Objective To identify the neural basis of autobiographical memory deficits in transient epileptic amnesia (TEA).

Method 11 people (mean age: 65.91; SD=7.63) diagnosed with transient epileptic amnesia, all of whom complained of extensive autobiographical memory loss, and 17 age and IQ matched controls were recruited. Participants were matched on standard measures of anterograde memory. Participants recalled 32 previously identified autobiographical memories, specific in time and place, from four different time periods (childhood, young adult, middle aged and recent), during fMRI scanning. Activations were analysed using SPM8 software, effective connectivity using dynamic causal modelling (DCM). Post-scan ratings of the subjective vividness, level of detail, pleasantness, personal significance and frequency of retrieval of the memories were recorded.

Results Both patients and controls activated core regions of the autobiographical memory network. However, patients had reduced activation in the right posterior parahippocampal gyrus (pPHG), particularly for more recent memories, together with decreased engagement of the right temporoparietal junction and the right cerebellum. In addition, we found reduced effective connectivity in patients between the right pPHG and the right middle temporal gyrus. There were no differences in the subjective ratings of memories between patients and control participants.

Conclusion The reduction of activity in the right pPHG is consistent with other evidence that TEA is a disorder of the medial temporal lobes (MTL) and further implicates the pPHG as a key region for contextual information. These MTL differences were most marked for recent and mid-life periods suggesting that, at least at the neural level, remote memories are more robust than recent memories. We also found reduced effective connectivity in patients between the right pPHG and the right middle temporal gyrus. This may reflect persisting effects of the seizures, the continued presence of sub-clinical epileptiform activity or the sequelae of subtle structural changes in the MTL in our patient group.