for other indications (B). Cognitive-behavioural therapy for insomnia is recommended as the first-line treatment for chronic insomnia in adults of any age (including patients with comorbidities), either applied in-person or digitally (A). When cognitive-behavioural therapy for insomnia is not sufficiently effective, a pharmacological intervention can be offered (A). Benzodiazepines (A), benzodiazepine receptor agonists (A), daridorexant (A) and low-dose sedating antidepressants (B) can be used for the short-term treatment of insomnia (≤ 4 weeks). Longer-term treatment with these substances may be initiated in some cases, considering advantages and disadvantages (B). Orexin receptor antagonists can be used for periods of up to 3 months or longer in some cases (A). Prolonged-release melatonin can be used for up to 3 months in patients ≥ 55 years (B). Antihistaminergic drugs, antipsychotics, fast-release melatonin, ramelteon and phytotherapeutics are not recommended for insomnia treatment (A). Light therapy and exercise interventions may be useful as adjunct therapies to cognitive-behavioural therapy for insomnia (B).

Evidence for an emotional adaptive function of dreams: a cross-cultural study.

The function of dreams is a longstanding scientific research question. Simulation theories of dream function, which are based on the premise that dreams represent evolutionary past selective pressures and fitness improvement through modified states of consciousness, have yet to be tested in cross-cultural populations that include small-scale forager societies. Here, we analyze dream content with cross-cultural comparisons between the BaYaka (Rep. of Congo) and Hadza (Tanzania) foraging groups and Global North populations, to test the hypothesis that dreams in forager groups serve a more effective emotion regulation function due to their strong social norms and high interpersonal support. Using a linear mixed effects model we analyzed 896 dreams from 234 individuals across these populations, recorded using dream diaries. Dream texts were processed into four psychosocial constructs using the Linguistic Inquiry and Word Count (LIWC-22) dictionary. The BaYaka displayed greater community-oriented dream content. Both the BaYaka and Hadza exhibited heightened threat dream content, while, at the same time, the Hadza demonstrated low negative emotions in their dreams. The Global North Nightmare Disorder group had increased negative emotion content, and the Canadian student sample during the COVID-19 pandemic displayed the highest anxiety dream content. In conclusion, this study supports the notion that dreams in non-clinical populations can effectively regulate emotions by linking potential threats with non-fearful contexts, reducing anxiety and negative emotions through emotional release or catharsis. Overall, this work contributes to our understanding of the evolutionary significance of this altered state of consciousness.

[Insomnia in psychiatry and psychotherapy]. / Insomnie en psychiatrie et psychothérapie.

Insomnia disorder is characterized by disturbed sleep continuity and associated daytime impairment. Insomnia is frequent in patients with psychiatric disorders ; 30-40% fulfill the criteria for insomnia disorder as a comorbidity. According to current guidelines, cognitive behavioral therapy for insomnia (CBT-I) is the first-line treatment, comprising sleep education, bedtime restriction, relaxation and cognitive restructuring. Despite guideline recommendations, CBT-I is insufficiently implemented, and insomnia is frequently over-treated with hypnotics. 'Become your own SLEEPexpert' is a behavioral treatment program based on CBT-I with the aim of empowering patients to take care of their own sleep health.

L'insomnie est un trouble de la continuité du sommeil et des troubles diurnes associés. Les symptômes sont fréquents chez les patients souffrant de troubles psychiatriques ; 30 à 40 % d'entre eux remplissant les critères du trouble de l'insomnie en tant que comorbidité. Selon les directives internationales, la thérapie cognitivo-comportementale de l'insomnie (TCC-I) est le traitement de première intention, comprenant l'éducation, la restriction du temps passé au lit, la relaxation et la restructuration cognitive. Malgré les recommandations, la TCC-I n'est pas suffisamment mise en œuvre et l'insomnie est souvent surtraitée avec des hypnotiques. « Become your own SLEEPexpert ¼ est un programme comportemental basé sur la TCC-I, dont l'objectif est de permettre aux patients de prendre en charge leur propre santé du sommeil.

