Generalized Epilepsy

1. Thalamic and Cortical Mechanisms in Absence Attacks

   1. Spontaneous Spike-and-Wave Discharges in Wistar Rats: A Model of Genetic Generalized Nonconvulsive Epilepsy

      • M. Vergnes, Ch. Marescaux, A. Depaulis, G. Micheletti, J.-M. Warter

      Pages 238-253

   2. Behavioral and Electrophysiological Studies of Absence Epilepsy

      • A. F. Mirsky, C. C. Duncan

      Pages 254-269

2. Photosensitivity

   1. Front Matter

      Pages 271-271

      PDF

   2. Focal Discharges in Photosensitive Generalized Epilepsy

      • R. Naquet, A. Valin

      Pages 273-285

   3. Photosensitive Epilepsy of the Baboon: A Generalized Epilepsy with a Motor Cortical Origin

      • C. Silva-Barrat, Ch. Menini

      Pages 286-297

   4. Role of Dopamine in Generalized Photosensitive Epilepsy: Electroencephalographic and Biochemical Aspects

      • L. F. Quesney, T. A. Reader

      Pages 298-313

   5. Inferences Regarding the Visual Precipitation of Seizures, Eye Strain, and Headaches

      • A. J. Wilkins, C. D. Binnie, C. E. Darby, D. Kasteleijn-Nolst Trenité

      Pages 314-326

3. Generalized Convulsive Seizures

   1. Front Matter

      Pages 327-327

      PDF

   2. Animal Models of Generalized Convulsive Seizures: Some Neuroanatomical Differentiation of Seizure Types

      • K. Gale

      Pages 329-343

   3. Mechanisms Underlying Generalized Tonic—Clonic Seizures in the Rat: Functional Significance of Calcium Ions

      • E.-J. Speckmann, J. Walden, D. Bingmann, A. Lehmenkühler, U. Altrup

      Pages 344-354

   4. Substantia Nigra-Mediated Control of Generalized Seizures

      • S. L. Moshé, E. F. Sperber

      Pages 355-367

   5. Mesencephalic Structures and Tonic—Clonic Generalized Seizures

      • F. Velasco, M. Velasco

      Pages 368-384

4. Metabolic and Neurochemical Studies

   1. Front Matter

      Pages 385-385

      PDF

   2. Metabolic Studies of Generalized Epilepsy

      • J. Engel Jr., R. F. Ochs, P. Gloor

      Pages 387-396

   3. PET Studies of Generalized Epilepsy Induced by Convulsant Drugs Acting at the GABA-Benzodiazepine Receptor Complex

      • M. Mazière, E. Brouillet, M. Kunimoto, M. Khalili-Varasteh, Ph. Hantraye, R. H. Dodd et al.

      Pages 397-406

   4. Postictal Compensatory Changes in Cortical Alpha-1 Receptors and Adrenergic-Mediated Phosphoinositol Metabolism Following Repeated Electroconvulsive Seizures in Rats

      • A. L. Sherwin, S. Dyve, F. Dubeau, W. Regenold, D. Guévremont

      Pages 407-422

5. Pharmacological Agents and Generalized Seizures

   1. Front Matter

      Pages 423-423

      PDF

   2. Cellular Actions of Petit Mal Anticonvulsants: Implication of Thalamic Low-Threshold Calcium Current in Generation of Spike-Wave Discharge

      • D. A. Coulter, J. R. Huguenard, D. A. Prince

      Pages 425-435

   3. Mechanisms of Anticonvulsant Action of Valproate: An Overview and Perspective

      • R. Čapek, B. Esplin

      Pages 436-459

   4. Sedative Drug Withdrawal Seizures: Cellular Eleptrophysiological Mechanisms

      • P. L. Carlen, M. F. Davies, I. Rougier-Naquet, J. N. Reynolds, I. Spigelman

      Pages 460-470

In recent years there has been intense interest in the basic mechanisms of epilepsy. Many symposia and monographs have been devoted to this topic. These reviews, however, have focused almost exclusively on studies performed in models of partial (or focal) epilepsy. It was natural that scientists interested in the fundamental mechanism of epileptogenesis at the cellular level were attracted to work on models in which the epileptogenic dysfunction could be confined to ever-smaller populations of neurons. Many of the most illuminating studies done in this field in the recent past have been carried out in vitro on brain slices or on dissociated neuronal cultures. Much valuable insight into the mechanisms of epileptogenesis has been obtained in this manner. One cannot, however, automatically assume that mechanisms elucidated in such exquisitely "focal" models are applicable to forms of epilepsy in which seizures from their very start involve the entire brain. One of the most difficult questions that arises in this context is how epileptogenic dysfunction, which can be understood in terms of mechanisms involving a few contiguous cells, can lead to what appears to be a simultaneous onset of seizure discharge in virtually all areas of the brain. Most of the workers who have made excellent contributions to the understanding of the cellular mechanisms involved in epileptogenesis have paid virtually no attention to this important problem.

• PET
• brain
• cortex
• electroencephalography (EEG)
• epilepsy
• neurons
• physiology
• positron emission tomography (PET)
• receptor

• Montreal Neurological Institute, Department of Neurophysiology, McGill University, Montreal, Canada

  Massimo Avoli, Pierre Gloor

• Department of Physiology, University of Patras Medical School, Patras, Greece

  George Kostopoulos

• Laboratoire de Physiologie Nerveuse, CNRS, Gif-sur-Yvette, France

  Robert Naquet

Policies and ethics