Le somnambulisme est une parasomnie commune, caractérisée par des éveils incomplets lors des stades de sommeil lent, au cours desquels les individus atteints présentent des comportements moteurs d’une complexité variable accompagnés de confusion et d’un jugement altéré. La littérature actuelle suggère que ce trouble serait associé à des particularités de l’activité en ondes lentes et des oscillations lentes, deux indices de l’intégrité du processus homéostatique et de la profondeur du sommeil. Toutefois, en raison de certaines lacunes méthodologiques dans les études existantes, le rôle de ces marqueurs électroencéphalographiques dans la pathophysiologie du somnambulisme reste à éclaircir. Notre premier article a donc investigué d’éventuelles anomalies de l’activité en ondes lentes et des oscillations lentes chez les somnambules, en comparant leur sommeil au cours de la nuit entière à celui de participants contrôles. De plus, comme les somnambules semblent réagir différemment (en termes de fragmentation du sommeil notamment) des dormeurs normaux à une pression homéostatique accrue, nous avons comparé l’activité en ondes lentes et les oscillations lentes en nuit de base et suite à une privation de sommeil de 38 heures. Les résultats de nos enregistrements électroencéphalographiques chez 10 somnambules adultes et neuf participants contrôles montrent une élévation de la puissance spectrale de l’activité en ondes lentes et de la densité des oscillations lentes en nuit de récupération par rapport à la nuit de base pour nos deux groupes. Toutefois, contrairement à plusieurs études précédentes, nous ne n’observons pas de différence entre somnambules et dormeurs normaux quant à l’activité en ondes lentes et aux oscillations lentes pour aucune des deux nuits. Au-delà ce certaines considérations méthodologiques ayant pu contribuer à ce résultat inattendu, nous croyons qu’il justifie un questionnement sur l’hétérogénéité des somnambules comme population. Notre deuxième article s’est penché sur les facteurs électroencéphalographiques transitoires susceptibles d’être associés au déclenchement des épisodes de somnambulisme. Nous avons comparé les fluctuations d’activité en ondes lentes et des oscillations lentes dans les minutes avant des épisodes de somnambulisme spontanés (c.a.d.: non associés à un stimulus identifiable) à celles survenant avant des éveils normaux comparables chez 12 somnambules adultes. Nous montrons que, comparativement aux éveils normaux, les épisodes de somnambulisme sont précédés d’un sommeil plus profond, tel qu’indiqué par une plus grande densité spectrale de l’activité en ondes lentes et une plus grande densité des oscillations lentes. Cet approfondissement du sommeil, spécifique aux épisodes de somnambulisme, semble survenir sur un laps de temps relativement long (>3 minutes), et non abruptement au cours des secondes précédant l’épisode. Ces données ouvrent un questionnement quant aux mécanismes en jeu dans la survenue des épisodes de somnambulisme spontanés. Globalement, cette thèse suggère que des phénomènes liés à l’activité en ondes lentes et aux oscillations lentes seraient liés au déclenchement des épisodes de somnambulisme, mais que des études supplémentaires devront être menées afin de délimiter le rôle précis que ces marqueurs jouent dans la pathophysiologie du somnambulisme. / Sleepwalking is a common parasomnia characterized by sudden but incomplete arousals out of non-rapid eye movement sleep during which predisposed individuals display motor behaviours of various complexity, accompanied by mental confusion and altered judgement. A growing body of evidence suggests that this condition could be associated with atypical patterns in slow wave activity and slow oscillations, both markers of the integrity of the homeostasis process and of sleep intensity. However, due to methodological limitations in past studies, the role of these electroencephalographic markers in the pathophysiology of sleepwalking remains unclear. Our first article aimed at describing slow wave activity and slow oscillations abnormalities in sleepwalkers by comparing whole night sleep in 10 adult sleepwalkers and 9 control participants. In addition, since past studies have shown that increased homeostatic pressure has differential effects on sleepwalkers versus normal controls (e.g., in terms of sleep fragmentation), we compared slow wave activity and slow oscillations during baseline sleep and recovery sleep after 38 hours of sleep deprivation in patients and controls. Results show that sleep