Abstract
Transient amnesic syndromes are striking clinical phenomena that are commonly encountered by physicians in acute medical settings. Diagnosis of such syndromes can be challenging, and their causes have been debated for over 50 years. Critical clinical distinctions, such as between transient global amnesia (TGA) and transient epileptic amnesia (TEA), as well as important clues to the underlying pathophysiology, have recently been revealed. TGA is characterized by the sudden onset of a profound anterograde and retrograde amnesia that lasts for up to 24 h, with neuroimaging after an acute TGA event showing transient perturbation of specific hippocampal circuits that are involved in memory processing. Some cases of transient amnesia are attributable to focal seizure activity and are termed TEA, which has a clinical presentation similar to that of TGA, but can be distinguished from the latter by the brevity and frequency of amnesic attacks. Moreover, TEA carries a risk of persistent memory impairment that can be mistaken for dementia. Here, we summarize clinically relevant aspects of transient amnesic syndromes, giving practical recommendations for diagnosis and patient management. We describe results from imaging and epidemiological studies that have shed light on the functional anatomy and pathophysiological mechanisms underlying these conditions.
Key Points
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In patients with transient amnesia, careful assessment of the amnesic deficit is mandatory to identify treatable conditions
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After an acute attack of transient global amnesia (TGA), hippocampal lesions can be detected on MRI, suggesting transient dysfunction of hippocampus-dependent memory circuits
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Transient epileptic amnesia (TEA) can often be distinguished from TGA by the brevity and frequency of the amnesic attacks
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In contrast to TGA, TEA carries a risk of developing persistent memory impairment, which can be mistaken for dementia
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Imaging and neuropsychological data indicate that focal hippocampal pathology occurs in both TGA and TEA
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Psychogenic amnesia typically involves profound retrograde amnesia, often with loss of personal identity, in the context of preserved new learning.
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Acknowledgements
We wish to thank G. Deuschl, J. Döhring, K. Witt, A. Zeman, and other colleagues for helpful input, support and for many inspiring discussions. This work has been supported by Deutsche Forschungsgemeinschaft SFB 654 (TP A14; awarded to T. Bartsch) and by the Faculty of Medicine, University of Kiel, Germany. C. Butler is funded by the National Institute for Health Research. All case examples included in this manuscript are fictional and provided for illustrative purposes only.
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T. Bartsch has received speakers honoraria from GlaxoSmithKline and Thieme. C. Butler declares no competing interests.
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Bartsch, T., Butler, C. Transient amnesic syndromes. Nat Rev Neurol 9, 86–97 (2013). https://doi.org/10.1038/nrneurol.2012.264
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DOI: https://doi.org/10.1038/nrneurol.2012.264
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