Postical aphasia and paresis: A clinical and intracerebral EEG study

Citation
C. Adam et al., Postical aphasia and paresis: A clinical and intracerebral EEG study, CAN J NEUR, 27(1), 2000, pp. 49-54
Citations number
38
Categorie Soggetti
Neurology,"Neurosciences & Behavoir
Journal title
CANADIAN JOURNAL OF NEUROLOGICAL SCIENCES
ISSN journal
03171671 → ACNP
Volume
27
Issue
1
Year of publication
2000
Pages
49 - 54
Database
ISI
SICI code
0317-1671(200002)27:1<49:PAAPAC>2.0.ZU;2-2
Abstract
Background: We examined the lateralizing value of postictal language and mo tor deficits and studied their underlying mechanisms. Patients and methods: The total sample consisted of 35 patients (26 temporals, 8 frontals, 1 par ietal) 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 diffu sion of the epileptic discharge recorded by intracerebral EEG. Language dom inance was determined by the intracarotid amobarbital test. Results: Postic tal aphasia was observed only when (1) seizure originated in the dominant h emisphere and (2) ictal activity spread to language areas (Wernicke and/or Broca areas). When the epileptic focus was in the nondominant hemisphere, n o 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 se izures were secondarily generalized. Conclusion: Postictal aphasia in tempo ral 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.