ISCHEMIC STROKE / STROKE MIMICS
Transient global amnesia (TGA)
Created 24/03/2021, last revision 02/06/2023
- 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
- anterograde amnesia
- 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 and 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
- negative in true TGA
- transient hypoperfusion of hippocampi and mesiotemporal structures
- standard MRI FLAIR is negative
- DWI (Diffusion Weighted Images)
- some studies report no lesions [Huber, 2002]
- other studies show situations similar to stroke [Jain, 2018] [Winbeck, 2005] [Bartsch, 2007]
- dot hyperintensity on DWI, hypointensity on ADC maps
- ADC normalization within 10 days
- in case of stroke in the posterior circulation, more extensive MRI lesions can be expected
Differential 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
- no treatment is needed for TGA
- treatment of TGA syndrome depends on its etiology (antiepileptic drugs, antiplatelet therapy, etc.)
