967 resultados para Électroencéphalographie (EEG)


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Subjects with autism often show language difficulties, but it is unclear how they relate to neurophysiological anomalies of cortical speech processing. We used combined EEG and fMRI in 13 subjects with autism and 13 control participants and show that in autism, gamma and theta cortical activity do not engage synergistically in response to speech. Theta activity in left auditory cortex fails to track speech modulations, and to down-regulate gamma oscillations in the group with autism. This deficit predicts the severity of both verbal impairment and autism symptoms in the affected sample. Finally, we found that oscillation-based connectivity between auditory and other language cortices is altered in autism. These results suggest that the verbal disorder in autism could be associated with an altered balance of slow and fast auditory oscillations, and that this anomaly could compromise the mapping between sensory input and higher-level cognitive representations.

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A variety of technologies have been developed to assist decision-making during the management of patients with acute brain injury who require intensive care. A large body of research has been generated describing these various technologies. The Neurocritical Care Society (NCS) in collaboration with the European Society of Intensive Care Medicine (ESICM), the Society for Critical Care Medicine (SCCM), and the Latin America Brain Injury Consortium (LABIC) organized an international, multidisciplinary consensus conference to perform a systematic review of the published literature to help develop evidence-based practice recommendations on bedside physiologic monitoring. This supplement contains a Consensus Summary Statement with recommendations and individual topic reviews on physiologic processes important in the care of acute brain injury. In this article we provide the evidentiary tables for select topics including systemic hemodynamics, intracranial pressure, brain and systemic oxygenation, EEG, brain metabolism, biomarkers, processes of care and monitoring in emerging economies to provide the clinician ready access to evidence that supports recommendations about neuromonitoring.

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Although neuroimaging research has evidenced specific responses to visual food stimuli based on their nutritional quality (e.g., energy density, fat content), brain processes underlying portion size selection remain largely unexplored. We identified spatio-temporal brain dynamics in response to meal images varying in portion size during a task of ideal portion selection for prospective lunch intake and expected satiety. Brain responses to meal portions judged by the participants as 'too small', 'ideal' and 'too big' were measured by means of electro-encephalographic (EEG) recordings in 21 normal-weight women. During an early stage of meal viewing (105-145ms), data showed an incremental increase of the head-surface global electric field strength (quantified via global field power; GFP) as portion judgments ranged from 'too small' to 'too big'. Estimations of neural source activity revealed that brain regions underlying this effect were located in the insula, middle frontal gyrus and middle temporal gyrus, and are similar to those reported in previous studies investigating responses to changes in food nutritional content. In contrast, during a later stage (230-270ms), GFP was maximal for the 'ideal' relative to the 'non-ideal' portion sizes. Greater neural source activity to 'ideal' vs. 'non-ideal' portion sizes was observed in the inferior parietal lobule, superior temporal gyrus and mid-posterior cingulate gyrus. Collectively, our results provide evidence that several brain regions involved in attention and adaptive behavior track 'ideal' meal portion sizes as early as 230ms during visual encounter. That is, responses do not show an increase paralleling the amount of food viewed (and, in extension, the amount of reward), but are shaped by regulatory mechanisms.

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PURPOSE: To investigate current practices and timing of neurological prognostication in comatose cardiac arrest patients. METHODS: An anonymous questionnaire was distributed to the 8000 members of the European Society of Intensive Care Medicine during September and October 2012. The survey had 27 questions divided into three categories: background data, clinical data, decision-making and consequences. RESULTS: A total of 1025 respondents (13%) answered the survey with complete forms in more than 90%. Twenty per cent of respondents practiced outside of Europe. Overall, 22% answered that they had national recommendations, with the highest percentage in the Netherlands (>80%). Eighty-nine per cent used induced hypothermia (32-34 °C) for comatose cardiac arrest patients, while 11% did not. Twenty per cent had separate prognostication protocols for hypothermia patients. Seventy-nine per cent recognized that neurological examination alone is not enough to predict outcome and a similar number (76%) used additional methods. Intermittent electroencephalography (EEG), brain computed tomography (CT) scan and evoked potentials (EP) were considered most useful. Poor prognosis was defined as cerebral performance category (CPC) 3-5 (58%) or CPC 4-5 (39%) or other (3%). When prognosis was considered poor, 73% would actively withdraw intensive care while 20% would not and 7% were uncertain. CONCLUSION: National recommendations for neurological prognostication after cardiac arrest are uncommon and only one physician out of five uses a separate protocol for hypothermia treated patients. A neurological examination alone was considered insufficient to predict outcome in comatose patients and most respondents advocated a multimodal approach: EEG, brain CT and EP were considered most useful. Uncertainty regarding neurological prognostication and decisions on level of care was substantial.

