Format
Sort by
Items per page

Send to

Choose Destination

Search results

Items: 1 to 20 of 61

1.
Int Rev Neurobiol. 2018;139:321-355. doi: 10.1016/bs.irn.2018.07.013. Epub 2018 Jul 31.

The Role of Sleep in Learning Placebo Effects.

Author information

1
PERFORM Center & Department of Exercise Science, Concordia University, Montreal, QC, Canada; Centre de Recherche de l'Institut Universitaire de Gériatrie de Montréal, Université de Montréal, Montreal, QC, Canada.
2
Centre de Recherche de l'Institut Universitaire de Gériatrie de Montréal, Université de Montréal, Montreal, QC, Canada; Faculté de Médecine Dentaire, Université de Montréal, Montreal, QC, Canada.
3
Faculté de Médecine Dentaire, Université de Montréal, Montreal, QC, Canada; Centre d'Etudes Avancées en Médecine du Sommeil, Hôpital du Sacré-Coeur de Montréal, Montreal, QC, Canada. Electronic address: gilles.lavigne@umontreal.ca.

Abstract

The placebo effect is a psychobiological phenomenon producing clinical benefits attributed to a wide range of neurobiological mechanisms. Independently from placebo effects, these mechanisms may also be under the influence of processes that can take place during sleep. The relationship between sleep and placebo effects has received very little attention. Three experimental studies, conducted on healthy subjects, have examined sleep changes following placebo conditioning associated with analgesic suggestions and the effects of sleep deprivation on placebo effects. A relation between rapid eye movement (REM) sleep, expectations of relief and placebo analgesia was observed in which REM sleep deprivation seems to improve placebo-induced expectations and analgesia. Moreover, analgesic expectations developed before sleep produced a reduction in cortical arousals evoked by noxious stimuli during REM sleep. In this article, we describe sleep and pain/analgesia interactions, the relationship between sleep and placebo analgesia, and finally the potential mechanisms underlying this relationship.

KEYWORDS:

Conditioning; Expectations; Pain; Placebo; REM sleep; Relief; Sleep

PMID:
30146053
DOI:
10.1016/bs.irn.2018.07.013
[Indexed for MEDLINE]
Icon for Elsevier Science
2.
Sleep. 2018 May 1;41(5). doi: 10.1093/sleep/zsy039.

Altered brain perfusion patterns in wakefulness and slow-wave sleep in sleepwalkers.

Author information

1
Center for Advanced Research in Sleep Medicine, Hôpital du Sacré-Cœur de Montréal, Montreal, Canada.
2
Department of Psychology, Université de Montréal, Montreal, Canada.
3
Faculty of Medicine, Université de Montréal, Montreal, Canada.
4
PERFORM Centre, Concordia University, Montreal, Canada.
5
McConnell Brain Imaging Centre, Montreal Neurological Institute, McGill University, Montreal, Canada.
6
Center for Studies in Behavioral Neurobiology, Concordia University, Montreal, Canada.
7
Centre de Recherche de l'Institut Universitaire de Gériatrie de Montréal and Department of Neurosciences, Université de Montréal, Montreal, Canada.

Abstract

Study Objectives:

The present study assessed brain perfusion patterns with single-photon emission computed tomography (SPECT) during sleepwalkers' post-sleep deprivation slow-wave sleep (SWS) and resting-state wakefulness.

Methods:

Following a 24 hr period of sleep deprivation, 10 sleepwalkers and 10 sex- and age-matched controls were scanned with a high-resolution SPECT scanner. Participants were injected with 99mTc-ethylene cysteinate dimer after 2 min of stable SWS within their first sleep cycle as well as during resting-state wakefulness, both after a subsequent 24 hr period of sleep deprivation.

Results:

When compared with controls' brain perfusion patterns during both SWS and resting-state wakefulness, sleepwalkers showed reduced regional cerebral perfusion in several bilateral frontal regions, including the superior frontal, middle frontal, and medial frontal gyri. Moreover, reduced regional cerebral perfusion was also found in sleepwalkers' left postcentral gyrus, insula, and superior temporal gyrus during SWS compared with controls. During resting-state wakefulness compared with controls, reduced cerebral perfusion was also found in parietal and temporal regions of sleepwalkers' left hemisphere, whereas the right parahippocampal gyrus showed increased regional cerebral perfusion.

Conclusions:

Our results reveal patterns of reduced regional cerebral perfusion in sleepwalkers' frontal and parietal areas when compared with controls, regions previously associated with SWS generation and episode occurrence. Additionally, reduced perfusion in the dorsolateral prefrontal cortex and insula during recovery SWS is consistent with the clinical features of somnambulistic episodes, including impaired awareness and reduced pain perception. Altered regional cerebral perfusion patterns during sleepwalkers' resting-state wakefulness may be related to daytime functional anomalies in this population.

PMID:
29514303
PMCID:
PMC5946932
[Available on 2019-03-03]
DOI:
10.1093/sleep/zsy039
Icon for Silverchair Information Systems
3.
Sleep Med. 2017 Nov;39:54-61. doi: 10.1016/j.sleep.2017.08.012. Epub 2017 Sep 9.

Sleep spindles may predict response to cognitive-behavioral therapy for chronic insomnia.

