Center for Advanced Research in Sleep Medicine

Montréal, Canada

Center for Advanced Research in Sleep Medicine

Montréal, Canada
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O'Reilly C.,Center for Advanced Research in Sleep Medicine | Nielsen T.,Center for Advanced Research in Sleep Medicine
Journal of Neuroscience Methods | Year: 2014

Background: A convergence of studies has revealed sleep spindles to be associated with sleep-related cognitive processing and even with fundamental waking state capacities such as intelligence. However, some spindle characteristics, such as propagation direction and delay, may play a decisive role but are only infrequently investigated because of technical complexities. New method: A new methodology for assessing sleep spindle propagation over the human scalp using noninvasive electroencephalography (EEG) is described. This approach is based on the alignment of time-frequency representations of spindle activity across recording channels. Results: This first of a two-part series concentrates on framing theoretical considerations related to EEG spindle propagation and on detailing the methodology. A short example application is provided that illustrates the repeatability of results obtained with the new propagation measure in a sample of 32 night recordings. A more comprehensive experimental investigation is presented in part two of the series. Comparison with existing method(s): Compared to existing methods, this approach is particularly well adapted for studying the propagation of sleep spindles because it estimates time delays rather than phase synchrony and it computes propagation properties for every individual spindle with windows adjusted to the specific spindle duration. Conclusions: The proposed methodology is effective in tracking the propagation of spindles across the scalp and may thus help in elucidating the temporal aspects of sleep spindle dynamics, as well as other transient EEG and MEG events. A software implementation (the Spyndle Python package) is provided as open source software. © 2013 Elsevier B.V.


O'Reilly C.,Center for Advanced Research in Sleep Medicine | Nielsen T.,Center for Advanced Research in Sleep Medicine
Journal of Neuroscience Methods | Year: 2014

Background: This communication is the second of a two-part series that describes and tests a new methodology for assessing the propagation of EEG sleep spindles. Whereas the first part describes the methodology in detail, this part proposes a thorough evaluation of the approach by applying it to a sample of laboratory sleep recordings. New method: The tested methodology is based on the alignment of time-frequency representations of spindle activity across recording channels and is used for assessing sleep spindle propagation over the human scalp using noninvasive EEG. Results: Spindle propagation displays features that suggest wave displacements of global synaptic potential fields. Propagation patterns that are coherent (as opposed to random), laterally symmetrical, and highly repeatable within and between subjects were observed. Propagation was slower from posterior to anterior and from central to lateral brain regions than in the opposite directions. Propagation speeds varying between 2.3 and 7.0. m/s were obtained. A distinct grouping of propagation properties was noted for a small cluster of frontal electrodes. No propagation between distantly separated scalp locations was observed. The values of spindle characteristics such as average frequency, RMS amplitude, frequency slope, and duration, depend largely on propagation direction but are only mildly correlated with propagation delay. Comparison with existing method(s): Results obtained are in line with many results published in the literature and offer new measures for describing sleep spindle behavior. Conclusions: Propagation properties provide new information about sleep spindle behavior and thus allow more precise automated assessments of spindle-related functions. © 2013 Elsevier B.V.


Nielsen T.,Center for Advanced Research in Sleep Medicine | Nielsen T.,University of Montréal
Frontiers in Neurology | Year: 2017

Adverse childhood experiences can deleteriously affect future physical and mental health, increasing risk for many illnesses, including psychiatric problems, sleep disorders, and, according to the present hypothesis, idiopathic nightmares. Much like post-traumatic nightmares, which are triggered by trauma and lead to recurrent emotional dreaming about the trauma, idiopathic nightmares are hypothesized to originate in early adverse experiences that lead in later life to the expression of early memories and emotions in dream content. Accordingly, the objectives of this paper are to (1) review existing literature on sleep, dreaming and nightmares in relation to early adverse experiences, drawing upon both empirical studies of dreaming and nightmares and books and chapters by recognized nightmare experts and (2) propose a new approach to explaining nightmares that is based upon the Stress Acceleration Hypothesis of mental illness. The latter stipulates that susceptibility to mental illness is increased by adversity occurring during a developmentally sensitive window for emotional maturation-the infantile amnesia period-that ends around age 31/2. Early adversity accelerates the neural and behavioral maturation of emotional systems governing the expression, learning, and extinction of fear memories and may afford short-term adaptive value. But it also engenders long-term dysfunctional consequences including an increased risk for nightmares. Two mechanisms are proposed: (1) disruption of infantile amnesia allows normally forgotten early childhood memories to influence later emotions, cognitions and behavior, including the common expression of threats in nightmares; (2) alterations of normal emotion regulation processes of both waking and sleep lead to increased fear sensitivity and less effective fear extinction. These changes influence an affect network previously hypothesized to regulate fear extinction during REM sleep, disruption of which leads to nightmares. This network consists of a fear circuit that includes amygdala, hippocampus, and medial prefrontal cortex and whose substantial overlap with the stress acceleration findings allows the latter to be incorporated into a wider, more developmentally coherent framework. © 2017 Nielsen.


