Transient Global Amnesia Clinical Presentation

The syndrome of transient global amnesia (TGA) was described initially by Morris Bender in the Journal of the Hillside Hospital in 1956. Fisher and Adams later wrote extensively about TGA in Acta Neurologica Scandinavica in 1964. Since that time, TGA has become 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.
• 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.^[13]
• 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.^[14] 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.^[15] 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.^{[16, 17]} 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.^[16]