These cases are often difficult to manage, both because of the coexistence of minor organic, psychological factors and the possibility of financial compensation for injuries, and because the underlying stressors are often not obvious on initial inquiry. The other is after a minor brain insult such as mild concussion in a predisposed person. The first is following a typical fugue with wandering and loss of personal identity, when disproportionate retrograde amnesia persists. Clinically, there may be two aetiological routes to the appearance of this syndrome. Often, spouses or close family members are not initially recognised and later the patient claims to have relearned who they are. There is considerable controversy concerning whether a brain lesion in isolation can ever cause this dissociation between anterograde and retrograde amnesia ( Reference KopelmanKopelman, 2002a). The amnesia is described as ‘focal’ because anterograde memory is relatively or completely spared. This is a persistent state in which the individual loses all retrograde memories. It emerged that, following a marital crisis in the context of an unstable marriage, she had disappeared from her home and taken a flight to the UK. One year later, relatives in the USA sent a missing person poster to the UK police and she was traced. She was eventually discharged from hospital and the retrograde memory loss persisted. An amytal interview was tried, again with no success. In an effort to trace her identity a picture was shown on national television, with no responses. Initially, she appeared depressed but this resolved with no medication. After being medically cleared she was admitted to a psychiatric unit. Staff contacted the police, who took her to an accident and emergency department. The only clues to her identity were a bag with a few clothes and a letter that turned out to be addressed to someone else. She had approached a staff member, telling them that she had no recollection of who she was or what she was doing. However, regardless of the term used, the question remains, at what point, in cases of doubt, should the clinician assume that a psychological stressor or a marker of neuropathology or brain pathology is the primary cause of the symptoms? A subsidiary to this is, does the amnesia have both psychological and neurological contributions to its aetiology?Ī 40-year-old woman ‘came round’ on the London Underground. The term ‘functional’ amnesia has the problem that the amnesia could in many respects be considered dysfunctional. Also, it does not specify whether the memory loss is produced (partly or entirely) consciously (‘factitious’ or ‘exaggerated’ amnesia) or purely unconsciously (‘hysterical’ amnesia). We favour ‘psychogenic’ amnesia, because it points to underlying psychological processes without assuming that any particular psychological mechanism is involved (a difficulty with ‘dissociative’ amnesia). Others prefer ‘medically unexplained amnesia’. Some have argued strongly for ‘functional’ amnesia as a description more acceptable to patients ( Reference Stone, Carson and SharpeStone 2005). Unfortunately, the presence of amnesia may make it difficult to identify the stress until either informants have come forward or the amnesia itself has resolved.īoth DSM–IV ( American Psychiatric Association, 2000) and ICD–10 ( World Health Organization, 1992) favour the term ‘dissociative’ amnesia. Each requires the exclusion of an underlying neurological cause and the identification of a precipitating stress that has resulted in amnesia. A number of terms have been used to describe medically unexplained amnesia, including ‘hysterical’, ‘psychogenic’, ‘dissociative’ and ‘functional’.
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