The Handbook of Memory Disorders


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An international panel of renowned scientists and clinicians offers an accessible, up-to-date and practical review of the key research and latest clinical developments in the field. Describes theoretical concepts, assessment processes, clinical management and therapy to produce results of considerable relevance to clinical practice and rehabilitation.

Describes retrograde amnesia/disorders of semantic memory/ memory changes in normal aging/depression & anxiety/etc.

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Editorial Reviews

From the Publisher
“…incorporates several changes and additions that reflect the progress that has been made…promises to be a valuable resource…” (The Quarterly Journal of Experimental Psychology, Vol 57A(5), 2004)
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Product Details

  • ISBN-13: 9780471967040
  • Publisher: Wiley, John & Sons, Incorporated
  • Publication date: 4/1/1999
  • Edition number: 1
  • Pages: 668
  • Product dimensions: 6.52 (w) x 9.74 (h) x 1.43 (d)

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Handbook of Memory Disorders

John Wiley & Sons

Copyright © 2002 John Wiley & Sons, Ltd.
All right reserved.

ISBN: 0-471-49819-X

Chapter One

The Psychology of Memory

Alan D. Baddeley Department of Experimental Psychology, University of Bristol, UK

In editing the first edition of this Handbook, we declared the aim of making available the substantial amount of information that had been acquired concerning memory deficits, not only to researchers with a specific interest in the area but also to a wider audience, including particularly clinicians for whom memory deficit is just one of many problems confronting their patients. Rather than requiring each of our authors to provide an account of the concepts underlying their study of memory, it seemed sensible to provide this information in a single chapter. Hence, if you are already familiar with the psychology of memory, or indeed have read the equivalent chapter in the previous edition, then I suggest you stop here. If not, then I will try to provide a brief overview of the concepts and techniques that are most widely used. Although it may not appear to be the case from sampling the literature, there is in fact a great deal of agreement as to what constitutes the psychology of memory, much of it developed through the interaction of the study of normal memory in the laboratory and of its breakdown in brain-damaged patients. A somewhat more detailed account can be found in Parkin &Leng (1993) and Baddeley (1999), while a more extensive overview is given by Baddeley (1997), and within the various chapters comprising the Handbook of Memory (Tulving & Craik, 2000).


The concept of human memory as a unitary faculty began to be seriously eroded in the 1960s with the proposal that long-term memory (LTM) and short-term memory (STM) represent separate systems. Among the strongest evidence for this dissociation was the contrast between two types of neuropsychological patient. Patients with the classic amnesic syndrome, typically associated with damage to the temporal lobes and hippocampi, appeared to have a quite general problem in learning and remembering new material, whether verbal or visual (Milner, 1966). They did, however, appear to have normal short-term memory (STM), as measured for example by digit span, the capacity to hear and immediately repeat back a unfamiliar sequence of numbers. Shallice & Warrington (1970) identified an exactly opposite pattern of deficit in patients with damage to the perisylvian region of the left hemisphere. Such patients had a digit span limited to one or two, but apparently normal LTM. By the late 1960s, the evidence seemed to be pointing clearly to a two-component memory system. Figure 1.1 shows the representation of such a system from an influential model of the time, that of Atkinson & Shiffrin (1968). Information is assumed to flow from the environment through a series of very brief sensory memories, that are perhaps best regarded as part of the perceptual system, into a limited capacity short-term store. They proposed that the longer an item resides in this store, the greater the probability of its transfer to LTM. Amnesic patients were assumed to have a deficit in the LTM system, and STM patients in the short-term store.

By the early 1970s, it was clear that the model had encountered at least two problems. The first of these concerned the learning assumption. Evidence suggested that merely holding an item in STM did not guarantee learning. Much more important was the processing that the item underwent. This is emphasized in the levels-of-processing framework proposed by Craik & Lockhart (1972). They suggested that probability of subsequent recall or recognition was a direct function of the depth to which an item was processed. Hence, if the subject merely noted the visual characteristics of a word, for example whether it was in upper or lower case, little learning would follow. Slightly more would be remembered if the word were also processed acoustically by deciding, for example, whether it rhymed with a specified target word. By far the best recall, however, followed semantic processing, in which the subject made a judgement about the meaning of the word, or perhaps related it to a specified sentence, or to his/her own experience.

This levels of processing effect has been replicated many times, and although the specific interpretation proposed is not universally accepted, there is no doubt that a word or experience that is processed in a deep way that elaborates the experience and links it with prior knowledge, is likely to be far better retained than one that receives only cursory analysis. The effect also occurs in the case of patients with memory deficits, making it a potentially useful discovery for those interested in memory rehabilitation, although it is important to remember that cognitive impairment may hinder the processes necessary for such elaboration. Indeed, it was at one point suggested that failure to elaborate might be at the root of the classic amnesic syndrome, although further investigation showed this was not the case (see Baddeley, 1997; and Chapter 16, this volume, for further discussion).

A second problem for the Atkinson & Shiffrin model was presented by the data on STM patients that had initially appeared to support it. Although such patients argued strongly for a dissociation between LTM and STM, the Atkinson & Shiffrin model assumed that STM was necessary, indeed crucial, for long-term learning, and indeed for many other cognitive activities. In fact, STM patients appeared to have normal LTM, and with one or two minor exceptions, such as working out change while shopping, had very few everday cognitive problems.

