Episodios aparentemente letales en las primeras dos horas de vida durante el contacto piel con piel. Incidencia y factores de riesgo

Objective

To evaluate an unexpected increase in the incidence of apparently life threatening events and sudden deaths in neonates during the first 2 hours after birth in our hospital. This increase occurred in the first 2 years after generalized skin-to-skin contact between mother and infant became routine practice.

Methods

Full information on all our patients was collected to evaluate possible risk factors. Differences in incidence in four successive periods comprising the previous 35 years, with 208220 live neonates, were also analyzed.

Results

In the last period, there was a statistically significant increase in the rate of apparently life threatening events and sudden deaths in neonates. Several potential risk factors were detected: skin-to-skin contact, primiparity, an increased incidence in night hours and the invariable occurrence of these events in the second period of neonatal adaptation (30 to 90 minutes of life). Of eight patients with apparently life-threatening events, two had neurological sequelae and another died.

Conclusion

Apparently life threatening events in the first 2 hours of life are uncommon but may have serious consequences. One of the main risk factors may be skin-to-skin contact between mother and infant in the delivery room during the early adaptation period. As such contact has been proven to be beneficial and without apparent risks, this practice should be promoted. However, maternity staff should be vigilant during skin-to-skin contact, especially if the mother is alone with her neonate or other risk factors are present.     

Finding a better drug for epilepsy: Antiepileptogenesis targets

For several decades, both in vitro and in vivo models of seizures and epilepsy have been employed to unravel the molecular and cellular mechanisms underlying the occurrence of spontaneous recurrent seizures (SRS)—the defining hallmark of the epileptic brain. However, despite great advances in our understanding of seizure genesis, investigators have yet to develop reliable biomarkers and surrogate markers of the epileptogenic process. Sadly, the pathogenic mechanisms that produce the epileptic condition, especially after precipitating events such as head trauma, inflammation, or prolonged febrile convulsions, are poorly understood. A major challenge has been the inherent complexity and heterogeneity of known epileptic syndromes and the differential genetic susceptibilities exhibited by patients at risk. Therefore, it is unlikely that there is only one fundamental pathophysiologic mechanism shared by all the epilepsies. Identification of antiepileptogenesis targets has been an overarching goal over the last decade, as current anticonvulsant medications appear to influence only the acute process of ictogenesis. Clearly, there is an urgent need to develop novel therapeutic interventions that are disease modifying—therapies that either completely or partially prevent the emergence of SRS. An important secondary goal is to develop new treatments that can also lessen the burden of epilepsy comorbidities (e.g., cognitive impairment, mood disorders) by preventing or reducing the deleterious changes during the epileptogenic process. This review summarizes novel antiepileptogenesis targets that were critically discussed at the XIth Workshop on the Neurobiology of Epilepsy (WONOEP XI) meeting in Grottaferrata, Italy. Further, emerging neurometabolic links among several target mechanisms and highlights of the panel discussion are presented.     

Ex vivo MR microimaging of neuronal damage after kainate-induced status epilepticus in rat: correlation with quantitative histology.

The present study was designed to investigate whether T(2)-weighted signal changes obtained by microimaging of paraformaldehyde-fixed brain correlate with the histologically quantified damage in a model of status epilepticus (SE) induced by kainic acid in the rat. Animals were killed at several time points up to 8 weeks after a single intraperitoneal kainate (KA) injection (9 mg/kg). Perfusion-fixed brains were embedded in gelatin for MR microimaging at 9.4T. After the MRI analysis, the gelatin was removed and the brains were cryoprotected and processed for quantitative histology. Severity of neuronal damage and gliosis were assessed from thionin-stained serial sections. Correlative analysis of microimaging and histology data was done in the hippocampus, amygdala, parietal rhinal cortex (PaRH), piriform cortex (Pir), and entorhinal cortex. The relative signal intensities in T(2)-weighted images correlate with the severity of neuronal damage in the matched histological sections (correlation coefficients of 0.752-0.826). Our data show that MR microimaging ex vivo detects the degree of neuronal damage and its anatomical distribution after KA-induced SE, thus providing a useful tool for detecting the dynamics of progressive neuronal damage after prolonged seizures.     

Genetics of epilepsy: epilepsy research foundation workshop report.

