ISCHEMIC STROKE / STROKE MIMICS

Transient global amnesia (TGA)

Created 24/03/2021, last revision 14/09/2022

  • transient global amnesia (TGA) is a sudden, temporary (< 24h) episode of memory loss with the absence of other neurological signs that can’t be attributed to a more common neurological condition, such as epilepsy or stroke
  • mostly non-recurrent
  • it can be triggered by an intense emotional experience
  • incidence ~ 5–11  per 100,000 in the general population, the incidence is increased in patients > 50 years of age
  • TGA is considered to be a benign disorder, recurrences are relatively uncommon (12–19%), and it is not associated with an increased risk of stroke  [Mangla, 2013]

Clinical presentation

  • sudden onset of memory loss, verified by a witness, duration < 24 h (mostly 3-6 h, rarely > 12h), usually with the gradual return of memory
    • anterograde amnesia
      • inability to form new memories and to recall the recent past
      • a common feature includes repetitive questioning, usually of the same question (“How did we get here?”, “What am I doing here?”)
    • retrograde amnesia
      • inability to recall the circumstances that immediately preceded the memory loss
  • retention of personal identity despite memory loss
  • normal cognition, such as the ability to recognize and name familiar objects and follow simple directions
  • the patient may be slightly restless, anxious, but adequately given the situation
  • absence of focal neurological deficits (hemiparesis, involuntary movements, problems with speech, apraxia, etc.)
  • no evidence of seizures during the period of amnesia, no history of active epilepsy
Hodges and Warlow diagnostic criteria for Transient Global Amnesia
  • attacks must be witnessed
  • anterograde amnesia must occur during an attack
  • cognitive impairment is limited to amnesia
  • no clouding of consciousness or loss of personal identity
  • no focal neurological signs/symptoms
  • no epileptic features
  • the attack must resolve < 24h
  • no recent head injury or active epilepsy

Etiology

  • there is a dysfunction of the medial part of the temporal lobes, particularly the hippocampus
  • the exact etiology and etiopathogenesis have not yet been clearly elucidated
    • spreading depression or transient vasospasms are considered
  • inconsistent MR DWI findings underline ambiguities about the etiology – there are MR DWI studies with negative results and studies showing an image similar to stroke  [Bartsch, 2007]
    • punctuate hyperintensity on DWI, hypointense on ADC map with normalization of ADC signal within ten days
    • it is not clear, however, whether these patients do not actually have TGA syndrome
  • it is always necessary to exclude TGA syndrome (stroke/TIA, epileptic seizure or nonconvulsive status epilepticus, and metabolic disorders)

Diagnostic evaluation

Computed tomography (CT)
  • negative in true TGA
SPECT, PET
  • transient hypoperfusion of hippocampi and mesiotemporal structures
MR DWI
DWI finding in TGA patient
Transient global amnesia (TGA)

Differencial diagnosis

  • exclusion of TGA syndrome (stroke, epilepsy, and other stroke mimics)
  • TGA is not associated with an increased risk of ischemic stroke  [Mangla, 2013]
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Management

  • in TGA no treatment is needed
  • treatment of TGA syndrome depends on its etiology (antiepileptic drugs, antiplatelet therapy etc.)
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