This issue was tackled by Baddeley & Hitch (1974), who were explicitly concerned with the relationship between STM and LTM. A series of experiments attempted to block STM in normal subjects by requiring them to recite digit sequences while performing other tasks, such as learning, reasoning or comprehending, that were assumed to depend crucially upon STM. Decrement occurred, with the impairment increasing with the length of the digit sequence that was being retained, suggesting that STM and LTM did interact. However, the effect was far from dramatic, again calling into question the standard model. Baddeley & Hitch proposed that the concept of a simple unitary STM be replaced by a more complex system which they termed "working memory", so as to emphasize its functional importance in cognitive processing. The model they proposed is shown in Figure 1.2.

Working memory is assumed to comprise an attentional controller, the central executive, assisted by two subsidiary systems, the phonological loop and the visuospatial sketchpad. The phonological (or articulatory) loop is assumed to comprise a store that holds memory traces for a couple of seconds, coupled with a subvocal rehearsal process. This is capable of maintaining the items in memory using subvocal speech, which can also be used to convert nameable but visually presented stimuli, such as letters or words, into a phonological code. STM patients were assumed to have a deficit in this system, whereas the remainder of working memory was assumed to be spared (Vallar & Baddeley, 1984). Subsequent research, based on STM patients, normal children and adults, and children with specific language impairment, suggest that the phonological loop system may have evolved for the purpose of language acquisition (Baddeley et al., 1998). A more detailed account of this system and its breakdown is given in Chapter 12, this volume.

The visuospatial sketchpad (or scratchpad) is assumed to allow the temporary storage and manipulation of visual and spatial information. Its function can be disrupted by concurrent visuospatial activity and, as in the case of the phonological loop, our understanding has been advanced by the study of neuropsychological patients. More specifically, there appear to be separate visual and spatial components, which may be differentially disrupted. A more detailed account of this system and the relevant neuropsychological evidence is given in Chapter 13, this volume.

The third component of the model, the central executive, was assumed to provide an attentional control system, both for the subsystems of working memory and for other activities. Baddeley (1986) suggested that a good account of it might be provided by the supervisory attentional system (SAS) proposed by Norman & Shallice (1986) to account for the attentional control of action. They assume that much activity is controlled by well-learned habits and schemata, guided by environmental cues. Novel actions that needed to respond to unexpected situations, however, depended upon the intervention of the limited-capacity SAS. This was assumed to be capable of overriding habits so as to allow novel actions in response to new challenges. Slips of action, such as driving to the office rather than the supermarket on a Saturday morning, were attributed to the failure of the SAS to override such habits. The problems in action control shown by patients with frontal lobe damage were also attributed to failure of the SAS; hence, perseverative activity might reflect the failure of the SAS to break away from the domination of action by environmental cues (Shallice, 1988).

Both Shallice himself and others have extended their account to include a range of potentially separable executive processes, hence providing an account of the range of differing deficits that may occur in patients with frontal lobe damage (Baddeley, 1996; Duncan, 1996; Shallice & Burgess, 1996). Given the far from straightforward mapping of anatomical location onto cognitive function, Baddeley & Wilson (1988) suggested that the term "frontal lobe syndrome" be replaced by the more functional term, "dysexecutive syndrome". For a recent review of this area, see Roberts et al. (1998) and Stuss & Knight (in press).

The implications of frontal lobe function and executive deficit for the functioning of memory are substantial, since the executive processes they control play a crucial role in the selection of strategy and stimulus processing that has such a crucial influence in effective learning. These issues are discussed in Chapters 15, 16 and 17, this volume.

More recently, a fourth component of WM has been proposed, the episodic buffer. This is assumed to provide a multimodal temporary store of limited capacity that is capable of integrating information from the subsidiary systems with that of LTM. It is assumed to be important for the chunking of information in STM (Miller, 1956). This is the process whereby we can take advantage of prior knowledge to package information more effectively and hence to enhance storage and retrieval. For example, a sequence of digits that comprised a number of familiar dates, such as 1492 1776 1945, would be easier to recall then the same 12 digits in random order. The episodic buffer is also assumed to play an important role in immediate memory for prose, allowing densely amnesic patients with well-preserved intelligence and/or executive capacities to show apparently normal immediate, although not delayed, recall of a prose passage that would far exceed the capacity of either of the subsidiary systems (Baddeley & Wilson, in press). It seems unlikely that the episodic buffer will reflect a single anatomical location, but it is probable that frontal areas will be crucially involved. For a more detailed account, see Baddeley (2000).


