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Transient Global Amnesia

  • Author: Roy Sucholeiki, MD; Chief Editor: Helmi L Lutsep, MD  more...
Updated: Apr 22, 2016


Transient global amnesia (TGA) has been a well-described phenomenon for more than 40 years. Clinically, it manifests with a paroxysmal, transient loss of memory function. Immediate recall ability is preserved, as is remote memory; however, patients experience striking loss of memory for recent events and an impaired ability to retain new information. In some cases, the degree of retrograde memory loss is mild.

Many patients are anxious or agitated and may repeatedly ask questions concerning transpiring events. Upon mental status examination, language function is preserved, which indicates a preservation of semantic and syntax memory. Attention is spared, visual-spatial skills are intact, and social skills are retained. Symptoms typically last less than 24 hours. As the syndrome resolves, the amnesia improves, but the patient may be left with a distinct lapse of recollection for events during the attack.

Generally, TGA is a solitary event, however, patients can experience more than one event with very similar symptoms and recovery.



The precise pathophysiology of transient global amnesia is not clear. The findings reported with positron emission tomography (PET), diffusion-weighted MRI (DWI), single photon emission computed tomography (SPECT) and MR spectroscopy (MRS) have indicated various brain regions that are affected in TGA.

  • On PET and DWI, blood flow to specific brain areas that involve memory appears to be disrupted transiently during TGA. This includes the thalamus and/or mesial temporal structures (in particular the amygdala and hippocampus).
  • Hakan et al demonstrated tiny increases in signal in the left parahippocampal gyrus and splenium of the corpus callosum on DWI in one patient. This method of imaging allows detection of hyperacute ischemic change. Liang et al and Yang et al have also recently used DWI to document tiny lesions in the hippocampus of patients with acute TGA. [1, 2] However, Eustache et al reported a PET study consistent with a spreading depression in the left lateral frontal cortex. This case also featured oligemia in the left occipital cortex. [3] Strupp et al found mainly medial temporal changes on DWI in 7 of 10 patients with TGA. They suggested that cellular edema or spreading depression could be responsible, not just ischemia. [4]
  • Winbeck et al found a significant incidence (10/28) of acute DWI changes in patients with TGA, which is comparable to the TIA group (21/74). Although the patients who presented with a TIA had a higher prevalence of vascular risk factors, those in the TGA group (who had DWI changes) were found to have significantly more carotid atherosclerosis. [5]
  • Nakada et al demonstrated via high-resolution T2-reversed MRI a high incidence of hippocampal cavities compared with their normal or disease controls. The authors conclude that their findings may indicate that TGA can be associated with neuronal loss in the CA1 region of the hippocampus. [6]
  • Generally, the territory of the vertebrobasilar system is most often rendered ischemic and dysfunctional. However, since ischemia typically does not progress to infarction, symptoms are expected to resolve completely.
  • Yamane et al reported rather diffuse cerebral hypoperfusion on SPECT that improved months later upon repeating the test in a patient with TGA. [7] Yang et al also reported hypoperfusion in the cerebellar vermis that recovered by the time of follow-up examination. [1]
  • Bartsch et al found that in 7 patients with TGA, 4 had a diffusion abnormality corresponding with a T2 lesion in the CA-1 sector of the hippocampus. In 3 of these patients, MRS revealed a lactate peak. The authors suggest that this represents an acute stress reaction of this particular area and indicates the pathological substrate of TGA. [8]

Overall, the variety of findings on functional imaging studies may support the notion that TGA is a syndrome with not only a variety of precipitating causes but also of differing mechanisms.




United States

Based on data from Rochester, Minnesota, Miller et al determined an incidence of 5.2 cases per 100,000 population. However, among individuals older than 50 years, the incidence was 23.5 cases per 100,000 population per year.[9]


Estimates vary, but Matiea-Guiu et al found a lower incidence in Alcoi, Spain, of 2.9 cases per 100,000 population.[10] On the other hand, Lauria et al found an incidence of 10 cases per 100,000 population in Belluno, Italy.[11]


As the name implies, transient global amnesia symptoms are transient.

The mean annual recurrence rate is thought to be low (approximately 4-5%). However, in the study by Miller et al, the calculated recurrence rate could be as high as 24% over a lifetime depending on inclusion criteria.[9] These occasional recurrences usually involve no long-term morbidity or death.

If transient ischemic attack (TIA) is suspected, then the patient should be evaluated for stroke risk factors. Likewise, if a seizure is suspected, appropriate testing should be initiated.

Age- and sex-related demographics

The typical age of occurrence is older than 50 years.