Author information

1
Department of Exercise Science, Concordia University, Montréal, QC, Canada; Department of Psychology, Concordia University, Montréal, QC, Canada; Center for Studies in Behavioral Neurobiology, Concordia University, Montréal, QC, Canada; PERFORM Center, Concordia University, Montréal, QC, Canada; Center for Clinical Research in Health, Concordia University, Montréal, QC, Canada; Centre de Recherches de l'Institut Universitaire de Gériatrie de Montréal, Montréal, QC, Canada; Department of Neurosciences, Université de Montréal, Montréal, QC, Canada. Electronic address: tt.dangvu@concordia.ca.
2
Department of Psychology, Concordia University, Montréal, QC, Canada; Center for Studies in Behavioral Neurobiology, Concordia University, Montréal, QC, Canada; PERFORM Center, Concordia University, Montréal, QC, Canada.
3
Department of Exercise Science, Concordia University, Montréal, QC, Canada; Center for Studies in Behavioral Neurobiology, Concordia University, Montréal, QC, Canada; PERFORM Center, Concordia University, Montréal, QC, Canada; Centre de Recherches de l'Institut Universitaire de Gériatrie de Montréal, Montréal, QC, Canada.
4
Department of Exercise Science, Concordia University, Montréal, QC, Canada; Department of Psychology, Concordia University, Montréal, QC, Canada; PERFORM Center, Concordia University, Montréal, QC, Canada; Centre de Recherches de l'Institut Universitaire de Gériatrie de Montréal, Montréal, QC, Canada.
5
Physip SA, Paris, France.
6
Department of Psychology, Concordia University, Montréal, QC, Canada; PERFORM Center, Concordia University, Montréal, QC, Canada; Center for Clinical Research in Health, Concordia University, Montréal, QC, Canada.

Abstract

BACKGROUND:

While cognitive-behavioral therapy for insomnia constitutes the first-line treatment for chronic insomnia, only few reports have investigated how sleep architecture relates to response to this treatment. In this pilot study, we aimed to determine whether pre-treatment sleep spindle density predicts treatment response to cognitive-behavioral therapy for insomnia.

METHODS:

Twenty-four participants with chronic primary insomnia participated in a 6-week cognitive-behavioral therapy for insomnia performed in groups of 4-6 participants. Treatment response was assessed using the Pittsburgh Sleep Quality Index and the Insomnia Severity Index measured at pre- and post-treatment, and at 3- and 12-months' follow-up assessments. Secondary outcome measures were extracted from sleep diaries over 7 days and overnight polysomnography, obtained at pre- and post-treatment. Spindle density during stage N2-N3 sleep was extracted from polysomnography at pre-treatment. Hierarchical linear modeling analysis assessed whether sleep spindle density predicted response to cognitive-behavioral therapy.

RESULTS:

After adjusting for age, sex, and education level, lower spindle density at pre-treatment predicted poorer response over the 12-month follow-up, as reflected by a smaller reduction in Pittsburgh Sleep Quality Index over time. Reduced spindle density also predicted lower improvements in sleep diary sleep efficiency and wake after sleep onset immediately after treatment. There were no significant associations between spindle density and changes in the Insomnia Severity Index or polysomnography variables over time.

CONCLUSION:

These preliminary results suggest that inter-individual differences in sleep spindle density in insomnia may represent an endogenous biomarker predicting responsiveness to cognitive-behavioral therapy. Insomnia with altered spindle activity might constitute an insomnia subtype characterized by a neurophysiological vulnerability to sleep disruption associated with impaired responsiveness to cognitive-behavioral therapy.

KEYWORDS:

Biomarkers; Electroencephalography; Insomnia; Neural oscillations; Sleep spindles

PMID:
29157588
DOI:
10.1016/j.sleep.2017.08.012
[Indexed for MEDLINE]
Icon for Elsevier Science
4.
Sleep. 2017 Oct 1;40(10). doi: 10.1093/sleep/zsx140.

Altered Regional Cerebral Blood Flow in Idiopathic Hypersomnia.

Author information

1
Center for Studies in Behavioral Neurobiology and Department of Exercise Science, Concordia University, Montreal, Quebec, Canada.
2
PERFORM Centre, Concordia University, Montreal, Quebec, Canada.
3
Centre de Recherche de l'Institut Universitaire de Gériatrie de Montréal, Montréal, Quebec, Canada.
4
Center for Advanced Research in Sleep Medicine, Hôpital du Sacré-Coeur de Montréal, Montreal, Quebec, Canada.
5
Department of Psychiatry, Université de Montréal, Montreal, Quebec, Canada.
6
Department of Psychology, Université de Montréal, Montreal, Quebec, Canada.
7
McConnell Brain Imaging Centre, Montreal Neurological Institute, McGill University, Montreal, Quebec, Canada.
8
Department of Neurosciences, Université de Montréal, Montreal, Quebec, Canada.

Abstract

Study Objectives:

Idiopathic hypersomnia is characterized by excessive daytime sleepiness, despite normal or long sleep time. Its pathophysiological mechanisms remain unclear. This pilot study aims at characterizing the neural correlates of idiopathic hypersomnia using single photon emission computed tomography.

Methods:

Thirteen participants with idiopathic hypersomnia and 16 healthy controls were scanned during resting wakefulness using a high-resolution single photon emission computed tomography scanner with 99mTc-ethyl cysteinate dimer to assess cerebral blood flow. The main analysis compared regional cerebral blood flow distribution between the two groups. Exploratory correlations between regional cerebral blood flow and clinical characteristics evaluated the functional correlates of those brain perfusion patterns. Significance was set at p < .05 after correction for multiple comparisons.

Results:

Participants with idiopathic hypersomnia showed regional cerebral blood flow decreases in medial prefrontal cortex and posterior cingulate cortex and putamen, as well as increases in amygdala and temporo-occipital cortices. Lower regional cerebral blood flow in the medial prefrontal cortex was associated with higher daytime sleepiness.

Conclusions:

These preliminary findings suggest that idiopathic hypersomnia is characterized by functional alterations in brain areas involved in the modulation of vigilance states, which may contribute to the daytime symptoms of this condition. The distribution of regional cerebral blood flow changes was reminiscent of the patterns associated with normal non-rapid-eye-movement sleep, suggesting the possible presence of incomplete sleep-wake transitions. These abnormalities were strikingly distinct from those induced by acute sleep deprivation, suggesting that the patterns seen here might reflect a trait associated with idiopathic hypersomnia rather than a non-specific state of sleepiness.

KEYWORDS:

idiopathic hypersomnia; single photon emission computed tomography; sleep disorders; sleepiness

PMID:
28958044
DOI:
10.1093/sleep/zsx140
[Indexed for MEDLINE]
Icon for Silverchair Information Systems
5.
Curr Psychiatry Rep. 2017 Jul;19(7):37. doi: 10.1007/s11920-017-0789-3.