News Article | January 21, 2016
Site: motherboard.vice.com

I wake up in darkness, and reach over the edge of my mattress, like I have every morning for the past two weeks. I feel around the inky void until I grab hold of a sleek white headset. It looks like a pair of snowboarding goggles, but without the lenses. I tap the “on” button, and the headset glows with a bright blue-green light. I slip the device on my head and let my eyes adjust to the light—which is now shining straight into my eyes—and groggily stumble to the bathroom. The light obscures my vision, and so I stumble over a boot along the way. When I look in the mirror, I can’t help thinking that, in terms of sci-fi cred, I look more SkyMall than Darth Maul. This has been my new morning routine—a slightly strange, and kind of silly, but earnest (I swear) attempt to reset my body’s internal clock so that I can go to bed earlier and wake up earlier the next day. You see, I’m a chronic night owl, often to my detriment; I often can’t get to bed before midnight without a little help. Recently, that’s meant taking melatonin supplements, a naturally occurring hormone believed to induce sleep in mammals. When I wake up for work, I’m tired as hell. The device on my face is called the Re-Timer. It was created by Leon Lack, a clinical psychologist at the Adelaide Institute for Sleep Health in Australia. The Re-Timer is supposed to re-adjust the wearer’s circadian rhythms—the 24 hour cycle of chemicals like melatonin and other physiological cues that together determine when you go to sleep and wake up—by shining bright blue and green light into the wearer's eyes. Researchers believe that light plays the largest role in regulating circadian rhythms related to sleep, and so the idea is that the Re-Timer tricks your brain into thinking it needs to go to sleep earlier or later by mimicking the conditions it’s used to in the natural world—sunlight at daybreak, for example. It’s basically a SAD lamp that you wear on your face, and retails for $299 USD. “We have a biological clock, and the master clock is in the brain, in the suprachiasmatic nucleus,” which is part of the hypothalamus said Julie Carrier, a professor of psychology at the University of Montreal’s Center for Advanced Research in Sleep Medicine. “There are other clocks in the body, we know that, but the master one is in the hypothalamus. And it’s a good thing we have these circadian rhythms, because it allows mammals and humans to do the correct action at the same time. For human beings, it’s good to be asleep at night, because we don’t see much.” The suprachiasmatic nucleus, or SCN, as it turns out, is connected to your eyes via photoreceptor cells that are sensitive to short wavelength blue and green light, Carrier told me. These cells are used to receiving cues from natural sunlight and communicating them to the SCN, but they’ll also respond to artificial light. The idea is that, by wearing a device like the Re-Timer, your circadian rhythms will respond in kind. “Bright light can be used to shift the timing of the body clock. There’s been a lot of research to show that, and ours was actually some of the earliest work in that area,” Lack said over a Skype conversation. “One of my students wrote his PhD in 1990 and showed that a single pulse of four hours of bright light at high intensity had the effect to earlier delay the body clock or shift it earlier, depending on when the light exposure occurred.” The Re-Timer is apparently based on this and other academic research spanning the past 25 years, and has a handful of peer-reviewed papers to back it up (most of them co-authored by Lack himself). To get to sleep earlier and wake up earlier (my goal), you’re supposed to wear the Re-Timer for up to an hour, within a half hour of your normal wake time. According to the company, you should see results after three or four days. The results after this period of time will likely be a change of 20 or 30 minutes in your sleep schedule, Lack said, because the light is less intense than what you see in a lab. However, if the glasses are worn for much longer, those changes could stretch to a couple hours. You’re probably wondering by now: how did it go for me? The most I can say is that results were promising, but inconclusive. I began wearing the glasses on a Sunday. After several days—occasionally cheating by wearing them later than the recommended half hour after waking up, if I was running late to work—I really couldn’t tell if anything was different. If I felt a little more energetic one morning, was it really because of a pricey device? As far as I could tell, I was inconveniencing myself without much benefit. At least my coworkers got a show, since wearing the Re-Timer to work quickly turned my desk into a zoo exhibit, and I was the main attraction: a dude with ominous green lights shining into his eyes. But then, something strange happened. On Sunday night, exactly a week after I started wearing the glasses, I was overcome by tiredness at 9:30 PM (about three hours shy of my normal bedtime) and went to sleep. I woke up at 5 AM. I initially wrote this off as coincidence, because I’d partied a little too hard over the weekend and not slept much. But on Monday and Tuesday, the phenomenon repeated itself. Was it because of the Re-Timer, or because I was catching up on sleep lost over a couple of weekend nights? I’m not sure I can say for certain—although, my experience somewhat mimics what Lack found in a 2007 paper published in Sleep and Biological Rhythms. In that study, subjects that received two hours of blue light after waking up for a week straight were able to shift their wake up time back by nearly three hours. However, after the study ended, the change didn’t stick. Coey gets her shine on. Photo: Raf Katigbak I also learned that going to bed at a reasonable hour just isn’t my style. I’m a night owl and I think I like it. But the science behind bright light therapy is solid, Carrier assured me, and according to her, it works. “[These products] are for sure legitimate,” Carrier said. “For most people, they are a good purchase, and they can be very useful during winter. But light outside will also be sufficient to achieve some of the effect that you want.” In the summer, for example, the same effect could likely be achieved by going outside for a run in the morning, Carrier said—or, hell, just standing outside your door and looking around. Whether you shell out for a fancy piece of tech to hack your body’s rhythms or go the all-natural route will probably depend on what season it is, and how you feel about looking like an extra from a low-rent Blade Runner remake. As for me, it really does seem like light, even from an LED, has some sort of tangible effect on your body—but that I already knew. I think I'll just stick with the sun, thanks.