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NlmCategory="UNASSIGNED">Sleep and sleep disorders are complex and highly variable phenotypes regulated by many genes and environment. The catechol-O-methyltransferase (COMT) gene is an interesting candidate, being one of the major mammalian enzymes involved in the catabolism of catecholamines. The activity of COMT enzyme is genetically polymorphic due to a guanine-to-adenine transition at codon 158, resulting in a valine (Val) to methionine (Met) substitution. Individuals homozygous for the Val allele show higher COMT activity, and lower dopaminergic signaling in prefrontal cortex (PFC) than subjects homozygous for the Met allele. Since COMT has a crucial role in metabolising dopamine, it was suggested that the common functional polymorphism in the COMT gene impacts on cognitive function related to PFC, sleep-wake regulation, and potentially on sleep pathologies. The COMT Val158Met polymorphism may predict inter-individual differences in brain electroencephalography (EEG) alpha oscillations and recovery processes resulting from partial sleep loss in healthy individuals. The Val158Met polymorphism also exerts a sexual dimorphism and has a strong effect on objective daytime sleepiness in patients with narcolepsy-cataplexy. Since the COMT enzyme inactivates catecholamines, it was hypothesized that the response to stimulant drugs differs between COMT genotypes. Modafinil maintained executive functioning performance and vigilant attention throughout sleep deprivation in subjects with Val/Val genotype, but less in those with Met/Met genotype. Also, homozygous Met/Met patients with narcolepsy responded to lower doses of modafinil compared to Val/Val carriers. We review here the critical role of the common functional COMT gene polymorphism, COMT enzyme activity, and the prefrontal dopamine levels in the regulation of sleep and wakefulness in normal subjects, in narcolepsy and other sleep-related disorders, and its impact on the response to psychostimulants.

