Sara Gasparini1, Edoardo Ferlazzo1, Ettore Beghi2, Vito Sofia3, Laura Mumoli4, Angelo Labate4, Vittoria Cianci1, Daniela Fatuzzo3, Marina Angela Bellavia1, Luciano Arcudi5, Emilio Russo6, Giovambattista De Sarro6, Antonio Gambardella4, Umberto Aguglia7. 1. Magna Græcia University of Catanzaro, Regional Epilepsy Center, Via Melacrino, Reggio Calabria, Italy. 2. Laboratory of Neurological Disorders, "Mario Negri" Institute, Via G. La Masa 19, Milan, Italy. 3. Department "GF.Ingrassia", Neurologic Clinic, University of Catania, Via S. Sofia 78, Catania, Italy. 4. Neurologic Clinic, Magna Græcia University of Catanzaro, Viale Europa, Catanzaro, Italy. 5. Stroke Unit Azienda Ospedaliera Bianchi Melacrino Morelli, Via Melacrino, Reggio Calabria, Italy. 6. Science of Health Department, School of Medicine, Magna Græcia University of Catanzaro, Viale Europa, Catanzaro, Italy. 7. Magna Græcia University of Catanzaro, Regional Epilepsy Center, Via Melacrino, Reggio Calabria, Italy. Electronic address: u.aguglia@tin.it.
Abstract
OBJECTIVE: To compare anatomo-electro-clinical findings between patients with epilepsy associated with leukoaraiosis only (EAL) and patients with a well-defined vascular lesion, i.e. post-stroke epilepsy (PSE). METHODS: Two hundred eighty-three subjects with epilepsy and cerebrovascular disease, consecutively seen in our epilepsy centres from January 2000 to March 2014, were retrospectively considered. Inclusion criteria were: history of one or more unprovoked seizures and MRI evidence of one or more vascular lesions. Exclusion criteria were: inadequate neuroimaging data, coexistence of nonvascular lesions, and psychogenic seizures. Subjects were divided in two groups: PSE and EAL, based onclinical and MRI findings. Epileptogenic focus was identified according to ictal semiology and EEG findings. In PSE group, coherence between the vascular lesion(s) and epileptogenic focus was scored as likely or unlikely. RESULTS: One hundred seventeen subjects were included: 58 had PSE, 59 EAL. Coherence was identified as likely in 38 (95%) and unlikely in 2 (5%). At univariate analysis, abnormal EEG and frontal localization were associated with a lower EAL probability [odds ratio (OR) 0.36, 95% confidence interval (CI) 0.15-0.87, p=0.02 and OR 0.12, 95% CI 0.04-0.37, p<0.001, respectively], while temporal localization was associated with a higher EAL probability (OR 4.0, 95% CI 1.8-9.0, p<0.001). Multivariate confirmed these associations. CONCLUSIONS: While in PSE epileptogenic focus is coherent with the vascular lesions, in EAL temporal lobe epilepsy predominates. In EAL, causal relationship between vascular lesions and epilepsy is not straightforward, and the role of adjunctive factors needs to be elucidated.
OBJECTIVE: To compare anatomo-electro-clinical findings between patients with epilepsy associated with leukoaraiosis only (EAL) and patients with a well-defined vascular lesion, i.e. post-stroke epilepsy (PSE). METHODS: Two hundred eighty-three subjects with epilepsy and cerebrovascular disease, consecutively seen in our epilepsy centres from January 2000 to March 2014, were retrospectively considered. Inclusion criteria were: history of one or more unprovoked seizures and MRI evidence of one or more vascular lesions. Exclusion criteria were: inadequate neuroimaging data, coexistence of nonvascular lesions, and psychogenic seizures. Subjects were divided in two groups: PSE and EAL, based onclinical and MRI findings. Epileptogenic focus was identified according to ictal semiology and EEG findings. In PSE group, coherence between the vascular lesion(s) and epileptogenic focus was scored as likely or unlikely. RESULTS: One hundred seventeen subjects were included: 58 had PSE, 59 EAL. Coherence was identified as likely in 38 (95%) and unlikely in 2 (5%). At univariate analysis, abnormal EEG and frontal localization were associated with a lower EAL probability [odds ratio (OR) 0.36, 95% confidence interval (CI) 0.15-0.87, p=0.02 and OR 0.12, 95% CI 0.04-0.37, p<0.001, respectively], while temporal localization was associated with a higher EAL probability (OR 4.0, 95% CI 1.8-9.0, p<0.001). Multivariate confirmed these associations. CONCLUSIONS: While in PSE epileptogenic focus is coherent with the vascular lesions, in EAL temporal lobe epilepsy predominates. In EAL, causal relationship between vascular lesions and epilepsy is not straightforward, and the role of adjunctive factors needs to be elucidated.
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