The term transient global amnesia was first coined by Fisher and Adams in 1964 to describe a clinical syndrome characterised by the abrupt onset of severe amnesia usually accompanied by repetitive questioning, occurring in middle aged or elderly people, and lasting several hours.1 The aetiology of transient global amnesia has been a topic of debate, but in the past few years the situation has become considerably clearer with the emergence of the following diagnostic criteria: (1) attacks must be witnessed and information available from an observer who was present for most of the attack, (2) there must be clear cut anterograde amnesia during the attack, (3) clouding of consciousness and loss of personal identity must be absent and the cognitive impairment limited to amnesia, (4) there should be no accompanying focal neurological symptoms and functionally relevant focal signs, (5) epileptic features must be absent, (6) attacks must resolve within 24 hours, and (7) patients with recent head injury or known active epilepsy are excluded.2 3 Epidemiological studies which have applied these criteria have established that thromboembolic cerebrovascular disease plays no part in the causation of transient global amnesia, but the incidence of migraine in patients with transient global amnesia is greater than would be expected in the general population. A small minority of cases with unusually brief, and recurrent, attacks eventually manifest temporal lobe epilepsy.3

Turning to the neuropsychological aspects, much has been learned about the organisation and neural basis of human memory since the initial description of transient global amnesia. It is clear that memory is not a unitary function but consists of interactive systems.4 5 One broad distinction, which derives from experimental studies of patients with amnesia, is that between explicit and implicit memory; explicit memory refers to memory available to conscious access; implicit …