The Sixth Epilepsy Research Foundation workshop, held in Oxford in March 2006, brought together basic scientists, geneticists, epidemiologists, statisticians, pharmacologists and clinicians to consider progress, issues and strategies for harnessing genetics to improve the understanding and treatment of the epilepsies. General principles were considered, including the fundamental importance of clear study design, adequate patient numbers, defi ned phenotypes, robust statistical data handling, and follow-up of genetic discoveries. Topics where some progress had been made were considered including chromosomal abnormalities, neurodevelopment, hippocampal sclerosis, juvenile myoclonic epilepsy, focal cortical dysplasia and pharmacogenetics. The ethical aspects of epilepsy genetics were reviewed. Principles and limitations of collaboration were discussed. Presentations and their matched discussions are produced here. There was optimism that further genetic research in epilepsy was not only feasible, but might lead to improvements in the lives of people with epilepsy.     

Cardioplegic arrest does not increase the risk of atrial fibrillation after coronary artery bypass surgery.

OBJECTIVE: Atrial fibrillation (AF) is the most common arrhythmia after coronary artery bypass grafting (CABG). It is a considerable source of morbidity, prolongs hospital stay and increases costs of treatment. Atrial cannulation, cardiopulmonary bypass and cardioplegic arrest have been suggested to play a role in the development of AF after CABG. The aim of this case-control study was to evaluate the role of cardiopulmonary bypass and cardioplegic arrest in the development of postoperative AF. METHODS: Data from 114 patients undergoing CABG without cardiopulmonary bypass and cardioplegic arrest (off-pump) between October, 1998 and December, 2002 were evaluated for the occurrence of postoperative AF. Each patient was individually matched by gender, age (+/-3 years), left ventricle ejection fraction (+/-5%), history of myocardial infarction, unstable angina, and beta-blocker medication with patients undergoing CABG with cardiopulmonary bypass and cardioplegic arrest (on-pump) during the same period. The data from off-pump and on-pump groups were compared. RESULTS: Off-pump and on-pump groups had similar preoperative characteristics. The number of distal anastomoses was lower in the off-pump (2.3+/-0.9) than in the on-pump (3.9+/-1.1, (P<0.001) group. However, the incidence of postoperative AF in the off-pump (36.8%) and the on-pump groups (36.0%) did not differ from each other. Old age was the only independent predictor of AF after CABG. CONCLUSIONS: Neither cardiopulmonary bypass nor cardioplegic arrest increases the risk of postoperative AF after CABG.     

Six DOF in vivo kinematics of the ankle joint complex: Application of a combined dual‐orthogonal fluoroscopic and magnetic resonance imaging technique

Accurate knowledge of in vivo ankle joint complex (AJC) biomechanics is critical for understanding AJC disease states and for improvement of surgical treatments. This study investigated 6 degrees‐of‐freedom (DOF) in vivo kinematics of the human AJC using a combined dual‐orthogonal fluoroscopic and magnetic resonance imaging (MRI) technique. Five healthy ankles of living subjects were studied during three in vivo activities of the foot, including maximum plantarflexion and dorsiflexion, maximum supination and pronation, and three weight‐bearing positions in simulated stance phases of walking. A three‐dimensional (3D) computer model of the AJC (including tibia, fibula, talus, and calcaneus) was constructed using 3D MR images of the foot. The in vivo AJC position at each selected position of the foot was captured using two orthogonally positioned fluoroscopes. In vivo AJC motion could then be reproduced by coupling the orthogonal images with the 3D AJC model in a virtual dual‐orthogonal fluoroscopic system. From maximum dorsiflexion to plantarflexion, the arc of motion of the talocrural joint (47.5 ± 2.2°) was significantly larger than that of the subtalar joint (3.1 ± 6.8°). Both joints showed similar degrees of internal–external and inversion–eversion rotation. From maximum supination to pronation, all rotations and translations of the subtalar joint were significantly larger than those of the talocrural joint. From heel strike to midstance, the plantarflexion contribution from the talocrural joint (9.1 ± 5.3°) was significantly larger than that of the subtalar joint (?0.9 ± 1.2°). From midstance to toe off, internal rotation and inversion of the subtalar joint (12.3 ± 8.3° and ?10.7 ± 3.8°, respectively) were significantly larger than those of the talocrural joint (?1.6 ± 5.9° and ?1.7 ± 2.7°). Strong kinematic coupling between the talocrural and subtalar joints was observed during in vivo AJC activities. The contribution of the talocrural joint to active dorsi‐plantarflexion was higher than that of the subtalar joint, whereas the contribution of the subtalar joint to active supination–pronation was higher than that of the talocrural joint. In addition, the talocrural joint demonstrated larger motion during the early part of stance phase while the subtalar joint contributes more motion during the later part of stance phase. The results add quantitative data to an in vivo database of normals that can be used in clinical diagnosis, treatment, and evaluation of the AJC after injuries. © 2006 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res