Transient Global Amnesia

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Basics

Description

  • Transient global amnesia (TGA) has the following features:
    • Episode of amnesia with abrupt onset
    • No focal neurologic signs or symptoms
    • Temporary, severe, anterograde amnesia:
      • Acute inability to form new memories
      • Permanent memory gap after the episode
    • Temporary short-range retrograde amnesia:
      • More recent memories at more risk
      • Previously encoded memories unavailable only temporarily
    • Gradually improves until only remaining memory deficit is the gap induced by the anterograde amnesia
      • Some retrograde loss may be permanent
    • Mean duration of symptoms: 4–6 hr
      • Majority resolve within 8 hr
  • Incidence between 3 and 8 per 100,000 people:
    • 75% occur in patients 50–70 yr old
    • 10% occur in patients <50 yr
    • Rare in patients <40 yr

Etiology

  • Multimodal MRI, SPECT, and PET have shown some abnormalities of regional blood flow in selectively vulnerable hippocampal structures
  • The exact etiology of TGA is unknown; speculated causes are controversial:
    • Vasoconstriction due to hyperventilation:
      • Psychogenic hyperventilation in setting of age-related cerebrovascular autoregulatory dysfunction
    • Hippocampal venous congestion with Valsalva:
      • Increased prevalence of internal jugular vein insufficiency on ultrasound
      • Intracranial venous reflux not seen
    • Migraine (in younger patients)
      • Destabilization of the CA1 sector of the hippocampus via glutamate release
      • Increased prevalence of migraine history in TGA patients
      • No increased frequency of TGA in patients with migraines
  • No correlation between TGA and thromboembolic cerebrovascular disease has been found
    • TGA patients in fact have a lower risk of future cerebrovascular events than TIA patients

-- To view the remaining sections of this topic, please or --

Basics

Description

  • Transient global amnesia (TGA) has the following features:
    • Episode of amnesia with abrupt onset
    • No focal neurologic signs or symptoms
    • Temporary, severe, anterograde amnesia:
      • Acute inability to form new memories
      • Permanent memory gap after the episode
    • Temporary short-range retrograde amnesia:
      • More recent memories at more risk
      • Previously encoded memories unavailable only temporarily
    • Gradually improves until only remaining memory deficit is the gap induced by the anterograde amnesia
      • Some retrograde loss may be permanent
    • Mean duration of symptoms: 4–6 hr
      • Majority resolve within 8 hr
  • Incidence between 3 and 8 per 100,000 people:
    • 75% occur in patients 50–70 yr old
    • 10% occur in patients <50 yr
    • Rare in patients <40 yr

Etiology

  • Multimodal MRI, SPECT, and PET have shown some abnormalities of regional blood flow in selectively vulnerable hippocampal structures
  • The exact etiology of TGA is unknown; speculated causes are controversial:
    • Vasoconstriction due to hyperventilation:
      • Psychogenic hyperventilation in setting of age-related cerebrovascular autoregulatory dysfunction
    • Hippocampal venous congestion with Valsalva:
      • Increased prevalence of internal jugular vein insufficiency on ultrasound
      • Intracranial venous reflux not seen
    • Migraine (in younger patients)
      • Destabilization of the CA1 sector of the hippocampus via glutamate release
      • Increased prevalence of migraine history in TGA patients
      • No increased frequency of TGA in patients with migraines
  • No correlation between TGA and thromboembolic cerebrovascular disease has been found
    • TGA patients in fact have a lower risk of future cerebrovascular events than TIA patients

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