Historical introduction

Fisher and Adams (1964) coined the term ‘transient global amnesia’ (TGA) to describe a syndrome which was reported independently by several authors in the 1950s (Bender, 1956; Guyotat & Courjon, 1956). This profound but temporary ‘defect of memory, involving the events of the recent past and the present’, had probably been classified previously as a manifestation of hysteria (Hodges, 1991). Once recognized, the syndrome proved highly distinctive and over 1500 cases have been described (Frederiks, 1993).

Many years before the delineation of TGA, Hughling-Jackson's classical description of the case of a physician with epilepsy, Dr Z., suggested that amnesia for episodes of complex and well-integrated behaviour can be a manifestation of temporal lobe epilepsy (TLE, Hughlings-Jackson, 1889). Fisher and Adams speculated that TGA might result from seizure activity disrupting ‘the recording and recall of recent events’. Subsequent research, outlined below, has shown that true TGA does not have an epileptic basis, but has also confirmed that epilepsy can cause a distinctive variety of transient amnesia. Numerous terms have been applied to episodes of epileptic amnesia including pure amnestic seizures (Palmini et al., 1992), ictal amnesia (Rowan, 1991), epileptic amnesic attacks (Pritchard et al., 1985; Galassi et al., 1986) and epileptic transient amnesia (Stracciari et al., 1990). The term suggested recently by Kapur, transient epileptic amnesia (TEA, Kapur, 1993), has been adopted, which highlights the similarity of this syndrome to, but also its distinction from, TGA.

In this chapter the clinical and neuropsychological features of TGA and TEA are reviewed and contrasted, their pathophysiology discussed and an approach to the management of patients with transient amnesia is outlined.