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Am J Clin Oncol 1988;11:614–7. 16. Sinkovics JG, Plager C, Ayala AG, et al. Ewing sarcoma: its course and treatment in 50 adult patients. Oncology 1980;37:114–9. doi:10.1016/j.jocn.2010.02.010 Focal retrograde amnesia: Extending the clinical syndrome of transient epileptic amnesia Michael Hornberger a,b , Armin Mohamed c , Laurie Miller c , John Watson c , Zoe Thayer c , John R. Hodges a,b, * a Prince of Wales Medical Research Institute, Corner of Barker Street and Easy Street, Randwick, New South Wales 2031, Australia b School of Medical Sciences, University of New South Wales, Kensington, New South Wales, Australia c Royal Prince Alfred Hospital, University of Sydney, New South Wales, Australia article info Article history: Received 16 November 2009 Accepted 8 March 2010 Keywords: Transient epileptic amnesia Retrograde amnesia Ictal epileptic activity Autobiographical memory Prodromal TEA abstract A 44-year-old woman presented with focal retrograde amnesia and complaints of rapid forgetting in the absence of episodes of transient cognitive disturbance. Her MRI and 2-deoxy-2-[18F]fluoro-D-glucose positron emission tomography (FDG-PET) were normal. On standard neuropsychological tests she per- formed within the normal range although a test of autobiographical memory confirmed impoverished recall especially involving recent life events. The electroencephalograph (EEG) recordings were sugges- tive of temporal lobe epilepsy but no clear diagnosis was established. After 4 years the patient’s recurrent brief episodes of disorientation, suggestive of transient epileptic amnesia (TEA), were corroborated by her sister. This diagnosis was confirmed by an ambulatory EEG that revealed ictal activity. Several important points emerge from this study. Focal retrograde amnesia can be a prodromal symp- tom of TEA which can precede the full-blown syndrome by several years. Moreover, transient attacks might not be reported if patients live alone. The ictal EEG findings further substantiate the epileptic nat- ure of the syndrome. Ó 2010 Elsevier Ltd. All rights reserved. 1. Introduction Transient epileptic amnesia (TEA) 1–3 is characterized by recurrent brief amnesic periods often on waking presenting in middle-aged or elderly subjects. Patients complain of dense gaps in autobiographical memories 4 and accelerated loss of new mem- ories over days or weeks, 5 although their performance on standard neuropsychological tests is within normal limits. 6 The question arises of whether some patients with isolated retrograde amnesia (RGA) may have a cryptic form of TEA as electroencephalograph (EEG) findings may be subtle. 7 We report a long-term study of a patient presenting with focal RGA and accel- erated forgetting but without other clinical manifestations of TEA. Definite proof of the diagnosis emerged only 4 years later when transient ‘‘attacks” were witnessed and ambulatory EEG revealed accompanying ictal activity. 2. Case report A 44-year-old woman presented in 2004 with a 12 months his- tory of focal RGA. She noticed that friends and family could recall events that she could not, even when prompted. She and family members denied transient amnesia or ictal phenomena and no changes in cognition, mood, appetite or sleep. The patient did not smoke, drank no alcohol and had no history of psychiatric illnesses. Her medical history included hypertension, a thyroidectomy and mild infrequent migraine without aura. Awake and sleep EEGs showed sharp waves in the left temporal region but seizures and epileptiform changes were not seen on an ambulatory EEG re- corded over 4 consecutive days. Her MRI and 2-deoxy-2-[18F]flu- oro-D-glucose positron emission tomography (FDG-PET) were normal. Neuropsychological assessment revealed average to high aver- age level on all measures (premorbid intellect, visuo-spatial, lan- guage, executive function and memory measures (Table 1)). Long-term memory testing indicated accelerated forgetting over seven days and impaired recent autobiographical memories (Fig. 1). * Corresponding author. Tel.: +61 2 9399 1132; fax: +61 2 9399 1047. E-mail address: j.hodges@powmri.edu.au (J.R. Hodges). Case Reports / Journal of Clinical Neuroscience 17 (2010) 1319–1321 1319