deprivation increases slow wave activity power density and slow oscillations density in both groups. However, contrary to our predictions, no group differences were noted on any of the two nights on slow wave activity or slow oscillations. Beyond methodological considerations which may partially account for this unexpected result, this study opens questions as to the homogeneity of sleepwalkers as a clinical population. Our second study focused on transient electroencephalographic fluctuations that may be associated with the onset of sleepwalking episodes. We compared slow wave activity and slow oscillations fluctuations in the moments leading up to spontaneous (that is, occurring without an identifiable internal or external stimuli) somnambulistic episodes recorded in the sleep laboratory in 12 adult sleepwalkers and comparing these patterns to those observed prior to non-behavioural awakenings observed in the same patients. We showed that when compared to non-behavioural awakenings from the same sleep stage and sleep period, somnambulistic episodes were preceded by deeper sleep, as indicated by higher slow wave activity power density and slow oscillations density. This deepening of sleepwalkers’ sleep occurs over a relatively long period of time (>3 minutes) before the episode, rather than abruptly in the seconds preceding episode onset. These findings raise key questions about fundamental mechanisms involved in the occurrence of spontaneously recorded somnambulistic episodes. Taken as a whole, the results from the work presented in this thesis show that electrophysiological processes related to slow wave activity and slow oscillations play a role in the occurrence of somnambulistic episodes. However, the functional significance of these electroencephalographic markers in the pathophysiology of sleepwalking remains to be clarified.

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Diverses études se sont penchées sur les paramètres EEG du sommeil en ondes lentes, y compris l’activité en ondes lentes en lien avec le somnambulisme, mais les résultats se révèlent inconsistants et contradictoires. Le premier objectif de la présente étude était d’analyser quantitativement l’EEG en sommeil en mesurant les fluctuations de puissance spectrale en delta (1-4 Hz) et delta lent (0.5-1 Hz) avant des épisodes de somnambulisme. Le second était de détecter les oscillations lentes (> 75 μV, fréquence d'environ 0.7-0.8 Hz) et très lentes (> 140 μV, fréquence d'environ 0.7-0.8 Hz) afin d'examiner leur changement d'amplitude et de densité avant de tels épisodes. Suite à une privation de sommeil de 25 heures, les enregistrements polysomnographiques de 22 adultes atteints de somnambulisme ont été scrutés. L’analyse des 200 secondes avant les épisodes révèle que ceux-ci ne sont pas précédés d’une augmentation graduelle de puissance spectrale en delta ni en delta lent, tant sur les dérivations frontale, centrale que pariétale. Toutefois, une hausse statistiquement significative de la densité des oscillations lentes et des oscillations très lentes a été observée au cours des 20 sec immédiatement avant le début des épisodes. Reste à déterminer le rôle exact de ces paramètres de l’EEG en sommeil par rapport à la manifestation et au diagnostic des parasomnies en sommeil lent. / Several studies have investigated slow-wave sleep EEG parameters, including slow-wave activity (SWA) in relation to somnambulism, but results have been both inconsistent and contradictory. The first goal of the present study was to conduct a quantitative analysis of sleepwalkers’ sleep EEG by studying fluctuations in spectral power for delta (1-4 Hz) and slow delta (0.5-1 Hz) before the onset of somnambulistic episodes. A secondary aim was to detect slow wave oscillations to examine their changes in amplitude and density prior to behavioral episodes of somnambulism. Twenty-two adult sleepwalkers were investigated polysomnographically following 25 h of sleep deprivation. Analysis of patients’ sleep EEG over the 200 sec prior to the episodes’ onset revealed that the episodes were not preceded by a gradual increase in spectral power for either delta or slow delta over frontal, central, or parietal leads. However, time course comparisons revealed significant changes in the density of slow and very slow wave oscillations, with significant increases occurring during the final 20 sec immediately preceding episode onset. The specificity of these sleep EEG parameters for the occurrence and diagnosis of NREM parasomnias remains to be determined.

