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What causes psychogenic amnesia?

The media love it. Films and novels fictionalise it. TV and newspapers want to follow a real patient around. They virtually always get it wrong (and the worst thing you can do for such a patient is put him/her on television). Psychogenic amnesia (also known as dissociative or functional amnesia) still intrigues and fascinates.

In 1926, Agatha Christie, the acclaimed novelist, disappeared for 11 days. Her home was in Berkshire; her car was found in Surrey; and she was discovered 11 days later in a hotel in Harrogate. She claimed amnesia for what had happened. The authenticity of her amnesia has been disputed, but the circumstances were typical of those that characterise a ‘fugue state’.

Many cases of psychogenic amnesia appear to migrate to central London, where they are often picked up by the police in central London parks or railway termini, and taken to St Thomas’s Hospital in its location opposite the Houses of Parliament. Harrison et al. (2017) have now reported 53 cases seen by Prof Kopelman and his team over the course of 20 years on a psychiatric receiving ward. This is by far the largest series of such patients to be described in recent times.

We found that there were four sub-groups of such patients. The first sub-group consisted of patients who, following a precipitating crisis, disappeared (rather like Agatha Christie) with loss of their sense of identity and memory, and travelled what were sometimes long distances. These patients are described as having a ‘fugue episode’, an expression derived from the Latin word ‘fuga’, meaning ‘flight’. These patients characteristically get better, either spontaneously or with therapeutic help – often within a few hours or days (we drew a cut-off point at four weeks).

Newspaper article about Archibald Christie and his wife Agatha Christie at Harrogate by Daily Herald (London) 15 December 1926, p. 1. Public domain via Wikimedia Commons.

A second group started out like the Fugue group (forgetting who they were, and sometimes travelling distances); although these patients rapidly ‘re-learned’ who they were, their amnesia persisted, much longer than four weeks. We have labelled this sub-group Fugue-to-Focal Retrograde Amnesia (F_FRA).

A third sub-group did not begin with a fugue-like episode, but had often suffered a very mild head trauma or neurological event just before their memory loss, which could not possibly account for their onset of Focal Retrograde Amnesia (FRA).

A final subgroup simply reported ‘gaps’ in their memories, which related, directly or indirectly, to stressful life events.

With regard to features of the amnesia, a person’s knowledge of who he/she was (personal identity) was lost only in the psychogenic cases, particularly the Fugue cases. The failure to recognise the family was most common in the psychogenic cases, particularly the two FRA subgroups, but occasionally happened in neurological cases. Interestingly, a history of past or precipitating head injury was actually more common in the psychogenic cases (just over 40%) than the neurological cases (10%). Factors like past or precipitating depression, relationship or family problems, financial or employment problems, occurred in all the groups, but were much more common in the psychogenic than the neurological cases or healthy participants.

With regard to performance on neuropsychological tests, we found that, during their amnesia, the psychogenic patients were mildly impaired on tests of new learning, particularly on word recall tests, compared with their scores three to six months later. However, their most devastating deficit was in remembering past facts about their lives or in recalling events they had experienced. The Fugue group performed particularly badly in trying to recall facts or events from any time period in their lives. The two FRA groups did badly on facts or events from childhood or their young adult life, but somewhat better for more recent events – this is the opposite pattern to neurological patients, who characteristically show relative sparing in remembering early memories, but do very badly on recent memories. However, after three to six months, the Fugue group had improved to normal in remembering facts about their past, and near-normal in remembering events from their past. The two FRA groups had also improved, but not so much as the Fugue group; and they still did better on recent memories, compared with earlier ones.

Taking all this together, it shows that the outcome in such cases is much better than generally assumed – at least if the cases are caught at an early stage in their disorder. The Fugue cases often recovered ‘spontaneously’ with very little or no specific treatment. The FRA cases had had a variety of treatments, including antidepressant medication. The pattern of results suggests that memory retrieval had been inhibited during the amnesia, perhaps because the patients had somehow been avoiding (consciously or subconsciously) thinking about stressful or traumatic events, and this in turn can induce forgetting, as recent experimental work has shown. The findings are also consistent with a ‘model’ in which a stressful life event or events at a time when a person is depressed (and sometimes suicidal) can trigger psychogenic amnesia, even if the person cannot then pinpoint what these stressors were. This psychogenic memory loss seems to happen more commonly in people who, for whatever reason, have had a past, brief episode of transient memory loss for a neurological reason, such as a very minor head injury. This latter factor may be the reason why these patients developed amnesia at a time of severe stress as opposed to some other psychogenic/functional disorder, such as non-epileptic seizures, psychogenic blindness, or various motor or sensory symptoms.

This remains a fascinating topic, but not necessarily in the way that the media envisage.

Featured image credit: ‘Memory’ by jarmoluk. CCO Public Domain via Pixabay.

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