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Postictal Aphasia and Paresis: A Clinical and Intracerebral EEG Study

Published online by Cambridge University Press:  04 August 2016

Christine Adam ,
Claude Adam ,
Isabelle Rouleau  and
Jean-Marc Saint-Hilaire
Christine Adam
Affiliation:
C.H.U.M. (Pavillon Notre-Dame), Service de Neurologie, Montréal, Québec, Canada Université de Montréal, Montréal, Québec, Canada
Claude Adam
Affiliation:
C.H.U.M. (Pavillon Notre-Dame), Service de Neurologie, Montréal, Québec, Canada
Isabelle Rouleau
Affiliation:
C.H.U.M. (Pavillon Notre-Dame), Service de Neurologie, Montréal, Québec, Canada Université du Québec à Montréal, Montréal, Québec, Canada
Jean-Marc Saint-Hilaire*
Affiliation:
C.H.U.M. (Pavillon Notre-Dame), Service de Neurologie, Montréal, Québec, Canada Université de Montréal, Montréal, Québec, Canada
*
C.H.U.M. (Pavillon Notre-Dame), Service de Neurologie, 1560, rue Sherbrooke est, Montréal (Québec) H2L4M1, Canada.
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Abstract:

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Background:

We examined the lateralizing value of postictal language and motor deficits and studied their underlying mechanisms.

Patients and methods:

The total sample consisted of 35 patients (26 temporals, 8 frontals, 1 parietal) with a good postsurgical outcome (Engel's class I and II). Postictal examination was blindly reviewed on videotapes. In 15 cases (29 seizures), postictal language manifestations were analyzed in relation with the diffusion of the epileptic discharge recorded by intracerebral EEG. Language dominance was determined by the intracarotid amobarbital test.

Results:

Postictal aphasia was observed only when (1) seizure originated in the dominant hemisphere and (2) ictal activity spread to language areas (Wernicke and/or Broca areas). When the epileptic focus was in the nondominant hemisphere, no postictal aphasia was observed even if there was secondary generalization of ictal activity affecting the language areas of the dominant hemisphere. Postictal motor deficits also had a strong lateralizing value even when seizures were secondarily generalized.

Conclusion:

Postictal aphasia in temporal epilepsies and postictal motor deficits in temporal and extra temporal epilepsies provided excellent lateralizing information. Postictal deficits appear to be the result of inhibitory mechanisms induced by previous ictal activity of the structures related to these functions.

Résumé:

RÉSUMÉ:Introduction:

Nous avons examiné la valeur de latéralisation post-ictale des déficits du langage et des déficits moteurs et nous avons étudié les mécanismes sous-jacents.

Patients et Méthodes:

L'échantillon comprenait 35 patients ayant subi avec succès une chirurgie (classe I et II de Engel), dont 26 ayant présenté un ictus temporal, 8 un ictus frontal et 1 un ictus pariétal. L'examen post-ictal a été révisé à l'aveugle sur bande vidéo. Dans 15 cas (29 crises), les manifestations post-ictales au niveau du langage ont été analysées en relation avec la diffusion de la décharge épileptique enregistrée par ÉEG intracérébral. La dominance pour le langage a été déterminée par le test intracarotidien à l'amobarbital.

Résultats:

L'aphasie post-ictale a été observée seulement quand 1) les crises originaient dans l'hémisphère dominant et 2) l'activité ictale s'étendait aux zones du langage (zones de Wernicke et/ou de Broca). Quand le foyer épileptique était situé dans l'hémisphère non dominant on n'a pas observé d'aphasie post-ictale, même quand il y avait généralisation secondaire de l'activité épileptique affectant les zones du langage de l'hémisphère dominant. Les déficits moteurs post-ictaux avaient également une grande valeur de latéralisation, même quand les crises étaient secondairement généralisées.

Conclusion:

L'aphasie post-ictale dans les épilepsies temporales et les déficits moteurs post-ictaux dans les épilepsies temporales et extratemporales fournissent de l'information précieuse sur la latéralisation. Les déficits post-ictaux semblent être le résultat de mécanismes inhibiteurs induits par une activité ictale antérieure des structures reliées à ces fonctions.

Type
Original Article
Information
Canadian Journal of Neurological Sciences , Volume 27 , Issue 1 , February 2000 , pp. 49 - 54
Copyright
Copyright © The Canadian Journal of Neurological 2000

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