Hélène Blais

Hôpital du Sacré-Cœur de Montréal

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Nadia Gosselin

Université de Montréal

Julie Carrier

Université de Montréal

Jacques Montplaisir

Hôpital du Sacré-Cœur de Montréal

Catherine Duclos

Inserm

Cynthia Thompson

Hôpital du Sacré-Cœur de Montréal

Caroline Arbour

Centre Intégré Universitaire de Santé et de Services Sociaux du Centre-Sud-de-l'Île-de-Montréal

Marie Dumont

Haute École Louvain en Hainaut

Erlan Sanchez

Centre Intégré Universitaire de Santé et de Services Sociaux du Centre-Sud-de-l'Île-de-Montréal

Héjar El-Khatib

Université de Montréal

Françis Bernard

Université de Montréal

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Université de Montréal

Hôpital du Sacré-Cœur de Montréal

Centre Intégré Universitaire de Santé et de Services Sociaux du Centre-Sud-de-l'Île-de-Montréal

Canadian Sleep & Circadian Network

Centre intégré universitaire de santé et de services sociaux du Nord-de-l’Île-de-Montréal

Centre Intégré Universitaire de Santé et de Services Sociaux du Saguenay–Lac-Saint-Jean

McGill University

Douglas Mental Health University Institute

Montreal Neurological Institute and Hospital

Université du Québec à Montréal

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1173 FATIGUE AND SLEEP SLOW OSCILLATIONS ARE ASSOCIATED WITH WHITE MATTER INTEGRITY FOLLOWING MODERATE TO SEVERE TRAUMATIC BRAIN INJURY

SLEEP (2017)

Erlan Sanchez Caroline Arbour Héjar El-Khatib Christophe Bedetti Hélène Blais

Chronic sleep-wake disturbances are among the most invalidating and frequently reported symptoms following a traumatic brain injury (TBI), but their pathophysiological mechanisms are still poorly understood. We aimed to explore potential mechanisms by which anatomical damage due to TBI, more specifically white matter damage, can cause the reported symptoms. Twenty-three subjects (17M/6F; age: 31 ± 11 years) were tested 23 ± 9 months following a moderate to severe TBI (Glasgow Coma Scale Score at hospital admission: 8.1 ± 2.9); twenty-seven age- and sex-matched healthy controls were also tested. Magnetic resonance imaging (3T) including a diffusion weighted sequence, 1-night polysomnography, and sleep questionnaires (Pittsburgh Sleep Quality Index, Fatigue Severity Scale and Epworth Sleepiness Scale) were used. Voxelwise t-tests and correlations were carried out with FSL, using tract-based spatial statistics and the Randomise tool. Extensive white matter damage (i.e. increased diffusivity and reduced anisotropy) was observed for most cerebral tracks in TBI subjects compared to controls. TBI subjects also had lower slow wave frequency (F=6.9; p=0.01), longer negative and positive phase durations (F=4.0–8.0; p=0.05-0.007), and reduced slope (F=4.8; p=0.03). In TBI participants, lower white matter integrity was associated with higher slow wave amplitude (r=0.46–0.79; p<0.05), longer positive and negative phase durations (r=0.69, p<0.05; r=0.55–0.67, p<0.05, respectively), as well as with higher subjective fatigue (r=0.06–0.08; p<0.05). These results suggest that TBI subjects with greater damage in white matter track integrity report more fatigue symptoms and have larger and elongated sleep slow waves. These slow waves may represent a mechanism that compensates for a possible higher mental effort exerted to accomplish tasks during the day. Our results bring new elements to explain the pathophysiology of post-TBI fatigue and sleep disturbances. Canadian Institutes of Health Research (CIHR), Fonds de Recherche Santé-Québec (FRSQ)

Epworth Sleepiness Scale

10.1093/sleepj/zsx050.1172

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Associations between REM‐sleep EEG spectral power, the cholinergic basal forebrain volume and episodic memory in ageing

