This paper reviews disorders of memory. After a brief survey of the clinical varieties of the amnesic syndrome, transient and persistent, selected theoretical issues will be considered by posing a series of questions. (i) What is impaired and what is spared in anterograde amnesia? (ii) Do temporal lobe, diencephalic and frontal lobe amnesias differ? (iii) How independently semantic is semantic memory? (iv) What determines the pattern and extent of retrograde memory loss? (v) Can retrograde amnesia ever be "isolated"? (vi) Does psychogenic amnesia involve the same mechanisms as organic amnesia? (vii) How and when do false memories arise? Commonalities as well as differences across separate literatures will be emphasized, and the case for a more "dynamic" (interactionist) approach to the investigation of amnesia will be advocated.

The relationship of these neuropathological, neurochemical, and metabolic abnormalities to cognitive functioning, with particular reference to specific aspects of memory processing, has been considered in some detail. Whereas structural and/or neurochemical abnormalities within the limbic/diencephalic circuits account for anterograde amnesia, some other factor, such as frontal lobe dysfunction, must underlie the severe retrograde memory loss which is characteristically found in this syndrome.

A detailed critique of the literature on focal retrograde amnesia is provided. Some of the cases commonly cited in this literature had, in fact, severely impaired anterograde memory, most often involving visuospatial material. Other cases showed poor anterograde memory in more moderate or subtle form, begging the question of whether "like" had really been compared with "like" across the retrograde and anterograde domains: there may be alternative explanations for the observed patterns of performance. One suggestion is that these patients suffer an impairment of long-term consolidation, an attractive hypothesis but one which requires much more rigorous testing than has occurred to date and which implies that the underlying problem is not specific to retrograde memory. Moreover, within the literature on cases of focal retrograde amnesia, differing patterns of performance on tests of autobiographical memory or remote semantic knowledge have been reported, and sometimes these may have reflected factors other than the sites of lesions. Many of the most convincing cases in this literature have been those in whom there was an initially severe anterograde amnesia as well as an extensive retrograde loss: in these cases, the critical issue is what determines differential patterns of recovery across these domains-it is likely that both physiological and psychological factors are important. A second, somewhat different, group are patients with semantic dementia, who show a pronounced recency effect in remote memory but, in these cases, the most parsimonious explanation may be in terms of predominantly semantic/linguistic and/or strategic factors. A third group are those with transient epileptic amnesia but, in these cases, the memory gaps may reflect past (anterograde) ictal activity. A fourth group are those in whom psychogenic factors may well be relevant. Although it is difficult to "prove" psychological causation, the logical difficulties in attributing causation where brain lesions are either very subtle or multiple have been considerably underestimated in the neuropsychological literature. Given these problems, in uncertain or equivocal cases, it is as critical to present the relevant psychological data for the reader to evaluate as it is to provide the pertinent memory test scores: this is underemphasised in many of the studies reviewed. Publication of cases in the absence of such data may lead to faulty clinical, neuropsychological, and cognitive conclusions. Abbreviations : AA: anterograde amnesia; AMI: Autobiographical Memory Interview; PTA: posttraumatic amnesia; RA: retrograde amnesia; RMT: Recognition Memory Test; TEA: transient epileptic amnesia; TGA: transient global amnesia; WMS: Wechsler Memory Scale.