With many thanks to the study participants, and the original study authors for generously sharing their data!

These results provide evidence for an inhibitory control mechanism operating to prevent the recognition of personally-relevant stimuli in dissociative amnesia.

By contrast, the inhibitory activation pattern persisted in the second participant, who did not show any memory recovery following this treatment.

Following treatment (interview under sedation), one participant recovered almost all of his memories. On repeating the task, he no longer showed activation of the retrieval inhibition network when reminded of current colleagues.

Critically, effective connectivity analyses provided evidence that the hippocampus was actively downregulated by the right anterior DLPFC when patients failed to recognise their current colleagues.

Reduced activation was observed across autobiographical memory regions including in the mPFC and the anterior hippocampus, demonstrating further functional alignment with the regions downregulated during retrieval stopping in the Think/No Think task.

When the participants were reminded of people from forgotten time-periods (their current colleagues), they engaged a network of regions very similar to those engaged when during laboratory-based retrieval inhibition tasks (mega-analysis of the Think/No-Think task).

Participant 1 experienced a 2-day fugue episode, following which he remained amnesic for the ~4.5 years preceding onset.
Participant 2 presented with a focal retrograde amnesia for the past 35 years of his life.

We re-analysed fMRI data from two people with generalised dissociative amnesia to test the theory that memory retrieval is inhibited via prefrontal control.

Generalised forms of dissociative amnesia involve memory loss for extended periods of the personal past, often several years or decades, in the absence of identifiable neuropathology. The underlying neurobiological mechanisms are poorly understood.