SynthesisNeurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology2022
Acute neurological disease as a trigger or co-occurrence of transient global amnesia: a case series and systematic review.
Synthesis in Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers, 1 of them a synthesis that pooled it.
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3 citing papers in PubMed, 1 synthesis or guideline pooled it, 5 citations in OpenAlex.
- Acute amnestic syndrome in fornix lesions: a systematic review of reported cases with a focus on differential diagnosis.Frontiers in neurology · 2024Pooled it
- Vertebral artery hypoplasia and hemodynamic impairment in transient global amnesia: a case control study.Frontiers in neurology · 2024Article
- Mitochondrial transport in neurons and evidence for its involvement in acute neurological disorders.Frontiers in neuroscience · 2023Review
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
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.
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