Human Cognitive Neuropsychology

A Textbook With Readings

Andrew W. Ellis, Andrew W. Young

• Publisher: Psychology Press
• Year: 2013
• ISBN:
  9781135887797
• Edition: 1
• Topic: Psychology
• Subtopic: History & Theory in Psychology
• Index: Psychology

This textbook augments the first edition through the inclusion of a set of reseach and review papers selected by the authors to supplement the contents of each chapter by providing a discussion of research issues and detailed investigation of individual cases. One or two papers supplement each chapter. A short introduction to each set makes clear the nature of their contribution and how they relate to each chapter's contents. Some of the papers are short reviews of theoretical contributions; others are case studies in the tradition of cognitive neuropsychology. At least three of the main trends discernible in cognitive neuropsychology in the 1990s are represented in the chosen papers. The first is the use of connectionist models to simulate patterns of impairment in brain-injured patients. The second is the growing convergence between cognitive neuropsychology and neuroscience: cognitive neuropsychologists are becoming increasingly interested in the brain processes that underlie the preserved and damaged psychological processes they study. The third trend is the involvement of cognitive neuropsychologists in work on therapy and rehabilitation.

1 What is Cognitive
Neuropsychology?

In any well-made machine one is ignorant of the working of most of the parts—the better they work the less we are conscious of them … it is only a fault which draws our attention to the existence of a mechanism at all.

Kenneth Craik, The Nature of Explanation (1943)

INTRODUCTION

On 5th August, 1982 a 19-year-old man who we shall refer to by his initials as PH was involved in an accident in which he was knocked off his motorcycle. He lost his right arm, and suffered a severe closed head injury. He was in a coma for over 12 days.

Like many head-injury patients PH has, with the help of rehabilitation services, made quite a good recovery. Some four years after his accident his language abilities seemed normal in conversation, and he could read without difficulty. His I.Q. on verbal tests (91) was probably close to what it was before the accident. His short-term memory abilities were normal and, although he scored poorly on formal tests involving long-term retention, he was able to remember the things that were important to his daily life without apparent difficulty.

However, one of PH's problems was most resistant to rehabilitation; he could not recognise people's faces. As soon as a familiar person spoke he would know who it was but, to PH, all faces seemed unfamiliar. He could tell if a face belonged to a man or a woman, an old or a young person, and he could describe the general appearance and facial features reasonably accurately. But PH had no sense of recognising people who had previously been very familiar to him. In neuropsychological terms, his accident had left PH Prosopagnosic—able to see, but unable to recognise many once-familiar faces (De Haan, Young, & Newcombe, 1987a).

EST was a well-educated, 65-year old man whose difficulties lay not in perception or recognition, but in speaking. His attempts to converse were hampered by the fact that he could no longer call to mind many words that had once been part of his ordinary, everyday vocabulary. The cause of EST's anomia (as his condition is known) was not a head injury, but a large slow-growing tumour in the left hemisphere of his brain which was successfully removed when he was 53 years old. Whereas normal people just occasionally find themselves caught in a “tip of the tongue ” state, temporarily unable to remember a word, EST seemed to be trapped in such a state almost every minute because EST's word-finding problems extended to commonplace words like “piano”, “spider”, and “lamp”. He knew perfectly well what such objects were, and what one could do with them, but was often unable to remember what they were called. His understanding of speech was good, and he could comprehend written words, though his attempts to read aloud were hindered by the same word-finding problems as affected his speaking (Kay & Ellis, 1987; Kay & Patterson, 1985).

The difficulties experienced by PH and EST are just two of the vast range of different problems that can be caused by brain injury. In this book we shall encounter many of them, though there are many more that we have not had space to include. Chapter 4, for example, reviews different forms of face recognition disorder, including the sort of prosopagnosia suffered by PH, whereas Chapters 5 and 9 examine disorders of speech production, including EST's type of anomia. Other conditions we shall look at include disorders affecting object recognition, spatial knowledge and orientation, speech comprehension, reading, writing, and memory.

Human cognitive neuropsychology is, however, much more than just a catalogue of the different problems that brain injury can give rise to. Cognitive neuropsychologists believe that by studying patients like PH and EST (with their co-operation and consent), fundamental insights can be gained into the way the human mind works. These insights should then feed back to provide a better understanding of the problems of brain-injured patients, and should lead in turn to the development of better therapies (e.g. Howard & Hatfield, 1987).

As an approach to understanding the mind and the brain, cognitive neuropsychology is both old and new—old to the extent that the issues it addresses are ones which have exercised the minds of philosophers, psychologists, neurologists and others for hundreds, even thousands, of years; and new because it is only within the last 15 years or so that cognitive neuropsychology has become established and has articulated its distinctive approach. This chapter is intended to acquaint the reader with what cognitive neuropsychologists are trying to do. We shall discuss the sort of questions they ask, the methods they adopt in trying to answer them, the assumptions they make, and some of the potential pitfalls that await them along the way. In doing so we shall try to be brief for two reasons. First, we believe that the vigour and usefulness of cognitive neuropsychology is best established through illustrating its practical application in different areas: If any converts are to be made, they will be won over by the demonstrations in later chapters of how cognitive neuropsychology can illuminate the processes involved in human perception, language, and memory. Secondly, cognitive neuropsychology is an approach in evolution. Matters to be reviewed in this chapter, such as the appropriate methodology and the underlying assumptions, are matters of lively current debate, and we are only too well aware that opinion on these topics is likely to continue to evolve in the years to come. But the fact that we can make extensive use in the chapters to come of observations and conclusions made by earlier researchers whose theoretical viewpoints were different from our own shows that the main substance of the book has a fair chance of surviving a wide range of changes in theoretical fashion.

