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Article type: Research Article
Authors: Cretin, Benjamina; b; c; d | Di Bitonto, Laurea; b; d | Blanc, Frederica; b; c; d | Magnin, Eloie; f; g; *
Affiliations: [a] Unité de Neuropsychologie, Service de Neurologie des Hôpitaux Universitaires de Strasbourg, Strasbourg, France | [b] Centre Mémoire, de Ressources et de Recherche d'Alsace (Strasbourg-Colmar), France | [c] Laboratoire ICube, CNRS-Université de Strasbourg, France | [d] Centre de Compétences des démences rares des Hôpitaux Universitaires de Strasbourg/Service de Neurologie, Hospices Civils de Colmar, France | [e] Centre Mémoire Ressousrces et Recherche (CMRR), CHU Besançon, Besançon, France | [f] Service de Neurologie, CHU Besançon, Besançon, France | [g] Centre Leenaards de la Mémoire, CHUV, Lausanne, Suisse
Correspondence: [*] Correspondence to: Eloi Magnin, MD, PhD, Department of Neurology, University Hospital of Besancon, 25000 Besancon, France. Tel.: +33381668098; Fax: +33381668470; E-mail: [email protected].
Abstract: Seizures can be an early symptom of Alzheimer's disease (AD) and can precede cognitive decline. Early epilepsy in AD can mimic transient epileptic amnesic syndrome (TEAS) or epileptic amnesic syndrome. We report the case of a patient who started a cerebrospinal fluid (CSF)-proven AD with partial seizures and TEAS that secondarily became a cortical posterior atrophy syndrome. CSF biomarkers showed a high amyloid production, amyloidopathy, and high level of total tau and p-Tau. This observation adds data to the complex AD-early epilepsy interactions and illustrates that atypical AD can cause a TEAS. Possible red flags for an underlying neurodegenerative process in TEAS are discussed.
Keywords: Alzheimer's disease, mild cognitive impairment, posterior cortical atrophy, temporal lobe epilepsy, transient epileptic amnesic syndrome
DOI: 10.3233/JAD-141953
Journal: Journal of Alzheimer's Disease, vol. 45, no. 2, pp. 521-526, 2015
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