Psychiatric Illness and Parasomnias: a Systematic Review.

Author information

1
School of Psychological Science, The University of Western Australia, 35 Stirling Highway, Crawley, Western Australia, 6009, Australia. flavie.waters@health.wa.gov.au.
2
Clinical Research Centre, Graylands Hospital, North Metropolitan Health Service-Mental Health, Perth, Western Australia, Australia. flavie.waters@health.wa.gov.au.
3
Psychiatric Unit I Department of Clinical and Experimental Medicine, University of Pisa, Via Roma 67, Pisa, Italy.
4
Center for Studies in Behavioral Neurobiology & PERFORM Center, Department of Exercise Science, Concordia University, 7141 Sherbrooke St. West, SP 165.27, Montreal, H4B 1R6, Canada.
5
Centre de Recherche de l'Institut Universitaire de Gériatrie de Montréal (CRIUGM), 4545 chemin Queen-Mary, M5815, Montreal, H3W 1W5, Canada.

Abstract

PURPOSE OF REVIEW:

Little is known about the presence of parasomnias such as nightmare disorder, sleep paralysis, REM sleep behavior disorder (RBD), and sleep-related eating disorders (SRED) in people with mental illness. A predominant view suggests that psychotropic medications might be contributing to parasomnias. This article summarizes knowledge regarding the relationships between psychiatric disorders and parasomnias, and possible confounds. A systematic search of the literature in the past 10 years identified 19 articles.

RECENT FINDINGS:

There were significantly elevated rates of parasomnias in psychiatric disorders (average prevalence of nightmares was 38.9%, sleep paralysis 22.3%, SRED 9.9%, sleepwalking 8.5%, and RBD 3.8%). Medication usage was only one of many risk factors (other sleep disorders, medical comorbidities, and substance abuse) which were associated with parasomnias. A strong association exists between mental illness and parasomnias which is not fully explained by medications. Prospective longitudinal studies are needed to develop a better understanding of the unique and shared variance from multiple risk factors.

KEYWORDS:

Eating disorder; Nightmare disorder; Paralysis; REM sleep behavior disorder; Somnambulism

PMID:
28534293
DOI:
10.1007/s11920-017-0789-3
[Indexed for MEDLINE]
Icon for Springer
6.
Ann Behav Med. 2017 Dec;51(6):912-924. doi: 10.1007/s12160-017-9915-z.

High-Frequency Heart Rate Variability Reactivity and Trait Worry Interact to Predict the Development of Sleep Disturbances in Response to a Naturalistic Stressor.

Author information

1
Department of Psychology, Concordia University, Montreal, Canada.
2
Department of Psychiatry, McGill University, Montreal, QC, Canada.
3
Douglas Mental Health University Institute, Montreal, QC, Canada.
4
Department of Exercise Science, Concordia University, Montreal, Canada.
5
Centre de Recherche de l'Institut Universitaire de Gériatrie de Montréal and Department of Neurosciences, Université de Montréal, Montreal, Canada.
6
PERFORM Center, Concordia University, Montreal, Canada.
7
Department of Psychology, Concordia University, Montreal, Canada. jp.gouin@concordia.ca.
8
PERFORM Center, Concordia University, Montreal, Canada. jp.gouin@concordia.ca.

Abstract

BACKGROUND:

High-frequency heart rate variability (HF-HRV) reactivity was proposed as a vulnerability factor for stress-induced sleep disturbances. Its effect may be amplified among individuals with high trait worry or sleep reactivity.

PURPOSE:

This study evaluated whether HF-HRV reactivity to a worry induction, sleep reactivity, and trait worry predict increases in sleep disturbances in response to academic stress, a naturalistic stressor.

METHOD:

A longitudinal study following 102 undergraduate students during an academic semester with well-defined periods of lower and higher academic stress was conducted. HF-HRV reactivity to a worry induction, trait worry using the Penn State Worry Questionnaire, and sleep reactivity using the Ford Insomnia Stress Reactivity Test were measured during the low stress period. Sleep disturbances using the Pittsburgh Sleep Quality Index were assessed twice during the lower stress period and three times during the higher stress period.

RESULTS:

Greater reductions in HF-HRV in response to the worry induction predicted increases in sleep disturbances from the lower to the higher academic stress period. Trait worry moderated this association: individuals with both higher trait worry and greater HF-HRV reactivity to worry had larger increases in stress-related sleep disturbances over time, compared to participants with lower trait worry and HF-HRV reactivity. A similar, but marginally significant effect was found for sleep reactivity.

CONCLUSION:

This study supports the role of HF-HRV reactivity as a vulnerability factor for stress-induced sleep disturbances. The combination of high trait worry and high HF-HRV reactivity to worry might identify a subgroup of individuals most vulnerable to stress-related sleep disturbances.

KEYWORDS:

Heart rate variability; Insomnia; Sleep disturbances; Sleep reactivity; Stress; Worry

PMID:
28527014
DOI:
10.1007/s12160-017-9915-z
[Indexed for MEDLINE]
Icon for Silverchair Information Systems
7.
Sci Rep. 2016 Oct 11;6:34948. doi: 10.1038/srep34948.

Cerebral Activity Associated with Transient Sleep-Facilitated Reduction in Motor Memory Vulnerability to Interference.

Author information

1
Cyclotron Research Centre, University of Liège, Liège, Belgium.
2
Functional Neuroimaging Unit, Centre de Recherche de l'Institut Universitaire de Gériatrie de Montreal, University of Montreal, Montreal, Canada.
3
Movement Control and Neuroplasticity Research Group, Department of Kinesiology, KU Leuven, Leuven, Belgium.
4
PERFORM Center and Center for Studies in Behavioral Neurobiology, Department of Exercise Science, Concordia University, Montreal, Canada.
5
Unité Mixte de Recherche-S 678, Institut National de la Santé et de la Recherche Médicale/University of Paris 6, Centre Hospitalier Universitaire Pitié-Salpêtrière, Paris, France.
6
UR2NF - Neuropsychology and Functional Neuroimaging Research Unit affiliated at CRCN - Center for Research in Cognition and Neurosciences, Neurosciences Institute, Université Libre de Bruxelles, Brussels, Belgium.
7
Laboratory for Functional Brain Imaging and Learning Research, The Brain-Behavior Center, University of Haifa, Haifa, Israel.
8
Occupational Therapy Department, Faculty of Social Welfare &Health Sciences, University of Haifa, Haifa, Israel.

