Get Adobe Acrobat ReaderResearch Areas - Theories of Memory
The 'standard' theory of declarative memory processing proposes that the hippocampus plays a key role in the acquisition and the early stages (seconds - weeks or months) of storage of both episodic and semantic memories. However this theory envisages that over time the representation of memories is transferred into the neocortex. A recently proposed alternative model, 'Multiple Trace' theory, accepts that semantic memories become dependent upon the neocortex over time, but proposes that recollection of detailed episodic memories requires the integrity of the hippocampus throughout our lifetimes. Independently of these theories, evidence has accumulated recently that reactivation of memory traces during sleep may contribute towards their consolidation.
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.
Episodes of TEA are associated with sleep. 37/50 patients in the TIME series reported attacks on waking; EEG abnormalities may be absent on wake but present on sleep EEGs. Although the role of sleep in memory processing remains controversial, there is growing evidence, from animal and human studies, that sleep-specific processes contribute to memory consolidation. The persistent amnesic phenomena observed in patients with TEA may be due to disturbance of sleep-specific memory processes.