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Transient Global Amnesia Clinical Presentation

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


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,[12] 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.[13]

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.[14]

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.[15] 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.[16] 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.[17]

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.

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