Abstract

Motor memory consolidation is characterized, in part, by a sleep-facilitated decrease in susceptibility to subsequent interfering experiences. Surprisingly, the cerebral substrates supporting this phenomenon have never been examined. We used fMRI to investigate the neural correlates of the influence of sleep on interference to motor memory consolidation. Healthy young adults were trained on a sequential motor task, and subsequently practiced a second competing sequence after an interval including diurnal sleep or wakefulness. Participants were then retested on the initial sequence 8 h and 24 h (including nocturnal sleep) after training. Results demonstrated that a post-training nap significantly protected memory against interference at 8 h and modulated the link between cerebral activity and behavior, such that a smaller post-interference decrease in cortico-striatal activity was associated with better performance. Interestingly, the protective effect of a nap was only transitory, as both groups performed similarly at 24 h. Activity in cortico-striatal areas that was disrupted during the day, presumably due to interference and accentuated in the absence of a nap, was restored overnight. Altogether, our findings offer the first evidence that cortico-striatal areas play a critical role in the transient sleep-facilitated reduction in motor memory vulnerability and in the overnight restoration of previously degraded memories.

PMID:
27725727
PMCID:
PMC5057137
DOI:
10.1038/srep34948
[Indexed for MEDLINE]
Free PMC Article
Icon for Nature Publishing Group Icon for PubMed Central
8.
Schizophr Bull. 2016 Sep;42(5):1098-109. doi: 10.1093/schbul/sbw076. Epub 2016 Jun 29.

What Is the Link Between Hallucinations, Dreams, and Hypnagogic-Hypnopompic Experiences?

Author information

1
Clinical Research Centre, Graylands Hospital, North Metro Health Service Mental Health, Perth, Australia; School of Psychiatry and Clinical Neurosciences, The University of Western Australia, Perth, Australia; flavie.waters@health.wa.gov.au.
2
Center for Studies in Behavioral Neurobiology, PERFORM Center and Department of Exercise Science, Concordia University; and Centre de Recherches de l'Institut Universitaire de Gériatrie de Montréal and Department of Neurosciences, University of Montreal, Montreal, QC, Canada;
3
Department of Psychology, University of Waterloo, Waterloo, ON, Canada;
4
Department of Psychology, Durham University, Durham, UK;
5
University of Sheffield, UK, Hamad Medical Corporation, Doha, Qatar;
6
Clinical Psychology, Northumberland, Tyne and Wear NHS Foundation Trust, and Institute of Neuroscience, Newcastle University, Newcastle upon Tyne, UK.

Abstract

By definition, hallucinations occur only in the full waking state. Yet similarities to sleep-related experiences such as hypnagogic and hypnopompic hallucinations, dreams and parasomnias, have been noted since antiquity. These observations have prompted researchers to suggest a common aetiology for these phenomena based on the neurobiology of rapid eye movement (REM) sleep. With our recent understanding of hallucinations in different population groups and at the neurobiological, cognitive and interpersonal levels, it is now possible to draw comparisons between the 2 sets of experiences as never before. In the current article, we make detailed comparisons between sleep-related experiences and hallucinations in Parkinson's disease, schizophrenia and eye disease, at the levels of phenomenology (content, sensory modalities involved, perceptual attributes) and of brain function (brain activations, resting-state networks, neurotransmitter action). Findings show that sleep-related experiences share considerable overlap with hallucinations at the level of subjective descriptions and underlying brain mechanisms. Key differences remain however: (1) Sleep-related perceptions are immersive and largely cut off from reality, whereas hallucinations are discrete and overlaid on veridical perceptions; and (2) Sleep-related perceptions involve only a subset of neural networks implicated in hallucinations, reflecting perceptual signals processed in a functionally and cognitively closed-loop circuit. In summary, both phenomena are non-veridical perceptions that share some phenomenological and neural similarities, but insufficient evidence exists to fully support the notion that the majority of hallucinations depend on REM processes or REM intrusions into waking consciousness.

KEYWORDS:

Parkinson’s disease; REM; consciousness; eye disease; hypnopompic and hypnagogic hallucination; misperception; nightmare; parasomnia; schizophrenia; sleep

PMID:
27358492
PMCID:
PMC4988750
DOI:
10.1093/schbul/sbw076
[Indexed for MEDLINE]
Free PMC Article
Icon for Silverchair Information Systems Icon for PubMed Central
9.
Sci Rep. 2016 Jun 1;6:26782. doi: 10.1038/srep26782.

Structural Brain Alterations Associated with Rapid Eye Movement Sleep Behavior Disorder in Parkinson's Disease.

Author information

1
Center for Studies in Behavioural Neurobiology, PERFORM Center and Dpt of Exercise Science, Concordia University, 7141 Sherbrooke St. West, Montréal, Québec, H4B 1R6 Canada.
2
Centre de Recherche de l'Institut Universitaire de Gériatrie de Montréal and Dpt of Neurosciences, Université de Montréal, 4545 Chemin Queen Mary, Montréal, Québec, H3W 1W4 Canada.
3
Montreal Neurological Institute, McGill University, 3801 University Street, Montréal, Québec, H3A 2B4 Canada.

