What transient amnesia tells us about autobiographical memory and brain plasticity

November, 2011

Brain scans of those suffering from transient global amnesia indicate a permanent role of the hippocampus in autobiographical memory, and demonstrate the brain’s ability to self-repair.

When a middle-aged woman loses her memory after sex, it naturally makes the headlines. Many might equate this sort of headline to “Man marries alien”, but this is an example of a rare condition — temporary, you will be relieved to hear — known as transient global amnesia. Such abrupt, localized loss of autobiographical memory is usually preceded by strenuous physical activity or stressful events. It generally occurs in middle-aged or older adults, but has been known to occur in younger people. In those cases, there may be a history of migraine or head trauma.

Following an earlier study in which 29 of 41 TGA patients were found to have small lesions in the CA1 region of the hippocampus, scanning of another 16 TGA patients has revealed 14 had these same lesions. It seems likely that all the patients had such lesions, but because they are very small and don’t last long, they’re easy to miss. The lesion is best seen after 24-72 hours, but is gone after 5-6 days.

At the start of one of these attacks, memory for the first 30 years of life was significantly impaired, but still much better than memory for the years after that. There was a clear temporal gradient, with memory increasingly worse for events closer in time. There was no difference between events in the previous year and events in the previous five years, but a clear jump at that five-year point.

The exact location of the lesions was significant: when the lesion was in the anterior part of the region, memory for recent events was more impaired.

The hippocampus is known to be crucially involved in episodic memory (memory for events), and an integral part of the network for autobiographical memory. In recent years, it has come to be thought that such memories are only hosted temporarily by the hippocampus, and over a few years come to be permanently lodged in the neocortex (the standard consolidation model). Evidence from a number of studies of this change at the five-year mark has been taken as support for this theory. According to this, then, older memories should be safe from hippocampal damage.

An opposing theory, however, is that the hippocampus continues to be involved in such memories, with both the neocortex and the hippocampus involved in putting together reconsolidated memories (the multiple trace model). According to this model, each retrieval of an episodic memory creates a new version in the hippocampus. The more versions, the better protected a memory will be from any damage to the hippocampus.

The findings from this study show that while there is indeed a significant difference between older and more recent memories, the CA1 region of the hippocampus continues to be crucial for retrieving older memories, and for our sense of self-continuity.

Interestingly, some studies have also found a difference between the left and right hemispheres, with the right hippocampus showing a temporal gradient and the left hippocampus showing constant activation across all time periods. Such a hemisphere difference was not found in the present study. The researchers suggest that the reason may lie in the age of the participants (average age was 68), reflecting a reduction in hemispheric asymmetry with age.

There’s another message in this study. In these cases of TGA, memory function is restored within 24 hours (and generally sooner, within 6-10 hours). This shows how fast the brain can repair damage. Similarly, the fact that such tiny lesions have temporary effects so much more dramatic than the more lasting effects of larger lesions, is also a tribute to the plasticity of the brain.

The findings are consistent with findings of a preferential degeneration of CA1 neurons in the early stages of Alzheimer's disease, and suggest a target for treatment.

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