Alzheimer s & Dementia (2021)

Claire André Marie‐Ève Martineau‐Dussault Véronique Daneault Hélène Blais Dominique Lorrain

Abstract Background Our research team has demonstrated that quantitative electroencephalography (qEEG) slowing during rapid‐eye movement (REM) sleep is a more powerful tool to discriminate patients with mild cognitive impairment (MCI) or Alzheimer Disease (AD) from healthy controls than waking EEG. Cortical activation during REM sleep highly depends on the cholinergic basal forebrain system (BFCS) neurons, while other neuronal systems are less active compared to wakefulness. However, the BFCS degenerates early in AD. Here, we tested the hypothesis that REM sleep EEG activity could be strongly associated with neurodegeneration of the BFCS, before the onset of dementia. Method 134 participants (mean age 68.45 ± 7.8 years; 52 women; 61 with MCI) underwent a polysomnography, structural magnetic resonance imaging, and a neuropsychological evaluation. T1‐weighted images were preprocessed using CAT12 and the DARTEL algorithm, and the JuBrain Anatomy Toolbox was used to extract bilateral BFCS volumes (i.e., Ch1‐2‐3, Ch4 and total volume). Based on prior evidence, theta (4‐8Hz) and alpha (8‐13Hz) absolute EEG power during REM sleep were computed on temporal electrodes (T3‐T4‐T5‐T6). A composite episodic memory score was calculated as the mean of Z‐scores obtained on the Rey Auditory Verbal Learning Test immediate and delayed free recalls. Multiple regressions were performed between (i) spectral power values or (ii) episodic memory performance, and basal forebrain volumes controlling for age, sex, the apnea‐hypopnea index, and the total intracranial volume. Complementary analyses were performed by stratifying the cohort by sex. Result Both Ch4 (r=0.24, p=0.006) and total BFCS (r=0.25, p=0.005) volumes were positively associated with episodic memory performance. Ch4 (r=‐0.21; p=0.025) and total BFCS (r=‐0.22; p=0.02) volumes were negatively associated with temporal theta power. Moreover, total BFCS (r=‐0.22; p=0.023) volumes were negatively associated with temporal alpha power. Sex‐stratified analyses revealed that the associations between BFCS volumes, REM‐sleep spectral power and episodic memory were significant in women, but not in men. Conclusion These results confirmed that cortical activation during REM sleep is sensitive to volume loss in the BFCS, a cholinergic region known to degenerate early in AD. Why this association was only observed in women is intriguing and will need further investigation.

10.1002/alz.057683

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REM sleep is associated with the integrity of the cholinergic basal forebrain in aMCI participants

Alzheimer s & Dementia (2022)

Claire André Marie‐Ève Martineau‐Dussault Véronique Daneault Hélène Blais Dominique Lorrain

Abstract Background The basal forebrain cholinergic system (BFCS) degenerates in Alzheimer’s disease (AD) before the onset of dementia. Interestingly, rapid‐eye movement (REM) sleep is highly dependent on cholinergic activity. In AD patients, REM sleep duration is reduced but the underlying brain mechanisms are still unclear. Our objective was to investigate the associations between REM‐sleep quantity and BFCS integrity in participants with amnestic mild cognitive impairment (aMCI) compared to healthy controls. Method Sixty‐two participants (31 cognitively healthy: 66.8 ± 7.2 years old, 13 women; 31 aMCI: 68.3 ± 8.8 years old, 7 women) underwent polysomnography and structural magnetic resonance imaging examinations. REM sleep duration (number of minutes) and proportion (%) were computed. All participants had a REM sleep apnea‐hypopnea index <15. T1‐weighted images were preprocessed using CAT12 and the DARTEL algorithm, and the mean intensity of BFCS subregions (i.e., Ch1‐2‐3, Ch4 and total BFCS) was extracted using the JuBrain Anatomy Toolbox. Multiple regressions were performed between BFCS subregional intensities and REM sleep indices controlling for age, sex and total intracranial volume, in the whole cohort and in the two groups separately. Result In the whole cohort, REM sleep duration and proportion were positively associated with Ch4 intensity (duration: r = 0.31, p = 0.017; proportion: r = 0.35, p = 0.007; Figure 1A and B) and total BFCS intensity (duration: r = 0.31, p = 0.016; proportion: r = 0.29, p = 0.024). Analyses stratified by cognitive status showed the same pattern in aMCI participants: REM sleep duration and proportion were positively associated with both Ch4 intensity (duration: r = 0.44, p = 0.018; proportion: r = 0.49, p = 0.009; Figure 1C and D) and total BFCS intensity (duration: r = 0.46, p = 0.014; proportion: r = 0.46, p = 0.013). No significant association, nor trend, was found in cognitively healthy participants (Figure 1C and D). Conclusion In aMCI participants, lower REM sleep duration and proportion were associated with a decreased integrity of the BFCS, especially the Nucleus Basalis of Meynert. Our results support the notion that REM sleep alterations are an early marker of the degeneration of the BFCS in prodromal AD, before the onset of dementia.

