Archives of Academic Emergency Medicine. 2020; 8(1): e66 CA S E RE P O RT Transient Global Amnesia in a Patient Presenting with Hy- pertensive Emergency; a Case Report Takafumi Obara1, Tsuyosi Nojima1, Hitoshi Koga2, Atsunori Nakao1, Hiromichi Naito1∗ 1. Department of Emergency, Critical Care and Disaster Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama, Japan. 2. Department of Emergency Medicine, St. Mary Hospital, Kurume, Fukuoka, Japan. Received: June 2020; Accepted: July 2020; Published online: 28 July 2020 Abstract: Transient global amnesia (TGA) is characterized by the abrupt onset of global amnesia, particularly anterograde amnesia. The pathophysiology of TGA is poorly understood and it could be caused by various factors and be associated with various diseases. We report a 58-year-old man who presented to the local emergency room with TGA lasting for several hours. The patient had complete anterograde amnesia without a past medical history of migraine or neurological findings. His systolic blood pressure on presentation was 220 mmHg, which was immediately treated with intravenous calcium ion influx inhibitor. Other than global amnesia, there was no evidence of neurological disturbance. Computed tomography and magnetic resonance imaging results were unremarkable. After treatment of his hypertension, his amnesia resolved within 12 hours. Emergency depart- ment physicians may encounter TGA. Correct diagnosis of the condition depends on recognizing the disease. Keywords: Amnesia, transient global; memory disorders; htpertension; arterial pressure; hypertension; stroke; emergen- cies Cite this article as: Obara T, Nojima T, Koga H, Nakao A, Naito H. Transient Global Amnesia in a Patient Presenting with Hypertensive Emer- gency; a Case Report. Arch Acad Emerg Med. 2020; 8(1): e66. 1. Introduction Transient global amnesia (TGA) is characterized by the abrupt onset of global amnesia, particularly anterograde am- nesia. It is usually a self-limiting condition and does not co- incide with other neurological symptoms or signs. While var- ious causes, such as migraine, focal ischemia, epilepsy, or metabolic aspects, have been proposed, the pathophysiology of TGA has not been fully elucidated. TGA is considered to be a result of multiple causes rather than a single mechanism (1). We treated the unique case of a patient with a typical his- tory of TGA associated with hypertensive emergencies. There have been only a few reports showing the relationship be- tween hypertension and TGA episodes (1-3). Since TGA presents very dramatically and is sometimes seen in the emergency department, emergency physicians must be fa- ∗Corresponding Author: Hiromichi Naito; Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Department of Emergency, Critical Care, and Disaster Medicine. 2-5-1 Shikata, Okayama, Japan 700-8558. Email: naito.hiromichi@gmail.com, Tel: +81-86-235-7426, Fax: +81-86-235-7427 miliar with this condition. Sharing our experience may help emergency physicians to successfully diagnose TGA by rec- ognizing its characteristic features and avoid unnecessary testing. 2. Case Presentation A 58-year-old man came to the emergency department with amnesia since 2 hours before admission. His past history in- cluded only hypertension and treatment with amlodipine (5 mg/day). Additionally, he had no family psychiatric history. He had woken up normally and had breakfast as usual prior to the onset of his amnesia. His family members noticed his repetitive questioning regarding where he was and how he got there, indicating his inability to encode new memories ("How did I come here?"; "Why I am here?"). On arrival, he was alert and calm. The patient presented no seizures, al- tered mental status, headache, or visual disturbances. His vital signs were as follows; body temperature 36.7◦C, blood pressure 220/118 mmHg, and heart rate 84 beats/minutes. Physical examination was unremarkable. Other than the re- cent memory disturbance, there were no abnormal neuro- logical signs such as sensory disturbance or muscle weak- This open-access article distributed under the