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• Negative central activity (NCA) is a frequent triphasic abnormal electroencephalographic feature of the extreme prematurity. • NCA is associated with severe intraventricular haemorrhage and may reflect the functional neural impact of vascular pathology. • The NCA association with adverse outcome argues for its consideration in brain function assessment and prognosis prediction. To characterize Negative Central Activity (NCA), an overlooked electroencephalographic activity of preterm newborns and investigate its relationship with brain injuries, dysfunction, and neurodevelopmental outcome. 109 preterm infants (23–28 weeks) were retrospectively included. NCA were selected at the negative peak on EEG. Individual averaged NCA were automatically characterized. Brain structural data were collected from cranial ultrasounds (cUS). The neurodevelopmental outcome at two years of age was assessed by the Denver Developmental Screening Test-II. Thirty-six (33%) children showed NCA: 6,721 NCA were selected, a median of 75 (interquartile range, 25/157.3) per EEG. NCA showed a triphasic morphology, with a mean amplitude and duration of the negative component of 24.6–40.0 µV and 222.7–257.3 ms. The presence of NCA on EEG was associated with higher intraventricular haemorrhage (IVH) grade on the first (P = 0.016) and worst neonatal cUS (P < 0.001) and poorer neurodevelopmental outcome (P < 0.001). NCA is an abnormal EEG feature of extremely preterm newborns that may correspond to the functional neural impact of a vascular pathology. The NCA relationships with an adverse outcome and the presence/severity of IVH argue for considering NCA in the assessment of pathological processes in the developing brain network and for early outcome prediction. [ABSTRACT FROM AUTHOR]

Electroencephalography is the only clinically available technique that can address the premature neonate normal and pathological functional development week after week. The changes in the electroencephalogram (EEG) result from gradual structural and functional modifications that arise during the last trimester of pregnancy. Here, we review the structural changes over time that underlie the establishment of functional immature neural networks, the impact of certain anatomical specificities (fontanelles, connectivity, etc.) on the EEG, limitations in EEG interpretation, and the utility of high-resolution EEG (HR-EEG) in premature newborns (a promising technique with a high degree of spatiotemporal resolution). In particular, we classify EEG features according to whether they are manifestations of endogenous generators (i.e. theta activities that coalesce with a slow wave or delta brushes) or come from a broader network. Furthermore, we review publications on EEG in premature animals because the data provide a better understanding of what is happening in premature newborns. We then discuss the results and limitations of functional connectivity analyses in premature newborns. Lastly, we report on the magnetoelectroencephalographic studies of brain activity in the fetus. A better understanding of complex interactions at various structural and functional levels during normal neurodevelopment (as assessed using electroencephalography as a benchmark method) might lead to better clinical care and monitoring for premature neonates. [ABSTRACT FROM AUTHOR]

We report on a 7-year-old female who presented paroxysmal episodes of loss of consciousness with clonic movements. The electroencephalogram (EEG) evidenced diffuse slow wave activations, with no symptoms. Epilepsy was suspected but antiepileptic drugs were ineffective. Video-EEG monitoring revealed that the syncope was triggered by stretching with a tachycardia that started during the stretch maneuver and diffuse slow waves on the EEG 2 s before the symptoms. Stretch syncope can result in striking manifestations with subcortically driven clonic movements that can be mistaken for signs of epilepsy. Stretching might lead to transient hypoxia of the brainstem; in turn, this might activate the thalamocortical loop and thus generate cardiovascular changes, EEG slow waves, and physical manifestations. [ABSTRACT FROM AUTHOR]

Myoclonic‐atonic epilepsy (MAE) is thought to have a genetic etiology. Mutations in CHD2, SLC2A1 and SLC6A1 genes have been reported in few patients showing often intellectual disability prior to MAE onset. We aimed to explore putative causal genetic factors in MAE. We performed array‐CGH and whole‐exome sequencing in 27 patients. We considered non‐synonymous variants, splice acceptor, donor site mutations, and coding insertions/deletions. A gene was causal when its mutations have been already linked to epilepsy or other brain diseases or when it has a putative function in neuronal excitability or brain development. We identified candidate disease‐causing variants in 11 patients (41%). Single variants were found in some known epilepsy‐associated genes (namely CHD2, KCNT1, KCNA2 and STXBP1) but not in others (SLC2A1 and SLC6A1). One new candidate gene SUN1 requires further validation. MAE shows underlying genetic heterogeneity with only few cases linked to mutations in genes reported in developmental and epileptic encephalopathies. [ABSTRACT FROM AUTHOR]

Introduction Le cerveau du nouveau-né prématuré subit un processus dynamique de maturation avec la mise en place de générateurs spécifiques au cours de développement. L’activité thêta temporale est l’un des premiers neurobiomarqueurs. Le but de cette étude était de mieux caractériser les localisations des générateurs de ces activités. Méthodes Des électroencéphalographies Haute Résolution (EEGHR) étaient enregistrées chez des prématurés âgés de 26 à 31 semaines d’âge corrigé (sAC), avec 40 à 64 électrodes. La position des électrodes était digitalisée sur 2 modèles de têtes réalistes (29 et 31 sAC). La localisation de source était effectuée, après moyennage pour chaque enfant, par méthode dipolaire. La localisation des sources par méthode dipolaire et MUSIC était effectuée sur les activités thêta après interpolation cubique puis grand moyennage par groupe d’enfants/par hémisphère. Résultats Les EEGHR de 14 prématurés comprenant en moyenne 125 activités thêta étaient analysés. Les générateurs des activités thêta, traitées par groupe d’enfant après moyennage, étaient localisés dans le prolongement du sillon temporal postérieur avec une localisation plus profonde pour les plus jeunes. Les modifications des caractéristiques du modèle de tête (conductivité osseuse, prise en compte du liquide cérébro-spinal) entraînaient des modifications relatives de la position du dipôle temporal. Conclusion Les générateurs des activités thêta temporales étaient localisés dans le prolongement du sillon temporal supérieur en regard du planum temporal dès 26 sAC. Ces biomarqueurs pouvaient correspondre indirectement au rôle de guidance fonctionnelle de la sous plaque afin de préparer la mise en place de la fonction auditive ou langagière corticale. [ABSTRACT FROM AUTHOR]

Temporal theta slow‐wave activity (TTA‐SW) in premature infants is a specific neurobiomarker of the early neurodevelopment of perisylvian networks observed as early as 24 weeks of gestational age (wGA). It is present at the turning point between non‐sensory driven spontaneous networks and cortical network functioning. Despite its clinical importance, the underlying mechanisms responsible for this spontaneous nested activity and its functional role have not yet been determined. The coupling between neural oscillations at different timescales is a key feature of ongoing neural activity, the characteristics of which are determined by the network structure and dynamics. The underlying mechanisms of cross‐frequency coupling (CFC) are associated with several putative functions in adults. In order to show that this generic mechanism is already in place early in the course of development, we analyzed electroencephalography recordings from sleeping preterm newborns (24–27 wGA). Employing cross‐frequency phase–amplitude coupling analyses, we found that TTAs were orchestrated by the SWs defined by a precise temporal relationship. Notably, TTAs were synchronized to the SW trough, and were suppressed during the SW peak. Spontaneous endogenous TTA‐SWs constitute one of the very early signatures of the developing temporal neural networks with key functions, such as language and communication. The presence of a fine‐tuned relationship between the slow activity and the TTA in premature neonates emphasizes the complexity and relative maturity of the intimate mechanisms that shape the CFC, the disruption of which can have severe neurodevelopmental consequences. [ABSTRACT FROM AUTHOR]