INTRODUÇÃO: Os Movimentos Periódicos dos Membros (PLM) são movimentos repetitivos, estereotipados, que ocorrem principalmente nos membros inferiores e associam-se freqüentemente à Síndrome das Pernas Inquietas (SPI), na qual os pacientes relatam necessidade de mover os membros, geralmente associada a desconforto que pode ser exacerbado com a inatividade e piora no fim da tarde ou à noite. PLM são relatados em pacientes com lesão medular, indicando um componente medular da desordem. Neste trabalho, PLM e SPI são analisados em pacientes com lesão medular. MÉTODOS: Neste estudo observacional realizado entre novembro de 2007 e novembro de 2008, comparou-se achados polissonográficos, Escala de Sonolência de Epworth, Questionário de Síndrome das Pernas Inquietas, entre 2 grupos de indivíduos com idade de 18 a 40 anos, sem outros distúrbios de sono: Grupo Controle (GC) e Grupo Lesão Medular (LM). RESULTADOS: LM contou com 9 homens e GC tinha 8 homens e 8 mulheres. Não houve diferença significativa entre as idades de cada grupo: LM com 28 ±7,382 anos e CG com 24,38 ± 4,031 anos. O grupo LM caracterizou-se por 3 lesões cervicais ASIA A, 5 lesões torácicas A e 1 lesão torácica B avaliados através da avaliação American Spinal Cord Injury Association ASIA, com tempo de lesão variando de 1 ano e 1 mês a 5 anos e 2 meses, com mediana de 4, 615 anos; as causas de lesão medular foram acidente de motocicleta (86,44%), mergulho (6,78%) e queda de bicicleta (6,78%). 77,80% de LM apresenta Movimentos Periódicos dos Membros (PLM) em comparação com 31,30% de GC (p=0,04; IC95% = 1,2-51,2). Não houve diferença significativa na gravidade de PLM entre os grupos (p>0,05). Em LM, não houve diferença significativa entre PLM índex NREM e PLM índex REM (p= 0,05). Na avaliação de sonolência, não houve diferença significativa entre os grupos (p>0,05); não houve correlação entre PLM e sonolência excessiva diurna (r= 0,02). LM apresentou 100% de frequência de SPI contra 17% de GC (p < 0,0001). Não houve diferença significativa entre os grupos na gravidade da SPI (p>0,05). Em relação ao número de microdespertares, não houve diferença significativa entre os grupos (p>0,05). Não houve diferença significativa entre os grupos na comparação de eficiência de sono (p>0,05), porém o subgrupo dos tetraplégicos de LM apresentou 9,97±2,17 minutos de tempo de latência enquanto o GC apresentou 3,65±2,43 minutos (p=0,01). CONCLUSÕES: a SPI e o PLM são mais frequentes em lesados medulares que na população em idade de 18 a 40 anos sem outros distúrbios de sono associados, o que pode sugerir que PLM e SPI estejam relacionados ao Centro Gerador de Padrão Medular. / INTRODUCTION: The Periodic Leg Movements (PLM) are repetitive, stereotyped movements that occur mainly in legs and are frequently associated to Restless Legs Syndrome (RLS) in which patients refer the need to move the limbs, usually associated to discomfort that might worse with inactivity and worse in the evening or night. PLM are reported in patients with spinal cord injury thus indicating a spinal component in the disorder. In this research PLM were analyzed in spinal cord injury patients. METHODS: In this observation study performed from November 2007 to November 2008, polysomnographic findings, Epworth Sleepiness Scale Score and an adapted form of International Restless Legs Syndrome Scale Score were compared between 2 groups formed by 18 to 40 years old volunteers without any other sleep disturbances: Control Group (CG) and Spinal Cord Injury Group (SCIG). RESULTS: The SCIG was composed by 9 men and the CG was composed by 8 men and 8 women. There was no statistically significant difference in ages of each group: SCIG 28 ±7,382 years and CG 24,38 ± 4,031 years. The SCGI group was characterized by 3 A cervical spinal cord injury (SCI), 5 A thoracic SCI and 1 B thoracic SCI classified according to American Spinal Cord Injury Association (ASIA) evaluation, presenting from 1 year and 1 month to 5 years and 2 months of injury time, with median of 4,615 years. The SCI were caused by motorcycle accident (86,44%), shallow water diving (6,78%) and bicycle fall (6,78%). In SCIG 77,80% presented PLM while 31,30% presented PLM in CG (p=0,041; CI95% = 1,2-51,2). There wasn´t significant difference in PLM severity between groups (p>0,05). In SCIG there wasn´t significant difference between PLM index NREM and PLM index REM (p>0,05). There wasn´t correlation between PLM and excessive diurnal somnolence (r=0,02). SCGI presented 100% of RLS comparing to 17% in CG (p < 0,0001). There was no significant difference in RLS severity between groups (p>0,05). There was no significant difference in arousal index between groups (p>0,05).There was no significant difference in sleep efficiency (p>0,05), however the subgroup of tetraplegic patients in SCIG presented 9,97±2,17 minutes while CG presented 3,65±2,43 minutes of sleep onset time (p=0,01). CONCLUSIONS: RLS and SPI are more recurrent in SCI patients than in general population from 18 to 40 years old without any other sleep disturbances. This might suggest that PLM and RLS are related to Spinal Cord Central Pattern Generator.

