ReviewJournal of clinical medicine2022
Forgetting the Unforgettable: Transient Global Amnesia Part I: Pathophysiology and Etiology.
Review in Journal of clinical medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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Who cites it
8 citing papers in PubMed, 21 citations in OpenAlex.
- Five-Year Prognosis of Transient Ischemic Attack and Transient Global Amnesia in a Finnish Population.Neuroepidemiology · 2026Article
- Memory and Resting-State Connectivity in Acute Transient Global Amnesia: A Case-Control fMRI Study.Annals of clinical and translational neurology · 2026Article
- Recurrent transient global amnesia related to dural arteriovenous fistula.Dementia & neuropsychologia · 2025Article
- Transient global amnesia after the right temporal epilepsy surgery: A case report.Epilepsia open · 2024Article
- Article
- Cerebral Small Vessel Disease Burden in Patients with Transient Global Amnesia and its Relationship with Recurrence.Current neurovascular research · 2024Article
- Guideline "Transient Global Amnesia (TGA)" of the German Society of Neurology (Deutsche Gesellschaft für Neurologie): S1-guideline.Neurological research and practice · 2023Article
- Transient Global Amnesia (TGA): Sex-Specific Differences in Blood Pressure and Cerebral Microangiopathy in Patients with TGA.Journal of clinical medicine · 2022Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Transient global amnesia (TGA) is a clinical syndrome characterized by the sudden onset of a temporary memory disorder with a profound anterograde amnesia and a variable impairment of the past memory. Since the first description, dating back over 60 years, several cases have beenreported in the literature. Nevertheless, TGA remains one of the most mysterious diseases in clinical neurology. The debate regarding the etiology of this disease has focused mainly on three different mechanisms: vascular (due to venous flow changes or focal arterial ischemia), epileptic, and migraine related. However, to date there is no scientific proof of any of these mechanisms. Furthermore, the demonstration by diffusion-weighted MRI of lesions in the CA1 field of the hippocampus cornu ammonis led us to hypothesize that the selective vulnerability of CA1 neurons to metabolic stress could play a role in the pathophysiology of TGA. In this review, we summarize current knowledge on the anatomy, vascularization and function of the hippocampus. Furthermore, we discuss the emerging theories on the etiology and the pathophysiological cascade leading to an impairment of hippocampal function during the attacks.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.