What are the causes of transient global amnesia (TGA)?

Updated: Jul 27, 2018
  • Author: Roy Sucholeiki, MD; Chief Editor: Helmi L Lutsep, MD  more...
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Answer

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]


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