Transient Global Amnesia

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Basics

Description

  • Transient global amnesia (TGA), first described in 1956, is a clinical syndrome characterized by sudden onset of marked reduction of anterograde and milder reduction of retrograde episodic long-term memory that lasts up to 24 hours (1).
  • Patient may have persistent vegetative symptoms (such as headaches, nausea, dizziness) and subclinical neuropsychological deficit lasting for days. Patient presents along with reduced executive functions.
  • No clear triggers have been identified, although several have been proposed (1):
    • Extenuating physical activity (most common) (1)
    • High levels of anxiety/stress (second most common) (1)
    • Rapid changes in body temperature (e.g., water contact/temperature change) (third most common) (1)
    • Migraines
    • Coitus (2)
  • Common risk factors that may have confounding effect like cardiovascular risk factors, diabetes, dyslipidemia, hypertension (HTN), atrial fibrillation have been studied and ruled out permitting to properly differentiated from transient ischemic attacks (TIAs).

Epidemiology

Incidence
  • TGA is not a rare entity as its incidence ranges from 10 to 32/100,000 per year among the age group 50 to 70 years (3).
  • Presents in the 7th decade of life most commonly, with mean age between 61 and 67 years
  • In an observational study, it occurred more in men than in women with a potential precipitating cause found in 50% of the cases.
  • Recurrence rate of 2.9–26.3% (1,4)

Prevalence
Unknown

Etiology and Pathophysiology

  • Regarding neuroanatomy: There are two areas of focus regarding memory and memory-guided behaviors which are hippocampal region and cortical hippocampal circuits (represented by posterior medial region network in temporal cortex and anterior temporal network).
  • It has been proposed that fragility and vulnerability of neurons located in cornu ammonis (CA1) area to metabolic stress (due to cytotoxic glutaminergic uptake or release) represents main landmark in pathophysiology leading to hippocampal function impairment (1). This largely represents watershed area in the brain (2).
  • Main arteries involved are represented by (i) anterior, middle, and posterior hippocampal arteries, all branching from posterior cerebral artery (PCA) responsible for hippocampal body circulation; (ii) anterior choroidal artery, responsible for hippocampal head circulation
  • Multiple etiology mechanism has been proposed for TGA (1):
    • Arterial ischemia and venous congestion with retrograde cerebral flow in any of the vessels described prior
    • Transient vascular constriction during hyperventilation episode
    • Hemorrhagic damage
    • TGA as a sequela from migraines due to decrease in activity throughout the cortex
    • Disruption of the learning circuit between amygdala, hippocampus, striatum, and prefrontal cortex
    • Reversible cerebral vasoconstriction syndrome

Risk Factors

  • Migraine history, having incidence ratio of 2.48; because it has been seen associated in 14% cases in retrospective studies (3)
  • Male sex (3)
  • Ischemic heart disease
  • Elevated levels of emotional stress
  • High level of physical effort
  • Phobic personality traits (1)
  • Prior CVA has been associated in 11% of cases in retrospective studies.

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