Fereshtehnejad S.-M.,Karolinska Institutet | Romenets S.R.,McGill University | Anang J.B.M.,McGill University | Latreille V.,Center for Advanced Research in Sleep Medicine | And 3 more authors.
JAMA Neurology | Year: 2015

Importance There is increasing evidence that Parkinson disease (PD) is heterogeneous in its clinical presentation and prognosis. Defining subtypes of PD is needed to better understand underlying mechanisms, predict disease course, and eventually design more efficient personalized management strategies. Objectives To identify clinical subtypes of PD, compare the prognosis and progression rate between PD phenotypes, and compare the ability to predict prognosis in our subtypes and those from previously published clustering solutions. Design, Setting, and Participants Prospective cohort study. The cohortswere from 2 movement disorders clinics in Montreal, Quebec, Canada (patients were enrolled during the period from 2005 to 2013). A total of 113 patients with idiopathic PD were enrolled. A comprehensive spectrum of motor and nonmotor features (motor severity, motor complications, motor subtypes, quantitative motor tests, autonomic and psychiatric manifestations, olfaction, color vision, sleep parameters, and neurocognitive testing) were assessed at baseline. After a mean follow-up time of 4.5 years, 76 patients were reassessed. In addition to reanalysis of baseline variables, a global composite outcome was created by merging standardized scores for motor symptoms, motor signs, cognitive function, and other nonmotor manifestations. Main Outcomes and Measures Changes in the quintiles of the global composite outcome and its components were compared between different subtypes. Results The best cluster solution found was based on orthostatic hypotension, mild cognitive impairment, rapid eyemovement sleep behavior disorder (RBD), depression, anxiety, and Unified Parkinson's Disease Rating Scale Part II and Part III scores at baseline. Three subtypes were defined as Mainly motor/slow progression, diffuse/malignant, and intermediate. Despite similar age and disease duration, patients with the diffuse/malignant phenotype were more likely to have mild cognitive impairment, orthostatic hypotension, and RBD at baseline, and at prospective follow-up, they showed a more rapid progression in cognition (odds ratio [OR], 8.7 [95%CI, 4.0-18.7]; P <.001), other nonmotor symptoms (OR, 10.0 [95%CI, 4.3-23.2]; P <.001), motor signs (OR, 4.1 [95%CI, 1.8-9.1]; P =.001), motor symptoms (OR, 2.9 [95%CI, 1.3-6.2]; P <.01), and the global composite outcome (OR, 8.0 [95%CI, 3.7-17.7]; P <.001). Conclusions and Relevance It is recommended to screen patients with PD for mild cognitive impairment, orthostatic hypotension, and RBD even at baseline visits. These nonmotor features identify a diffuse/malignant subgroup of patients with PD for whom the most rapid progression rate could be expected. © 2015 American Medical Association. All rights reserved.


