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Subarachnoid Hemorrhage After Transient Global Maetani et al. BMC Neurology (2018) 18:36 https://doi.org/10.1186/s12883-018-1042-3 CASE REPORT Open Access Subarachnoid hemorrhage after transient global amnesia caused by cerebral venous congestion: case report Yuta Maetani1, Masahiro Nakamori1*, Tomoaki Watanabe1, Hayato Matsushima1, Eiji Imamura1 and Shinichi Wakabayashi2 Abstract Background: Transient global amnesia is reported to be caused by cerebral venous congestion. Internal jugular venous flow reversal in particular with the Valsalva maneuver leads to cerebral venous congestion. In addition, Valsalva maneuver can also induce subarachnoid hemorrhage. Transient global amnesia and subarachnoid hemorrhage might have common a pathophysiology in cerebral venous congestion. Case presentation: We report here the case of a 57-year-old woman who twice experienced convexal subarachnoid hemorrhage just after straining at stool following an episode of transient global amnesia. Digital subtraction angiography showed left temporal congestion. Left jugular vein ultrasonography revealed reflux with the Valsalva maneuver only in acute phase, indicating transient cerebral venous congestion. Conclusions: Subarachnoid hemorrhage followed by transient global amnesia indicates a common factor between them. Transient venous congestion is discussed in order to explain this rare phenomenon. Keywords: Transient global amnesia, Subarachnoid hemorrhage, Cerebral venous congestion, Valsalva maneuver, Straining Background maneuver that leads to cerebral venous congestion Transient global amnesia (TGA) is a clinical syndrome can also induce SAH [3]. characterized by the sudden onset of reduced episodic Thus, TGA and SAH might be induced by venous memory. Several possibilities, such as cerebral ischemia congestion. However, there are few reports of the rela- and epileptic episode are suggested as the etiology of tion between TGA and SAH. Although TGA as a pres- TGA, but the pathophysiology is still elusive. Internal entation of SAH has been reported, to the best of our jugular venous flow reversal that leads to cerebral ven- knowledge, SAH after TGA has been never reported. ous congestion can contribute to TGA [1]. Particularly, We report the case of a patient with SAH after TGA fol- the Valsalva maneuver leads to internal jugular venous lowing straining at stool. flow reversal in patients with TGA [2]. Subarachnoid hemorrhage (SAH) is mainly caused by the rupture of a cerebral aneurysm or cerebral ar- Case presentation teriovenous malformation, but sometimes the origin A 57-year-old woman was admitted to our hospital cannot be detected despite detailed examinations such due to sudden-onset amnesia. She had no past as digital subtraction angiography (DSA). Valsalva medical history, except for dyslipidemia, had taken no medicine, including pills and nutritional supplements. She had neither smoked nor drank. She was an elementary school teacher. Before developing amnesia, * Correspondence: [email protected] she visited another elementary school for a workshop. 1Department of Neurology, Suiseikai Kajikawa Hospital, 1-1-23, Higashisendamachi, Naka-ku, Hiroshima 730-0053, Hiroshima, Japan She did not clearly remember the situation at the on- Full list of author information is available at the end of the article set of TGA. At the first medical examination, she © The Author(s). 2018 Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated. Maetani et al. BMC Neurology (2018) 18:36 Page 2 of 6 presented with no neurologic deficit, except for am- artery angiography in the last part of the venous phase nesia. Magnetic resonance imaging (MRI), electro- revealed reflux from the inferior petrosal vein into the encephalogram, and laboratory findings were normal. cavernous (Fig. 4a, b). Left vertebral artery angiography We diagnosed the patient with TGA. The patient’s revealed that hypoplastic left sinus caused venous blood symptom disappeared after about 6 hours. Diffusion- flow into supplementary path, that is, the basilar venous weighted imaging (DWI) carried out the next day re- plexus in addition to normal flow into bilateral trans- vealed a high-density spot in the left hippocampus verse sinus (Fig. 4c, d), which indicated the left temporal (Fig. 1), which indicated TGA. She was discharged venous congestion. However, perfusion-weighted im- two days after onset. aging did not show distinct congestion in the lesion of Several hours after discharge, the patient had a sudden cSAH. terrible headache. The patient