Most (75%) cases of transient global amnesia occur in people aged 50 to 70; this disorder rarely occurs in people < 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 neurons in the CA1 area of the hippocampus 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 transient global amnesia include
However, usually no trigger is identified.
Patients often present after a triggering event.
The classic presentation in transient global amnesia is
But a less severe retrograde amnesia may be the presenting symptom.
Episodes usually last for 1 to 8 hours but may last from 30 minutes to 24 hours (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
Diagnosis of transient global amnesia is primarily clinical. Neurologic examination Introduction to the Neurologic Examination The neurologic examination begins with careful observation of the patient entering the examination area and continues during history taking. The patient should be assisted as little as possible... read more typically does not detect any abnormalities other than disturbed memory. Brain ischemia Diagnosis Ischemic stroke is sudden neurologic deficits that result from focal cerebral ischemia associated with permanent brain infarction (eg, positive results on diffusion-weighted MRI). Common causes... read more must be ruled out.
Laboratory tests should include complete blood count (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; if brain ischemia is present, MRI may show focal hyperintense lesions correlating with restricted diffusion in the lateral hippocampus. During the first 24 hours 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, when the patient has recovered, is unknown.
The electroencephalogram (EEG) usually shows nonspecific abnormalities and is unnecessary unless a seizure is suspected or episodes recur.
Prognosis is good. Symptoms typically last < 24 hours. 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.
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