No sex predilection has been observed. However, one study found that particular triggers may be associated with men and women. For men, transient global amnesia occurs more often after a physical precipitating event. In women, episodes may be more associated with emotional precipitating events, a history of anxiety, or pathological personality.


Contributor Information and Disclosures

Roy Sucholeiki, MD Director, Comprehensive Seizure and Epilepsy Program, The Neurosciences Institute at Central DuPage Hospital

Roy Sucholeiki, MD is a member of the following medical societies: American Academy of Neurology, American Neuropsychiatric Association, American Epilepsy Society

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Howard S Kirshner, MD Professor of Neurology, Psychiatry and Hearing and Speech Sciences, Vice Chairman, Department of Neurology, Vanderbilt University School of Medicine; Director, Vanderbilt Stroke Center; Program Director, Stroke Service, Vanderbilt Stallworth Rehabilitation Hospital; Consulting Staff, Department of Neurology, Nashville Veterans Affairs Medical Center

Howard S Kirshner, MD is a member of the following medical societies: Alpha Omega Alpha, American Neurological Association, American Society of Neurorehabilitation, American Academy of Neurology, American Heart Association, American Medical Association, National Stroke Association, Phi Beta Kappa, Tennessee Medical Association

Disclosure: Nothing to disclose.

Chief Editor

Helmi L Lutsep, MD Professor and Vice Chair, Department of Neurology, Oregon Health and Science University School of Medicine; Associate Director, OHSU Stroke Center

Helmi L Lutsep, MD is a member of the following medical societies: American Academy of Neurology, American Stroke Association

Disclosure: Medscape Neurology Editorial Advisory Board for: Stroke Adjudication Committee, CREST2.

Additional Contributors

Carmel Armon, MD, MSc, MHS Chair, Department of Neurology, Assaf Harofeh Medical Center, Tel Aviv University Sackler Faculty of Medicine, Israel

Carmel Armon, MD, MSc, MHS is a member of the following medical societies: American Academy of Neurology, Massachusetts Medical Society, American Academy of Sleep Medicine, American Stroke Association, American Association of Neuromuscular and Electrodiagnostic Medicine, American Clinical Neurophysiology Society, American College of Physicians, American Epilepsy Society, American Medical Association, American Neurological Association, Sigma Xi

Disclosure: Received research grant from: Neuronix Ltd, Yoqnea'm, Israel.

  1. Yang Y, Kim JS, Kim S, Kim YK, Kwak YT, Han IW. Cerebellar Hypoperfusion during Transient Global Amnesia: An MRI and Oculographic Study. J Clin Neurol. 2009 Jun. 5(2):74-80. [Medline]. [Full Text].

  2. Liang JF, Shen AL, Lin SK. Bilateral hippocampal abnormalities on diffusion-weighted MRI in transient global amnesia: report of a case. Acta Neurol Taiwan. 2009 Jun. 18(2):127-9. [Medline].

  3. Eustache F, Desgranges B, Petit-Taboué MC, et al. Transient global amnesia: implicit/explicit memory dissociation and PET assessment of brain perfusion and oxygen metabolism in the acute stage. J Neurol Neurosurg Psychiatry. 1997 Sep. 63(3):357-67. [Medline].

  4. Strupp M, Bruning R, Wu RH, et al. Diffusion-weighted MRI in transient global amnesia: elevated signal intensity in the left mesial temporal lobe in 7 of 10 patients. Ann Neurol. 1998 Feb. 43(2):164-70. [Medline].

  5. Winbeck K, Etgen T, von Einsiedel HG, et al. DWI in transient global amnesia and TIA: proposal for an ischaemic origin of TGA. J Neurol Neurosurg Psychiatry. 2005 Mar. 76(3):438-41. [Medline].

  6. Nakada T, Kwee IL, Fujii Y, Knight RT. High-field, T2 reversed MRI of the hippocampus in transient global amnesia. Neurology. 2005 Apr 12. 64(7):1170-4. [Medline].

  7. Yamane Y, Ishii K, Shimizu K, Sofue K, Yoshikawa T, Miyamoto N, et al. Global cerebral hypoperfusion in a patient with transient global amnesia. J Comput Assist Tomogr. 2008 May-Jun. 32(3):415-7. [Medline].

  8. Bartsch T, Alfke K, Wolff S, Rohr A, Jansen O, Deuschl G. Focal MR spectroscopy of hippocampal CA-1 lesions in transient global amnesia. Neurology. 2008 Mar 25. 70(13):1030-5. [Medline].

  9. Miller JW, Petersen RC, Metter EJ, et al. Transient global amnesia: clinical characteristics and prognosis. Neurology. 1987 May. 37(5):733-7. [Medline].

  10. Matias-Guiu J, Blanquer J, Falip R, et al. Incidence of transient global amnesia in a Alcoi (Spain). Acta Neurol Scand. 1992 Aug. 86(2):221. [Medline].

