From the Guidelines
Transient global amnesia is a benign condition that resolves spontaneously within 24 hours, and no specific treatment is required, but medical evaluation is necessary to rule out more serious conditions like stroke or seizures. This condition is characterized by sudden, brief episodes of memory loss without other neurological symptoms, typically affecting adults over 50. During an episode, patients remain alert but cannot form new memories and may repeatedly ask the same questions 1. The exact cause of transient global amnesia remains unclear, but potential triggers include emotional stress, physical exertion, sudden temperature changes, and sexual activity.
Key Considerations
- The condition is temporary and resolves on its own, with patients rarely experiencing mild memory deficits afterward.
- Medical evaluation is crucial to exclude other conditions, such as stroke or seizures, which may present with similar symptoms.
- Brain imaging and EEG may be performed to rule out other conditions, but these tests are typically normal in transient global amnesia 1.
- Patients should be kept safe during episodes, and a companion should stay with them until symptoms resolve.
- The pathophysiological mechanism responsible for transient global amnesia has not been elucidated, and it is not clear whether this syndrome is related to extracranial carotid and vertebral artery disease (ECVD) at all 1.
Management
- No medications are needed to treat transient global amnesia, as it resolves spontaneously.
- Medical evaluation should focus on ruling out more serious conditions, such as stroke or seizures.
- Patients should be monitored and kept safe during episodes, with a companion staying with them until symptoms resolve.
- Further testing, such as brain imaging and EEG, may be necessary to exclude other conditions, but these tests are typically normal in transient global amnesia 1.
From the Research
Definition and Characteristics of Transient Global Amnesia
- Transient Global Amnesia (TGA) is a benign and temporary loss of anterograde memory with the preservation of remote memories and immediate recall 2.
- It is characterized by the acute inability to form new memories, which can last up to 24 hours 3, 4.
- TGA confers no known long-term risks, but when abnormal signs or symptoms are present, they take precedence and guide the formulation of a differential diagnosis and investigation 3, 4.
Diagnosis and Management
- The diagnosis of TGA is dependent on eliminating other more serious etiologies, including toxic ingestions, acute strokes, complex partial seizures, and central nervous system infections 3, 4.
- The criteria created by Hodge and Warlow in 1990 can be used to diagnose TGA, which requires the episode of memory loss to be witnessed and involve anterograde amnesia, with no evidence of neurological signs or deficits, features of epilepsy, active epilepsy, or recent head injury 2.
- A minimalist approach is reasonable in witnessed TGA with classic features, avoiding overtesting, inappropriate medication, and medical interventions in favor of observation, ensuring patient safety, and reassuring patients and their families 3, 4.
Causes and Precipitants
- Precipitants of TGA include physical exertion, valsalva-like maneuvers, emotional stress, significant physical exertion, exposure to extreme temperatures, high-altitude conditions, acute illness, or sexual intercourse 2, 5.
- The pathophysiology of TGA is not well understood but may be related to impaired venous drainage of the hippocampus 5.
- There is an association between TGA and migraine headaches as well as takotsubo cardiomyopathy, but no apparent increased risk of cerebrovascular events occurs in patients who have had an episode of TGA 5.
Imaging Findings
- Classical MRI changes in TGA consist of unilateral or bilateral punctuate areas of hyperintensity in the hippocampal cornu ammonis 1 (CA1) region on diffusion-weighted imaging 6.
- Recognition of these imaging features is of the utmost importance for radiologists to allow for an accurate diagnosis and differentiation from ischemic pathology 6.