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(1979)
Selective distribution of projections from amygdala to prefrontal cortex in rhesus monkeys
W. Spielmeyer
Histopathologie des NervensystemsJournal of Nervous and Mental Disease, 57
(1968)
Atlas stCrCo-taxique
Y. Ben‐Ari, É. Tremblay, O. Ottersen, B. Meldrum (1980)
The role of epileptic activity in hippocampal and ‘remote’ cerebral lesions induced by kainic acidBrain Research, 191
H. Gastaut, A. Meyer, E. Beck (1959)
EXPERIMENTAL PSYCHOMOTOR EPILEPST IN THE CAT ELECTRO‐CLINICAL AND ANATOMO‐PATHOLOGICAL CORRELATIONSJournal of Neuropathology and Experimental Neurology, 18
(2019)
Cerebral HypoxiaDefinitions
D. Riche, J. Huguenin, J. Lavieille (1968)
Atlas stéréotaxique du cerveau de babouin (Papio papio)
J. Nadler, D. Shelton, B. Perry, C. Cotman (1980)
Regional distribution of [3H]kainic acid after intraventricular injection.Life sciences, 26 2
Brian Meidrum, Roger Vigouroux, J. Brierley (1973)
Systemic factors and epileptic brain damage. Prolonged seizures in paralyzed, artificially ventilated baboons.Archives of neurology, 29 2
W. Spielmeyer
Histopathologie des Nervensystems: Erster Band Allgemeiner Teil
(1966)
La corne d’Am-mon et le noyau amygdalien: effets cliniques et ilectriques de leur stimulation chez I’homme
C. Munari, J. Bancaud, A. Bonis, P. Buser, J. Talairach, G. Szikla, A. Philippe (1979)
Role du noyau amygdalien dans la survenue de manifestations oro-alimentaires au cours des crises épileptiques chez l'homme*Revue d'Electroencéphalographie et de Neurophysiologie Clinique, 9
M. Scheibel, Paul Crandall, A. Scheibel (1974)
The Hippocampal‐Dentate Complex in Temporal Lobe EpilepsyEpilepsia, 15
G. Blennow, J. Brierley, B. Meldrum, B. Siesjö (1978)
Epileptic brain damage: the role of systemic factors that modify cerebral energy metabolism.Brain : a journal of neurology, 101 4
J. Nadler, B. Perry, C. Cotman (1978)
Intraventricular kainic acid preferentially destroys hippocampal pyramidal cellsNature, 271
Brian Meidrum, James Brierlev (1973)
Prolonged epileptic seizures in primates. Ischemic cell change and its relation to ictal physiological events.Archives of neurology, 28 1
Menini e t al: Pathological Changes after Focal Epilepsy 509
(1954)
Investigation of the primate amygdala . Movements of the face and jaws
(1978)
Contr6le radiographique sim-plifiC pour l’exploration stereotaxique du babouin, et les injections intracCrCbro-ventriculaires chez I’animal chronique
Takashi Hayashi (1954)
EFFECTS OF SODIUM GLUTAMATE ON THE NERVOUS SYSTEMThe Keio Journal of Medicine, 3
D. Daly (1975)
Ictal clinical manifestations of complex partial seizures.Advances in neurology, 11
Etude des post - dbcharges Clectriques provoquCes par stirnulation du complex nucleaire amygdalien chez le chat
Scheibel Scheibel, Crandall Crandall, Scheibel Scheibel (1974)
The hippocampaldentate complex in temporal lobe epilepsy. A Golgi studyEpilepsia, 15
S. Wuerthele, K. Lovell, M. Jones, K. Moore (1978)
A histological study of kainic acid-induced lesions in the rat brainBrain Research, 149
B. Meldrum, Horton Rw, Brierley Jb (1974)
Epileptic brain damage in adolescent baboons following seizures induced by allylgycine.Brain : a journal of neurology, 97 2
Y. Ben‐Ari, É. Tremblay, O. Ottersen, R. Naquet (1979)
Evidence suggesting secondary epileptogenic lesions after kainic acid: pretreatment with diazepam reduces distant but not local brain damageBrain Research, 165
M. Baldy‐Moulinier, L. Arias, P. Passouant (1973)
Hippocampal Epilepsy Produced by OuabainEuropean Neurology, 9
R.N.DeJ. (1954)
Epilepsy and the Functional Anatomy of the Human BrainNeurology, 4
M. Falconer, E. Serafetinides, J. Corsellis (1964)
ETIOLOGY AND PATHOGENESIS OF TEMPORAL LOBE EPILEPSY.Archives of neurology, 10
(1968)
Acch epilep - tiques induits par la stimulation du noyau amygdalien et de la come d ’ Ammon
In Papio papio baboons chronically prepared for cortical and deep electroencephalographic recording, injection of kainic acid into the amygdala (7 animals) or temporal pole (2 animals) gave rise to focal epileptic discharges lasting 15 to 150 hours. Electrographically, the seizure activity spread ipsilaterally and contralaterally within the limbic system but did not become generalized. The principal associated motor signs were arrest of movement and oral automatisms. Histological examination after two to ten days demonstrated lesions (neuron loss and gliosis) at the injection site that varied according to the amount of kainic acid injected (2 to 68 μg). “Remote” lesions occurred in the ipsilateral hippocampus (end‐folium and Sommer sector) and neocortex (occipital and frontal regions). The hippocampal lesions were comparable to those previously described as consequent to status epilepticus.
Annals of Neurology – Wiley
Published: Nov 1, 1980
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