LATE SEIZURE RECURRENCE AND THE POSSIBILITY OF SECONDARY EPILEPTOGENESIS AT THE EDGE OF THE PREVIOUS RESECTION AFTER TEMPORAL LOBECTOMY IN PATIENTS WITH MESIAL TEMPORAL SCLEROSIS
Abstract number :
2.412
Submission category :
Year :
2003
Submission ID :
1049
Source :
www.aesnet.org
Presentation date :
12/6/2003 12:00:00 AM
Published date :
Dec 1, 2003, 06:00 AM
Authors :
Barbara C. Jobst, Brenna C. McDonald, Andrew J. Saykin, Tamas A. Gonda, Karen L. Gilbert, Vijay M. Thadani, Laurence D. Cromwell, David W. Roberts, Peter D. Williamson Section of Neurology, Dartmouth- Hitchcock Medical Center, Lebanon, NH; Department of P
A small percentage of patients with mesial temporal sclerosis become initially seizure free after temporal lobectomy, but seizures may recur despite being seizure free for extended periods of time after surgery. Recurrence could be due to false localization of the true seizure onset outside the initially resected area. Secondary epileptogenesis at the edge of the initial resection has also been suggested. This study correlates late seizure recurrence with MRI abnormalities at the edge of the resection.
Volumetric analysis of hyperintense signal on FLAIR MRI at the edge of the resection, likely to represent gliosis, was performed in 13 patients with pathologically confirmed mesial temporal sclerosis. 7 patients were initially seizure free but had a late seizure recurrence ([gt]1 year seizure free, mean follow up 77.8 months). As control group, eight seizure free patients were evaluated (mean follow up: 72.2 months).
Mean seizure recurrence was at 38.7 months (12-144 months) after surgery. Hyperintense FLAIR signals at the edge of the resection were greatly variable (range: 0.125 cm3-9.6 cm3) in patients with and without seizure recurrence. Seizure recurrence did not correlate with the extent of signal abnormalities (mean volume seizure free: 2.04 cm3 seizure recurrence 2.48 cm3; p=0.79). Signal abnormalities were independent of the timespan after surgery (Pearson coefficient: 0.14; p=0.87) and surgical procedure (selective amydalohippocampectomy versus standard temporal lobectomy), but extent of signal change was significantly correlated with age (p=0.04). One patient underwent repeat invasive evaluation after seizure recurrence 12 years after temporal lobectomy. Seizure onset was proven to be in the ipsilateral insula not at the edge of the resection.
The mechanism of late seizure recurrence in patients with mesial temporal sclerosis is still unclear. This study could not correlate imaging abnormalities at the edge of the previous resection with seizure recurrence, and other mechanisms besides secondary epileptogenesis at the edge of the resection may play a crucial role in late seizure recurrence.
[Supported by: Hitchcock Foundation]