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Since the discovery of hypocretins/orexins (Hcrt/Ox) in 1998, several narcoleptic mouse models, such as Hcrt-KO, Hcrtrl-KO, Hcrtr2-KO and double receptors KO mice, and orexin-ataxin transgenic mice were generated. The available Hcrt mouse models do not allow the dissection of the specific role of Hcrt in each target region. Dr. Anne Vassalli generated loxP-flanked alleles for each Hcrt receptor, which are manipulated by Cre recombinase to generate mouse lines with disrupted Hcrtrl or Hcrtr2 (or both) in cell type-specific manner. The role of noradrenaline (NA) and dopamine (OA) in ttie regulation of vigilance states is well documented. The purpose of this thesis is to explore the role of the Hcrt input into these two monoaminergic systems. Chronic loss of Hcrtrl in NA neurons consolidated paradoxical sleep (PS), and altered wakefulness brain activity in baseline, during the sleep deprivation (SD), and when mice were challenged by a novel environment, or exposed to nest-building material. The analysis of alterations in the sleep EEG delta power showed a consistent correlation with the changes in the preceding waking quality in these mice. Targeted inactivation of Hcrt input into DA neurons showed that Hcrtr2 inactivation present the strongest phenotype. The loss of Hcrtr2 in DA neurons caused modified brain activities in spontaneous wakefulness, during SD, and in novel environmental conditions. In addition to alteration of wakefulness quality and quantity, conditional inactivation of Hcrtr2 in DA neurons caused an increased in time spent in PS in baseline and a delayed and less complete PS recovery after SD. In the first 30 min of sleep recovery, single (i.e. for Hcrtrl or Hcrtr2) conditional knockout receptor mice had opposite changes in delta activity, including an increased power density in the fast delta range with specific inactivation of Hcrtr2, but a decreased power density in the same range with specific inactivation of Hcrtrl in DA cells. These studies demonstrate a complex impact of Hcrt receptors signaling in both NA and DA system, not only on quantity and quality of wakefulness, but also on PS amount regulation as well as on SWS delta power expression. -- Depuis la découverte des hypocrétines/orexines (Hcrt/Ox) en 1998, plusieurs modèles de souris, narcoleptiques telles que Hcrt-KO, Hcrtr2-KO et récepteurs doubles KO et les souris transgéniques orexine-ataxine ont été générés. Les modèles de souris Hcrt disponibles ne permettaient pas la dissection du rôle spécifique de l'Hcrt dans chaque noyau neuronal cible. Notre laboratoire a généré des allèles loxP pour chacun des 2 gènes codant pour les récepteurs Hcrtr, qui sont manipulés par recombinase Cre pour générer des lignées de souris avec Hcrtrl inactivé, ou Hcrtr2 inactivé, (ou les deux), spécifiquement dans un type cellulaire particulier. Le rôle de la noradrénaline (NA) et la dopamine (DA) dans la régulation des états de vigilance est bien documentée. Le but de cette thèse est d'étudier le rôle de l'afférence Hcrt dans ces deux systèmes monoaminergiques au niveau de l'activité cérébrale telle qu'elle apparaît dans l'électroencéphalogramme (EEG). Mon travail montre que la perte chronique de Hcrtrl dans les neurones NA consolide le sommeil paradoxal (PS), et l'activité cérébrale de l'éveil est modifiée en condition spontanée, au cours d'une experience de privation de sommeil (SD), et lorsque les souris sont présentées à un nouvel environnement, ou exposées à des matériaux de construction du nid. Ces modifications de l'éveil sont corrélées à des modifications de puissance de l'activité delta du sommeil lent qui le suit. L'inactivation ciblée des Hcrtrs dans les neurones DA a montré que l'inactivation Hcrtr2 conduit au phénotype le plus marqué. La perte de Hcrtr2 dans les neurones DA mène à des modification d'activité cérébrale en éveil spontané, pendant SD, ainsi que dans des conditions environnementales nouvelles. En plus de l'altération de la qualité de l'éveil et de la quantité, l'inactivation conditionnelle de Hcrtr2 dans les neurones DA a provoqué une augmentation du temps passé en sommeil paradoxal (PS) en condition de base, et une reprise retardée et moins complète du PS après SD. Dans les 30 premières minutes de la récupération de sommeil, les modèles inactivés pour un seul des récepteurs (ie pour Hcrtrl ou Hcrtr2 seulement) montrent des changements opposés en activité delta, en particulier une densité de puissance accrue dans le delta rapide avec l'inactivation spécifique de Hcrtr2, mais une densité de puissance diminuée dans cette même gamme chez les souris inactivées spécifiquement en Hcrtrl dans les neurones DA. Ces études démontrent un impact complexe de l'inactivation de la neurotransmission au niveau des récepteurs d'Hcrt dans les deux compartiments NA et DA, non seulement sur la quantité et la qualité de l'éveil, mais aussi sur la régulation de quantité de sommeil paradoxal, ainsi que sur l'expression de la puissance delta pendant le sommeil lent.

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The Commission on Classification and Terminology and the Commission on Epidemiology of the International League Against Epilepsy (ILAE) have charged a Task Force to revise concepts, definition, and classification of status epilepticus (SE). The proposed new definition of SE is as follows: Status epilepticus is a condition resulting either from the failure of the mechanisms responsible for seizure termination or from the initiation of mechanisms, which lead to abnormally, prolonged seizures (after time point t1 ). It is a condition, which can have long-term consequences (after time point t2 ), including neuronal death, neuronal injury, and alteration of neuronal networks, depending on the type and duration of seizures. This definition is conceptual, with two operational dimensions: the first is the length of the seizure and the time point (t1 ) beyond which the seizure should be regarded as "continuous seizure activity." The second time point (t2 ) is the time of ongoing seizure activity after which there is a risk of long-term consequences. In the case of convulsive (tonic-clonic) SE, both time points (t1 at 5 min and t2 at 30 min) are based on animal experiments and clinical research. This evidence is incomplete, and there is furthermore considerable variation, so these time points should be considered as the best estimates currently available. Data are not yet available for other forms of SE, but as knowledge and understanding increase, time points can be defined for specific forms of SE based on scientific evidence and incorporated into the definition, without changing the underlying concepts. A new diagnostic classification system of SE is proposed, which will provide a framework for clinical diagnosis, investigation, and therapeutic approaches for each patient. There are four axes: (1) semiology; (2) etiology; (3) electroencephalography (EEG) correlates; and (4) age. Axis 1 (semiology) lists different forms of SE divided into those with prominent motor systems, those without prominent motor systems, and currently indeterminate conditions (such as acute confusional states with epileptiform EEG patterns). Axis 2 (etiology) is divided into subcategories of known and unknown causes. Axis 3 (EEG correlates) adopts the latest recommendations by consensus panels to use the following descriptors for the EEG: name of pattern, morphology, location, time-related features, modulation, and effect of intervention. Finally, axis 4 divides age groups into neonatal, infancy, childhood, adolescent and adulthood, and elderly.

