Acute neurological disease as a trigger or co-occurrence of transient global amnesia: a case series and systematic review View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2022-07-15

AUTHORS

Silvio Piffer, Stefania Nannoni, Francesco Maulucci, Valérie Beaud, Olivier Rouaud, Carlo W. Cereda, Philippe Maeder, Patrik Michel

ABSTRACT

BackgroundTransient global amnesia (TGA) represents a benign neurological syndrome of unknown pathophysiology, often accompanied by vanishing hippocampal punctate lesions on diffusion-weighted imaging (hippocampal punctate diffusion lesion, HPDL). The recent literature suggests that TGA may be triggered by acute neurological conditions.ObjectiveTo study patients with TGA triggered by an acute neurological disease.MethodsWe retrospectively reviewed patients from two neurology centres with TGA (with or without HPDL) in whom an acute neurological condition could be identified as trigger. We also performed a systematic review of the literature of this situation using predefined search terms.ResultsWe identified 38 patients (median age 62 years, 55.3% female): 6 from our centres and 32 from the literature. Acute neurovascular diseases that preceded or were associated with TGA included ischemic and haemorrhagic strokes, convexity subarachnoid haemorrhage, and reversible cerebral vasoconstriction syndrome. As non-vascular acute neurological diseases, we identified migraine and peripheral-origin vertigo. The clinical manifestation of the neurological trigger showed a variable temporal relation with TGA onset; in some cases preceding and in others co-occurring with TGA manifestation. In some cases, presumed neurological triggers were asymptomatic and diagnosed from the neuroimaging done for the TGA.ConclusionsAcute vascular and non-vascular neurological events may trigger TGAs or may occur simultaneously. In the first case, such an acute neurological disease may activate direct pathways within the nervous systems leading to TGA, or alternatively elicit a bodily sympathetic overactivity cascade. In the second case, both neurological events may be the result of a common external stressor. More... »

PAGES

1-9

Identifiers

URI

http://scigraph.springernature.com/pub.10.1007/s10072-022-06259-6

DOI

http://dx.doi.org/10.1007/s10072-022-06259-6

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1149500739

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/35838848


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