Abstract

Characterized by dream-enactment motor manifestations arising from rapid eye movement (REM) sleep, REM sleep behavior disorder (RBD) is frequently encountered in Parkinson's disease (PD). Yet the specific neurostructural changes associated with RBD in PD patients remain to be revealed by neuroimaging. Here we identified such neurostructural alterations by comparing large samples of magnetic resonance imaging (MRI) scans in 69 PD patients with probable RBD, 240 patients without RBD and 138 healthy controls, using deformation-based morphometry (p < 0.05 corrected for multiple comparisons). All data were extracted from the Parkinson's Progression Markers Initiative. PD patients with probable RBD showed smaller volumes than patients without RBD and than healthy controls in the pontomesencephalic tegmentum, medullary reticular formation, hypothalamus, thalamus, putamen, amygdala and anterior cingulate cortex. These results demonstrate that RBD is associated with a prominent loss of volume in the pontomesencephalic tegmentum, where cholinergic, GABAergic and glutamatergic neurons are located and implicated in the promotion of REM sleep and muscle atonia. It is additionally associated with more widespread atrophy in other subcortical and cortical regions whose loss also likely contributes to the altered regulation of sleep-wake states and motor activity underlying RBD in PD patients.

PMID:
27245317
PMCID:
PMC4887790
DOI:
10.1038/srep26782
[Indexed for MEDLINE]
Free PMC Article
Icon for Nature Publishing Group Icon for PubMed Central
10.
Neural Plast. 2016;2016:7328725. doi: 10.1155/2016/7328725. Epub 2016 Mar 10.

Spindle Oscillations in Sleep Disorders: A Systematic Review.

Author information

1
PERFORM Center and Center for Studies in Behavioural Neurobiology, Department of Exercise Science and Department of Psychology, Concordia University, Montréal, QC, Canada H4B 1R6; Centre de Recherche de l'Institut Universitaire de Gériatrie de Montréal and Department of Neurosciences, Université de Montréal, Montreal, QC, Canada H3W 1W5.

Abstract

Measurement of sleep microarchitecture and neural oscillations is an increasingly popular technique for quantifying EEG sleep activity. Many studies have examined sleep spindle oscillations in sleep-disordered adults; however reviews of this literature are scarce. As such, our overarching aim was to critically review experimental studies examining sleep spindle activity between adults with and without different sleep disorders. Articles were obtained using a systematic methodology with a priori criteria. Thirty-seven studies meeting final inclusion criteria were reviewed, with studies grouped across three categories: insomnia, hypersomnias, and sleep-related movement disorders (including parasomnias). Studies of patients with insomnia and sleep-disordered breathing were more abundant relative to other diagnoses. All studies were cross-sectional. Studies were largely inconsistent regarding spindle activity differences between clinical and nonclinical groups, with some reporting greater or less activity, while many others reported no group differences. Stark inconsistencies in sample characteristics (e.g., age range and diagnostic criteria) and methods of analysis (e.g., spindle bandwidth selection, visual detection versus digital filtering, absolute versus relative spectral power, and NREM2 versus NREM3) suggest a need for greater use of event-based detection methods and increased research standardization. Hypotheses regarding the clinical and empirical implications of these findings, and suggestions for potential future studies, are also discussed.

PMID:
27034850
PMCID:
PMC4806273
DOI:
10.1155/2016/7328725
[Indexed for MEDLINE]
Free PMC Article
Icon for Hindawi Limited Icon for PubMed Central
11.
Sleep. 2016 Jan 1;39(1):161-71. doi: 10.5665/sleep.5340.

Cortical Thinning and Altered Cortico-Cortical Structural Covariance of the Default Mode Network in Patients with Persistent Insomnia Symptoms.

Author information

1
Sungshin Women's University, Department of Psychology, Seoul, Korea.
2
Stanford University, Department of Psychiatry, Palo Alto, CA.
3
University of California San Francisco, Department of Radiology and Biomedical Imaging, San Francisco, CA.
4
Center for Studies in Behavioral Neurobiology, PERFORM Center & Department of Exercise Science, Concordia University, Montreal, Canada.
5
Centre de Recherche de l'Institut Universitaire de Gériatrie de Montréal & Department of Neurosciences, University of Montreal, Montreal, Canada.
6
Samsung Medical Center, Department of Neurology, Sungkyunkwan University School of Medicine, Seoul, Korea.
7
Korea University Ansan Hospital, Institute of Human Genomic Study, Seoul, Korea.
8
Korea University Ansan Hospital, Department of Internal Medicine, Seoul, Korea.

Abstract

STUDY OBJECTIVES:

Recent studies have suggested that structural abnormalities in insomnia may be linked with alterations in the default-mode network (DMN). This study compared cortical thickness and structural connectivity linked to the DMN in patients with persistent insomnia (PI) and good sleepers (GS).

METHODS:

The current study used a clinical subsample from the longitudinal community-based Korean Genome and Epidemiology Study (KoGES). Cortical thickness and structural connectivity linked to the DMN in patients with persistent insomnia symptoms (PIS; n = 57) were compared to good sleepers (GS; n = 40). All participants underwent MRI acquisition. Based on literature review, we selected cortical regions corresponding to the DMN. A seed-based structural covariance analysis measured cortical thickness correlation between each seed region of the DMN and other cortical areas. Association of cortical thickness and covariance with sleep quality and neuropsychological assessments were further assessed.

RESULTS:

Compared to GS, cortical thinning was found in PIS in the anterior cingulate cortex, precentral cortex, and lateral prefrontal cortex. Decreased structural connectivity between anterior and posterior regions of the DMN was observed in the PIS group. Decreased structural covariance within the DMN was associated with higher PSQI scores. Cortical thinning in the lateral frontal lobe was related to poor performance in executive function in PIS.

CONCLUSION:

Disrupted structural covariance network in PIS might reflect malfunctioning of antero-posterior disconnection of the DMN during the wake to sleep transition that is commonly found during normal sleep. The observed structural network alteration may further implicate commonly observed sustained sleep difficulties and cognitive impairment in insomnia.

KEYWORDS:

MRI; default mode network; insomnia; neuroimaging; structural covariance

PMID:
26414892
PMCID:
PMC4678334
DOI:
10.5665/sleep.5340
[Indexed for MEDLINE]
Free PMC Article
Icon for Silverchair Information Systems Icon for PubMed Central
12.
PLoS One. 2015 Aug 4;10(8):e0133474. doi: 10.1371/journal.pone.0133474. eCollection 2015.

Sleep Deprivation Reveals Altered Brain Perfusion Patterns in Somnambulism.