had strained at stool just Jugular vein ultrasonography revealed reflux only with before onset. She came back to our hospital immedi- the Valsalva maneuver in left internal jugular vein (Fig. 5). ately. At the time of the second admission, the patient Reflux was confirmed according to a previous report [4]. was alert and had a blood pressure of 140/88mmHg. The internal jugular venous valve was not found. The Her heart rate and oxygen saturation were normal. She other examinations, such as electrocardiography, Holter had a throbbing headache, but exhibited no signs of electrocardiography, transthoracic echocardiography, neurologic deficit, including amnesia. Computed tomog- carotid artery ultrasonography, leg venous ultrasonog- raphy (CT) and MRI revealed convexal subarachnoid raphy, whole-body CT scan, and electroencephalogram hemorrhage (cSAH) in the right frontal lobe (Fig. 2a). were normal. The signal in this lesion was hyperintense on fluid- The headache steadily improved and the patient was attenuated inversion recovery and T2-weighted images, discharged. Repeated brain imaging tests, including CT, and hypointense on T2* susceptibility-weighted images MRI, MRA, and MRV indicated no relapse of cSAH, (Fig. 2b-d). This indicates hemorrhage and not throm- new lesion, reversible lesion, contraction, or thrombosis. bosis. There were no signs of leukoaraiosis or micro- The left internal jugular venous reflux following the Val- bleeds on MRI and no vessel abnormalities, such as salva maneuver on ultrasonography disappeared four aneurysms or arteriovenous fistula/malformation on months later. Medical history and the test results are magnetic resonance angiography (MRA) (Fig. 3) and summarized in the Additional file 1. magnetic resonance venography (MRV). Laboratory findings, including those regarding the coagulating sys- Discussion and Conclusion tem, were normal. On day 2 of the second admission, a Secondary TGA is likely to be caused by stroke, strong headache re-occurred when the patient strained epilepsy, migraine, or abnormal cerebral venous re- at stool. CT and MRI revealed another cSAH in the right flux. CA-1 subfield of the hippocampus is related to frontal lobe (Figs. 2e-h). There were no findings such as TGA, and is affected by hypoxemia-induced metabolic aneurysms, anomalies, or sinus thrombosis on DSA. stress, β-amyloid-induced neurotoxicity, and ischemia However, DSA revealed hypoplastic left transvers sinus [1]. However, the predominant hypothesis is that and congestion in the left temporal lobe. Left carotid TGA most commonly occurs due to abnormal Fig. 1 Brain magnetic resonance imaging (MRI) showed a high-density spot in the left hippocampus on diffusion-weighted imaging at the first admission Maetani et al. BMC Neurology (2018) 18:36 Page 3 of 6 Fig. 2 Head computed tomography and magnetic resonance imaging showed twice convexal subarachnoid hemorrhage on day1 of second admission (a-d), on day2 of second admission (e-h). Lesions have high density on computed tomography (a, e), a hyperintense signal on fluid-attenuated inversion recovery (b, e) and T2-weighted image (d, h) (arrow), and a hypointense signal on T2* susceptibility-weighted image (arrow head), which indicate not thrombosis but hemorrhage cerebral venous drainage from the temporal lobes [1, incompetency, this phenomenon is more common in pa- 5]. Increased intrathoracic pressure, such as that tients with TGA than in controls or patients with transi- caused by Valsalva maneuver, could trigger retrograde ent ischemic attack [2]. Since the Valsalva maneuver venous flow in patients with valve incompetence in causes internal jugular venous flow reversal in patients the internal jugular veins. The resulting venous con- with TGA [2], in this case, it was not clear whether the gestion would preferentially affect the function of the patient performed the Valsalva maneuver before the on- medial temporal lobes, thus triggering the anterograde set of TGA. A high-density spot was found in her left amnesia [1]. In this case, DSA showed congestion in hippocampus on DWI and left internal jugular venous the temporal lobe. flow reversal was noted with ultrasonography only dur- Internal jugular venous flow reversal and internal ing the acute phase. This was in agreement with a diag- jugular vein valve incompetency can contribute to TGA. nosis of TGA. Although not all patients with TGA show internal jugu- However, a high-density spot on DWI also indicated lar venous flow reversal or internal jugular vein valve ischemic
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