![]() One final hypothesis is that TGA is a type of migrainous aura, occurring due to cortical spreading depression, leading to cellular metabolic stress in vulnerable CA-1 sector neurons. Some studies have found TGA patients to have higher vascular risk factors and greater frequency of carotid atherosclerosis, suggesting an atherosclerotic embolic event as a cause. Ischaemia from thromboembolism constitutes a contrasting hypothesis on pathogenesis. Support for this comes from the observation that many TGA cases are precipitated by Valsalva-like activities, particularly physical or emotional stressors, which would temporarily cause thoracic-pressure elevation. One hypothesis is that retrograde venous flow leads to venous congestion, possibly due to increased thoracic pressure or jugular valve incompetence, which in turn causes a transient ischemia due to hypoperfusion. Multiple mechanisms have been proposed for the aetiology of TGA. Other patients might develop long-lasting memory problems, especially those with recurrence. For instance, memory and executive function impairment may objectively last up to five days post-TGA onset, despite patients subjectively reporting normal memory. It is hypothesized that, as these neurons are in locations vital for memory consolidation, small lesions may significantly impair memory function, though any effects on prognosis are unknown. Diffusion-weighted imaging (DWI) on magnetic resonance imaging (MRI) provides specific, consistent findings of 1–5 mm focal lesion in the hippocampal CA-1 sector, which resolve 7–10 days after onset of TGA, with no long-term structural changes. Imaging investigations are used to support the clinical diagnosis of TGA. While TGA occurs as a single event for many, estimates of recurrence have ranged from 2.9 to 26.3%, but some studies were retrospective. The estimated minimum annual incidence of TGA is 3.4 per 100,000, though this is likely to be much higher as some people will not present to the hospital and others will be misdiagnosed. Meta-analysis has found no predominance for either gender. Typically, it occurs in individuals aged 50–80 years, with decreased incidence in younger and older populations. Transient global amnesia (TGA) presents as sudden onset anterograde amnesia, with some features of retrograde amnesia, without residual cognitive impairment, of duration < 24 h. The Creative Commons Public Domain Dedication waiver ( ) applies to the data made available in this article, unless otherwise stated in a credit line to the data. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. Long-Term Outcome in Patients With Transient Global Amnesia: A Population-Based Study. | Open in Read by QxMDĪrena JE, Brown RD, Mandrekar J, Rabinstein AA. Syndromes of transient amnesia: towards a classification. High-field, T2 reversed MRI of the hippocampus in transient global amnesia. Transient global amnesia: clinical characteristics and prognosis. Miller JW, Petersen RC, Metter EJ, Millikan CH, Yanagihara T. ![]()
0 Comments
Leave a Reply. |
AuthorWrite something about yourself. No need to be fancy, just an overview. ArchivesCategories |