The mechanisms underlying generalized forms of dissociative (‘psychogenic’) amnesia are poorly understood. One theory suggests that memory retrieval is inhibited via prefrontal control. Findings from cognitive neuroscience offer a candidate mechanism for this proposed retrieval inhibition. By applying predictions based on these experimental findings, we examined the putative role of retrieval suppression in dissociative amnesia.

We analyzed fMRI data from two previously reported cases of dissociative amnesia. Patients had been shown reminders from forgotten and remembered time periods (colleagues and school friends). We examined the neuroanatomical overlap between regions engaged in the unrecognized compared to the recognized condition, and the regions engaged during retrieval suppression in laboratory-based tasks. Effective connectivity analyses were performed to test the hypothesized modulatory relationship between the right anterior dorsolateral prefrontal cortex (raDLPFC) and the hippocampus. Both patients were scanned again following treatment, and analyses were repeated.

We observed substantial functional alignment between the inhibitory regions engaged during laboratory-based retrieval suppression tasks, and those engaged when patients failed to recognize their current colleagues. This included significant activation in the raDLPFC and right ventrolateral prefrontal cortex, and a corresponding deactivation across autobiographical memory regions (hippocampus, medial PFC). Dynamic causal modeling confirmed the hypothesized modulatory relationship between the raDLPFC and the hippocampus. This pattern was no longer evident following memory recovery in the first patient, but persisted in the second patient who remained amnesic.

Findings are consistent with an inhibitory mechanism driving down activity across core memory regions to prevent the recognition of personally relevant stimuli.

Dissociative Amnesia remains an enigmatic and controversial entity. It is classically described as responsible for autobiographic amnesia associated with a traumatic event.

To report a clinical case and review the literature.

We collected data from the patient’s clinical file with his informed consent. We conducted a non-systematic review of the literature.

A 46-years-old patient presents to the emergency department for sudden global retrograde amnesia, with multiple domain amnestic syndrome (impairing verbal and visual memory, processing speed, mental flexibility, calculus, executive functions and language). He was initially admitted for a suspected infectious meningoencephalitis, which was not confirmed. Later an autoimmune encephalitis was pursued. Brain MRI showed a nonspecific left temporal and hipocampal hyperintensity and the EEG a mild left temporal dysfunction. The autoimmune encephalitis panel was negative and the formal diagnostic criteria were not met. The neurologic examination at discharge presented only with autobiographical and semantic amnesia. On the mental state examination, he presented with depressive symptoms reactive to the situation. There was no evident traumatic event apart from a promotion received the day before the amnesia started. He was prescribed escitalopram 10 mg/day. The amnesia was maintained at 9 months follow-up.

Our case report illustrates a case of amnesia without evident organic or psychogenic cause, assumed as a dissociative amnesia. Further studies are necessary to clarify the pathophysiology of this condition and develop specific treatments.

No significant relationships.