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OBJECTIVE: Although sleep is a biomarker for general health and pathological conditions, its changes across age and gender are poorly understood. METHODS: Subjective evaluation of sleep was assessed by questionnaires in 5,064 subjects, and 2,966 were considered without sleep disorders. Objective evaluation was performed by polysomnography in 2,160 subjects, and 1,147 were considered without sleep disorders. Only subjects without sleep disorders were included (aged 40-80 years). RESULTS: Aging was strongly associated with morning preference. Older subjects, especially women, complained less about sleepiness, and pathological sleepiness was significantly lower than in younger subjects. Self-reported sleep quality and daytime functioning improved with aging. Sleep latency increased with age in women, while sleep efficiency decreased with age in both genders. Deep slow-wave sleep decreased with age, but men were more affected. Spectral power densities within slow waves (< 5 Hz) and fast spindles (14-14.75 Hz) decreased, while theta-alpha (5-1 Hz) and beta (16.75-25 Hz) power in non-rapid eye movement sleep increased with aging. In REM sleep, aging was associated with a progressive decrease in delta (1.25-4.5 Hz) and increase in higher frequencies. CONCLUSIONS: Our findings indicate that sleep complaints should not be viewed as part of normal aging but should prompt the identification of underlying causes.

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O objetivo deste trabalho foi determinar a existência de concordância entre os métodos radioisotópico e radiológico e, em caso positivo, avaliar a utilidade do SPECT ictal na determinação do foco epileptogênico. Foram realizados SPECT ictal, ressonância magnética (RM) e ressonância magnética com espectroscopia de prótons (RME) em seis pacientes com epilepsia de lobo temporal refratária. O SPECT ictal foi realizado após a retirada das drogas antiepilépticas durante monitoramento por vídeo-EEG, utilizando-se o 99mTc-ECD, administrado aos pacientes no início da crise. As imagens de RM foram obtidas em T1, T2 e FLAIR, com cortes de 3 e 5 mm de espessura, e a RME foi realizada com técnica PRESS, com voxel único posicionado no hipocampo, bilateralmente. A análise estatística incluiu os valores de Kappa (k), erro-padrão (ep) e o nível de significância (p) para a lateralização do foco. Os achados foram analisados com base na localização por EEG da descarga ictal, no tempo de duração da crise (109-280 s; média: 152 s) e no tempo de administração do traçador (30-262 s; média: 96 s). Obtivemos dados correlatos em quatro pacientes (67%), com valores de k = 0,67, ep = 0,38 e p = 0,041. Concluímos que existe concordância entre SPECT ictal, RM e RME, e a utilidade do procedimento radioisotópico está relacionada aos casos em que o EEG não é diagnóstico e quando há discordância ou indefinição diagnóstica na análise comparativa entre EEG, RM e RME.

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INTRODUCTION: The aim of this study was to evaluate if there is a significant effect of lunar phases on subjective and objective sleep variables in the general population. METHODS: A total of 2125 individuals (51.2% women, age 58.8 ± 11.2 years) participating in a population-based cohort study underwent a complete polysomnography (PSG) at home. Subjective sleep quality was evaluated by a self-rating scale. Sleep electroencephalography (EEG) spectral analysis was performed in 759 participants without significant sleep disorders. Salivary cortisol levels were assessed at awakening, 30 min after awakening, at 11 am, and at 8 pm. Lunar phases were grouped into full moon (FM), waxing/waning moon (WM), and new moon (NM). RESULTS: Overall, there was no significant difference between lunar phases with regard to subjective sleep quality. We found only a nonsignificant (p = 0.08) trend toward a better sleep quality during the NM phase. Objective sleep duration was not different between phases (FM: 398 ± 3 min, WM: 402 ± 3 min, NM: 403 ± 3 min; p = 0.31). No difference was found with regard to other PSG-derived parameters, EEG spectral analysis, or in diurnal cortisol levels. When considering only subjects with apnea/hypopnea index of <15/h and periodic leg movements index of <15/h, we found a trend toward shorter total sleep time during FM (FM: 402 ± 4, WM: 407 ± 4, NM: 415 ± 4 min; p = 0.06) and shorter-stage N2 duration (FM: 178 ± 3, WM: 182 ± 3, NM: 188 ± 3 min; p = 0.05). CONCLUSION: Our large population-based study provides no evidence of a significant effect of lunar phases on human sleep.

