Abstract
Objective: To characterize the clinical, EEG, and neuroimaging profiles of transient epileptic amnesia (TEA).Methods: We performed a retrospective analysis of patients diagnosed with TEA at the Mayo Clinic Minnesota from January 1, 1998 to September 21, 2017. Diagnostic criteria included the presence of recurrent episodes of transient amnesia with preservation of other cognitive functions and evidence for epilepsy [epileptiform abnormalities on EEG, clinical features of seizures, or symptomatic response to anti-seizure medications (ASMs)].Results: Nineteen patients were identified (14 men, 5 women) with median onset age 66 years and median time to diagnosis 2 years. Thirteen patients (68%) reported persistent cognitive/behavioral symptoms, including 4 (21%) for whom these were the chief presenting complaints. EEG revealed epileptiform abnormalities involving the frontal and/or temporal regions in 12/19 individuals (63%), including activation during sleep in all of these cases. In numerous cases, sleep and prolonged EEG evaluations identified abnormalities not previously seen on shorter or awake-state studies. Brain MRI revealed focal abnormalities in only 4/19 cases (21%). FDG-PET identified focal hypometabolism in 2/8 cases where it was performed, both involving the frontal and/or temporal regions. Anti-seizure therapy, most often with a single agent, resulted in improvement (reduction in spell frequency and/or subjective improvement in interictal cognitive/behavioral complaints) in all 17 cases with available follow-up.Conclusions: TEA is a treatable cause of amnestic spells in older adults. This syndrome is frequently associated with persistent interictal cognitive/behavioral symptoms and thus can be mistaken for common mimics. In the appropriate clinical context, our findings support the use of early prolonged EEG with emphasis on sleep monitoring as a key diagnostic tool. FDG-PET may also complement MRI in distinguishing TEA from neurodegenerative disease when suspected.
Highlights
Transient epileptic amnesia (TEA) is a clinical presentation of focal epilepsy of presumed temporal origin which is characterized by self-resolving episodes of retrograde and/or anterograde amnesia [1]
Sleep is known to be crucial for memory consolidation [13], and frequent nocturnal subclinical seizures have been proposed as mechanisms for unremitting accelerated longterm forgetting and autobiographical memory impairment in TEA [4, 11]
Comorbid sleep pathologies such as obstructive sleep apnea can impact seizure frequency [14]. These concepts suggest that prolonged EEG including sufficient sleep recording may be crucial both for initial diagnosis, when short-term studies are unrevealing, and for assessing for uncontrolled subclinical seizures if interictal cognitive and behavioral symptoms do not improve despite anti-seizure medications (ASMs) initiation
Summary
Transient epileptic amnesia (TEA) is a clinical presentation of focal epilepsy of presumed temporal origin which is characterized by self-resolving episodes of retrograde and/or anterograde amnesia [1]. Reminiscent of events of transient global amnesia (TGA), the spells of TEA tend to be shorter (often 1 h or less), more commonly recurrent, associated with waking, and responsive to anti-seizure medications (ASMs) [2, 3]. In addition to the transient amnestic spells which are the hallmark of this disorder, most patients with TEA experience some degree of chronic memory difficulties. Distinctive forms of memory dysfunction associated with TEA include loss over days to weeks of recently learned information (known as accelerated long-term forgetting) and loss of memories of remote life events (known as autobiographical memory impairment) [4, 5]. Other less specific cognitive and behavioral complaints can be present and may precede the identification of amnestic spells by years [6]
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