Sleep Initiation and Maintenance Disorders: Montplaisir J

Dang-Vu TT, Desseilles M, Petit D, Mazza S, Montplaisir J, Maquet P. · Cyclotron Research Centre B30, University of Liege - Sart Tilman, 4000 Liege, Belgium. · Sleep Med. · Pubmed #17470413 No free full text.

Abstract: The development of neuroimaging techniques has made possible the characterization of cerebral function throughout the sleep-wake cycle in normal human subjects. Indeed, human brain activity during sleep is segregated within specific cortical and subcortical areas in relation to the sleep stage, sleep physiological events and previous waking activity. This approach has allowed sleep physiological theories developed from animal data to be confirmed, but has also introduced original concepts about the neurobiological mechanisms of sleep, dreams and memory in humans. In contrast, at present, few neuroimaging studies have been dedicated to human sleep disorders. The available work has brought interesting data that describe some aspects of the pathophysiology and neural consequences of disorders such as insomnia, sleep apnea and narcolepsy. However, the interpretation of many of these results is restricted by limited sample size and spatial/temporal resolution of the employed technique. The use of neuroimaging in sleep medicine is actually restrained by concerns resulting from the technical experimental settings and the characteristics of the diseases. Nevertheless, we predict that future studies, conducted with state of the art techniques on larger numbers of patients, will be able to address these issues and contribute significantly to the understanding of the neural basis of sleep pathologies. This may finally offer the opportunity to use neuroimaging, in addition to the clinical and electrophysiological assessments, as a helpful tool in the diagnosis, classification, treatment and monitoring of sleep disorders in humans.

Montplaisir J. · Sleep Disorders Centre, University of Montreal, Montreal, Canada. · Sleep Med. · Pubmed #15301995 No free full text.

Abstract: Abnormal motor behaviors during sleep can be classified into four categories, ranging from myoclonic jerks to complex and integrated motor behaviors There have been recent developments in several of these conditions, in particular restless legs syndrome (RLS) and rapid-eye-movement sleep behavior disorder (RBD). RLS is one of the major causes of insomnia. Familial aggregation of RLS has been demonstrated by several groups, and molecular genetics studies have suggested the presence of susceptibility genes on chromosomes 12q and 14q. Pharmacologic and brain imaging studies suggest the involvement of dopaminergic mechanisms in RLS, but recent work has focused on brain iron metabolism. Studies indicate that RBD patients may eventually develop Parkinson's disease (PD). Conversely, RBD has been found in patients already diagnosed with PD. Single-photon emission computed tomography and positron emission tomography studies have shown a decrease in binding to presynaptic dopamine transporter in both idiopathic RBD and PD. Patients with RBD (associated or unassociated with PD) also have neuropsychological deficits. RBD may therefore represent the prodrome of a neurodegenerative disease leading to multiple system atrophy and Lewy body dementia. Understanding the underlying pathophysiology of abnormal sleep motor behaviors may prove useful in the management of insomnia.

Montplaisir J, Hawa R, Moller H, Morin C, Fortin M, Matte J, Reinish L, Shapiro CM. · Department of Psychiatry, University of Toronto, ECW-3D Bathurst Street, Toronto, Ontario M5T 2SB, Canada. · Hum Psychopharmacol. · Pubmed #12532313 No free full text.

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Gagnon JF, Montplaisir J, Bédard MA. · Centre d'étude du sommeil et des rythmes biologiques, Hôpital du Sacré-Coeur de Montréal, Québec, Canada. · Rev Neurol (Paris). · Pubmed #11965170 No free full text.

Abstract: During the past 10 years, there has been an increasing interest in the study of rapid-eye-movement (REM) sleep in neurodegenerative diseases and more particulary in Parkinson's disease (PD). This interest is justified by the strong association observed between these diseases and REM sleep behavior disorder (RBD). In the first section of this paper, a critical review of the literature on the presence of REM sleep disorders in PD is presented. Studies that show an association between PD and RBD are reviewed. Studies that report the presence of other REM sleep disorders in PD (short latency, abnormal length and/or proportion of REM sleep, increasing occurrence of hallucinations) are then discussed. Limitations of the criteria proposed by Rechtschaffen et Kales (1968) for the quantification of REM sleep are also presented. Some authors believe that dopaminergic (DA) agents used in the treatment of PD (levodopa, bromocriptine, pergolide, pramipexole and selegiline) could be a responsable factor for the occurence of REM sleep disorders observed in this disease. The literature concerning the impact of these DA agents on human REM sleep is therefore critically reviewed. It is concluded that DA agents cannot explain on their own the presence of REM sleep disorders in PD. Other causes, among which the disturbance of some neurochemical systems linked to the neuropathological process of the disease, must be considered in order to explain these REM sleep disorders. In the second section of this paper, we present the different pathophysiological hypotheses proposed to explain REM sleep disorders in PD, such as a dysfunction of the cholinergic, noradrenergic, serotonergic, dopaminergic or GABAergic neurons. Emphasis is placed on the role of cholinergic neurons of the pedunculopontine and laterodorsal tegmental nuclei, structures shown to be particularly impaired in PD. Neurophysiological, neuroanatomical and neuropharmacological studies demonstrate that these neurons are strongly implicated in the different REM sleep parameters (muscular atonia, electroencephalographic desynchronisation, ponto-geniculo-occipital spikes). Finally, future research directions are proposed.