Fox K.C.R.,University of British Columbia | Nijeboer S.,University of British Columbia | Solomonova E.,Center for Advanced Research in Sleep Medicine | Solomonova E.,University of Montréal | And 3 more authors.
Frontiers in Human Neuroscience | Year: 2013

Isolated reports have long suggested a similarity in content and thought processes across mind wandering (MW) during waking, and dream mentation during sleep. This overlap has encouraged speculation that both 'daydreaming' and dreaming may engage similar brain mechanisms. To explore this possibility, we systematically examined published first-person experiential reports of MW and dreaming and found many similarities: in both states, content is largely audiovisual and emotional, follows loose narratives tinged with fantasy, is strongly related to current concerns, draws on long-term memory, and simulates social interactions. Both states are also characterized by a relative lack of meta-awareness. To relate first-person reports to neural evidence, we compared meta-analytic data from numerous functional neuroimaging (PET, fMRI) studies of the default mode network (DMN, with high chances of MW) and rapid eye movement (REM) sleep (with high chances of dreaming). Our findings show large overlaps in activation patterns of cortical regions: similar to MW/DMN activity, dreaming and REM sleep activate regions implicated in self-referential thought and memory, including medial prefrontal cortex (PFC), medial temporal lobe structures, and posterior cingulate. Conversely, in REM sleep numerous PFC executive regions are deactivated, even beyond levels seen during waking MW. We argue that dreaming can be understood as an 'intensified' version of waking MW: though the two share many similarities, dreams tend to be longer, more visual and immersive, and to more strongly recruit numerous key hubs of the DMN. Further, whereas MW recruits fewer PFC regions than goal-directed thought, dreaming appears to be characterized by an even deeper quiescence of PFC regions involved in cognitive control and metacognition, with a corresponding lack of insight and meta-awareness. We suggest, then, that dreaming amplifies the same features that distinguish MW from goal-directed waking thought. © 2013 Fox, Nijeboer, Solomonova, Domhoff and Christoff.


Carr M.,Center for Advanced Research in Sleep Medicine | Carr M.,University of Montréal | Nielsen T.,Center for Advanced Research in Sleep Medicine | Nielsen T.,University of Montréal
Sleep | Year: 2015

Study Objectives: The goals of the study were to assess semantic priming to emotion and nonemotion cue words using a novel measure of associational breadth for participants who either took rapid eye movement (REM) or nonrapid eye movement (NREM) naps or who remained awake, and to assess the relation of priming to REM sleep consolidation and REM sleep inertia effects. Design: The associational breadth task was applied in both a priming condition, where cue words were signaled to be memorized prior to sleep (primed), and a nonpriming condition, where cue words were not memorized (nonprimed). Cue words were either emotional (positive, negative) or nonemotional. Participants were randomly assigned to either an awake (WAKE) or a sleep condition, which was subsequently split into NREM or REM groups depending on stage at awakening. Setting: Hospital-based sleep laboratory. Participants: Fifty-eight healthy participants (22 male) ages 18 to 35 y (mean age = 23.3 ± 4.08 y). Measurements and Results: The REM group scored higher than the NREM or WAKE groups on primed, but not nonprimed emotional cue words; the effect was stronger for positive than for negative cue words. However, REM time and percent correlated negatively with degree of emotional priming. Priming occurred for REM awakenings but not for NREM awakenings, even when the latter sleep episodes contained some REM sleep. Conclusions: Associational breadth may be selectively consolidated during REM sleep for stimuli that have been tagged as important for future memory retrieval. That priming decreased with REM time and was higher only for REM sleep awakenings is consistent with two explanatory REM sleep processes: REM sleep consolidation serving emotional downregulation and REM sleep inertia. © 2015, Associated Professional Sleep Societies, LLC. All rights reserved.