10.1002/alz.067250

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Daytime vigilance in chronotypes: Diurnal variations and effects of behavioral sleep fragmentation

Behavioural Brain Research (2008)

Valérie Mongrain Jonathan Noujaim Hélène Blais Marie Dumont

Vigilance (psychology)

Chronotype

Psychomotor vigilance task

Alertness

10.1016/j.bbr.2008.02.007

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Sleep in the Acute Phase of Severe Traumatic Brain Injury

Neurorehabilitation and neural repair (2015)

Catherine Wiseman‐Hakes Catherine Duclos Hélène Blais Marie Dumont Françis Bernard

Background and Objectives. The onset of pervasive sleep-wake disturbances associated with traumatic brain injury (TBI) is poorly understood. This study aimed to ( a) determine the feasibility of using polysomnography in patients in the acute, hospitalized stage of severe TBI and ( b) explore sleep quality and sleep architecture during this stage of recovery, compared to patients with other traumatic injuries. Methods. A cross-sectional case-control design was used. We examined the sleep of 7 patients with severe TBI (17-47 years; 20.3 ± 15.0 days postinjury) and 6 patients with orthopedic and/or spinal cord injuries (OSCI; 19-58 years; 16.9 ± 4.9 days postinjury). One night of ambulatory polysomnography was performed at bedside. Results. Compared to OSCI patients, TBI patients showed a significantly longer duration of nocturnal sleep and earlier nighttime sleep onset. Sleep efficiency was low and comparable in both groups. All sleep stages were observed in both groups with normal proportions according to age. Conclusion. Patients in the acute stage of severe TBI exhibit increased sleep duration and earlier sleep onset, suggesting that the injured brain enhances sleep need and/or decreases the ability to maintain wakefulness. As poor sleep efficiency could compromise brain recovery, further studies should investigate whether strategies known to optimize sleep in healthy individuals are efficacious in acute TBI. While there are several inherent challenges, polysomnography is a useful means of examining sleep in the early stage of recovery in patients with severe TBI.

Sleep

10.1177/1545968315619697

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Sleep-wake disturbances in hospitalized patients with traumatic brain injury: association with brain trauma but not with an abnormal melatonin circadian rhythm

SLEEP (2019)