Psychobiological personality traits of children and adolescents with disorders of arousal.

INTRODUCTION: Disorders of arousal (DOA) are parasomnias that emerge from incomplete arousal out of Non-Rem Sleep (NREM) and lead to a broad variety of emotional and motor behaviours. Increasing evidence supports the hypothesis that specific psychopathological traits contribute to the multifactorial origin of these phenomena. The aim of the current multicenter study was to compare the personality profile of children and adolescents with and without DOA using the Junior Temperament and Character Inventory (JTCI). METHODS: We enrolled 36 patients with a diagnosis of DOA (mean age of 11 ± 3 years, 64% males), and 36 healthy age and gender matched control subjects (mean age of 11.2 ± 3.6, years, 67% males). Their parents completed the Paris Arousal Disorder Severity Scale (PADSS), the Sleep Disturbance Scale for Children (SDSC) and the JTCI. RESULTS: Patients with DOA reached significantly higher levels compared to their control group in total PADSS (p < 0.0001) and in total SDSC (p < 0.0001). They also displayed higher scores in novelty seeking (p = 0.005), harm avoidance (p = 0.01), self-transcendence (p = 0.006) JTCI subscales, and lower scores on the self-directedness subscale (p = 0.004). CONCLUSION: Our pediatric sample with DOA exhibited specific psychobiological personality traits compared to age and gender matched subjects without DOA. These results shed light on new possible etiopathogenetic mechanisms, as TCI traits have been linked to specific genetic variants and brain circuits, like the reward system. Prospective studies are required to assess the effect of targeted psychological/psychiatric treatment on DOA symptomatology.

Enhancing imagery rehearsal therapy for nightmares with targeted memory reactivation.

Nightmare disorder (ND) is characterized by dreams with strong negative emotions occurring during rapid eye movement (REM) sleep. ND is mainly treated by imagery rehearsal therapy (IRT), where the patients are asked to change the negative story line of their nightmare to a more positive one. We here used targeted memory reactivation (TMR) during REM sleep to strengthen IRT-related memories and accelerate remission of ND. Thirty-six patients with ND were asked to perform an initial IRT session and, while they generated a positive outcome of their nightmare, half of the patients were exposed to a sound (TMR group), while no such pairing took place for the other half (control group). During the next 2 weeks, all patients performed IRT every evening at home and were exposed to the sound during REM sleep with a wireless headband, which automatically detected sleep stages. The frequency of nightmares per week at 2 weeks was used as the primary outcome measure. We found that the TMR group had less frequent nightmares and more positive dream emotions than the control group after 2 weeks of IRT and a sustained decrease of nightmares after 3 months. By demonstrating the effectiveness of TMR during sleep to potentiate therapy, these results have clinical implications for the management of ND, with relevance to other psychiatric disorders too. Additionally, these findings show that TMR applied during REM sleep can modulate emotions in dreams.

Targeted Memory Reactivation During REM Sleep in Patients With Social Anxiety Disorder.