Zadra A.,Center for Advanced Research in Sleep Medicine | Zadra A.,University of Montréal | Desautels A.,Center for Advanced Research in Sleep Medicine | Desautels A.,University of Montréal | And 4 more authors.
The Lancet Neurology | Year: 2013

Somnambulism, or sleepwalking, can give rise to a wide range of adverse consequences and is one of the leading causes of sleep-related injury. Accurate diagnosis is crucial for proper management and imperative in an ever-increasing number of medicolegal cases implicating sleep-related violence. Unfortunately, several widely held views of sleepwalking are characterised by key misconceptions, and some established diagnostic criteria are inconsistent with research findings. The traditional idea of somnambulism as a disorder of arousal might be too restrictive and a comprehensive view should include the idea of simultaneous interplay between states of sleep and wakefulness. Abnormal sleep physiology, state dissociation, and genetic factors might explain the pathophysiology of the disorder. © 2013 Elsevier Ltd.


Nielsen T.,University of Montréal | Nielsen T.,Center for Advanced Research in Sleep Medicine
Frontiers in Neurology | Year: 2012

We assessed dream recall frequency (DRF) and dream theme diversity (DTD) with an internet questionnaire among a cohort of 28,888 male and female participants aged 10- 79 years in a cross-sectional design. DRF increased from adolescence (ages 10-19) to early adulthood (20-29) and then decreased again for the next 20years. The nature of this decrease differed for males and females. For males, it began earlier (30-39), proceeded more gradually, and reached a nadir earlier (40-49) than it did for females. For females, it began later (40-49), dropped more abruptly, and reached nadir later (50-59). Marked sex differences were observed for age strata 10-19 through 40-49 and year-by-year analyses estimated the window for these differences to be more precisely from 14 to 44 years. DTD decreased linearly with age for both sexes up to 50-59 and then dropped even more sharply for 60-79. There was a sex difference favoring males on this measure but only for ages 10-19. Findings replicate, in a single sample, those from several previous studies showing an increase in DRF from adolescence to early adulthood, a subsequent decrease primarily in early and middle adulthood, and different patterns of age-related decrease in the two sexes. Age-related changes in sleep structure, such as decreasing %REM sleep which parallel the observed dream recall changes, might help explain these findings, but these sleep changes are much smaller and more gradual in nature. Changes in the phase and amplitude of circadian rhythms of REM propensity and generational differences in life experiences may also account for some part of the findings. That decreases in DTD parallel known age-related decreases in episodic and autobiographical memory may signify that this new diversity measure indexes an aspect of autobiographical memory that also influences dream recall. © 2012 Nielsen.


Gagnon J.-F.,Center for Advanced Research in Sleep Medicine | Bertrand J.-A.,Center for Advanced Research in Sleep Medicine | Marchand D.G.,Center for Advanced Research in Sleep Medicine
Frontiers in Neurology | Year: 2012

Rapid eye movement (REM) sleep behavior disorder (RBD) is a parasomnia characterized by excessive muscle activity and undesirable motor events during REM sleep. RBD occurs in approximately 0.5% of the general population, with a higher prevalence in older men. RBD is a frequent feature of dementia with Lewy bodies (DLB), but is only rarely reported in Alzheimer's disease. RBD is also a risk factor for a-synuclein-related diseases, such as DLB, Parkinson's disease (PD), and multiple system atrophy. Therefore, RBD has major implications for the diagnosis and treatment of neurodegenerative disorders and for understanding specific neurodegeneration patterns. Several markers of neurodegeneration have been identified in RBD, including cognitive impairments such as deficits in attention, executive functions, learning capacities, and visuospatial abilities. Approximately 50% of RBD patients present mild cognitive impairment. Moreover, RBD is also associated with cognitive decline in PD. © 2012 Gagnon, Bertrand and Génier Marchand.

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