As in the case of STM, LTM has proved to be profitably fractionable into separate components. Probably the clearest distinction is that between explicit (or declarative) and implicit (or non-declarative) memory. Once again, neuropsychological evidence has proved crucial. It has been known for many years that densely amnesic patients are able to learn certain things; e.g. the Swiss psychiatrist Claparède (1911) pricked the hand of a patient while shaking hands one morning, finding that she refused to shake hands the next day but could not recollect why. There was also evidence that such patients might be able to acquire motor skills (Corkin, 1968). Probably the most influential work, however, stemmed from the demonstration by Warrington & Weiskrantz (1968) that densely amnesic patients were capable of showing learning of either words or pictures, given the appropriate test procedure. In their initial studies, patients were shown a word or a line drawing, and subsequently asked to identify a degraded version of the item in question. Both patients and control subjects showed enhanced identification of previously presented items, to a similar degree. This procedure, which is typically termed "priming", has since been investigated widely in both normal subjects and across a wide range of neuropsychologically impaired patients (for review, see Schacter, 1994).

It has subsequently become clear that a relatively wide range of types of learning may be preserved in amnesic patients, ranging from motor skills, through the solution of jigsaw puzzles (Brooks & Baddeley, 1976) to performance on concept formation (Kolodny, 1994) and complex problem-solving tasks (Cohen & Squire, 1980); a review of this evidence is provided by Squire (1992). The initial suggestion, that these may all represent a single type of memory, now seems improbable. What they appear to have in common is that the learning does not require the retrieval of the original learning episode, but can be based on implicit memory that may be accessed indirectly through performance, rather than depending on recollection. Anatomically, the various types of implicit memory appear to reflect different parts of the brain, depending upon the structures that are necessary for the relevant processing. While pure amnesic patients typically perform normally across the whole range of implicit measures, other patients may show differential disruption. Hence Huntingdon's disease patients may show problems in motor learning while semantic priming is intact, whereas patients suffering from Alzheimer's disease show the opposite pattern (see Chapters 26 and 27, this volume).

In contrast to the multifarious nature and anatomical location of implicit memory systems, explicit memory appears to depend crucially on a system linking the hippocampi with the temporal and frontal lobes, the so-called Papez circuit (see Chapter 2, this volume). Tulving (1972) proposed that explicit memory itself can be divided into two separate systems, episodic and semantic memory, respectively. The term "episodic memory" refers to our capacity to recollect specific incidents from the past, remembering incidental detail that allows us in a sense to relive the event or, as Tulving phrases it, to "travel back in time".


Excerpted from Handbook of Memory Disorders Copyright © 2002 by John Wiley & Sons, Ltd.. Excerpted by permission.
All rights reserved. No part of this excerpt may be reproduced or reprinted without permission in writing from the publisher.
Excerpts are provided by Dial-A-Book Inc. solely for the personal use of visitors to this web site.

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Table of Contents

About the Editors
List of Contributors
Preface to the First Edition
Sect. I Theoretical Background 1
Ch. 1 The Psychology of Memory 3
Ch. 2 Neurobiological Foundations of Human Memory 17
Ch. 3 Functional Neuroimaging of Memory 57
Ch. 4 The Medial Temporal Lobe and Memory for Facts and Events 81
Ch. 5 Connectionist Models of Memory Disorders 101
Ch. 6 Psychopharmacology of Human Memory 123
Sect. II Varieties of Memory Disorder 143
Ch. 7 The Amnesic Syndrome: Overview and Subtypes 145
Ch. 8 Theories of Anterograde Amnesia 167
Ch. 9 Retrograde Amnesia 189
Ch. 10 Transient Global Amnesia 209
Ch. 11 Recovery of Memory Function in Neurological Disease 233
Ch. 12 Neuropsychological Impairments of Verbal Short-term Memory 249
Ch. 13 Neuropsychological Impairments of Visual and Spatial Working Memory 271
Ch. 14 Disorders of Semantic Memory 293
Ch. 15 The Cognitive Neuroscience of Confabulation: A Review and a Model 315
Ch. 16 The Cognitive Neuropsychology of False Memories: Theory and Data 343
Ch. 17 Frontal Lobes and Memory 363
Ch. 18 Posttraumatic Amnesia and Residual Memory Deficit after Closed Head Injury 381
Ch. 19 Schizophrenia 413
Ch. 20 Memory and Emotional Disorder 437
Ch. 21 Psychogenic Amnesia 451
Sect. III Development and Memory 473
Ch. 22 Memory Development During the Childhood Years 475
Ch. 23 Children with Intellectual Disabilities 501
Ch. 24 Developmental Amnesias and Acquired Amnesias of Childhood 521
Ch. 25 Memory in Elderly People 543
Ch. 26 The Memory Deficit in Alzheimer's Disease 569
Ch. 27 Memory Disorders in Subcortical Dementia 591
Sect. IV Assessment and Management of Memory Problems 615
Ch. 28 Assessment of Memory Disorders 617
Ch. 29 Separating Memory form Other Cognitive Disorders 637
Ch. 30 Management of Remediation of Memory Problems in Brain-injured Adults 655
Ch. 31 Assessment and Management of Memory Problems in Children 683
Ch. 32 Assessment and Intervention in Dementia of Alzheimer Type 711
Ch. 33 Reducing the Impact of Cognitive Impairment in Dementia 741
Ch. 34 External Memory Aids and Computers in Memory Rehabilitation 757
Ch. 35 Emotional and Social Consequences of Memory Disorders 785
Author Index 809
Subject Index 835
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