Background: Social anxiety disorder (SAD) is characterized by a significant amount of fear when confronted to social situations. Exposure therapy, which is based on fear extinction, does not often lead to full remission. Here, based on evidence showing that rapid eye movement (REM) sleep promotes the consolidation of extinction memory, we used targeted memory reactivation (TMR) during REM sleep to enhance extinction learning in SAD. Methods: Forty-eight subjects with SAD were randomly assigned to two groups: control or TMR group. All patients had two successive exposure therapy sessions in a virtual reality (VR) environment, where they were asked to give a public talk in front of a virtual jury. At the end of each session, and only in the TMR group (N = 24), a sound was paired to the positive feedback phase of therapy (i.e., approval of their performance), which represented the memory to be strengthened during REM sleep. All participants slept at home with a wearable headband device which automatically identified sleep stages and administered the sound during REM sleep. Participants' anxiety level was assessed using measures of parasympathetic (root mean square of successive differences between normal heartbeats, RMSSD) and sympathetic (non-specific skin conductance responses, ns-SCRs) activity, and subjective measures (Subjective Units of Distress Scale, SUDS), during the preparation phase of their talks before (T1) and after (T2) one full-night's sleep and after 1 week at home (T3). Participants also filled in a dream diary. Results: We observed an effect of time on subjective measures of anxiety (SUDS). We did not find any difference in the anxiety levels of the two groups after 1 week of TMR at home. Importantly, the longer the total duration of REM sleep and the more stimulations the TMR group had at home, the less anxious (increased RMSSD) these participants were. Finally, fear in dreams correlated positively with ns-SCRs and SUDS at T3 in the TMR group. Conclusion: TMR during REM sleep did not significantly modulate the beneficial effect of therapy on subjective anxiety. Yet, our results support that REM sleep can contribute to extinction processes and substantiate strong links between emotions in dreams and waking stress levels in these patients.

NREM sleep stages specifically alter dynamical integration of large-scale brain networks.

Functional dissociations in the brain observed during non-rapid eye movement (NREM) sleep have been associated with reduced information integration and impaired consciousness that accompany increasing sleep depth. Here, we explored the dynamical properties of large-scale functional brain networks derived from transient brain activity using functional magnetic resonance imaging. Spatial brain maps generally display significant modifications in terms of their tendency to occur across wakefulness and NREM sleep. Unexpectedly, almost all networks predominated in activity during NREM stage 2 before an abrupt loss of activity is observed in NREM stage 3. Yet, functional connectivity and mutual dependencies between these networks progressively broke down with increasing sleep depth. Thus, the efficiency of information transfer during NREM stage 2 is low despite the high attempt to communicate. Critically, our approach provides relevant data for evaluating functional brain network integrity and our findings robustly support a significant advance in our neural models of human sleep and consciousness.

EEG microstates of dreams.

Why do people sometimes report that they remember dreams, while at other times they recall no experience? Despite the interest in dreams that may happen during the night, it has remained unclear which brain states determine whether these conscious experiences will occur and what prevents us from waking up during these episodes. Here we address this issue by comparing the EEG activity preceding awakenings with recalled vs. no recall of dreams using the EEG microstate approach. This approach characterizes transiently stable brain states of sub-second duration that involve neural networks with nearly synchronous dynamics. We found that two microstates (3 and 4) dominated during NREM sleep compared to resting wake. Further, within NREM sleep, microstate 3 was more expressed during periods followed by dream recall, whereas microstate 4 was less expressed. Source localization showed that microstate 3 encompassed the medial frontal lobe, whereas microstate 4 involved the occipital cortex, as well as thalamic and brainstem structures. Since NREM sleep is characterized by low-frequency synchronization, indicative of neuronal bistability, we interpret the increased presence of the "frontal" microstate 3 as a sign of deeper local deactivation, and the reduced presence of the "occipital" microstate 4 as a sign of local activation. The latter may account for the occurrence of dreaming with rich perceptual content, while the former may account for why the dreaming brain may undergo executive disconnection and remain asleep. This study demonstrates that NREM sleep consists of alternating brain states whose temporal dynamics determine whether conscious experience arises.

Failure of fear extinction in insomnia: An evolutionary perspective.

The pathophysiology of insomnia remains poorly understood, yet emerging cross-disciplinary approaches integrating natural history, observational studies in traditional populations, gene-phenotype expression and experiments are opening up new avenues to investigate the evolutionary origins of sleep disorders, with the potential to inform innovations in treatment. Previous authors have supported that acute insomnia is a normal biopsychosocial response to a perceived or real threat and may thus represent an adaptive response to stress. We further extend this hypothesis by claiming that insomnia reflects a fear-related evolutionary survival mechanism, which becomes persistent in some vulnerable individuals due to failure of the fear extinction function. Possible treatments targeting fear extinction are proposed, such as pharmacotherapy and emotion-based cognitive behavioral therapy.

