Transient Global Amnesia Clinical Presentation
- Author: Roy Sucholeiki, MD; Chief Editor: Helmi L Lutsep, MD more...
Transient global amnesia (TGA) is a well-described syndrome, but one whose exact etiology is not yet completely understood.
TGA specifically affects memory function. As mentioned previously, patients can register information, but retentive memory ability is affected dramatically.
Many mechanisms have been proposed, but no single cause can explain fully all the features of TGA. These include migraine variant, temporal lobe seizure, and TIA. If a patient is young or has repeated attacks, then the possibility of seizure or even migraine is higher. Some authors have stated that patients with TGA have age and risk factor profiles similar to those of patients with stroke or TIA, but patients with TGA have a low incidence of strokes on follow-up.
There is a demonstrated association between TGA and migraine. In one nationwide cohort study, migraine was associated with an increased risk of TGA, particularly in female patients aged 40-60 years.
Precipitants of TGA frequently include physical exertion, overwhelming emotional stress, pain, cold-water exposure, sexual intercourse, and Valsalva maneuver. These triggers may have a common physiologic feature: increased venous return to the superior vena cava.
The effects of drugs must be considered. For instance, sedative-hypnotic medications, either over-the-counter or prescribed for sleep (especially if used in conjunction with a transoceanic flight), or premedication with midazolam for medical procedures, may cause similar symptoms. Excessive alcohol can cause a blackout phenomenon. Hence, any history of drug-related amnesia may help clarify mitigating causes.
Sporadic reports of TGA occur very rarely in a variety of circumstances such as dobutamine-atropine stress echocardiography, infusion of DMSO-cryopreserved autologous peripheral blood stem cells, breathing of hyperoxic mixtures (Nitrox) in diving, intrathecal baclofen treatments, and withdrawal symptoms from a beta-blocker. In this report, the authors suggest that vasospasm might be an etiology versus venous conjestion.
Social history and family history is relevant. Pantoni et al found that patients with TGA have a higher incidence of personal or family background of psychiatric conditions compared with patients who have had a TIA. Prognostically, patients with TGA are less likely to experience a cardiovascular or cerebrovascular event compared with patients who have had a TIA.
Neurologic examination of the patient typically fails to demonstrate any abnormalities (other than memory dysfunction).
If any lateralizing or focal findings are noted on the examination, then the diagnosis of transient global amnesia should be questioned.
The exact mechanism that produces transient global amnesia is unclear.
The most compelling evidence in favor of migraine is that patients who suffer from a TGA event have a slightly higher incidence of a previous migraine. However, patients with TGA rarely report an associated headache. They also do not report nausea, photophobia, or phonophobia.
Seizure (eg, temporal lobe) is unlikely. TGA events are not associated with alteration of consciousness or stereotypical movements. EEG does not demonstrate epileptiform activity.
TIA as indicative of cerebrovascular disease is unlikely. Studies have demonstrated that patients with TGA have fewer cerebrovascular risk factors than those with known cerebrovascular or coronary artery disease. The prognosis for TGA is often better than for TIAs.
One theory proposed by Lewis is that venous congestion causes disrupted blood flow to the thalamic or mesial temporal structures. More recently, one study used cranial 3-dimensional time-of-flight (TOF) MR angiography (MRA) to try to detect any intracranial retrograde venous flow in 10 patients with TGA. By using left brachiocephalic vein occlusion, retrograde intracranial venous flow was found only in patients (5 of 10) versus controls. The authors suggest that this may indicate that patients have an impairment of cerebral venous outflow that make them at risk for a TGA event.
The frequently cited triggers for TGA can increase either sympathetic activity and/or intrathoracic pressure. This, in turn, could cause back-pressure in the jugular venous system, disrupting intracranial arterial flow with secondary venous congestion/ischemia to memory areas in the brain.
Conditions predisposing to this scenario might include venous anatomy anomalies, integrity of jugular vein valves, timing of the trigger, and severity of the inciting event. In support of the above concept of venous congestion are Schreiber et al's finding of a higher prevalence of internal jugular vein valve incompetence in patients with TGA versus normal controls and Cejas et al's similar findings.[17, 18] However, the authors of this study could find no particular internal jugular vein valve incompetence associated venous circulatory patterns that could indicate a direct cause/effect with TGA.
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].
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].
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].
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].
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].
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].
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].
Miller JW, Petersen RC, Metter EJ, et al. Transient global amnesia: clinical characteristics and prognosis. Neurology. 1987 May. 37(5):733-7. [Medline].
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].
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].
Shuping JR, Rollinson RD, Toole JF. Transient global amnesia. Ann Neurol. 1980 Mar. 7(3):281-85. [Medline].
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].
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].
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].
Lewis SL. Aetiology of transient global amnesia. Lancet. 1998 Aug 1. 352(9125):397-9. [Medline].
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].
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].
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].
Adams RD, Victor M, Ropper AH. Transient global amnesia. Principles of Neurology. New York: McGraw-Hill; 1997: 429-30.
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].
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].
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].
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].
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].
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].
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].
Schmidtke K, Ehmsen L. Transient global amnesia and migraine. A case control study. Eur Neurol. 1998 Jul. 40(1):9-14. [Medline].
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].
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].
Zweifler RM. Management of acute stroke. South Med J. 2003 Apr. 96(4):380-5. [Medline].