Abstracts
Résumé
Chez l’homme, certaines crises épileptiques apparaissent pendant le sommeil à ondes lentes. Nos recherches expérimentales ont démontré une transformation de l’activité cérébrale électrique qui caractérise le sommeil vers des paroxysmes de type épileptique. L’origine des crises se situe dans le cortex cérébral. Les paroxysmes se propagent d’un groupe de neurones à un autre, avant de déboucher dans le thalamus. Les neurones thalamiques de relais sont inhibés pendant les crises corticales, ce qui pourrait expliquer la perte de conscience dans l’épilepsie de type absence (petit-mal).
Summary
Epileptic seizures mainly develop during slow-wave sleep. Our experiments, using multi-site, extra- and intracellular recordings, show a transformation without discontinuity from sleep patterns to seizures. The cerebral cortex is the minimal substrate of paroxysms with spike-wave complexes at ~3 Hz. Simultaneously, thalamocortical neurons are steadily inhibited and cannot relay signals from the outside world to cortex. This may explain the unconsciousness during certain types of epilepsy.
Appendices
Références
- 1. Niedermeyer E. Epileptic seizure disorders. In: Niedermeyer E, Lopes da Silva F, eds. Electroencephalography: basic principles, clinical applications and related fields. Baltimore: Williams and Wilkins, 1999: 476-585.
- 2. Steriade M. Neuronal substrates of sleep and epilepsy. Cambridge (United Kingdom): Cambridge University Press, 2003: 522 p.
- 3. Steriade M. Interneuronal epileptic discharges related to spike-and-wave cortical seizures in behaving monkeys. Electroencephalogr Clin Neurophysiol 1974; 37: 247-63.
- 4. IFSECN. A glossary of terms most commonly used by clinical electroen-cephalographers. Electroencephalogr Clin Neurophysiol 1974; 37: 538-48.
- 5. Steriade M, Contreras D. Spike-wave complexes and fast runs of cortically generated seizures. I. Role of neocortex and thalamus. J Neurophysiol 1998; 80: 1439-55.
- 6. Steriade M, Amzica F. Dynamic coupling among neocortical neurons during evoked and spontaneous spike-wave seizure activity. J Neurophysiol 1994; 72: 2051-69.
- 7. Neckelmann D, Amzica F, Steriade M. Spike-wave complexes and fast components of cortically generated seizures. III. Synchronizing mechanisms. J Neurophysiol 1998; 80: 1480-94.
- 8. Steriade M, Amzica F, Neckelmann D, Timofeev I. Spike-wave complexes and fast runs of cortically generated seizures. II. Extra- and intracellular patterns. J Neurophysiol 1998; 80: 1456-79.
- 9. Kettenmann H, Ransom BR. Neuroglia. New York: Oxford University Press, 1995: 1079.
- 10. Amzica F, Steriade M. Neuronal and glial membrane potentials during sleep and paroxysmal oscillations in the cortex. J Neurosci 2000; 20: 6648-65.
- 11. Amzica F, Massimini M, Manfridi A. Spatial buffering during slow and paroxysmal oscillations in cortical networks of glial cells in vivo. J Neurosci 2002; 22: 1042-53.
- 12. Timofeev I, Grenier F, Steriade M. The role of chloride-dependent inhibition and the activity of fast-spiking neurons during cortical spike-wave seizures. Neuroscience 2002; 114: 1115-32.
- 13. Johnston D, Brown TH. Giant spike potential hypothesis for epileptiform activity. Science 1981; 211: 294-7.
- 14. Timofeev I, Bazhenov M, Sejnowski TJ, Steriade M. Cortical Ih takes part in the generation of paroxysmal activities. Proc Natl Acad Sci USA 2002; 99: 9533-7.
- 15. Steriade M, Contreras D. Relations between cortical and thalamic cellular events during transition from sleep pattern to paroxysmal activity. J Neurosci 1995; 15: 623-42.
- 16. Timofeev I, Grenier F, Steriade M. Spike-wave complexes and fast runs of cortically generated seizures. IV. Paroxysmal fast runs in cortical and thalamic neurons. J Neurophysiol 1998; 80: 1495-513.
- 17. Pinault D, Leresche N, Charpier S, et al. Intracellular recordings in thalamic neurones during spontaneous spike and wave discharges in rats with absence epilepsy. J Physiol 1998; 509: 449-56.
- 18. Crunelli V, Leresche N. Childhood absence epilepsy: genes, channels, neurons and networks. Nat Rev Neurosci 2002; 3: 371-82.
- 19. Coulter DA, Huguenard JR, Prince DA. Characterization of ethosuximide reduction of low-threshold calcium current in thalamic neurons. Ann Neurol 1989; 25: 582-93.
- 20. de la Peña E, Geijo-Barrientos E. Laminar localization, morphology, and physiological properties of pyramidal neurons that have low-threshold calcium current in the guinea-pig medial frontal cortex. J Neurosci 1996; 16: 5301-11.
- 21. Destexhe A, Contreras D, Steriade M. LTS cells in cerebral cortex and their role in generating spike-and-wave oscillations. Neurocomputing 2001; 38-40: 555-63.
- 22. Steriade M. The intact and sliced brain. Cambridge (Massachusetts): The MIT Press, 2001: 366 p.
- 23. Steriade M. The GABAergic reticular nucleus: a preferential target of corticothalamic projctions. Proc Natl Acad Sci USA 2001; 98: 3625-7.