Author information

1
Center for Advanced Research in Sleep Medicine, Hôpital du Sacré-Cœur de Montréal, Montréal, Quebec, Canada; Center for Studies in Behavioral Neurobiology, PERFORM Center & Department of Exercise Science, Concordia University, Montréal, Quebec, Canada; Centre de Recherche de l'Institut Universitaire de Gériatrie de Montréal and Department of Neurosciences, Université de Montréal, Montréal, Quebec, Canada.
2
Center for Advanced Research in Sleep Medicine, Hôpital du Sacré-Cœur de Montréal, Montréal, Quebec, Canada; Department of Psychology, Université de Montréal, Montréal, Quebec, Canada.
3
Department of Psychology, Université de Montréal, Montréal, Quebec, Canada.
4
Center for Advanced Research in Sleep Medicine, Hôpital du Sacré-Cœur de Montréal, Montréal, Quebec, Canada.
5
Montreal Neurological Institute, McGill University, Montréal, Quebec, Canada; Department of Nuclear Medicine, Centre Hospitalier de l'Université de Montréal, Montréal, Québec, Canada.
6
Center for Advanced Research in Sleep Medicine, Hôpital du Sacré-Cœur de Montréal, Montréal, Quebec, Canada; Department of Psychiatry and Canada Research Chair in Sleep Medicine, Université de Montréal, Montréal, Quebec, Canada.

Abstract

BACKGROUND:

Despite its high prevalence, relatively little is known about the pathophysiology of somnambulism. Increasing evidence indicates that somnambulism is associated with functional abnormalities during wakefulness and that sleep deprivation constitutes an important drive that facilitates sleepwalking in predisposed patients. Here, we studied the neural mechanisms associated with somnambulism using Single Photon Emission Computed Tomography (SPECT) with 99mTc-Ethylene Cysteinate Dimer (ECD), during wakefulness and after sleep deprivation.

METHODS:

Ten adult sleepwalkers and twelve controls with normal sleep were scanned using 99mTc-ECD SPECT in morning wakefulness after a full night of sleep. Eight of the sleepwalkers and nine of the controls were also scanned during wakefulness after a night of total sleep deprivation. Between-group comparisons of regional cerebral blood flow (rCBF) were performed to characterize brain activity patterns during wakefulness in sleepwalkers.

RESULTS:

During wakefulness following a night of total sleep deprivation, rCBF was decreased bilaterally in the inferior temporal gyrus in sleepwalkers compared to controls.

CONCLUSIONS:

Functional neural abnormalities can be observed during wakefulness in somnambulism, particularly after sleep deprivation and in the inferior temporal cortex. Sleep deprivation thus not only facilitates the occurrence of sleepwalking episodes, but also uncovers patterns of neural dysfunction that characterize sleepwalkers during wakefulness.

PMID:
26241047
PMCID:
PMC4524685
DOI:
10.1371/journal.pone.0133474
[Indexed for MEDLINE]
Free PMC Article
Icon for Public Library of Science Icon for PubMed Central
13.
J Sleep Res. 2015 Dec;24(6):658-65. doi: 10.1111/jsr.12315. Epub 2015 Jun 19.

Sleep deprivation impairs inhibitory control during wakefulness in adult sleepwalkers.

Author information

1
Department of Psychology, Université de Montréal, Montreal, Canada.
2
Center for Advanced Research in Sleep Medicine, Hôpital du Sacré-Cœur, Montreal, Canada.
3
Center for Studies in Behavioral Neurobiology, PERFORM Center and Department of Exercise Science, Concordia University, Montreal, Canada.
4
Department of Neurosciences, Université de Montréal and Neurology Service, Hôpital du Sacré-Coeur, Montreal, Canada.
5
Department of Psychiatry, Université de Montréal, Montreal, Canada.

Abstract

Sleepwalkers often complain of excessive daytime somnolence. Although excessive daytime somnolence has been associated with cognitive impairment in several sleep disorders, very few data exist concerning sleepwalking. This study aimed to investigate daytime cognitive functioning in adults diagnosed with idiopathic sleepwalking. Fifteen sleepwalkers and 15 matched controls were administered the Continuous Performance Test and Stroop Colour-Word Test in the morning after an overnight polysomnographic assessment. Participants were tested a week later on the same neuropsychological battery, but after 25 h of sleep deprivation, a procedure known to precipitate sleepwalking episodes during subsequent recovery sleep. There were no significant differences between sleepwalkers and controls on any of the cognitive tests administered under normal waking conditions. Testing following sleep deprivation revealed significant impairment in sleepwalkers' executive functions related to inhibitory control, as they made more errors than controls on the Stroop Colour-Word Test and more commission errors on the Continuous Performance Test. Sleepwalkers' scores on measures of executive functions were not associated with self-reported sleepiness or indices of sleep fragmentation from baseline polysomnographic recordings. The results support the idea that sleepwalking involves daytime consequences and suggest that these may also include cognitive impairments in the form of disrupted inhibitory control following sleep deprivation. These disruptions may represent a daytime expression of sleepwalking's pathophysiological mechanisms.

KEYWORDS:

cognition; parasomnias; sleepiness; somnambulism; vigilance

PMID:
26087833
DOI:
10.1111/jsr.12315
[Indexed for MEDLINE]
Free full text
Icon for Wiley
14.
Sleep Med. 2015 May;16(5):659-64. doi: 10.1016/j.sleep.2015.02.001. Epub 2015 Feb 7.

High-frequency heart rate variability during worry predicts stress-related increases in sleep disturbances.