terms of the Creative Commons Attribution NonCommercial 3.0 License (CC BY-NC 3.0). Downloaded from: http://journals.sbmu.ac.ir/aaem T. Obara et al. 2 ness. All his higher cortical functions like reasoning, calcu- lations, language, and abstract thinking were intact. On in- terview, he could not recall why he had come to the hos- pital; however, he clearly stated his name, his work history, and his address. The patient could identify his family mem- bers. His biochemical and hematological indices were within normal limits. Intravenous nicardipine (2 mg) was adminis- tered and his systolic blood pressure (SBP) dropped to 140- 150 mmHg. Brain computed tomography (CT) scan demon- strated no hemorrhage or space occupied by a brain lesion. Magnetic resonance imaging (MRI) showed the absence of any localizing signs. His memory impairment fully recovered within 24 hours af- ter the onset of symptoms. However, he did not remem- ber the episode, including admission to the hospital and un- dergoing several examinations. On the day after admission, since recovery of his memory function was confirmed by in- terview, the patient was discharged on foot. In the three months of follow-up, he has been well without further am- nesia episodes. 3. Discussion Our case fully met the Hodges and Warlow TGA diagnostic criteria (4), which include a capable observer witnessing the attack, no neurological symptoms during or after the attack, anterograde amnesia, no personal identity loss, no recent head injury, no history of seizures or active epilepsy, absence of epileptic features, and resolution of TGA within 24 hours. Our patient did not have any head injury or seizure episodes for at least 10 years. We ruled out electrolyte/metabolic abnormality based on normal biochemical test and arterial blood gas analysis results. The following differential diagnoses were identified for our patient: complex partial seizures, acute confusional state, transient ischemic attack (TIA), transient epileptic amnesia (TEA), psychogenic amnesia, toxic metabolic states, and mi- graine. TEA is an indication of temporal lobe epilepsy, and patients will have multiple episodes of amnesia; symptoms commonly last for less than an hour or rapidly recur, which did not happen in our case. Psychogenic amnesia is charac- terized by profound retrograde amnesia with personal iden- tity loss but intact anterograde memory; these symptoms do not correspond to those of our patient. We ruled out TIA, which manifests additional focal neurological deficits dur- ing an attack, as our patient had no motor or sensory loss. Episodic memory dysfunction in TGA presents transiently. In contrast, it may present acutely in concussion, sub-acutely in thiamine deficiency, or chronically in Alzheimer’s disease. Since the pathophysiology of TGA is obscure, many hy- potheses have been proposed. A number of precipitating factors are closely related to TGA, including physical exer- cise, migraines, sexual intercourse, acute pain, emotional stress, cervical hyperextension, and coughing (5-7). Our patient did not have this type of episode based on infor- mation obtained from family members and no factor other than increased blood pressure, can fully explain the occur- rence of TGA in our patient. Plausible hypotheses for the pathogenesis of TGA are migraine-like mechanism and cere- bral hypoxic-ischemic insult. Studies using neuroimaging technologies like single photon emission CT scan show im- paired blood flow in the parahippocampus, hippocampus, and mediobasal temporal region in TGA patients (7). Sim- ilarly, diffusion-weighted MRI has demonstrated metabolic stress and structural changes in patients with TGA (8). It has been useful for confirming ischemic amnesia (9). As- sessment of internal jugular venous flow has shown block- age and resulting venous ischemia to hippocampal or bilat- eral diencephalic structures occurring due to Valsalva ma- neuvers, which may contribute to TGA development (7, 10). The rare incidence of microembolic signals in TGA patients indicates that embolism plays no essential role in TGA de- velopment (11). His anterograde memory rapidly and com- pletely returned within 24 hours, but he was not able to re- member the memory loss episode. Like our patient, patients in previous studies have reported that their retrograde mem- ory was slow to recover to normal. Arterial hypertension is a prominent finding in patients with TGA and may be an associated risk factor (12). Nedelmann et al. demonstrated that 21 of 22 patients with TGA (60% fe- male, mean age 62.4 years) had high SBP (180.9/98.3 mmHg mean pressure three hours after symptom onset). Moreover, systolic values above 200 mmHg were found in one-third of patients. These clinical observations may suggest that ele- vated blood pressure is a common factor in the early stage of this condition (3). 4. Conclusion We encountered the unique case of a patient with a typical TGA history associated with hypertensive emergencies. Our report may help emergency physicians to successfully diag- nose the condition by recognizing its characteristic features. 5. Declarations 5.1. Acknowledgements No funding supported this study. 5.2. Consent Consent was obtained from the participant in this study. This open-access article distributed under the terms of the Creative Commons Attribution NonCommercial 3.0 License (CC BY-NC 3.0). Downloaded from: http://journals.sbmu.ac.ir/aaem 3 Archives of Academic Emergency Medicine. 2020; 8(1): e66 5.3. Other relationships All authors have declared that they have no other relation- ships or activities that could appear to have influenced the submitted work. 5.4. Authors contribution All authors met the criteria for authorship contribution based on recommendations of international committee of medical journal editors. Authors’ ORCIDs Takafumi Obara: 0000-0001-5760-1980 Tsuyosi Nojima: 0000-0003-0768-0179 Hitoshi Koga: 0000-0002-2686-5905 Atsunori Nakao: 0000-0002-6818-2985 Hiromichi Naito: 0000-0002-7308-1716 5.5. Funding None. References 1. Arena JE, Rabinstein AA. Transient global amnesia. Mayo Clin Proc. 2015;90(2):264-72. 2. Nakamizo T, Tsuzuki I, Koide T. Transient Global Amnesia with Reversible White Matter Lesions: A Variant of Pos- terior Reversible Encephalopathy Syndrome? Case Rep Neurol Med. 2015;2015:541328. 3. Nedelmann M, Kaps M. Elevated blood pressure as a prominent finding in patients with transient global am- nesia. Eur J Neurol. 2007;14(7):e22. 4. Hodges JR, Warlow CP. Syndromes of transient amnesia: towards a classification. A study of 153 cases. J Neurol Neurosurg Psychiatry. 1990;53(10):834-43. 5. Espiridion ED, Gupta J, Bshara A, Danssaert Z. Tran- sient Global Amnesia in a 60-year-old female with Post- traumatic Stress Disorder. Cureus. 2019;11(9):e5792. 6. Yi M, Sherzai AZ, Ani C, Shavlik D, Ghamsary M, Lazar E, et al. Strong Association Between Migraine and Transient Global Amnesia: A National Inpatient Sample Analysis. J Neuropsychiatry Clin Neurosci. 2019;31(1):43-8. 7. Sander K, Sander D. New insights into transient global amnesia: recent imaging and clinical findings. Lancet Neurol. 2005;4(7):437-44. 8. Bartsch T, Deuschl G. Transient global amnesia: func- tional anatomy and clinical implications. Lancet Neurol. 2010;9(2):205-14. 9. Michel P, Beaud V, Eskandari A, Maeder P, Demonet JF, Eskioglou E. Ischemic Amnesia: Causes and Outcome. Stroke. 2017;48(8):2270-3. 10. Winbeck K, Etgen T, von Einsiedel HG, Rottinger M, Sander D. DWI in transient global amnesia and TIA: pro- posal for an ischaemic origin of TGA. J Neurol Neurosurg Psychiatry. 2005;76(3):438-41. 11. Jovanovic ZB, Pavlovic AM, Vujisic Tesic BP, Pekmezovic TP, Kostic Boricic MV, Cvitan EZ, et al. Comprehensive Ultrasound Assessment of the Craniocervical Circula- tion in Transient Global Amnesia. J Ultrasound Med. 2018;37(2):479-86. 12. Melo TP, Ferro JM, Ferro H. Transient global amnesia. A case control study. Brain. 1992;115 Pt 1:261-70. This open-access article distributed under the terms of the Creative Commons Attribution NonCommercial 3.0 License (CC BY-NC 3.0). Downloaded from: http://journals.sbmu.ac.ir/aaem Introduction Case Presentation Discussion Conclusion Declarations References