José Groswasser

Incongruent cerebral growth in sudden infant death syndrome

Sudden infant death syndrome remains a leading cause of postneonatal mortality in developed countries. Its etiopathogenic mechanisms are unknown. In this neuropathologic study, we noticed that the weights of the brains of infants who died from sudden infant death syndrome (n = 97) were invariably heavier in comparison with those of a group of age-matched controls (n = 23) issuing from the same local population. Brain edema was not a major element, and there were no significant microscopic or macroscopic cerebral anomalies in the brains from either of the study groups. Head circumference did not show a parallel increase in infants with sudden infant death syndrome. The excessive brain weight might reflect abnormal cerebral development and could be detrimental to vital neural control. In a previous study, we disclosed cytokine overexpression in the brains of these victims. Whether increased brain weight is linked to cytokine up-regulation remains, however, a moot case and merits further exploration.

Detection of obstructive apnea events in sleeping infants from thoracoabdominal movements

The aim of the study was to determine whether in infants, the evaluation of thoracoabdominal movements alone, with no measurement of airflow, could be used to identify obstructive sleep apnea events (OA). Two different methods were used: first, we initially quantified thoracoabdominal asynchrony. Although 79.3% of OAs showed a significant increase of thoracoabdominal asynchrony, only 10.9% of the events scored by the identification of phase opposition were true OAs. Next, we developed two artificial neural networks (ANNs) as classifiers for the study of the thoracoabdominal signals. The first network was trained to locate obstructive and central apnea events. It correctly detected 75% of the OAs; however, only 6.2% of the detected events were true OAs. When a second network was used, OAs could not be discriminated from other portions of the signals showing similar phase characteristics. It was concluded that the information available in uncalibrated signals of thoracic and abdominal respiratory movements was insufficient to unambiguously detect OA events in sleeping infants.

Sudden infant death syndrome from epidemiology to pathophysiology

Despite the dramatic decline in the incidence of sudden infant death syndrome (SIDS) by 50–90% over the past two decades, SIDS continues to be the leading cause of death in infants aged between 1 month and 1 year in developed countries.

158 Is Sighing a Resetting Mechanism of the Autonomic Nervous System

Sighs are important components of normal breathing. They occur isolated or associated with respîratory pauses. Functional residual capacity and lung compliance increase after sighs. Sighs have been shown to be part of an arousal reaction in infants and to induce heart rate modifications. We investigated the influence of sighs on the autonomic balance in infants.METHODS: 107 sighs (a single breath of at least twice the amplitude of the preceding breaths, not followed by an apnea) from 23 term infants were selected. The selection was made in conditions known not to interfere with spontaneous HR variability (quiet sleep,absence of movements, apnea or false detections of QRS during the 2 preceding and following minutes. Spectral analysis of RR variability was performed on the 2 minutes preceding and the 2 minutes following the sigh. To study the role of the ANS in the development of a sigh, spectral analysis of the period just before the sigh and of the 2 preceding minutes were compared.RESULTS: The 2 minutes following the sigh were characterized by an increased RR interval (p 0.001), an increased total power (p <0.01),an increased LF (p0.01), unchanged HF, increased HF/LF (p <0.001), increased LF normalized (p< 0.001),decreased HF normalized (p<0.001). When comparing the interval sigh minus 4 to 2 minutes with the interval sigh minus 2 to 0 minutes, the opposite evolution of autonomic balance was observed.DISCUSSION: The results of the spectral analysis indicate that sighs are followed by an increase in orthosympatic tone and a decrease in parasympatic tone. On the opposite, the period preceding sighs is caracterized by a decrease in orthosympatic tone and an increase in parasympatic tone.CONCLUSION: These results indicate that sighs could play a resetting role for the autonomic nervous system during quiet sleep in normal infants.

La mort subite du nourrisson(MSN) Données récentes en physiologie

Resume Les campagnes de prevention contre la Mort Subite du Nourrisson (MSN) ont conduit a une diminution significative du nombre de deces inattendus et inexpliques du nourrisson pendant le sommeil. Malgre une recherche intensive dans ce domaine, la comprehension des mecanismes responsables d’une MSN est encore incomplete. Les resultats des recherches epidemiologiques, genetiques, efectrophysio-logiques et anatomopathologiques les plus recentes seront revus. De ces donnees, un modele pour la MSN peut etre elabore : le deces resulterait de la survenue concomitante de trois facteurs (une vulnerabilite prenatale, une periode critique du developpement et des facteurs de stress postnataux) et de 3 mecanismes potentiels (une deficience respiratoire, autonome et des mecanismes d’eveil). Le reveil etant souvent la derniere chance de survie d’un individu soumis a un stress vital, une deficience de ce mecanisme pourrait etre un des facteurs cles du processus conduisant a une MSN. Un nourrisson dont les controles cardiorespiratoires et les mecanismes d’eveil sont alteres peut etre a risque de MSN. Des facteurs genetiques, metaboliques, nutritionnels ou toxiques pourraient etre responsables de lesions prenatales du systeme nerveux central et en particulier du tronc cerebral. Ces deficiences resteraient latentes dans les premieres semaines de vie, jusqu’a une periode du developpement particulierement critique entre 2 et 6 mois, quand des changements significatifs surviennent au niveau de la structure du sommeil, des controles respiratoire et cardiaque. L’incident a de grande chance de survenir lorsque l’enfant est expose a une infection ou a un milieu environnemental defavorable qui aggravera l’instabilite des controles cardiorespiratoires et d’eveils.