Transient global amneisa pathophysiology
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Hasnain Ali Moryani, MBBS.
Overview of Pathophysiology
The underlying pathophysiology of transient global amnesia (TGA) remains uncertain. No single mechanism fully explains the abrupt and transient disturbance of memory, and early seizure-based theories have not been supported by electroencephalographic data. Current concepts focus on transient dysfunction of the medial temporal structures and related networks, often framed in terms of unusual vascular or ischemic phenomena. Supportive evidence comes from stroke-risk analyses, delayed hippocampal lesions on diffusion-weighted MRI, perfusion and connectivity imaging, migraine-related mechanisms such as cortical spreading depression, and proposed (but not yet confirmed) venous congestion of the temporal lobes. [1] [2] [3] [4] [5] [6] [7] [8] [9] [10]
Pathophysiology of Transient Global Amnesia
- No adequate pathophysiological explanation of transient global amnesia has emerged.
- Early theories attributing episodes to seizures are not supported by electroencephalography or other neurophysiologic techniques.
- Most current premises involve unconventional vascular or ischemic mechanisms affecting the medial temporal lobes, thalamus, or posterior cerebral circulation.[3][4]
- Analyses of several series indicate that the risk of subsequent ischemic stroke is not clearly increased, although one large propensity-matched study suggested a minimally higher risk. [1] [4] [5]
- Delayed, small hippocampal lesions on diffusion-weighted MRI, appearing many hours after the episode, provide tentative support for a vascular mechanism, but it is unclear whether they represent ischemia or altered neuronal physiology.[10]
- Functional imaging has shown bitemporal hypoperfusion during episodes.[6]
- Network-based studies demonstrate reduced connectivity of the hippocampi and parahippocampal gyri bilaterally, as well as altered connectivity of the amygdala and parts of the lateral temporal lobe.[7]
- Migraine has been linked to transient global amnesia through the proposed mechanism of cortical spreading depression, but supporting evidence remains circumstantial. [2] [3]
- A proposed venous-reflux mechanism suggests transient vascular congestion of the temporal lobes due to retrograde jugular venous flow or jugular valve incompetence; however, this has not been confirmed.[8] [9]
- Occasional episodes occurring immediately after vertebral artery angiography support a vascular mechanism or cortical irritation similar to that seen in migraine-related phenomena.[3]
References
- ↑ 1.0 1.1 Zorzon M, Antonutti L, Masè G, Biasutti E, Vitrani B, Cazzato G (September 1995). "Transient global amnesia and transient ischemic attack. Natural history, vascular risk factors, and associated conditions". Stroke. 26 (9): 1536–42. doi:10.1161/01.str.26.9.1536. PMID 7660394.
- ↑ 2.0 2.1 Liampas I, Siouras AS, Siokas V, Tsouris Z, Rikos D, Brotis A, Aloizou AM, Dastamani M, Dardiotis E (January 2022). "Migraine in transient global amnesia: a meta-analysis of observational studies". J Neurol. 269 (1): 184–196. doi:10.1007/s00415-020-10363-y. PMID 33388926 Check
|pmid=value (help). - ↑ 3.0 3.1 3.2 3.3 Bartsch T, Deuschl G (February 2010). "Transient global amnesia: functional anatomy and clinical implications". Lancet Neurol. 9 (2): 205–14. doi:10.1016/S1474-4422(09)70344-8. PMID 20129169.
- ↑ 4.0 4.1 4.2 Mangla A, Navi BB, Layton K, Kamel H (February 2014). "Transient global amnesia and the risk of ischemic stroke". Stroke. 45 (2): 389–93. doi:10.1161/STROKEAHA.113.003916. PMC 3946840. PMID 24309586.
- ↑ 5.0 5.1 Lee SH, Kim KY, Lee JW, Park SJ, Jung JM (April 2022). "Risk of ischaemic stroke in patients with transient global amnesia: a propensity-matched cohort study". Stroke Vasc Neurol. 7 (2): 101–107. doi:10.1136/svn-2021-001006. PMC 9067272 Check
|pmc=value (help). PMID 34702748 Check|pmid=value (help). - ↑ 6.0 6.1 Stillhard G, Landis T, Schiess R, Regard M, Sialer G (April 1990). "Bitemporal hypoperfusion in transient global amnesia: 99m-Tc-HM-PAO SPECT and neuropsychological findings during and after an attack". J Neurol Neurosurg Psychiatry. 53 (4): 339–42. doi:10.1136/jnnp.53.4.339. PMC 1014174. PMID 2341849.
- ↑ 7.0 7.1 Peer M, Nitzan M, Goldberg I, Katz J, Gomori JM, Ben-Hur T, Arzy S (May 2014). "Reversible functional connectivity disturbances during transient global amnesia". Ann Neurol. 75 (5): 634–43. doi:10.1002/ana.24137. PMID 24623317.
- ↑ 8.0 8.1 Sander D, Winbeck K, Etgen T, Knapp R, Klingelhöfer J, Conrad B (December 2000). "Disturbance of venous flow patterns in patients with transient global amnesia". Lancet. 356 (9246): 1982–4. doi:10.1016/S0140-6736(00)03313-4. PMID 11130530.
- ↑ 9.0 9.1 Schreiber SJ, Doepp F, Klingebiel R, Valdueza JM (April 2005). "Internal jugular vein valve incompetence and intracranial venous anatomy in transient global amnesia". J Neurol Neurosurg Psychiatry. 76 (4): 509–13. doi:10.1136/jnnp.2004.043844. PMC 1739578. PMID 15774436.
- ↑ 10.0 10.1 Szabo K, Hoyer C, Caplan LR, Grassl R, Griebe M, Ebert A, Platten M, Gass A (July 2020). "Diffusion-weighted MRI in transient global amnesia and its diagnostic implications". Neurology. 95 (2): e206–e212. doi:10.1212/WNL.0000000000009783. PMID 32532848 Check
|pmid=value (help).