Author information

1
Department of Psychology, Concordia University, 7141 Sherbrooke St W, Montréal H4B 1R6, Canada; Center for Clinical Research in Health, Concordia University, 7141 Sherbrooke St W, Montréal H4B 1R6, Canada; PERFORM Center, Concordia University, 7141 Sherbrooke St W, Montréal H4B 1R6, Canada. Electronic address: jp.gouin@concordia.ca.
2
Department of Psychology, Concordia University, 7141 Sherbrooke St W, Montréal H4B 1R6, Canada.
3
PERFORM Center, Concordia University, 7141 Sherbrooke St W, Montréal H4B 1R6, Canada; Center for Studies in Behavioral Neurobiology and Department of Exercise Science, Concordia University, 7141 Sherbrooke St W, Montréal H4B 1R6, Canada; Centre de Recherche de l'Institut Universitaire de Gériatrie de Montréal, 4545 chemin Queen-Mary, Montréal H3W 1W5, Canada.
4
Department of Psychology, Concordia University, 7141 Sherbrooke St W, Montréal H4B 1R6, Canada; Center for Clinical Research in Health, Concordia University, 7141 Sherbrooke St W, Montréal H4B 1R6, Canada; PERFORM Center, Concordia University, 7141 Sherbrooke St W, Montréal H4B 1R6, Canada; Center for Studies in Behavioral Neurobiology and Department of Exercise Science, Concordia University, 7141 Sherbrooke St W, Montréal H4B 1R6, Canada; Centre de Recherche de l'Institut Universitaire de Gériatrie de Montréal, 4545 chemin Queen-Mary, Montréal H3W 1W5, Canada.

Abstract

OBJECTIVE:

The aim of this study was to evaluate whether high-frequency heart rate variability (HF-HRV) during waking restfulness and during worry predicts increases in sleep disturbances in response to a stressful life event.

METHODS:

A longitudinal study following up 22 individuals from well-defined periods of lower and higher stress was conducted. HF-HRV during waking restfulness and in response to a worry induction was measured during a low-stress period. Sleep disturbances were assessed using the Pittsburgh Sleep Quality Index (PSQI) and the Insomnia Severity Index (ISI) during low-stress and high-stress periods.

RESULTS:

During both the low- and high-stress periods, lower HF-HRV during worry was associated with greater PSQI scores. Importantly, lower HF-HRV during the worry induction prospectively predicted greater increases in the PSQI score from the low-stress to the high-stress periods.

CONCLUSION:

HF-HRV during worry might represent an index of vulnerability to stress-induced sleep disturbances.

KEYWORDS:

Autonomic function; Heart rate variability; Insomnia; Stress; Worry

PMID:
25819418
DOI:
10.1016/j.sleep.2015.02.001
[Indexed for MEDLINE]
Icon for Elsevier Science
15.
Front Hum Neurosci. 2015 Feb 10;9:68. doi: 10.3389/fnhum.2015.00068. eCollection 2015.

Sleep spindles predict stress-related increases in sleep disturbances.

Author information

1
Department of Exercise Science, Concordia University , Montréal, QC , Canada ; Center for Studies in Behavioral Neurobiology, Concordia University , Montréal, QC , Canada ; PERFORM Center, Concordia University , Montréal, QC , Canada ; Centre de Recherche de l'Institut Universitaire de Gériatrie de Montréal , Montréal, QC , Canada ; Center for Clinical Research in Health, Concordia University , Montréal, QC , Canada ; Department of Psychology, Concordia University , Montréal, QC , Canada.
2
Department of Exercise Science, Concordia University , Montréal, QC , Canada ; Center for Studies in Behavioral Neurobiology, Concordia University , Montréal, QC , Canada ; PERFORM Center, Concordia University , Montréal, QC , Canada ; Centre de Recherche de l'Institut Universitaire de Gériatrie de Montréal , Montréal, QC , Canada.
3
Department of Psychology, Concordia University , Montréal, QC , Canada.
4
Physip SA , Paris , France.
5
PERFORM Center, Concordia University , Montréal, QC , Canada ; Center for Clinical Research in Health, Concordia University , Montréal, QC , Canada ; Department of Psychology, Concordia University , Montréal, QC , Canada.

Abstract

BACKGROUND AND AIM:

Predisposing factors place certain individuals at higher risk for insomnia, especially in the presence of precipitating conditions such as stressful life events. Sleep spindles have been shown to play an important role in the preservation of sleep continuity. Lower spindle density might thus constitute an objective predisposing factor for sleep reactivity to stress. The aim of this study was therefore to evaluate the relationship between baseline sleep spindle density and the prospective change in insomnia symptoms in response to a standardized academic stressor.

METHODS:

Twelve healthy students had a polysomnography recording during a period of lower stress at the beginning of the academic semester, along with an assessment of insomnia complaints using the insomnia severity index (ISI). They completed a second ISI assessment at the end of the semester, a period coinciding with the week prior to final examinations and thus higher stress. Spindle density, amplitude, duration, and frequency, as well as sigma power were computed from C4-O2 electroencephalography derivation during stages N2-N3 of non-rapid-eye-movement (NREM) sleep, across the whole night and for each NREM sleep period. To test for the relationship between spindle density and changes in insomnia symptoms in response to academic stress, spindle measurements at baseline were correlated with changes in ISI across the academic semester.

RESULTS:

Spindle density (as well as spindle amplitude and sigma power), particularly during the first NREM sleep period, negatively correlated with changes in ISI (p < 0.05).

CONCLUSION:

Lower spindle activity, especially at the beginning of the night, prospectively predicted larger increases in insomnia symptoms in response to stress. This result indicates that individual differences in sleep spindle activity contribute to the differential vulnerability to sleep disturbances in the face of precipitating factors.

KEYWORDS:

EEG; insomnia; sleep; spindles; stress

16.
PLoS One. 2014 Oct 30;9(10):e110748. doi: 10.1371/journal.pone.0110748. eCollection 2014.

Fasting enhances TRAIL-mediated liver natural killer cell activity via HSP70 upregulation.

Author information

1
Department of Gastroenterological and Transplant Surgery, Applied Life Sciences, Institute of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.
2
Department of Surgery, Hiroshima City Hospital, Hiroshima, Japan.

