Neurological research and practice · 2023
Guideline "Transient Global Amnesia (TGA)" of the German Society of Neurology (Deutsche Gesellschaft für Neurologie): S1-guideline.
СтатьяНазвание и аннотация: Перевод в очереди
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Sander Dirk, Bartsch Thorsten, Connolly Florian, Enzinger Christian, Fischer Urs, Nellessen Nils, Poppert Holger, Szabo Kristina, Topka Helge
Аннотация
INTRODUCTION: In 2022 the DGN (Deutsche Gesellschaft für Neurologie) published an updated Transient Global Amnesia (TGA) guideline. TGA is characterized by a sudden onset of retrograde and anterograde amnesia for a period of one to a maximum of 24 h (with an average of 6 to 8 h). The incidence is estimated between 3 and 8 per 100,000 population/year. TGA is a disorder that occurs predominantly between 50 and 70 years.
RECOMMENDATIONS: The diagnosis of TGA should be made clinically. In case of an atypical clinical presentation or suspicion of a possible differential diagnosis, further diagnostics should be performed immediately. The detection of typical unilateral or bilateral punctate DWI/T2 lesions in the hippocampus (especially the CA1 region) in a proportion of patients proves TGA. The sensitivity of MRI is considered higher when performed between 24 and 72 h after onset. If additional DWI changes occur outside the hippocampus, a vascular etiology should be considered, and prompt sonographic and cardiac diagnostics should be performed EEG may help to differentiate TGA from rare amnestic epileptic attacks, especially in recurrent amnestic attacks. TGA in patients < 50 years of age is a rarity, therefore it is mandatory to rapidly search for other causes in particular in younger patients. The cause of TGA is still unknown. Numerous findings in recent years point to a multifactorial genesis. Because the pathomechanism of TGA is not yet clearly known, no evidence-based therapeutic or prophylactic recommendations can be made.
CONCLUSIONS: There is no evidence for chronic sequelae of TGA with respect to cerebral ischemia, chronic memory impairment, or the onset of dementia-related syndromes.
RECOMMENDATIONS: The diagnosis of TGA should be made clinically. In case of an atypical clinical presentation or suspicion of a possible differential diagnosis, further diagnostics should be performed immediately. The detection of typical unilateral or bilateral punctate DWI/T2 lesions in the hippocampus (especially the CA1 region) in a proportion of patients proves TGA. The sensitivity of MRI is considered higher when performed between 24 and 72 h after onset. If additional DWI changes occur outside the hippocampus, a vascular etiology should be considered, and prompt sonographic and cardiac diagnostics should be performed EEG may help to differentiate TGA from rare amnestic epileptic attacks, especially in recurrent amnestic attacks. TGA in patients < 50 years of age is a rarity, therefore it is mandatory to rapidly search for other causes in particular in younger patients. The cause of TGA is still unknown. Numerous findings in recent years point to a multifactorial genesis. Because the pathomechanism of TGA is not yet clearly known, no evidence-based therapeutic or prophylactic recommendations can be made.
CONCLUSIONS: There is no evidence for chronic sequelae of TGA with respect to cerebral ischemia, chronic memory impairment, or the onset of dementia-related syndromes.