Transient global amnesia is anterograde and usually retrograde amnesia that begins suddenly and lasts up to 24 h. Diagnosis is primarily clinical but includes laboratory tests and CT, MRI, or both to evaluate central circulation. The amnesia typically remits spontaneously but may recur. There is no specific treatment, but underlying abnormalities are corrected.
Most (75%) cases of transient global amnesia occur in people aged 50 to 70; and this disorder rarely occurs in patients < 40.
The etiology of transient global amnesia is not clear. Suggested mechanisms include those related to migraine, hypoxia and/or ischemia, venous flow abnormalities, or seizures, as well as psychologic factors. Recent data suggest that vulnerability of CA1 neurons to metabolic stress is pivotal; the resulting damage triggers a cascade of changes that lead to impaired hippocampal function.
A distinct benign form of transient global amnesia can follow excessive alcohol ingestion, moderately large sedative doses of barbiturates, use of several illicit drugs, or sometimes relatively small doses of benzodiazepines (especially midazolam and triazolam).
Events that can trigger this amnesia include sudden immersion in cold or hot water, physical exertion, emotional or psychologic stress, pain, medical procedures, sexual intercourse, and a Valsalva maneuver.
Symptoms and Signs
Patients often present after a triggering event. The classic presentation is abrupt onset of severe anterograde amnesia. But a less severe retrograde amnesia may be the presenting symptom. Episodes usually last for 1 to 8 h but may last from 30 min to 24 h (rarely). Patients are often disoriented to time and place but usually not to personal identity. Many patients are anxious or agitated and may repeatedly ask questions about transpiring events. Language function, attention, visual-spatial skills, and social skills are retained. Impairments gradually resolve as the episode subsides.
The benign transient amnesia after substance ingestion is distinct because it is selectively retrograde (ie, for events during and preceding intoxication), relates specifically to drug-accompanied events, does not cause confusion (once acute intoxication resolves), and recurs only if similar amounts of the same drug are ingested.
Diagnosis is primarily clinical. Neurologic examination typically does not detect any abnormalities other than disturbed memory. Brain ischemia must be ruled out (see Diagnosis).
Laboratory tests should include CBC, coagulation tests, and evaluation for hypercoagulable states.
Brain CT, brain MRI, or both are usually done. High-resolution diffusion-weighted MRI should be done to rule out brain ischemia if it is suspected; MRI may show focal hyperintense lesions correlating with restricted diffusion in the lateral hippocampus. During the first 24 h after symptom onset, MRI detects hippocampal lesions in only 12% of patients. Detection increases to 81% if MRI is done 3 days later and uses thinner 3-mm sections and higher b-values. Why lesions are more visible 3 days later is unknown.
EEG usually shows nonspecific abnormalities and is unnecessary unless a seizure is suspected or episodes recur.
Prognosis is good. Symptoms typically last < 24 h. As the disorder resolves, the amnesia lessens, but memory for events during the episode may be lost. Usually, episodes do not recur, unless the cause is seizures or migraines. Overall lifetime recurrence rate is about 5 to 25%. Risk of stroke is not increased.
No specific treatment is indicated. However, underlying ischemia (see Treatment) or seizure (see Treatment) should be treated.
Last full review/revision July 2013 by Juebin Huang, MD, PhD
Content last modified August 2013