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Introduction : la survenue de crises convulsives chez le nouveau-né est plus fréquente que chez l’enfant et l’adolescent. Leur incidence est en moyenne de 3,5/1000 naissances vivantes, de 1,5/1000 chez le nouveau-né à terme (1,2). Les études contrôlées randomisées, qui comparent les différents médicaments antiépileptiques administrés en période néonatale, sont peu nombreuses. Actuellement les molécules antiépileptiques d’urgence utilisées de manière courante, sont les médicaments pour lesquels les praticiens ont le plus d’expérience. Objectifs : l’objectif principal de l’étude était d’évaluer la réponse au traitement anti-épileptique d’urgence, selon le protocole utilisé dans le service chez le nouveau-né > 34 semaines d’aménorrhée (SA) en fonction de chaque étiologie (encéphalopathie anoxo-ischémique (EAI), accident vasculaire cérébral (AVC), hématome/hémorragie cérébrale, pathologie métabolique, syndromes épileptiques néonataux, malformation cérébrale corticale, infection intracérébrale bactérienne et virale). Méthodes : nous avons mené une étude observationnelle rétrospective monocentrique au sein du service de Réanimation et Pédiatrie Néonatales et du service de Neuropédiatrie du Centre Hospitalo-universitaire Robert-Debré (Paris, France) de janvier 2015 à décembre 2018. L’efficacité du traitement antiépileptique d’urgence (phénobarbital, puis phénytoïne puis clonazépam) était définie par l’arrêt des manifestations électro-cliniques dans un délai de 2 heures et l’absence de récidive de crise sous traitement bien mené pendant une durée de 24 heures. Les variables dichotomiques étaient comparées à l’aide d’un test exact de Fisher. Le seuil de significativité était p = 0,05. Résultats : 78 patients ont été inclus. 32 % d’EAI (n = 25), 23 % d’AVC (n = 18), 9 % de pathologie métabolique (n = 7) et d’hématome/hémorragie intracérébral (n = 7), 6,4 % de malformation cérébrale (n = 5) et de syndromes épileptiques néonataux (n = 5), 2,6 % d’infection intracérébrale bactérienne (n = 2) et 11,5 % d’absence de diagnostic étiologique (n = 9) ont été retrouvés. La réponse au traitement d’urgence était : 88,2 % des AVC (n = 15), 75 % des EAI (n = 18), 75 % des syndromes épileptiques néonataux (n = 3), 83,3 % des hématomes/hémorragies cérébrales (n = 5), 28,6 % des maladies métaboliques (n = 2). Aucun des patients ayant une malformation cérébrale n’a répondu au traitement antiépileptique d’urgence. Il n’y a pas de différence significative dans la réponse globale au traitement antiépileptique d’urgence entre les groupes « AVC » et « EAI » (p = 0,43). De même pour la réponse à la première ligne de traitement par phénobarbital (p = 0,78), à la deuxième ligne par phénytoïne (p = 0,21) et à la troisième par clonazépam (p =1). Conclusion : cette étude suggère que notre protocole local d’urgence de traitement des crises convulsives néonatales est efficace dans certaines étiologies (AVC, EAI, syndromes épileptiques néonataux et hématome/hémorragie cérébrale). En revanche, il semble inefficace en cas de malformation cérébrale ou insuffisant en cas de pathologie métabolique.

Introduction: our objectif was to identify risk factors of hypoxic-ischemic encephalopathy (HIE) in neonates with umbilical arterial pH =7.00. Patients and method: we performed a case-control study over a period of 5 years, including children =36 weeks born with an umbilical pH =7,00. Cases are infants who developed moderate or severe HIE. Controls did not develop moderate or severe HIE. Results: 41 cases and 98 controls were identified. Factors associated with moderate or severe HIE were: the occurrence of an acute event (34.1% vs 9.2% ORa = 6.4 [1.8-22.5]), maternal fever (24.4% vs 11.2% ORa= 3.5 [1.0-11.9]), meconium amniotic fluid (37.5% vs 15.6% ORa = 2.9 [1.0-8.6]) and the time between emergency caesarean section decision and birth (18.9 min vs 13.1 min p= 0.03). Children with moderate or severe HIE had lower mean umbilical pH (6.87 vs 6.93 p

Early brain injury including white matter damage (WMD) appears strongly correlated to perinatal hypoxia-ischemia and adverse neurological outcomes in preterm survivors. Indeed, WMD has been widely associated with subtle to major motor disturbances, sensory, behavioral and cognitive impairments in preterm infants who afterward develop cerebral palsy (CP). Prenatal ischemia (PI) has been shown to reproduce the main features of WMD observed in preterm infants. The present study was aimed at determining in adult rats the impact of PI on brain axons, musculoskeletal histology and locomotor activity. PI was induced by unilateral intrauterine artery ligation at E17 in pregnant rats. We found axonal degeneration and reactive astrogliosis in several white matter regions of adult PI rats. We found mild myopathic and secondary joint changes, including increased variability in myofiber size in several hind limb muscles, decreased myofibers numbers but increased Pax 7 cells and myofiber size in the gastrocnemius, and mild knee and ankle chondromalacia. Although treadmill locomotion appeared normal, several kinematic parameters, such as stride length, amplitude, velocity and leg joint angles were altered in adult PI rats compared to shams. Using intra- and inter-group variability of kinematic parameters, PI seemed to impair the maturation of locomotion on the treadmill. In addition, PI rats exhibited spontaneous hyperactivity in open-field test. Musculoskeletal changes appeared concomitant with mild impairments in gait and posture. Our rodent model of WMD based on PI reproduces the mild motor deficits and musculoskeletal changes observed in many preterm infants with a perinatal history of hypoxia-ischemia, and contributes towards a better understanding of the interplay between brain injury, musculoskeletal histopathology and gait disturbances encountered subsequently.