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Brain injury is frequently observed after sepsis and may be primarily related to the direct effects of the septic insult on the brain (e.g., brain edema, ischemia, seizures) or to secondary/indirect injuries (e.g., hypotension, hypoxemia, hypocapnia, hyperglycemia). Management of brain injury in septic patients is first focused to exclude structural intracranial complications (e.g., ischemic/hemorrhagic stroke) and possible confounders (e.g., electrolyte alterations or metabolic disorders, such as dysglycemia). Sepsis-associated brain dysfunction is frequently a heterogeneous syndrome. Despite increasing understanding of main pathophysiologic determinants, therapy is essentially limited to protect the brain against further cerebral damage, by way of "simple" therapeutic manipulations of cerebral perfusion and oxygenation and by avoiding over-sedation. Non-invasive monitoring of cerebral perfusion and oxygenation with transcranial Doppler (TCD) and near-infrared spectroscopy (NIRS) is feasible in septic patients. Electroencephalography (EEG) allows detection of sepsis-related seizures and holds promise also as sedation monitoring. Brain CT-scan detects intra-cerebral structural lesions, while magnetic resonance imaging (MRI) provides important insights into primary mechanisms of sepsis-related direct brain injury, (e.g., cytotoxic vs. vasogenic edema) and the development of posterior reversible encephalopathy. Together with EEG and evoked potentials (EP), MRI is also important for coma prognostication. Emerging clinical evidence suggests monitoring of the brain in septic patients can be implemented in the ICU. The objective of this review was to summarize recent clinical data about the role of brain monitoring - including TCD, NIRS, EEG, EP, CT, and MRI - in patients with sepsis and to illustrate its potential utility for the diagnosis, management and prognostication.

