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Calcified neurocysticercotic lesions and postsurgery seizure control in temporal lobe epilepsy

From Departments of Neurology (Drs. Leite, Terra–Bustamante, Fernandes, Sakamoto, and Takayanagui), Surgery (Dr. Assirati), Pathology (Dr. Chimelli), and Clinical Medicine (Dr. Santos), University of São Paulo School of Medicine at Ribeirão Preto, Brazil.

Address correspondence and reprint requests to Dr. João P. Leite, Department of Neurology, University of São Paulo School of Medicine at Ribeirão Preto, Ribeirão Preto, Campus Universitário, CEP 14049-900, Brazil; e-mail: jpleite{at}fmrp.usp.br

BACKGROUND: Several studies suggest that neurocysticercosis is the main cause of symptomatic epilepsy in developing countries. In such areas, calcified cysticercotic lesions (CCL) are frequently found in patients with complex partial seizures associated with hippocampal sclerosis (HS). The authors studied whether there are clinical and pathologic differences between HS patients with and without CCL.

METHODS: The authors determined the clinical and pathologic findings of 30 patients with HS and compared them with 32 patients with HS + CCL. Hippocampi from both groups were measured for fascia dentata 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 years in HS and at 11.9 years in HS + CCL. No significant differences were found for fascia dentata Timm staining and hippocampal cell densities. Good postsurgery outcome (Engel I classification) did not differ between groups, with this result occurring in 76.6% of patients with HS and 81.2% of patients with HS + CCL.

CONCLUSIONS: The presence of CCL does not influence the clinical and pathologic profile of patients with hippocampal atrophy. Clinical histories and postsurgical outcomes were similar to those of patients with classic HS, suggesting that the CCL is probably, in this set of patients, a coincidental pathology and does not have a role in epileptogenesis.–1491

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