  11. Lauria G, Gentile M, Fassetta G, et al. Incidence of transient global amnesia in the Belluno province, Italy: 1985 through 1995. Results of a community-based study. Acta Neurol Scand. 1997 May. 95(5):303-10. [Medline].

  12. Shuping JR, Rollinson RD, Toole JF. Transient global amnesia. Ann Neurol. 1980 Mar. 7(3):281-85. [Medline].

  13. Lin KH, Chen YT, Fuh JL, Li SY, Chen TJ, Tang CH, et al. Migraine is associated with a higher risk of transient global amnesia: a nationwide cohort study. Eur J Neurol. 2014 May. 21(5):718-24. [Medline].

  14. Saura D, Peñafiel P, Morales A, Albert L, Martínez F, de la Morena G. Transient global amnesia after dobutamine--atropine stress echocardiography. Eur J Echocardiogr. 2008 Jul. 9(4):567-8. [Medline].

  15. Pantoni L, Bertini E, Lamassa M, et al. Clinical features, risk factors, and prognosis in transient global amnesia: a follow-up study. Eur J Neurol. 2005 May. 12(5):350-6. [Medline].

  16. Lewis SL. Aetiology of transient global amnesia. Lancet. 1998 Aug 1. 352(9125):397-9. [Medline].

  17. Schreiber SJ, Doepp F, Klingebiel R, Valdueza JM. Internal jugular vein valve incompetence and intracranial venous anatomy in transient global amnesia. J Neurol Neurosurg Psychiatry. 2005 Apr. 76(4):509-13. [Medline].

  18. Cejas C, Cisneros LF, Lagos R, Zuk C, Ameriso SF. Internal Jugular Vein Valve Incompetence Is Highly Prevalent in Transient Global Amnesia. Stroke. 2009 Nov 19. [Medline].

  19. Choi BS, Kim JH, Jung C, Kim SY. High-Resolution Diffusion-Weighted Imaging Increases Lesion Detectability in Patients with Transient Global Amnesia. AJNR Am J Neuroradiol. 2012 Apr 26. [Medline].

  20. Adams RD, Victor M, Ropper AH. Transient global amnesia. Principles of Neurology. New York: McGraw-Hill; 1997: 429-30.

  21. Ay H, Furie KL, Yamada K, Koroshetz WJ. Diffusion-weighted MRI characterizes the ischemic lesion in transient global amnesia. Neurology. 1998 Sep. 51(3):901-3. [Medline].

  22. Chung CP, Hsu HY, Chao AC, et al. Detection of intracranial venous reflux in patients of transient global amnesia. Neurology. 2006 Jun 27. 66(12):1873-7. [Medline].

  23. Grande LA, Loeser JD, Samii A. Recurrent transient global amnesia with intrathecal baclofen. Anesth Analg. 2008 Apr. 106(4):1284-7, table of contents. [Medline].

  24. Hinge HH, Jensen TS, Kjaer M, et al. The prognosis of transient global amnesia. Results of a multicenter study. Arch Neurol. 1986 Jul. 43(7):673-6. [Medline].

  25. Lauria G, Gentile M, Fassetta G, et al. Transient global amnesia and transient ischemic attack: a community- based case-control study. Acta Neurol Scand. 1998 Jun. 97(6):381-5. [Medline].

  26. Otrock ZK, Beydoun A, Barada WM, Masroujeh R, Hourani R, Bazarbachi A. Transient global amnesia associated with the infusion of DMSO-cryopreserved autologous peripheral blood stem cells. Haematologica. 2008 Mar. 93(3):e36-7. [Medline].

  27. Quinette P, Guillery-Girard B, Dayan J, et al. What does transient global amnesia really mean? Review of the literature and thorough study of 142 cases. Brain. 2006. 129:1640-58. [Medline].

  28. Schmidtke K, Ehmsen L. Transient global amnesia and migraine. A case control study. Eur Neurol. 1998 Jul. 40(1):9-14. [Medline].

  29. Spigno F, De Lucchi M, Migliazzi L, Cocito L. Transient global amnesia after breathing hyperoxic mixtures in otherwise regular dives. Clin Neurol Neurosurg. 2008 Mar. 110(3):259-61. [Medline].

  30. Vyhnálek M, Bojar M, Jerabek J, Hort J. Long lasting recurrent familiar transient global amnesia after betablocker treatment withdrawal: case report. Neuro Endocrinol Lett. 2008 Feb. 29(1):44-6. [Medline].

  31. Zweifler RM. Management of acute stroke. South Med J. 2003 Apr. 96(4):380-5. [Medline].

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