Fear in dreams and in wakefulness: Evidence for day/night affective homeostasis.

Recent neuroscientific theories have proposed that emotions experienced in dreams contribute to the resolution of emotional distress and preparation for future affective reactions. We addressed one emerging prediction, namely that experiencing fear in dreams is associated with more adapted responses to threatening signals during wakefulness. Using a stepwise approach across two studies, we identified brain regions activated when experiencing fear in dreams and showed that frightening dreams modulated the response of these same regions to threatening stimuli during wakefulness. Specifically, in Study 1, we performed serial awakenings in 18 participants recorded throughout the night with high-density electroencephalography (EEG) and asked them whether they experienced any fear in their dreams. Insula and midcingulate cortex activity increased for dreams containing fear. In Study 2, we tested 89 participants and found that those reporting higher incidence of fear in their dreams showed reduced emotional arousal and fMRI response to fear-eliciting stimuli in the insula, amygdala and midcingulate cortex, while awake. Consistent with better emotion regulation processes, the same participants displayed increased medial prefrontal cortex activity. These findings support that emotions in dreams and wakefulness engage similar neural substrates, and substantiate a link between emotional processes occurring during sleep and emotional brain functions during wakefulness.

Increased heartbeat-evoked potential during REM sleep in nightmare disorder.

Nightmares are characterized by the experience of strong negative emotions occurring mainly during REM sleep. Some people suffer from nightmare disorder, which is defined by the repeated occurrence of nightmares and by significant distress in wakefulness. Yet, whether frequent nightmares relate to a general increase in emotional reactivity or arousal during sleep remains unclear. To address this question, we recorded heartbeat-evoked potentials (HEPs) during wakefulness, NREM and REM sleep in patients with nightmare disorder and healthy participants. The HEP represents a cortical (EEG) response to the heartbeat and indexes brain-body interactions, such as interoceptive processing and intrinsic levels of arousal. HEP amplitude is typically increased during states of high emotional arousal and motivation, and is decreased in depression. Here we compared the amplitude of HEPs between nightmare patients and healthy controls separately during AWAKE, NREM, REM periods, and found higher HEP amplitude in nightmare patients compared to healthy controls over a cluster of frontal regions only during REM sleep. This effect was not paralleled by any group difference in cardiac control measures (e.g. heart rate variability, interbeat interval). These findings corroborate the notion that nightmares are essentially a REM pathology and suggest that increased emotional arousal during REM sleep, as measured by HEP, is a physiological condition responsible for frequent nightmares. This result also supports that HEP may be used as a biomarker of increased emotional and sensory processing during REM sleep in these patients.

The Phenomenal Contents and Neural Correlates of Spontaneous Thoughts across Wakefulness, NREM Sleep, and REM Sleep.

Thoughts occur during wake as well as during dreaming sleep. Using experience sampling combined with high-density EEG, we investigated the phenomenal qualities and neural correlates of spontaneously occurring thoughts across wakefulness, non-rapid eye movement (NREM) sleep, and REM sleep. Across all states, thoughts were associated with activation of a region of the midcingulate cortex. Thoughts during wakefulness additionally involved a medial prefrontal region, which was associated with metacognitive thoughts during wake. Phenomenologically, waking thoughts had more metacognitive content than thoughts during both NREM and REM sleep, whereas thoughts during REM sleep had a more social content. Together, these results point to a core neural substrate for thoughts, regardless of behavioral state, within the midcingulate cortex, and suggest that medial prefrontal regions may contribute to metacognitive content in waking thoughts.

The neural correlates of dreaming.