INTRODUÇÃO: Os Movimentos Periódicos dos Membros (PLM) são movimentos repetitivos, estereotipados, que ocorrem principalmente nos membros inferiores e associam-se freqüentemente à Síndrome das Pernas Inquietas (SPI), na qual os pacientes relatam necessidade de mover os membros, geralmente associada a desconforto que pode ser exacerbado com a inatividade e piora no fim da tarde ou à noite. PLM são relatados em pacientes com lesão medular, indicando um componente medular da desordem. Neste trabalho, PLM e SPI são analisados em pacientes com lesão medular. MÉTODOS: Neste estudo observacional realizado entre novembro de 2007 e novembro de 2008, comparou-se achados polissonográficos, Escala de Sonolência de Epworth, Questionário de Síndrome das Pernas Inquietas, entre 2 grupos de indivíduos com idade de 18 a 40 anos, sem outros distúrbios de sono: Grupo Controle (GC) e Grupo Lesão Medular (LM). RESULTADOS: LM contou com 9 homens e GC tinha 8 homens e 8 mulheres. Não houve diferença significativa entre as idades de cada grupo: LM com 28 ±7,382 anos e CG com 24,38 ± 4,031 anos. O grupo LM caracterizou-se por 3 lesões cervicais ASIA A, 5 lesões torácicas A e 1 lesão torácica B avaliados através da avaliação American Spinal Cord Injury Association ASIA, com tempo de lesão variando de 1 ano e 1 mês a 5 anos e 2 meses, com mediana de 4, 615 anos; as causas de lesão medular foram acidente de motocicleta (86,44%), mergulho (6,78%) e queda de bicicleta (6,78%). 77,80% de LM apresenta Movimentos Periódicos dos Membros (PLM) em comparação com 31,30% de GC (p=0,04; IC95% = 1,2-51,2). Não houve diferença significativa na gravidade de PLM entre os grupos (p>0,05). Em LM, não houve diferença significativa entre PLM índex NREM e PLM índex REM (p= 0,05). Na avaliação de sonolência, não houve diferença significativa entre os grupos (p>0,05); não houve correlação entre PLM e sonolência excessiva diurna (r= 0,02). LM apresentou 100% de frequência de SPI contra 17% de GC (p < 0,0001). Não houve diferença significativa entre os grupos na gravidade da SPI (p>0,05). Em relação ao número de microdespertares, não houve diferença significativa entre os grupos (p>0,05). Não houve diferença significativa entre os grupos na comparação de eficiência de sono (p>0,05), porém o subgrupo dos tetraplégicos de LM apresentou 9,97±2,17 minutos de tempo de latência enquanto o GC apresentou 3,65±2,43 minutos (p=0,01). CONCLUSÕES: a SPI e o PLM são mais frequentes em lesados medulares que na população em idade de 18 a 40 anos sem outros distúrbios de sono associados, o que pode sugerir que PLM e SPI estejam relacionados ao Centro Gerador de Padrão Medular. / INTRODUCTION: The Periodic Leg Movements (PLM) are repetitive, stereotyped movements that occur mainly in legs and are frequently associated to Restless Legs Syndrome (RLS) in which patients refer the need to move the limbs, usually associated to discomfort that might worse with inactivity and worse in the evening or night. PLM are reported in patients with spinal cord injury thus indicating a spinal component in the disorder. In this research PLM were analyzed in spinal cord injury patients. METHODS: In this observation study performed from November 2007 to November 2008, polysomnographic findings, Epworth Sleepiness Scale Score and an adapted form of International Restless Legs Syndrome Scale Score were compared between 2 groups formed by 18 to 40 years old volunteers without any other sleep disturbances: Control Group (CG) and Spinal Cord Injury Group (SCIG). RESULTS: The SCIG was composed by 9 men and the CG was composed by 8 men and 8 women. There was no statistically significant difference in ages of each group: SCIG 28 ±7,382 years and CG 24,38 ± 4,031 years. The SCGI group was characterized by 3 A cervical spinal cord injury (SCI), 5 A thoracic SCI and 1 B thoracic SCI classified according to American Spinal Cord Injury Association (ASIA) evaluation, presenting from 1 year and 1 month to 5 years and 2 months of injury