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      Ischemic Evidence of Transient Global Amnesia: Location of the Lesion in the Hippocampus

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          Abstract

          Background and purpose

          Transient global amnesia (TGA) is a rare amnestic syndrome characterized by the sudden onset of a selective anterograde and retrograde amnesia with a time course of up to 24 hours. Recent studies have found a high frequency of small high-signal abnormalities in the hippocampus on diffusion-weighted imaging (DWI), and accordingly ischemia has been proposed as an etiology of TGA. We hypothesized that TGA lesions occur preferentially in the CA1 region of the hippocampus, which is known to be susceptible to ischemia.

          Methods

          Twenty consecutive patients with a clinical diagnosis of TGA underwent DWI both within 24 hours of symptom onset and 3 days later. Twenty patients with high-signal abnormalities in the hippocampus on the initial DWI underwent subsequent DWI and T2-weighted imaging in the coronal plane to precisely localize the lesions.

          Results

          Seventeen patients had small high-signal abnormalities (with diameters of 1-3 mm) in the hippocampus unilaterally on DWI. One of these patients had two lesions in one hippocampus. Three of the 20 patients had lesions bilaterally in the hippocampus, 1 of whom had 3 bilateral lesions. A total of 25 lesions were identified: 5 in the hippocampal head, 19 in the body, and 1 in the tail. Six patients had unilateral lesions on the left,11 patients had them on the right, and 3 patients had bilateral lesions.

          Conclusions

          In this study, lesions associated with TGA were localized mostly to the lateral portion of the hippocampus, corresponding to CA1. This finding supports the ischemic etiology of TGA, but the underlying pathophysiologic mechanism requires further investigation.

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          Most cited references16

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          Syndromes of transient amnesia: towards a classification. A study of 153 cases.

          Of 153 patients presenting with acute transient amnesia, 114 fulfilled the proposed strict diagnostic criteria for transient global amnesia (TGA). The prognosis of this group was excellent with the exception of a small subgroup (7%), largely identifiable because of atypically brief or recurrent attacks, who developed epilepsy of temporal lobe type on follow up. Computerised tomography (CT) scans performed on 95 patients were normal, evidence for covert alcoholism was lacking and there was a familial incidence of approximately 2%. By contrast, the group of 39 patients who did not meet the criteria for TGA had a significantly worse prognosis with a high incidence of major vascular events. The groups could not be distinguished on the basis of behavioural characteristics during the attack. The following classification was proposed: 1) pure TGA--attacks fulfilling the strict criteria, and of more than one hour in duration which do not require detailed investigation, 2) probable epileptic amnesia--attacks of less than an hour or rapidly recurrent, 3) probable transient ischaemic amnesia, a minority of cases with additional focal neurological deficits during the attack.
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            Detection of delayed focal MR changes in the lateral hippocampus in transient global amnesia.

            There is still limited knowledge on the location and etiology of transient global amnesia (TGA). MR studies including diffusion-weighted imaging (DWI) have been unable to demonstrate consistently the location and underlying pathology of TGA. To investigate patients with TGA using serial DWI performed from the day of symptom onset through days 1 and 2. After reporting negative DWI results in a previous study, the authors used a modified study design to investigate patients with TGA using serial DWI performed from the day of symptom onset through days 1 and 2. Of 31 consecutive patients studied, 26 developed a small, punctate DWI lesion in the lateral aspect of the hippocampal formation (pes and fimbria hippocampi) on either side (left, n = 15; right, n = 6) or bilaterally (n = 5). Lesions were rarely noted in the hyperacute phase (n = 2), but all became visible regularly at 48 hours. The study confirms the involvement of hippocampal parenchyma in the pathophysiology of TGA. The delayed detectability of the lesions may explain the incongruence of previous MR DWI studies in TGA patients.
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              Aetiology of transient global amnesia.

              The pathophysiology of transient global amnesia (TGA) has been obscure since the definition of this syndrome more than 30 years ago. Current hypotheses include migraine, seizure, or transient cerebral arterial ischaemia. However, none of these potential mechanisms explain both the absence of other neurological signs or symptoms during TGA, and its frequent precipitating activities: many of which would be expected to result in marked increases in venous return from the arms to the superior vena cava. Patients with TGA also commonly have a Valsalva manoeuvre at the onset of attacks. I suggest that a Valsalva manoeuvre, blocking venous return through the superior vena cava, may allow brief retrograde transmission of high venous pressure from the arms to the cerebral venous system, resulting in venous ischaemia to the diencephalon or mesial temporal lobes and to TGA.
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                Author and article information

                Journal
                J Clin Neurol
                JCN
                Journal of Clinical Neurology (Seoul, Korea)
                Korean Neurological Association
                1738-6586
                2005-5013
                June 2008
                20 June 2008
                : 4
                : 2
                : 59-66
                Affiliations
                [a ]Department of Neurology, Soonchunhyang University College of Medicine, Seoul, Korea.
                [b ]Department of Neurology, Seoul National University College of Medicine, Seoul, Korea.
                [c ]Department of Radiology, Seoul National University College of Medicine, Seoul, Korea.
                Author notes
                Address for correspondence: SangYun Kim, MD, PhD, Department of Neurology, College of Medicine, Seoul National University, Seoul National University Bundang Hospital, 300 Gumi-dong, Bundang-gu, Seongnam-si, Gyeonggi-do, 463-707, Korea. Tel: +82-31-787-7462, Fax: +82-31-719-6815, neuroksy@ 123456snu.ac.kr
                Article
                10.3988/jcn.2008.4.2.59
                2686867
                19513305
                c5fc4821-f3ad-4416-af84-d85b1f90f355
                Copyright © 2008 Korean Neurological Association
                History
                : 04 September 2007
                : 23 May 2008
                Categories
                Original Article

                Neurology
                transient global amnesia,hippocampus,ca1
                Neurology
                transient global amnesia, hippocampus, ca1

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