[6] Some people report short-lived retrograde amnesia so deep that they do not recognize their home or family members, though personal identity is preserved.
Observers may, however, notice some pallor of the skin, a brief 'loss of contact' such as not seeming to be aware of the person witnessing the attack, or some automatic movements such as swallowing, lip-smacking or fidgeting of the hands.
[4] Such unusual presentations "may be due to ongoing seizure activity (non-convulsive status epilepticus) or persistent post-ictal dysfunction of memory-related brain structures.
"All recordings showed seizure activity, which in 8/10 cases involved both temporal lobes and in the others remained unilateral (1 left and one right-sided).
[6][13] (Other sources of amnestic symptoms include herpes encephalitis, hypoxia, vascular or basal forebrain lesions, deep midline tumors, early dementia, and Korsakoff syndrome which is secondary to thiamine deficiency, most often the result of alcohol use disorder.
[1]) The anatomical and pathophysiological basis of TEA is presumed to be similar to transient global amnesia (TGA), that is, it is likely to be primarily hippocampal in origin, but with more variable involvement of limbic and adjacent temporal lobe neocortical structures.
[4][6] The IQ of people diagnosed with TEA tends to be in the high average to superior range, perhaps due to selection bias.
[2] Typically these tests examine the ability to store information for up to 30 minutes but the problem of accelerated long-term forgetting in TEA patients is not generally noticeable at this point.
It is possible that a pre-existing condition affecting the temporal lobe may both cause attacks of TEA and interfere with the handling of memories.
[4][15] 70%[4] of people with TEA notice a patchy but persistent loss of memories of events from their past personal experiences[5][18] and this autobiographical amnesia has been reported in all cases in which accelerated forgetting was also present.
[16]These memory deficits have been shown to extend across the entire lifespan and there are significant impairments across a wide range of different types of contextual information including event, place, perceptual and thought/emotion details.
[20] When asked to produce personal memories relating to a particular word (for example, "boat"), a 68-year-old epileptic patient failed to retrieve any episodes from his twenties or thirties.
The mechanism and etiology of this phenomenon remain controversial, especially as it is impossible to rule out prior subclinical epileptic activity which could be responsible for a failure to consolidate those seemingly forgotten memories.
[19] A recent imaging study that aimed to provide insight into the neural basis of these autobiographical memory deficits revealed that patients had significantly reduced activation in the right medial temporal lobes (and more specifically the right posterior parahippocampal cortex) and effective connectivity analysis indicated that there was reduced connectivity between this right parahippocampal region and the right middle temporal gyrus, which has been linked to semantic memory.
However, for semantic information that has an episodic component, such as knowledge of whether people are dead or alive, patients with TEA often show significant deficits.
[23] TEA responds well to low doses of medicine used to treat epilepsy, (such as carbamazepine, lamotrigine or sodium valproate)[24] resulting in a cessation of seizure activity in 45 of 47 patients.
The features of the amnesic episodes, the high frequency of olfactory hallucinations during attacks and findings from electroencephalography suggest that a medial temporal lobe focus is responsible for the seizures.
It could be that epileptiform activity originating in the medial temporal lobe has the potential to disrupt the distributed neocortical traces required to maintain detailed autobiographical memories.
However it is not evident, in this theory, that partial damage to the hippocampus – of the kind that might plausibly cause of the phenomena of TEA – should lead to selective erasure of previously salient autobiographical memories.
The stability of some memories suggests further that 'focal retrograde amnesia' as it has been termed[7][16][19] may be "due to erasure of representations rather than to a defective retrieval mechanism.
"[5] One issue raised by this hypothesis includes whether the reported amnesia in fact predates the TEA attack, and is possibly due to prior subclinical epileptic activity; it also highlights a variety of methodological concerns about studies of amnesia based largely on single case studies and cases with varying etiologies.
Recent studies of patients with medial temporal pathology have suggested that the hippocampal formation has a life long role in the storage of autobiographical memories.
Further work investigating the relationships between seizure frequency, EEG activity, structural changes in the temporal lobes, and the severity of accelerated forgetting and autobiographical memory loss, is required to clarify these issues.
"[28] TEA is related to sleep in nearly three-quarters of cases, and persistent memory problems could be the result of nocturnal, subclinical attacks disrupting on-going consolidation processes.
Alternatively, amnesia upon waking may reflect persistent post-ictal dysfunction of medial temporal lobe structures following a seizure during sleep.