Catherine Duclos Marie Dumont Jean Paquet Hélène Blais Solenne Van der Maren

Abstract Study Objectives To test whether the sleep-wake cycle disruption in patients hospitalized with traumatic brain injury (TBI) (1) is also found in patients with traumatic injuries other than TBI (non-TBI) and (2) is associated with a weaker or abnormal circadian clock signal. Methods Forty-two non-mechanically ventilated and non-sedated patients hospitalized for moderate-to-severe TBI were compared to 34 non-TBI patients. They wore wrist actigraphs for 9.4 ± 4.2 days, starting 19.3 ± 12.6 days post-injury. Of these, 17 TBI and 14 non-TBI patients had their urine collected every hour for 25 hours, starting 18.3 ± 12.3 days post-injury. We calculated urinary 6-sulfatoxymelatonin concentration to obtain total 24-hour excretion, excretion onset, offset, duration, amplitude, and acrophase. Using Student’s t-tests, we compared groups on actigraphy (daytime activity ratio, nighttime total sleep time, and fragmentation index) and melatonin variables. We investigated associations between melatonin and actigraphy variables using Pearson’s correlations. Results TBI patients had poorer daytime activity ratio (TBI: 77.5 ± 9.4%; non-TBI: 84.6 ± 6.9%), shorter nighttime total sleep time (TBI: 353.5 ± 96.6 min; non-TBI: 421.2 ± 72.2 min), and higher fragmentation index (TBI: 72.2 ± 30.0; non-TBI: 53.5 ± 23.6) (all p-values < 0.01). A melatonin rhythm was present in both groups, and no group differences were found on melatonin variables. No associations were found between melatonin and actigraphy variables in TBI patients. Conclusion Moderate-to-severe TBI patients have more serious sleep-wake disturbances than non-TBI patients hospitalized in the same environment, suggesting that the brain injury itself alters the sleep-wake cycle. Despite their deregulated 24-hour sleep-wake cycle, TBI patients have a normal circadian clock signal.

10.1093/sleep/zsz191

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1133 The Recovery of Sleep Oscillations in Acute to Chronic Traumatic Brain Injury

SLEEP (2020)

Erlan Sanchez Catherine Duclos Solenne Van der Maren Héjar El-Khatib Caroline Arbour

Abstract Introduction Slow waves and spindles are essential oscillations occurring during NREM sleep that may be disrupted by moderate to severe traumatic brain injury (TBI). We investigated these oscillations in the acute and chronic trauma stage. Methods Four groups were tested with whole-night polysomnography: hospitalized patients with acute TBI (n=10, 29.7±13.8y) or severe orthopedic injuries (n=15, 39.9±17.1y), chronic TBI including 9 returning from the acute TBI group (n=43, 31.9±13.5y), and healthy controls (n=36, 30.5±12.7y). Characteristics for slow waves (density, amplitude, slope, frequency, duration) and spindles (density, amplitude, frequency, duration) were quantified over N2 and N3 sleep for the first three sleep cycles, and groups were compared using one-way ANOVAs. Results One-way ANOVAs showed group effects only for slow wave density (F=4.11 to 6.04, p=0.009 to 0.0008)) and spindle density (F=3.3 to 8.8, p=0.02 to 0.00003). These effects were present for the 2nd and 3rd sleep cycles, but not the 1st. More specifically, slow wave density in acute TBI was higher than in controls, and returned to normal levels in the chronic stage. Conversely, spindle density in acute TBI was lower than in controls and returned to normal levels in the chronic stage. No group difference was observed for the orthopedic group. Conclusion Our results suggest that immediately after a severely disruptive event such as a TBI, the brain needs additional deeper sleep to recover, resulting in more slow waves but also in less spindles. These changes are only present in the 2nd and 3rd sleep cycles, reflecting an absence of the expected dissipation of slow waves, which may suggest increased homeostatic sleep pressure due to the brain injury. Limits to interpretation include the hospital environment and medication, but the absence of changes in the orthopedic group under similar conditions emphasizes the effect of the brain injury itself. Support Canadian Institutes of Health Research (CIHR) and Fonds de Recherche Québec-Santé (FRQS)

Sleep

Sleep spindle

10.1093/sleep/zsaa056.1127

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Cardiac autonomic dysfunction in idiopathic REM sleep behavior disorder

Movement Disorders (2010)

Ronald B. Postuma Paola A. Lanfranchi Hélène Blais Jean‐François Gagnon Jacques Montplaisir