Consciousness never fades during waking. However, when awakened from sleep, we sometimes recall dreams and sometimes recall no experiences. Traditionally, dreaming has been identified with rapid eye-movement (REM) sleep, characterized by wake-like, globally 'activated', high-frequency electroencephalographic activity. However, dreaming also occurs in non-REM (NREM) sleep, characterized by prominent low-frequency activity. This challenges our understanding of the neural correlates of conscious experiences in sleep. Using high-density electroencephalography, we contrasted the presence and absence of dreaming in NREM and REM sleep. In both NREM and REM sleep, reports of dream experience were associated with local decreases in low-frequency activity in posterior cortical regions. High-frequency activity in these regions correlated with specific dream contents. Monitoring this posterior 'hot zone' in real time predicted whether an individual reported dreaming or the absence of dream experiences during NREM sleep, suggesting that it may constitute a core correlate of conscious experiences in sleep.

Baclofen-Associated Onset of Central Sleep Apnea in Alcohol Use Disorder: A Case Report.

A 61-year-old patient with alcohol use disorder (AUD) was referred for suspicion of sleep apnea syndrome (SAS). He had incurred three road accidents attributed to sleepiness over the previous year, shortly after initiation of high-dose (100 mg b.i.d.) treatment with baclofen, a molecule increasingly used in the management of AUD. Polysomnography revealed a severe central SAS (CSAS) with an apnea-hypopnea index (AHI) of 81.6/h. Baclofen was suggested as a possible cause of the CSAS, and after its withdrawal, a second polysomnography was done, showing the disappearance of the central apneas and a shift to severe obstructive SAS (AHI 43.9/h), for which a positive airway pressure (CPAP) treatment was initiated. A third polysomnography was performed under CPAP after reintroduction of baclofen (50 mg b.i.d.) by the patient, showing reappearance of the CSAS (AHI 42.1/h). This case report illustrates the deleterious effect of baclofen on breathing physiology during sleep. Since it is typically prescribed off label at high doses to a population of patients potentially using other substances that inhibit the ventilatory drive, this possible adverse effect is a major concern. When considering the use of baclofen in patients with AUD, the potential for sleep-disordered breathing should be weighed and carefully monitored.

Increased Reward-Related Behaviors during Sleep and Wakefulness in Sleepwalking and Idiopathic Nightmares.

BACKGROUND: We previously suggested that abnormal sleep behaviors, i.e., as found in parasomnias, may often be the expression of increased activity of the reward system during sleep. Because nightmares and sleepwalking predominate during REM and NREM sleep respectively, we tested here whether exploratory excitability, a waking personality trait reflecting high activity within the mesolimbic dopaminergic (ML-DA) system, may be associated with specific changes in REM and NREM sleep patterns in these two sleep disorders. METHODS: Twenty-four unmedicated patients with parasomnia (12 with chronic sleepwalking and 12 with idiopathic nightmares) and no psychiatric comorbidities were studied. Each patient spent one night of sleep monitored by polysomnography. The Temperament and Character Inventory (TCI) was administered to all patients and healthy controls from the Geneva population (n = 293). RESULTS: Sleepwalkers were more anxious than patients with idiopathic nightmares (Spielberger Trait anxiety/STAI-T), but the patient groups did not differ on any personality dimension as estimated by the TCI. Compared to controls, parasomnia patients (sleepwalkers together with patients with idiopathic nightmares) scored higher on the Novelty Seeking (NS) TCI scale and in particular on the exploratory excitability/curiosity (NS1) subscale, and lower on the Self-directedness (SD) TCI scale, suggesting a general increase in reward sensitivity and impulsivity. Furthermore, parasomnia patients tended to worry about social separation persistently, as indicated by greater anticipatory worry (HA1) and dependence on social attachment (RD3). Moreover, exploratory excitability (NS1) correlated positively with the severity of parasomnia (i.e., the frequency of self-reported occurrences of nightmares and sleepwalking), and with time spent in REM sleep in patients with nightmares. CONCLUSIONS: These results suggest that patients with parasomnia might share common waking personality traits associated to reward-related brain functions. They also provide further support to the notion that reward-seeking networks are active during human sleep.