Lanfranchi PA, Pennestri MH, Fradette L, Dumont M, Morin CM, Montplaisir J. · Department of Medicine, Division of Cardiology, Hôpital du Sacré-Coeur de Montréal and Université de Montréal, Québec, Canada. · Sleep. · Pubmed #19544752 No free full text.

Abstract: OBJECTIVE: To assess as whether insomniacs have higher nighttime blood pressure (BP) and a blunted day-to-night BP reduction, recognized markers of increased risk of cardiovascular morbidity and mortality. DESIGN: Prospective case-control study. SETTING: University hospital-based sleep research laboratory. PARTICIPANTS: Thirteen normotensive subjects with chronic primary insomnia (9 women, 42 +/- 7 y) and 13 sex- and age-matched good sleepers. MEASUREMENTS AND RESULTS: Subjects underwent 2-week sleep diary and 3 sleep studies to provide subjective and objective sleep variables, and 24-h beat-to-beat BP recording to provide daytime, night-time and day-to-night BP changes ([nighttime-daytime]/daytime)*100) (BP dipping). Spectral analysis of the electroencephalogram (EEG) was also performed during sleep of night 3 to assess EEG activity in the beta frequency (16-32 Hz), a measure of brain cortical activation. Nighttime SBP was higher (111 +/- 15 vs 102 +/- 12 mm Hg, P < 0.01) and day-to-night SBP dipping was lower (-8% +/- 6% vs -15% +/- 5%, P < 0.01) in insomniacs than good sleepers. Insomniacs also had higher activity in EEG beta frequency (P < 0.05). Higher nighttime SBP and smaller SBP dipping were independently associated with increased EEG beta activity (P < 0.05). CONCLUSIONS: Higher nighttime SBP and blunted day-to-night SBP dipping are present in normotensive subjects with chronic insomnia and are associated with a hyperactivity of the central nervous system during sleep. An altered BP profile in insomniacs could be one mechanism implicated in the link between insomnia and cardiovascular morbidity and mortality documented in epidemiological studies.

Laberge L, Petit D, Simard C, Vitaro F, Tremblay RE, Montplaisir J. · Centre d'étude du sommeil, Hôpital du Sacré-Coeur, Montréal, Québec, Canada. · J Sleep Res. · Pubmed #11285056 No free full text.

Abstract: This study examines the developmental changes of sleep patterns as a function of gender and puberty and assesses the prevalence of sleep habits and sleep disturbances in early adolescence. It also investigates the relationship between sleep patterns, sleep habits and difficulty falling asleep and nocturnal awakenings. The present analyses are based on results available for 588 boys and 558 girls for whom mothers completed questions concerning demographics and sleep at annual intervals when their child was aged 10--13 years. The results indicated that nocturnal sleep times decreased, bedtimes were delayed and differences between weekend and school day sleep schedules progressively increased with age. Gender and puberty were both associated with the timing of sleep on weekends. Girls presented longer weekend time in bed (TIB) and later weekend wake time than boys. Similarly, subjects with higher pubertal status showed longer weekend TIB and later weekend wake time than subjects with lower pubertal status. Difficulty falling asleep was associated with later weekend wake time and with sleeping with a night light. In conclusion, the gender differences commonly reported in adolescents' sleep patterns are most likely explained by girls' higher pubertal status. This study emphasizes the link between puberty and a putative physiological need for more sleep, in presence of a general reduction of sleep times during adolescence. From age 10--13 years, the delay and lengthening of the sleep period on weekends in comparison to schooldays is associated with difficulty falling asleep.

Montplaisir J. · No affiliation provided · CMAJ. · Pubmed #10976252 links to  free full text

This publication has no abstract.