Item does not contain fulltext PURPOSE: To analyze white matter pathologic abnormalities by using diffusion-tensor (DT) imaging in a multicenter prospective cohort of comatose patients following cardiac arrest or traumatic brain injury (TBI). MATERIALS AND METHODS: Institutional review board approval and informed consent from proxies and control subjects were obtained. DT imaging was performed 5-57 days after insult in 49 cardiac arrest and 40 TBI patients. To control for DT imaging-processing variability, patients' values were normalized to those of 111 control subjects. Automated segmentation software calculated normalized axial diffusivity (lambda1) and radial diffusivity (lambda perpendicular) in 19 predefined white matter regions of interest (ROIs). DT imaging variables were compared by using general linear modeling, and side-to-side Pearson correlation coefficients were calculated. P values were corrected for multiple testing (Bonferroni). RESULTS: In central white matter, lambda1 differed from that in control subjects in six of seven TBI ROIs and five of seven cardiac arrest ROIs (all P < .01). The lambda perpendicular differed from that in control subjects in all ROIs in both patient groups (P < .01). In hemispheres, lambda1 was decreased compared with that in control subjects in three of 12 TBI ROIs (P < .05) and nine of 12 cardiac arrest ROIs (P < .01). The lambda perpendicular was increased in all TBI ROIs (P < .01) and in seven of 12 cardiac arrest ROIs (P < .05). Cerebral hemisphere lambda1 was lower in cardiac arrest than in TBI in six of 12 ROIs (P < .01), while lambda perpendicular was higher in TBI than in cardiac arrest in eight of 12 ROIs (P < .01). Diffusivity values were symmetrically distributed in cardiac arrest (P < .001 for side-to-side correlation) but not in TBI patients. CONCLUSION: DT imaging findings are consistent with the known predominance of cerebral hemisphere axonal injury in cardiac arrest and chiefly central myelin injury in TBI. This consistency supports the validity of DT imaging for differentiating axon and myelin damage in vivo in humans. 01 februari 2014

Year in review in Intensive Care Medicine, 2008 : II. Experimental, acute respiratory failure and ARDS, mechanical ventilation and endotracheal intubation

International audience; The amino acid glutamate, the major excitatory neurotransmitter in the central nervous system, activates receptors coupled to calcium influx. Excessive activation of glutamate receptors in conditions such as severe epileptic seizures or stroke can kill neurons in a process called excitotoxicity. However, subtoxic levels of activation of the N-methyl-D-aspartate (NMDA) type of glutamate receptor elicit adaptive responses in neurons that enhance their ability to withstand more severe stress. A variety of stimuli induce adaptive responses to protect neurons. For example, sublethal ischemic episodes or a mild epileptic insult can protect neurons in a process referred to as tolerance. The molecular mechanisms that protect neurons by these different stressful stimuli are largely unknown but they share common features such as the transcription factor, nuclear factor kappa B (NF-kappaB), which is activated by ischemic and epileptic preconditioning as well as exposure to subtoxic NMDA concentrations. In this article, we describe stress-induced neuroprotective mechanisms highlighting the role of brain-derived neurotrophic factor (BDNF), a protein that plays a crucial role in neuronal survival and maintenance, neurogenesis and learning and memory.

TREK-1 is a member of the two-pore domain potassium (K(2P)) channel family that is mechano-, heat, pH, voltage and lipid sensitive. It is highly expressed in the central nervous system and probably encodes one of the previously described arachidonic acid-activated K(+) channels. Polyunsaturated fatty acids and lysophospholipids protect the brain against global ischaemia. Since both lipids are openers of TREK-1, it has been suggested that this K(2P) channel is directly involved in neuroprotection. Recently, however, this view has been challenged by a report claiming that TREK-1 and its activation by arachidonic acid is inhibited by hypoxia. In the present study, we demonstrate that the bubbling of saline with gases results in the loss of arachidonic acid from solution. Using experimental conditions which obviate this experimental artefact we demonstrate that TREK-1 is resistant to hypoxia and is strongly activated by arachidonic acid even at low P(O(2)) (< 4 Torr). Furthermore, hypoxia fails to affect basal as well as 2,4,6-trinitrophenol- and acid-stimulated TREK-1 currents. These data are supportive for a possible role of TREK-1 in ischaemic neuroprotection and in cell signalling via arachidonic acid.