time, with median of 4,615 years. The SCI were caused by motorcycle accident (86,44%), shallow water diving (6,78%) and bicycle fall (6,78%). In SCIG 77,80% presented PLM while 31,30% presented PLM in CG (p=0,041; CI95% = 1,2-51,2). There wasn´t significant difference in PLM severity between groups (p>0,05). In SCIG there wasn´t significant difference between PLM index NREM and PLM index REM (p>0,05). There wasn´t correlation between PLM and excessive diurnal somnolence (r=0,02). SCGI presented 100% of RLS comparing to 17% in CG (p < 0,0001). There was no significant difference in RLS severity between groups (p>0,05). There was no significant difference in arousal index between groups (p>0,05).There was no significant difference in sleep efficiency (p>0,05), however the subgroup of tetraplegic patients in SCIG presented 9,97±2,17 minutes while CG presented 3,65±2,43 minutes of sleep onset time (p=0,01). CONCLUSIONS: RLS and SPI are more recurrent in SCI patients than in general population from 18 to 40 years old without any other sleep disturbances. This might suggest that PLM and RLS are related to Spinal Cord Central Pattern Generator.

Les cauchemars sont des rêves très dysphoriques, bien remémorés au réveil, dont le contenu est souvent caractérisé par la présence de menace à la survie, la sécurité ou l’intégrité physique. Les cauchemars surviendraient surtout durant le sommeil paradoxal. Bien qu’il s’agisse pour la plupart des gens d’une expérience rare et bénigne, il est de plus en plus apparent que les cauchemars entretiennent des liens avec la psychopathologie. Plusieurs populations psychiatriques ont une fréquence des cauchemars supérieure à la population générale. Au-delà d’être simplement associés à la psychopathologie, les cauchemars peuvent par exemple prédire le développement du trouble de stress post-traumatique, constituer un facteur de risque pour le suicide, ou amplifier des difficultés de régulation émotionnelle. Ainsi, les cauchemars peuvent être pertinents pour la clinique. Malgré cela, leur pathophysiologie demeure un sujet peu exploré. Plus spécifiquement, il existe peu de recherche portant sur leurs corrélats neuronaux. Selon le modèle neurocognitif des cauchemars, les cauchemars constitueraient un échec de la fonction normale des rêves, qui serait d’aider à la régulation émotionnelle en mêlant le contenu de mémoires émotionnellement négatives à celui d’autres mémoires plus neutres, permettant ainsi l’extinction de ces mémoires négatives. La fonction du rêve, et donc la présence de cauchemars, reposerait sur un réseau limbique-préfrontal composé du cortex préfrontal médian et cingulaire antérieur, de l’hippocampe et de l’amygdale. L’objectif de cette thèse est d’étudier les mécanismes cérébraux potentiellement impliqués dans les cauchemars de manière à tester le modèle neurocognitif des cauchemars. Dans une première étude, nous avons utilisé l’analyse spectrale pour comparer l’activité EEG à l’éveil et durant le sommeil entre 18 participants rapportant des cauchemars fréquents et 15 participants contrôles. Les résultats démontrent davantage d’activité 2-5Hz à l’éveil, en sommeil lent et en sommeil paradoxal, principalement aux électrodes centrales et frontales, chez les participants avec cauchemars comparativement aux participants contrôles. Ces résultats étaient plus apparents en sommeil paradoxal. Ces résultats répliquent partiellement une étude antérieure démontrant une activité 3-4Hz plus importante pour des participants avec cauchemars que des contrôles. L’apport original de l’étude réside surtout dans sa démonstration d’altérations de l’activité EEG visibles autant durant l’éveil que durant le sommeil, ce qui constitue un appui à la continuité éveil-sommeil avancée par le modèle neurocognitif des cauchemars. Dans une deuxième étude, nous avons utilisé la tomographie par émission monophotonique pour enregistrer le flux sanguin cérébral régional (une mesure indirecte de l’activité neuronale) de 18 participants