Center for Advanced Research in Sleep Medicine

Montréal, Canada

Center for Advanced Research in Sleep Medicine

Montréal, Canada

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News Article | January 21, 2016

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.

Lord C.,University of Montréal | Sekerovic Z.,University of Montréal | Carrier J.,University of Montréal | Carrier J.,Center for advanced research in sleep medicine
Pathologie Biologie | Year: 2014

This review aims to discuss how endogenous and exogenous testosterone exposures in men and estrogens/progesterone exposures in women interact with sleep regulation. In young men, testosterone secretion peaks during sleep and is linked to sleep architecture. Animal and human studies support the notion that sleep loss suppresses testosterone secretion. Testosterone levels decline slowly throughout the aging process, but relatively few studies investigate its impact on age-related sleep modifications. Results suggest that poorer sleep quality is associated with lower testosterone concentrations and that sleep loss may have a more prominent effect on testosterone levels in older individuals. In women, sex steroid levels are characterized by a marked monthly cycle and reproductive milestones such as pregnancy and menopause. Animal models indicate that estrogens and progesterone influence sleep. Most studies do not show any clear effects of the menstrual cycle on sleep, but sample sizes are too low, and research designs often inhibit definitive conclusions. The effects of hormonal contraceptives on sleep are currently unknown. Pregnancy and the postpartum period are associated with increased sleep disturbances, but their relation to the hormonal milieu still needs to be determined. Finally, studies suggest that menopausal transition and the hormonal changes associated with it are linked to lower subjective sleep quality, but results concerning objective sleep measures are less conclusive. More research is necessary to unravel the effects of vasomotor symptoms on sleep. Hormone therapy seems to induce positive effects on sleep, but key concerns are still unresolved, including the long-term effects and efficacy of different hormonal regimens. © 2014.

O'Reilly C.,Center for Advanced Research in Sleep Medicine | Nielsen T.,Center for Advanced Research in Sleep Medicine
2013 8th International Workshop on Systems, Signal Processing and Their Applications, WoSSPA 2013 | Year: 2013

This communication investigates the impact on classifier evaluation of a high asymmetry between positive and negatives classes. It points out some necessary precautions when reporting classifier performances using threshold-dependent statistics defined with the confusion matrix. It stresses that, in highly unbalanced datasets, reporting the positive predictive value (PPV) is more appropriate than reporting specificity. More elaborate variables such as F-measure and Matthews' correlation coefficient may also provide a reliable portrait. It further concludes that, in many cases, only a small portion of the receiver operating characteristic (ROC) curve is actually useful, unless very low PPV are judged acceptable. Two remedies are proposed to complement the ROC curve: using a positive tradeoff curve (defined herein) or adding iso-PPV lines (i.e., lines of constant PPV) on the ROC graph. The observations reported in this study contribute to understanding of the impact of asymmetry on classifier performances. They also cast some doubt on the pertinence, when dealing with highly asymmetric problems, of using the area under the ROC curve for threshold-independent assessment of classifier performances. © 2013 IEEE.

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.

Simard V.,Université de Sherbrooke | Bernier A.,University of Montréal | Belanger M.-E.,University of Montréal | Carrier J.,University of Montréal | Carrier J.,Center for Advanced Research in Sleep Medicine
Journal of Pediatric Psychology | Year: 2013

Objective To investigate relations between children's attachment and sleep, using objective and subjective sleep measures. Secondarily, to identify the most accurate actigraphy algorithm for toddlers. Methods 55 mother-child dyads took part in the Strange Situation Procedure (18 months) to assess attachment. At 2 years, children wore an Actiwatch for a 72-hr period, and their mothers completed a sleep diary. Results The high sensitivity (80) and smoothed actigraphy algorithms provided the most plausible sleep data. Maternal diaries yielded longer estimated sleep duration and shorter wake duration at night and showed poor agreement with actigraphy. More resistant attachment behavior was not associated with actigraphy-assessed sleep, but was associated with longer nocturnal wake duration as estimated by mothers, and with a reduced actigraphy-diary discrepancy. Conclusions Mothers of children with resistant attachment are more aware of their child's nocturnal awakenings. Researchers and clinicians should select the best sleep measurement method for their specific needs. © 2013 The Author. Published by Oxford University Press on behalf of the Society of Pediatric Psychology. All rights reserved.

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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