More than 50% of persons with idiopathic REM sleep behavior disorder (RBD) will develop Parkinson's disease or Lewy body dementia. Symptom screens and metaiodobenzylguanine (MIBG)-scintigraphy suggest autonomic abnormalities in idiopathic RBD, but it is unclear whether autonomic abnormalities can predict neurodegenerative disease. From a cohort of 99 patients with idiopathic RBD, we selected those who developed parkinsonism or dementia. These were matched by age, sex, and follow-up duration to patients with RBD who remained disease free and to matched controls. From the polysomnographic trace performed at baseline evaluation, measures of beat-to-beat RR variability including time domains (mean RR-interval and RR-standard deviation) and frequency domains (low and high frequency components) were retrospectively assessed. Twenty-one patients with idiopathic RBD who developed neurodegenerative disease were included (Parkinson's disease-11, multiple system atrophy-1, and dementia-9). Age at PSG was 66 years, and 86% were male. PSG was performed on average 6.7 years before defined neurodegenerative disease. Comparing all patients with idiopathic RBD to controls, there were significant reductions in RR-standard deviation (24.6 ± 2.2 ms vs. 35.2 ± 3.5 ms, P = 0.006), very low frequency components (238.6 ± 99.6 ms(2) vs. 840.1 ± 188.3 ms(2), P < 0.001), and low frequency components (127.8 ± 26.3 ms(2) vs. 288.7 ± 66.2 ms(2), P = 0.032). However, despite clear differences between patients with idiopathic RBD and controls, there were no differences in any measure between those who did or did not develop disease. RR-variability analysis demonstrates substantial autonomic dysfunction in idiopathic RBD. However, this dysfunction is identical in patients who will or will not develop defined neurodegenerative disease. This suggests that autonomic dysfunction is linked with RBD independent of associated Parkinson's disease or Lewy body dementia.

Lewy body

10.1002/mds.23347

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Sleep in Hospitalized Patients With Acute Moderate-Severe Traumatic Brain Injury:Relationship With Cognitive and Neurorecovery

Archives of Physical Medicine and Rehabilitation (2014)

Catherine Wiseman‐Hakes Catherine Duclos Pierre-Olivier Geaudreault Julie Carrier Hélène Blais

Sleep

10.1016/j.apmr.2014.07.163

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Rest-Activity Cycle Disturbances in the Acute Phase of Moderate to Severe Traumatic Brain Injury

Neurorehabilitation and neural repair (2013)

Catherine Duclos Marie Dumont Hélène Blais Jean Paquet Elyse Laflamme

Sleep-wake disturbances are among the most persistent sequelae after traumatic brain injury (TBI) and probably arise during the hospital stay following TBI. These disturbances are characterized by difficulties sleeping at night and staying awake during the day.The aim of the present study was to document rest-activity cycle consolidation in acute moderate/severe TBI using actigraphy and to assess its association with injury severity and outcome.In all, 16 hospitalized patients (27.1 ± 11.3 years) with moderate/severe TBI wore actigraphs for 10 days, starting in the intensive care unit (ICU) when continuous sedation was discontinued and patients had reached medical stability. Activity counts were summed for daytime (7:00-21:59 hours) and nighttime periods (22:00-6:59 hours). The ratio of daytime period activity to total 24-hour activity was used to quantify rest-activity cycle consolidation. An analysis of variance was carried out to characterize the evolution of the daytime activity ratio over the recording period.Rest-activity cycle was consolidated only 46.6% of all days; however, a significant linear trend of improvement was observed over time. Greater TBI severity and longer ICU and hospital lengths of stay were associated with poorer rest-activity cycle consolidation and evolution. Patients with more rapid return to consolidated rest-activity cycle were more likely to have cleared posttraumatic amnesia and have lower disability at hospital discharge.Patients with acute moderate/severe TBI had an altered rest-activity cycle, probably reflecting severe fragmentation of sleep and wake episodes, which globally improved over time. A faster return to rest-activity cycle consolidation may predict enhanced brain recovery.

10.1177/1545968313517756

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Citations (88)