title: Transient epileptic amnesia: regional brain atrophy and its relationship to memory deficits.
abstract: Transient epileptic amnesia (TEA) is a recently recognised form of epilepsy of which the principle manifestation is recurrent, transient episodes of isolated memory loss. In addition to the amnesic episodes, many patients describe significant interictal memory difficulties. Performance on standard neuropsychological tests is often normal. However, two unusual forms of memory deficit have recently been demonstrated in TEA: (i) accelerated long-term forgetting (ALF): the excessively rapid loss of newly acquired memories over a period of days or weeks and (ii) remote autobiographical memory loss: a loss of memories for salient, personally experienced events of the past few decades. The neuroanatomical bases of TEA and its associated memory deficits are unknown. In this study, we first assessed the relationship between subjective and objective memory performance in 41 patients with TEA. We then analysed MRI data from these patients and 20 matched healthy controls, using manual volumetry and voxel-based morphometry (VBM) to correlate regional brain volumes with clinical and neuropsychological data. Subjective memory estimates were unrelated to performance on standard neuropsychological tests but were partially predicted by mood, ALF and remote autobiographical memory. Manual volumetry identified subtle hippocampal volume loss in the patient group. Both manual volumetry and VBM revealed correlations between medial temporal lobe atrophy and standard anterograde memory scores, but no relation between atrophy and ALF or remote autobiographical memory. These results add weight to the hypothesis that TEA is a syndrome of mesial temporal lobe epilepsy. Furthermore, they suggest that although standard anterograde memory test performance is related to the degree of mesial temporal lobe damage, this is not true for ALF and autobiographical amnesia. It is possible that these unusual memory deficits have a more diffuse physiological basis rather than being a consequence of discrete structural damage.
authors.affiliation: Department of Clinical Neurosciences, Western General Hospital, Edinburgh, UK. chris.butler@ed.ac.uk
authors.forename: C R
authors.initials: CR
authors.lastname: Butler
authors.forename: A
authors.initials: A
authors.lastname: Bhaduri
authors.forename: J
authors.initials: J
authors.lastname: Acosta-Cabronero
authors.forename: P J
authors.initials: PJ
authors.lastname: Nestor
authors.forename: N
authors.initials: N
authors.lastname: Kapur
authors.forename: K S
authors.initials: KS
authors.lastname: Graham
authors.forename: J R
authors.initials: JR
authors.lastname: Hodges
authors.forename: A Z
authors.initials: AZ
authors.lastname: Zeman
mesh_terms: D000368:Aged; D000647:Amnesia / Q000473:pathology*; D001284:Atrophy; D001921:Brain / Q000473:pathology*; D016022:Case-Control Studies; D004827:Epilepsy / Q000473:pathology*; D005260:Female; D006801:Humans; D007091:Image Processing, Computer-Assisted; D008279:Magnetic Resonance Imaging; D008297:Male; D008568:Memory; D008875:Middle Aged; D009483:Neuropsychological Tests; D011581:Psychological Tests