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We all make decisions of varying levels of importance every day. Because making a decision implies that there are alternative choices to be considered, almost all decision involves some conflicts or dissatisfaction. Traditional economic models esteem that a person must weight the positive and negative outcomes of each option, and based on all these inferences, determines which option is the best for that particular situation. However, individuals rather act as irrational agents and tend to deviate from these rational choices. They somewhat evaluate the outcomes' subjective value, namely, when they face a risky choice leading to losses, people are inclined to have some preference for risk over certainty, while when facing a risky choice leading to gains, people often avoid to take risks and choose the most certain option. Yet, it is assumed that decision making is balanced between deliberative and emotional components. Distinct neural regions underpin these factors: the deliberative pathway that corresponds to executive functions, implies the activation of the prefrontal cortex, while the emotional pathway tends to activate the limbic system. These circuits appear to be altered in individuals with ADHD, and result, amongst others, in impaired decision making capacities. Their impulsive and inattentive behaviors are likely to be the cause of their irrational attitude towards risk taking. Still, a possible solution is to administrate these individuals a drug treatment, with the knowledge that it might have several side effects. However, an alternative treatment that relies on cognitive rehabilitation might be appropriate. This project was therefore aimed at investigate whether an intensive working memory training could have a spillover effect on decision making in adults with ADHD and in age-matched healthy controls. We designed a decision making task where the participants had to select an amount to gamble with the chance of 1/3 to win four times the chosen amount, while in the other cases they could loose their investment. Their performances were recorded using electroencephalography prior and after a one-month Dual N-Back training and the possible near and far transfer effects were investigated. Overall, we found that the performance during the gambling task was modulated by personality factors and by the importance of the symptoms at the pretest session. At posttest, we found that all individuals demonstrated an improvement on the Dual N-Back and on similar untrained dimensions. In addition, we discovered that not only the adults with ADHD showed a stable decrease of the symptomatology, as evaluated by the CAARS inventory, but this reduction was also detected in the control samples. In addition, Event-Related Potential (ERP) data are in favor of an change within prefrontal and parietal cortices. These results suggest that cognitive remediation can be effective in adults with ADHD, and in healthy controls. An important complement of this work would be the examination of the data in regard to the attentional networks, which could empower the fact that complex programs covering the remediation of several executive functions' dimensions is not required, a unique working memory training can be sufficient. -- Nous prenons tous chaque jour des décisions ayant des niveaux d'importance variables. Toutes les décisions ont une composante conflictuelle et d'insatisfaction, car prendre une décision implique qu'il y ait des choix alternatifs à considérer. Les modèles économiques traditionnels estiment qu'une personne doit peser les conséquences positives et négatives de chaque option et en se basant sur ces inférences, détermine quelle option est la meilleure dans une situation particulière. Cependant, les individus peuvent dévier de ces choix rationnels. Ils évaluent plutôt les valeur subjective des résultats, c'est-à-dire que lorsqu'ils sont face à un choix risqué pouvant les mener à des pertes, les gens ont tendance à avoir des préférences pour le risque à la place de la certitude, tandis que lorsqu'ils sont face à un choix risqué pouvant les conduire à un gain, ils évitent de prendre des risques et choisissent l'option la plus su^re. De nos jours, il est considéré que la prise de décision est balancée entre des composantes délibératives et émotionnelles. Ces facteurs sont sous-tendus par des régions neurales distinctes: le chemin délibératif, correspondant aux fonctions exécutives, implique l'activation du cortex préfrontal, tandis que le chemin émotionnel active le système limbique. Ces circuits semblent être dysfonctionnels chez les individus ayant un TDAH, et résulte, entre autres, en des capacités de prise de décision altérées. Leurs comportements impulsifs et inattentifs sont probablement la cause de ces attitudes irrationnelles face au risque. Cependant, une solution possible est de leur administrer un traitement médicamenteux, en prenant en compte les potentiels effets secondaires. Un traitement alternatif se reposant sur une réhabilitation cognitive pourrait être appropriée. Le but de ce projet est donc de déterminer si un entrainement intensif de la mémoire de travail peut avoir un effet sur la prise de décision chez des adultes ayant un TDAH et chez des contrôles sains du même âge. Nous avons conçu une tâche de prise de décision dans laquelle les participants devaient sélectionner un montant à jouer en ayant une chance sur trois de gagner quatre fois le montant choisi, alors que dans l'autre cas, ils pouvaient perdre leur investissement. Leurs performances ont été enregistrées en utilisant l'électroencéphalographie avant et après un entrainement d'un mois au Dual N-Back, et nous avons étudié les possibles effets de transfert. Dans l'ensemble, nous avons trouvé au pré-test que les performances au cours du jeu d'argent étaient modulées par les facteurs de personnalité, et par le degré des sympt^omes. Au post-test, nous avons non seulement trouvé que les adultes ayant un TDAH montraient une diminutions stable des symptômes, qui étaient évalués par le questionnaire du CAARS, mais que cette réduction était également perçue dans l'échantillon des contrôles. Les rsultats expérimentaux mesurés à l'aide de l'éléctroencéphalographie suggèrent un changement dans les cortex préfrontaux et pariétaux. Ces résultats suggèrent que la remédiation cognitive est efficace chez les adultes ayant un TDAH, mais produit aussi un effet chez les contrôles sains. Un complément important de ce travail pourrait examiner les données sur l'attention, qui pourraient renforcer l'idée qu'il n'est pas nécessaire d'utiliser des programmes complexes englobant la remédiation de plusieurs dimensions des fonctions exécutives, un simple entraiment de la mémoire de travail devrait suffire.

