Transient Epileptic Amnesia - Implications For Theories of Memory

Implications For Theories of Memory

These forms of memory deficit raise issues about the nature of memories in the neuroanatomy and how conflicting observations can be reconciled with either the standard or the multiple trace models. It has been noted that "People with temporal lobe epilepsy provide a natural laboratory for the study of human memory." TEA, as a form of temporal lobe epilepsy, is of particular interest as one must consider both the loss of long-encoded memories (as long as 40 years or one's whole life) and the simultaneous failure of recently-encoded but not immediately short-term memories. The issue of topographical amnesia, which would seem to involve parts of the brain not usually associated with other TEA symptoms, was referred to earlier. These are often considered different kinds of memories with distinct neuroanatomical loci, so that a model to explain both conditions with one etiology is elusive.

The major issues are summarized on the TIME website:

The cluster of memory problems occurring in patients with TEA - episodes of transient amnesia, accelerated forgetting and autobiographical amnesia - challenges both standard and multiple trace models of memory. 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. On the 'standard model' of memory consolidation, which proposes that the medial temporal lobes play a time-limited role in memory processing, accelerated forgetting, occurring over days-1 week (TIME data), is a plausible result of structural or functional pathology in the medial temporal lobes. The associated autobiographical memory impairment is, however, a more puzzling consequence of medial temporal lobe pathology on this theory. 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. Multiple trace theory, on the other hand predicts that disturbances of anterograde and retrograde episodic memory will go hand in hand. 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. Thus neither of the leading current models of retrograde memory readily accounts for our observations.

There is support in the pattern of these deficits for "dissociation between the mechanisms subserving anterograde memory and those required to evoke remote episodic memories, and strengthens the evidence for a dissociation between knowledge of public and of personal events." The stability of some memories and suggests further that 'focal retrograde amnesia' as it has been termed may be " due to erasure of representations rather than to a defective retrieval mechanism. Whether epileptic activity per se is responsible for this phenomenon requires further investigation." 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.

ALF and focal retrograde amnesia after TEA offer clues as to the nature of memory consolidation.

According to the standard view of memory consolidation, extensive retrograde amnesia is likely to be the result of damage to cortical memory representations or, more plausibly, the links between individual sensory elements that constitute an autobiographical episode. 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. It is plausible therefore that medial temporal damage, whether occurring as a result of recurrent seizures and/or underlying subtle vascular damage, could result in both accelerated forgetting and retrograde amnesia. 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.

This view of consolidation has been disputed, as it seems to suggest consolidation occurs over long spans of time, not just minutes or days, and "requires physiological changes lasting years or decades." Such long-term consolidation processes would seem to require multiple stages of consolidation, which remain hypothetical.

A central concern in theories of memory consolidation is the role of sleep. "(O)ne set of observations suggests that consolidation may occur over any time interval, whereas another body of data suggests that these processes require sleep…. Clearly, both cannot be true. Resolving the inherent conflict between these perspectives strikes at the very heart of how biological mechanisms process memories after their initial encoding." 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. Furthermore, as noted, abnormal EEG readings in people with TEA occur primarily in sleep EEG. However, the "reason for the close relationship of TEA with sleep is unclear. It may be that the transition from sleep to waking acts as a trigger to a seizure focus in the medial temporal lobe. Alternatively, amnesia upon waking may reflect persistent post-ictal dysfunction of medial temporal lobe structures following a seizure during sleep."