MECHANISMS OF ICTAL SPEECH ARREST IN LANGUAGE-DOMINANT ONSET TEMPORAL EPILEPSY
Abstract number :
2.087
Submission category :
Year :
2002
Submission ID :
1347
Source :
www.aesnet.org
Presentation date :
12/7/2002 12:00:00 AM
Published date :
Dec 1, 2002, 06:00 AM
Authors :
Brenda Y. Wu, Stephen Eisenschenk, Chris J. Sackellares, Eileen Fennell, Steven N. Roper, Robin L. Gilmore. Department of Neurology, University of Florida, Gainesville, FL; Department of Clinical and Health Psychology, Department of Neurosurgery, Universi
RATIONALE: Ictal speech with automatism and preserved responsiveness (APR) has been proposed as a reliable lateralizing sign with possible 100% specificity in non-language-dominant onset (NLDO) temporal lobe epilepsy (TLE). In our experience, similar semiology may be present in patients with language-dominant onset (LDO) TLE. Possible mechanisms of impaired ictal speech are explored here by studying cases with fluent ictal speech. At the end, the participants should be aware that ictal speech with preserved responsiveness may occur in TLE of language-dominant hemisphere.
METHODS: We reviewed clinical semiology and intracranial video EEGs of 46 adult patients for whom language dominance had been determined by Wada testing. Between January 1999 and March 2002, these patients were evaluated by bilateral depth with scalp electrodes or unilateral grids [plusminus] subdural strips. During ictal events, patients were tested for orientation, ability to count and ability to follow commands.
RESULTS: Fourteen patients had extra-temporal foci and are not discussed. Of the 32 patients with TLE, 9 had left, 17 right and 6 bilateral onsets. The cerebral dominance for language was left hemisphere in all patients. Among the 15 patients with unilateral left-onset or bilateral temporal onset seizures, 2 patients presented with ictal speech with APR during LDO seizures. For patient A who had similar semiology in either left- or right-onset hippocampal (hc) seizures, the presence of propagated epileptiform activity in the ipsilateral temporal cortex did not consistently abolish her ictal speech. Patient B with a left-onset hc epileptic focus maintained his baseline mentation and speech throughout seizures. With these seizuresm there was no propagation of epileptiform discharges to ipsilateral neocortex. However, he did completely lose responsiveness in seizures with secondary generalization to the contralateral hemisphere.
CONCLUSIONS: Fluent ictal speech in TLE is not a pathognomonic lateralizing sign for NLDO seizures. It may occasionally be seen in patients whose focus is within the language-dominant hemisphere. Propagation of epileptiform activity to the ipsilateral temporal neocortex may impair responsiveness but may not necessarily impair fluency. Distribution or rhythmicity and morphology of epileptiform activity in the temporal neocortex may be associated with varying degrees of ictal aphasia in LDO TLE.[table1]