Pyle LM, Laghari FJ, Kinem DJ (2018) Concomitant transient global amnesia and takotsubo cardiomyopathy following a stressful event. Ĭourand P-Y, Sibellas F, Gonidec S et al (2014) Acute myocardial infarction: a precipitating event for transient global amnesia. Jeong M, Kim WS, Kim A et al (2018) Medical procedure-related transient global amnesia. Cerebrovasc Dis 33:104-115–508 īartsch T, Döhring J, Reuter S et al (2015) Selective neuronal vulnerability of human hippocampal CA1 neurons: lesion evolution, temporal course, and pattern of hippocampal damage in diffusion-weighted MR imaging. įörster A, Griebe M, Gass A, et al (2012) Diffusion-weighted imaging for the differential diagnosis of disorders affecting the hippocampus. Michel P, Beaud V, Eskandari A et al (2017) Ischemic amnesia: causes and outcome. Szabo K, Förster A, Jäger T et al (2009) Hippocampal lesion patterns in acute posterior cerebral artery stroke: clinical and MRI findings. Szabo K, Hoyer C, Caplan LR et al (2020) Diffusion-weighted MRI in transient global amnesia and its diagnostic implications. Higashida K, Okazaki S, Todo K et al (2020) A multicenter study of transient global amnesia for the better detection of magnetic resonance imaging abnormalities. īartsch T, Alfke K, Stingele R et al (2006) Selective affection of hippocampal CA-1 neurons in patients with transient global amnesia without long-term sequelae. Sedlaczek OL, Hirsch JG, Grips E et al (2004) Detection of delayed focal MR changes in the lateral hippocampus in transient global amnesia. Quinette P, Guillery-Girard B, Dayan J et al (2006) What does transient global amnesia really mean? Review of the literature and thorough study of 142 cases. ![]() īartsch T, Deuschl G (2010) Transient global amnesia: functional anatomy and clinical implications. J Neurol Neurosurg Psychiatry 53:834–843. Hodges JR, Warlow CP (1990) Syndromes of transient amnesia: towards a classification. In: In Vinken PJ, Bruyn GW, Klawans HL (eds) Handbook of clinical neurology. In the second case, both neurological events may be the result of a common external stressor.Ĭaplan LB (1985) Transient global amnesia. 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. ConclusionsĪcute vascular and non-vascular neurological events may trigger TGAs or may occur simultaneously. In some cases, presumed neurological triggers were asymptomatic and diagnosed from the neuroimaging done for the TGA. 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. As non-vascular acute neurological diseases, we identified migraine and peripheral-origin vertigo. Acute neurovascular diseases that preceded or were associated with TGA included ischemic and haemorrhagic strokes, convexity subarachnoid haemorrhage, and reversible cerebral vasoconstriction syndrome. We identified 38 patients (median age 62 years, 55.3% female): 6 from our centres and 32 from the literature. We also performed a systematic review of the literature of this situation using predefined search terms. ![]() We retrospectively reviewed patients from two neurology centres with TGA (with or without HPDL) in whom an acute neurological condition could be identified as trigger. To study patients with TGA triggered by an acute neurological disease. The recent literature suggests that TGA may be triggered by acute neurological conditions. ![]() Transient 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).
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