Sleep and emotional functions.

In this chapter, we review studies investigating the role of sleep in emotional functions. In particular, evidence has recently accumulated to show that brain regions involved in the processing of emotional and reward-related information are activated during sleep. We suggest that such activation of emotional and reward systems during sleep underlies the reprocessing and consolidation of memories with a high affective and motivational relevance for the organism. We also propose that these mechanisms occurring during sleep promote adapted cognitive and emotional responses in the waking state, including overnight performance improvement, creativity, and sexual functions. Activation across emotional-limbic circuits during sleep also appears to promote emotional maturation and the emergence of consciousness in the developing brain.

Esse est percipi: a neurophilosophical model of psychosis.

Philosophers, psychiatrists and neuroscientists have all expressed interest in and formulated hypotheses on the nature of hallucinations, but no sufficient integration of these models exists to this date. The objective of this article is to present a neurophilosophical model of psychosis linking the neurobiology with the phenomenology of hallucinations and delusions. It is proposed that psychotic hallucinations could be regarded as 'intrusions' of subjective idealism, a condition where reality is mind dependent, into realism, a condition where reality is mind independent. Furthermore, delusions would be an attempt by the person to make sense of these intrusions. This approach is supported by phenomenological evidence of increased self-relatedness in hallucinations and delusions, and by current neurobiological evidence on the role of the reward system, default mode network and corollary discharge circuit in positive symptomatology. This model has clinical, research and therapeutic implications, and also demonstrates how scientific results can be informed and enhanced by philosophical theories and vice versa.

Spectral analysis of the sleep onset period in primary insomnia.

OBJECTIVE: To compare the EEG power spectra characteristics of the sleep onset period (SOP) in patients with sleep onset insomnia (SOI), sleep maintenance insomnia (SMI) and good sleepers (GS). METHODS: The time course of EEG power density (1-40Hz) during the SOP was examined in thirty subjects (SOI patients: N=10, SMI patients: N=10, GS: N=10). RESULTS: The EEG power of the beta2 frequency band (18-29.75 Hz) was significantly lower in SOI than in SMI in the period preceding sleep onset. The alpha power was significantly higher for the SMI group compared to GS before sleep onset. Despite the lack of statistical significance, several differences in EEG dynamics were observed in SOI compared to two other groups: delta power increased slower after sleep onset; beta2 and 3 (18-29.75 and 30-39.75 Hz) power decrease less abruptly before sleep onset; beta1 (15-17.75 Hz) power increase through the whole SOP. CONCLUSIONS: The lower level of beta2 frequency band in SOI and the differences in dynamics in delta and beta bands may suggest that a mechanism other than hyperarousal participates in etiology of SOI. SIGNIFICANCE: SOI and SMI patients have different spectral characteristics in SOP, thus future studies should avoid the inclusion of mixed insomnia samples.

Friedrich Nietzsche and his illness: a neurophilosophical approach to introspection.

There are some arguments that Friedrich Nietzsche suffered from the autosomal dominant vascular microangiopathy: Cerebral Autosomal Dominant Arteriopathy with Subcortical Infarcts and Leukoencephalopathy (CADASIL). Here, a hypothesis is formulated supporting that CADASIL presenting with symptoms of bipolar disorder and Gastaut-Geschwind syndrome would contribute to the increased insight and creativity of a philosopher whose perceptions and intuitions often bear out the results of modern neuroscience. Alterations of the brain default and reward networks would account for such an increased level of introspection and creativity. A new framework on approaching illness is proposed, which, in conformity with Nietzsche's positive view, outlines the enabling aspects of some otherwise highly disabling neuropsychiatric disorders.