Calcified neurocysticercotic lesions and postsurgery seizure control in temporal lobe epilepsy

Citation
Jp. Leite et al., Calcified neurocysticercotic lesions and postsurgery seizure control in temporal lobe epilepsy, NEUROLOGY, 55(10), 2000, pp. 1485-1491
Citations number
40
Categorie Soggetti
Neurology,"Neurosciences & Behavoir
Journal title
NEUROLOGY
ISSN journal
00283878 → ACNP
Volume
55
Issue
10
Year of publication
2000
Pages
1485 - 1491
Database
ISI
SICI code
0028-3878(20001128)55:10<1485:CNLAPS>2.0.ZU;2-V
Abstract
Background: Several studies suggest that neurocysticercosis is the main cau se of symptomatic epilepsy in developing countries. In such areas, calcifie d cysticercotic lesions (CCL) are frequently found in patients with complex partial seizures associated with hippocampal sclerosis (HS). The authors s tudied whether there are clinical and pathologic differences between HS pat ients with and without CCL. Methods: The authors determined the clinical an d pathologic findings of 30 patients with HS and compared them with 32 pati ents with HS + CCL. Hippocampi from both groups were measured for fascia de ntata Timm staining and cell density in hippocampal subfields. Results: In the HS + CCL group, single or multiple CCL were found in all lobes with no lobar predominance. An initial precipitating event occurred in 83.3% of HS and in 62.5% of HS + CCL. First complex partial seizure occurred at 10.1 ye ars in HS and at 11.9 years in HS + CCL. No significant differences were fo und for fascia dentata Timm staining and hippocampal cell densities. Good p ostsurgery outcome (Engel I classification) did not differ between groups, with this result occurring in 76.6% of patients with HS and 81.2% of patien ts with HS + CCL. Conclusions: The presence of CCL does not influence the c linical and pathologic profile of patients with hippocampal atrophy. Clinic al histories and postsurgical outcomes were similar to those of patients wi th classic HS, suggesting that the CCL is probably, in this set of patients , a coincidental pathology and does not have a role in epileptogenesis.