Edoardo Ferlazzo1,2,3, Sara Gasparini1,2, Ettore Beghi4, Chiara Sueri2, Emilio Russo5, Antonio Leo5, Angelo Labate1,3, Antonio Gambardella1,3, Vincenzo Belcastro6, Pasquale Striano7, Maurizio Paciaroni8, Laura Rosa Pisani9, Umberto Aguglia1,2,3. 1. Department of Medical and Surgical Sciences, Magna Graecia University, Catanzaro, Italy. 2. Regional Epilepsy Centre, Bianchi-Melacrino-Morelli Hospital, Reggio Calabria, Italy. 3. Institute of Molecular Bioimaging and Physiology of the National Research Council (IBFM-CNR), Catanzaro, Italy. 4. Laboratory of Neurological Disorders, IRCCS - Mario Negri Institute for Pharmacological Research Via La Masa, Milan, Italy. 5. Science of Health Department, School of Medicine, Magna Graecia University of Catanzaro, Viale Europa, Catanzaro, Italy. 6. Neurology Unit, Department of Neurosciences, S. Anna Hospital, Ravona, Como, Italy. 7. Department of Neurosciences, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health, G. Gaslini Institute, University of Genova, Genova, Italy. 8. Stroke Unit and Division of Cardiovascular Medicine, University of Perugia, Perugia, Italy. 9. IRCCS Centro Neurolesi Bonino-Pulejo, Messina, Italy.
Abstract
OBJECTIVE: Seizures may occur in close temporal association with a stroke or after a variable interval. Moreover, epilepsy is often encountered in patients with leukoaraiosis. Although early post-stroke seizures have been studied extensively, less attention has been paid to post-stroke epilepsy (PSE) and to epilepsy associated with leukoaraiosis (EAL). The aim of this paper is to review data concerning pathophysiology, prognosis, and treatment of PSE and EAL. METHODS: We performed an extensive literature search to identify experimental and clinical articles on PSE and EAL. We also conducted a systematic review of risk factors for PSE and EAL among eligible studies. RESULTS: PSE is caused by enhanced neuronal excitability within and near the scar. The role played by white matter changes in EAL remains to be elucidated. Meta-analysis showed that cortical involvement (odds ratio [OR] 3.71, 95% confidence interval [CI] 2.34-5.90, p < 0.001), cerebral hemorrhage (OR 2.41, 95% CI 1.57-3.70, p < 0.001), and early seizures (OR 4.43, 95% CI 2.36-8.32, p < 0.001) are associated with an increased risk of PSE. As regards EAL, no prospective, population-based studies evaluated the role of different variables on seizure risk. Studies about the management of PSE are limited. PSE is generally well controlled by drugs. Data about risk factors, prognosis, and treatment of EAL are lacking. SIGNIFICANCE: Pathophysiology and risk factors are well defined for PSE but need to be elucidated for EAL. Management of PSE and EAL relies on the clinician's judgment and should be tailored on an individual basis. Wiley Periodicals, Inc.
OBJECTIVE:Seizures may occur in close temporal association with a stroke or after a variable interval. Moreover, epilepsy is often encountered in patients with leukoaraiosis. Although early post-stroke seizures have been studied extensively, less attention has been paid to post-stroke epilepsy (PSE) and to epilepsy associated with leukoaraiosis (EAL). The aim of this paper is to review data concerning pathophysiology, prognosis, and treatment of PSE and EAL. METHODS: We performed an extensive literature search to identify experimental and clinical articles on PSE and EAL. We also conducted a systematic review of risk factors for PSE and EAL among eligible studies. RESULTS: PSE is caused by enhanced neuronal excitability within and near the scar. The role played by white matter changes in EAL remains to be elucidated. Meta-analysis showed that cortical involvement (odds ratio [OR] 3.71, 95% confidence interval [CI] 2.34-5.90, p < 0.001), cerebral hemorrhage (OR 2.41, 95% CI 1.57-3.70, p < 0.001), and early seizures (OR 4.43, 95% CI 2.36-8.32, p < 0.001) are associated with an increased risk of PSE. As regards EAL, no prospective, population-based studies evaluated the role of different variables on seizure risk. Studies about the management of PSE are limited. PSE is generally well controlled by drugs. Data about risk factors, prognosis, and treatment of EAL are lacking. SIGNIFICANCE: Pathophysiology and risk factors are well defined for PSE but need to be elucidated for EAL. Management of PSE and EAL relies on the clinician's judgment and should be tailored on an individual basis. Wiley Periodicals, Inc.
Authors: Maximilian Lenz; Marina Ben Shimon; Felix Benninger; Miri Y Neufeld; Efrat Shavit-Stein; Andreas Vlachos; Nicola Maggio Journal: J Mol Med (Berl) Date: 2019-10-31 Impact factor: 4.599
Authors: Charlotte Germonpré; Silke Proesmans; Charlotte Bouckaert; Mathieu Sprengers; Paul Boon; Robrecht Raedt; Veerle De Herdt Journal: Front Neurosci Date: 2021-06-18 Impact factor: 4.677