Abstract

Acute starvation, which is frequently observed in clinical practice, sometimes augments the cytolytic activity of natural killer cells against neoplastic cells. In this study, we investigated the molecular mechanisms underlying the enhancement of natural killer cell function by fasting in mice. The total number of liver resident natural killer cells in a unit weight of liver tissue obtained from C57BL/6J mice did not change after a 3-day fast, while the proportions of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)+ and CD69+ natural killer cells were significantly elevated (n = 7, p <0.01), as determined by flow cytometric analysis. Furthermore, we found that TRAIL- natural killer cells that were adoptively transferred into Rag-2-/- γ chain-/- mice could convert into TRAIL+ natural killer cells in fasted mice at a higher proportion than in fed mice. Liver natural killer cells also showed high TRAIL-mediated antitumor function in response to 3-day fasting. Since these fasted mice highly expressed heat shock protein 70 (n = 7, p <0.05) in liver tissues, as determined by western blot, the role of this protein in natural killer cell activation was investigated. Treatment of liver lymphocytes with 50 µg/mL of recombinant heat shock protein 70 led to the upregulation of both TRAIL and CD69 in liver natural killer cells (n = 6, p <0.05). In addition, HSP70 neutralization by intraperitoneally injecting an anti- heat shock protein 70 monoclonal antibody into mice prior to fasting led to the downregulation of TRAIL expression (n = 6, p <0.05). These findings indicate that acute fasting enhances TRAIL-mediated liver natural killer cell activity against neoplastic cells through upregulation of heat shock protein 70.

PMID:
25356750
PMCID:
PMC4214715
DOI:
10.1371/journal.pone.0110748
[Indexed for MEDLINE]
Free PMC Article
Icon for Public Library of Science Icon for PubMed Central
17.
Pathol Biol (Paris). 2014 Oct;62(5):262-9. doi: 10.1016/j.patbio.2014.05.013. Epub 2014 Aug 14.

Neuroimaging findings in primary insomnia.

Author information

1
Department of Exercise Science, Concordia University, 7141 Sherbrooke St W, Montreal, Quebec, H4B 1R6 Canada; Center for Studies in Behavioral Neurobiology, Concordia University, 7141 Sherbrooke St W, Montreal, Quebec, H4B 1R6 Canada.
2
Department of Psychology, Concordia University, 7141 Sherbrooke St W, Montreal, Quebec, H4B 1R6 Canada.
3
Department of Exercise Science, Concordia University, 7141 Sherbrooke St W, Montreal, Quebec, H4B 1R6 Canada; Center for Studies in Behavioral Neurobiology, Concordia University, 7141 Sherbrooke St W, Montreal, Quebec, H4B 1R6 Canada; Institut Universitaire de Gériatrie de Montréal, Université de Montréal, 4565, chemin Queen-Mary, Montreal, Quebec, H3W 1W5 Canada. Electronic address: tt.dangvu@concordia.ca.

Abstract

State-of-the-art neuroimaging techniques have accelerated progress in the study and understanding of sleep in humans. Neuroimaging studies in primary insomnia remain relatively few, considering the important prevalence of this disorder in the general population. This review examines the contribution of functional and structural neuroimaging to our current understanding of primary insomnia. Functional studies during sleep provided support for the hyperarousal theory of insomnia. Functional neuroimaging also revealed abnormalities in cognitive and emotional processing in primary insomnia. Results from structural studies suggest neuroanatomical alterations in primary insomnia, mostly in the hippocampus, anterior cingulate cortex and orbitofrontal cortex. However, these results are not well replicated across studies. A few magnetic resonance spectroscopy studies revealed abnormalities in neurotransmitter concentrations and bioenergetics in primary insomnia. The inconsistencies among neuroimaging findings on insomnia are likely due to clinical heterogeneity, differences in imaging and overall diversity of techniques and designs employed. Larger samples, replication, as well as innovative methodologies are necessary for the progression of this perplexing, yet promising area of research.

KEYWORDS:

Hyperactivation; Hyperarousal; Imagerie par résonance magnétique; Insomnia; Insomnie; Magnetic resonance imaging; Magnetic resonance spectroscopy; Neuroimagerie; Neuroimaging; Positron emission tomography; Single-photon emission computed tomography; Sleep; Sleep disorder; Sommeil; Spectroscopie en résonance magnétique nucléaire; Tomographie d’émission monophotonique; Tomographie par émission de positrons; Troubles du sommeil

PMID:
25129873
DOI:
10.1016/j.patbio.2014.05.013
[Indexed for MEDLINE]
Icon for Elsevier Science
18.
Front Psychol. 2013 Jul 25;4:474. doi: 10.3389/fpsyg.2013.00474. eCollection 2013.

Sleep and dreaming are for important matters.

Author information

1
Sleep Laboratory, Division of Neuropsychiatry, Department of Psychiatry, University Hospitals of Geneva Geneva, Switzerland ; Department of Neuroscience, University of Geneva Geneva, Switzerland ; Swiss Center for Affective Sciences, University of Geneva Geneva, Switzerland.

Abstract

Recent studies in sleep and dreaming have described an activation of emotional and reward systems, as well as the processing of internal information during these states. Specifically, increased activity in the amygdala and across mesolimbic dopaminergic regions during REM sleep is likely to promote the consolidation of memory traces with high emotional/motivational value. Moreover, coordinated hippocampal-striatal replay during NREM sleep may contribute to the selective strengthening of memories for important events. In this review, we suggest that, via the activation of emotional/motivational circuits, sleep and dreaming may offer a neurobehavioral substrate for the offline reprocessing of emotions, associative learning, and exploratory behaviors, resulting in improved memory organization, waking emotion regulation, social skills, and creativity. Dysregulation of such motivational/emotional processes due to sleep disturbances (e.g., insomnia, sleep deprivation) would predispose to reward-related disorders, such as mood disorders, increased risk-taking and compulsive behaviors, and may have major health implications, especially in vulnerable populations.

KEYWORDS:

creativity; dreaming; emotion; learning; memory; reward system; sleep

19.
Sleep. 2013 Jul 1;36(7):965-966.

Structural Brain Modifications in Primary Insomnia: Myth or Reality?

Author information

1
Department of Exercise Science and Center for Studies in Behavioral Neurobiology, Concordia University, Montreal, Canada.

Supplemental Content

Loading ...
Support Center