avec cauchemars fréquents durant le visionnement d’images émotionnellement négatives ou neutres. Les résultats démontrent que la sévérité des cauchemars est associée négativement au FSCr de régions inclues dans le modèle neurocognitif (cortex cingulaire antérieur et préfrontal médian), mais aussi d’autres régions corticales (frontales, temporales, insula). En résumé, cette thèse apporte un appui partiel au modèle neurocognitif des cauchemars, mais souligne également certaines limites du modèle et propose de nouvelles avenues de recherche pour comprendre les mécanismes neuronaux des cauchemars. Cette thèse souligne aussi des implications cliniques à l’étude des corrélats neuronaux des cauchemars, notamment par rapport à la compréhension des traitements (pharmacologiques ou non-pharmacologiques). / Nightmares are defined as highly dysphoric dreams that are well-remembered upon awakening, frequently involving threats to survival, security or physical integrity. They are thought to happen most frequently during rapid eye movement sleep. For most people, nightmares are a rare occurrence and are mostly benign. However, research shows that nightmares are linked to psychopathology. Many psychiatric populations have an elevated nightmare frequency compared to the general population. In addition to being associated with psychopathology, nightmares can for example predict the development of post-traumatic stress disorder, be a risk factor for suicide, or diminish emotional regulation capabilities. Therefore, nightmares can be relevant to clinical practice. However, research about their pathophysiology is lacking. More specifically, there is a lack of research on the neural correlates of nightmares. According to the neurocognitive model of nightmares, nightmares are a breakdown of the normal function of dreams. Dreams are thought to help emotional regulation by combining emotionally negative memories with more neutral memories, thereby extinguishing these negative memories. The function of dreams, and therefore the occurrence of nightmares, is thought to be supported by a limbic-prefrontal circuit comprising medial prefrontal and anterior cingulate cortices, hippocampus, and amygdala. The aim of this dissertation is to study brain mechanisms involved in nightmares, thereby testing the neurocognitive model of nightmares. In study 1, we used spectral analysis to compare EEG activity in wake and sleep between 18 frequent nightmare recallers and 15 control participants. The results show higher 2-5Hz activity during wake, non-REM and REM sleep, mainly for central and frontal derivations, for frequent nightmare recallers compared to controls. Differences were most apparent for REM sleep. These results partly replicate past work showing heightened 3-4Hz activity in frequent nightmare recallers compared to controls. It improves upon past work by demonstrating cross-state alterations of EEG activity, thereby supporting the cross-state continuity assumption of the neurocognitive model of nightmares. In study 2, we used single photon emission tomography to obtain regional cerebral blood flow (an indirect measure of neuronal activity) from 18 frequent nightmare recallers while they were viewing pictures with a negative or neutral emotional valence. Results demonstrate that the severity of nightmares is negatively associated with brain regions included (medial prefrontal and anterior cingulate cortices) and not included (frontal, temporal and insular regions) in the neurocognitive model of nightmares. In sum, this dissertation offers partial support to the neurocognitive model of nightmares, while also highlighting limits of the model and proposing ideas for future investigations on the neural correlates of nightmares. This dissertation also discusses some clinical implications of the study of the neural correlates of nightmares, most importantly providing a better understanding of nightmare-reducing treatments (pharmacological or non-pharmacological).