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RATIONALE: Limited-channel portable monitors (PMs) are increasingly used as an alternative to polysomnography (PSG) for the diagnosis of obstructive sleep apnoea (OSA). However, recommendations for the scoring of PM recordings are still lacking. Pulse-wave amplitude (PWA) drops, considered as surrogates for EEG arousals, may increase the detection sensitivity for respiratory events in PM recordings. OBJECTIVES: To investigate the performance of four different hypopnoea scoring criteria, using 3% or 4% oxygen desaturation levels, including or not PWA drops as surrogates for EEG arousals, and to determine the impact of measured versus reported sleep time on OSA diagnosis. METHODS: Subjects drawn from a population-based cohort underwent a complete home PSG. The PSG recordings were scored using the 2012 American Academy of Sleep Medicine criteria to determine the apnoea-hypopnoea index (AHI). Recordings were then rescored using only parameters available on type 3 PM devices according to different hypopnoea criteria and patients-reported sleep duration to determine the 'portable monitor AHIs' (PM-AHIs). MAIN RESULTS: 312 subjects were included. Overall, PM-AHIs showed a good concordance with the PSG-based AHI although it tended to slightly underestimate it. The PM-AHI using 3% desaturation without PWA drops showed the best diagnostic accuracy for AHI thresholds of ≥5/h and ≥15/h (correctly classifying 94.55% and 93.27% of subjects, respectively, vs 80.13% and 87.50% with PWA drops). There was a significant but modest correlation between PWA drops and EEG arousals (r=0.20, p=0.0004). CONCLUSION: Interpretation of PM recordings using hypopnoea criteria which include 3% desaturation without PWA drops as EEG arousal surrogate showed the best diagnosis accuracy compared with full PSG.

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OBJECTIVES: The aims of this study were to determine the etiology, clinical features, and predictors of outcome of new-onset refractory status epilepticus. METHODS: Retrospective review of patients with refractory status epilepticus without etiology identified within 48 hours of admission between January 1, 2008, and December 31, 2013, in 13 academic medical centers. The primary outcome measure was poor functional outcome at discharge (defined as a score >3 on the modified Rankin Scale). RESULTS: Of 130 cases, 67 (52%) remained cryptogenic. The most common identified etiologies were autoimmune (19%) and paraneoplastic (18%) encephalitis. Full data were available in 125 cases (62 cryptogenic). Poor outcome occurred in 77 of 125 cases (62%), and 28 (22%) died. Predictors of poor outcome included duration of status epilepticus, use of anesthetics, and medical complications. Among the 63 patients with available follow-up data (median 9 months), functional status improved in 36 (57%); 79% had good or fair outcome at last follow-up, but epilepsy developed in 37% with most survivors (92%) remaining on antiseizure medications. Immune therapies were used less frequently in cryptogenic cases, despite a comparable prevalence of inflammatory CSF changes. CONCLUSIONS: Autoimmune encephalitis is the most commonly identified cause of new-onset refractory status epilepticus, but half remain cryptogenic. Outcome at discharge is poor but improves during follow-up. Epilepsy develops in most cases. The role of anesthetics and immune therapies warrants further investigation.

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Our inability to adequately treat many patients with refractory epilepsy caused by focal cortical dysplasia (FCD), surgical inaccessibility and failures are significant clinical drawbacks. The targeting of physiologic features of epileptogenesis in FCD and colocalizing functionality has enhanced completeness of surgical resection, the main determinant of outcome. Electroencephalography (EEG)-functional magnetic resonance imaging (fMRI) and magnetoencephalography are helpful in guiding electrode implantation and surgical treatment, and high-frequency oscillations help defining the extent of the epileptogenic dysplasia. Ultra high-field MRI has a role in understanding the laminar organization of the cortex, and fluorodeoxyglucose-positron emission tomography (FDG-PET) is highly sensitive for detecting FCD in MRI-negative cases. Multimodal imaging is clinically valuable, either by improving the rate of postoperative seizure freedom or by reducing postoperative deficits. However, there is no level 1 evidence that it improves outcomes. Proof for a specific effect of antiepileptic drugs (AEDs) in FCD is lacking. Pathogenic mutations recently described in mammalian target of rapamycin (mTOR) genes in FCD have yielded important insights into novel treatment options with mTOR inhibitors, which might represent an example of personalized treatment of epilepsy based on the known mechanisms of disease. The ketogenic diet (KD) has been demonstrated to be particularly effective in children with epilepsy caused by structural abnormalities, especially FCD. It attenuates epigenetic chromatin modifications, a master regulator for gene expression and functional adaptation of the cell, thereby modifying disease progression. This could imply lasting benefit of dietary manipulation. Neurostimulation techniques have produced variable clinical outcomes in FCD. In widespread dysplasias, vagus nerve stimulation (VNS) has achieved responder rates >50%; however, the efficacy of noninvasive cranial nerve stimulation modalities such as transcutaneous VNS (tVNS) and noninvasive (nVNS) requires further study. Although review of current strategies underscores the serious shortcomings of treatment-resistant cases, initial evidence from novel approaches suggests that future success is possible.