QUESTIONS AND POSSIBLE ANSWERS

Assuming we have spent some time investigating a case like the anomic patient EST mentioned earlier, two questions arise naturally:

1. What has happened to this patient to cause him to show the particular symptoms he does?

2. Can his pattern of impaired and intact capabilities teach us anything about the way the normal mind and brain are organised?

If we consider first the question of what has happened to EST to cause his anomia, then it soon becomes clear that the question can be answered in at least two very different ways. Brain scans have shown that the tumour which caused EST's anomia occupied a large area in his left cerebral hemisphere, affecting in particular the temporal and temporoparietal areas (Kay & Patterson, 1985). As we have seen, the consequence of the resulting brain injury was that EST could no longer remember, or “find”, many words which had once been well-established parts of his vocabulary. Is it better to say of EST, “He is anomic because of damage to his left cerebral hemisphere” or “He is anomic because of damage to the psychological processes which mediate spoken word finding?” Although there are those who believe that one of these two modes of explanation is intrinsically superior to the other, we would suggest that they are both valid in their own way. Only the second explanation is a cognitive neuropsychological explanation, however. Accordingly, the emphasis in this book will be on explaining the symptoms of brain-injured patients in terms of impairment to psychological operations which are necessary for normal, efficient perception, language and memory, though we shall see that there are times when a knowledge of the relevant anatomy and physiology is of positive benefit when it would be churlish to ignore biological evidence.

Our main subject matter, however, is cognitive neuropsychology. Cognitive psychology (without the neuro- prefix) is the study of those mental processes which underlie and make possible our everyday ability to recognise familiar objects and familiar people, to find our way around in the world, to speak, read and write, to plan and execute actions, to think, make decisions and remember (Eysenck, 1984; Smyth, Morris, Levy, & Ellis, 1987). Neuropsychology is the study of how particular brain structures and processes mediate behaviour, and encompasses such things as appetites and emotions as well as cognitive aspects of mental life. As its name suggests, cognitive neuropsychology represents a conver-gence of cognitive psychology and neuropsychology. In Campbell's (1987a) words: “Neuropsychology is cognitive to the extent that it purports to clarify the mechanisms of cognitive functions such as thinking, reading, writing, speaking, recognising, or remembering, using evidence from neuropathology.”

Cognitive neuropsychology has, then, two basic aims (Coltheart, 1986; Ellis, 1983). The first is to explain the patterns of impaired and intact cognitive performance seen in brain-injured patients in terms of damage to one or more of the components of a theory or model of normal cognitive functioning. Thus PH's prosopagnosia and EST's anomia might be explained in terms of damage to one or more of the processes required to effect normal face recognition and speech production, respectively.

The second aim of cognitive neuropsychology is largely responsible for the recent upsurge of interest in the approach. It is to draw conclusions about normal, intact cognitive processes from the patterns of impaired and intact capabilities seen in brain-injured patients. In pursuing this second aim, the cognitive neuropsychologist wishes to be in a position to assert that observed patterns of symptoms could not occur if the normal, intact cognitive system were not organised in a certain way. We shall make claims of this sort with respect to patients PH and EST in Chapters 4 and 5.

Dissociations and Associations

Assertions about the way the intact mind must be organised are often based on what are termed dissociations. If patient X is impaired on task 1 but performs normally on task 2, then we may claim to have a dissociation between the two tasks. For instance, if task 1 is reading words and task 2 is recognising famous faces, then we would state that patient X shows a dissociation between reading, which is impaired, and face recognition, which is intact. On such evidence alone, many cognitive neuropsychologists would feel justified in saying that the normal cognitive system must be organised with face recognition and written word recognition handled by different sets of cognitive processes, thereby allowing one set to be impaired while the other continues to function normally.

Other cognitive neuropsychologists might be more circumspect, however. They would point out that logically possible alternative accounts of patient X can be put forward. It might be, for example, that written word recognition is in some way easier than face recognition and that X's brain injury has rendered him incapable of difficult recognition tasks, while leaving him still able to perform easy ones. This type of alternative account could be ruled out, however, if a second patient, Y, could be discovered in whom written word recognition was intact whereas face recognition was impaired. That patient when contrasted with patient X would provide us with a double dissociation between face recognition and written word recognition. There is no doubt that double dissociations are more reliable indicators that there are cognitive processes involved in the performance of task 1 that are not involved in the performance of task 2, and vice versa (Shallice, 1979a; Teuber, 1955; Weiskrantz, 1968). Double dissociations can also be established without requiring that either patient should perform normally on either task: It would often be sufficient to show that patient Y performed reliably and significantly better on task 1 than on task 2 whereas patient X performed reliably and significantly better on task 2 than on task 1 [for the technically-minded, Jones (1983) discusses cases in which this would not be sufficient evidence].

There are times, however, when arguments based on such things as the relative simplicity of two tasks seem so implausible that cognitive neuropsychologists are willing to venture claims about normal cognitive organisation on the basis of single dissociations (where a patient performs well on one set of tasks but badly on another), and we shall encounter several examples of such reasoning later in the book. Also, it would be unwise to regard the search for double dissociations as some sort of royal road to understanding the structure of the mind. Having unearthed a double dissociation, there is a lot of work to be done in determining just what cognitive processes mediate aspects of tasks 1 and 2 independently, and what processes, if any, the two tasks share in common. This requires intensive investigation of the patients in order to discover just why they perform badly when they do, and just where in the total cognitive system their breakdowns have occurred.

Much more problematical than arguments based on either double or single dissociations are arguments based on associations between symptoms. It is common in neuropsychology to discover that patients who are impaired on task 1 are also typically impaired on tasks 3, 4 and 5. Now, it might be that this association of deficits occurs because a cognitive process required for the successful execution of task 1 is also required for the successful execution of tasks 3, 4 and 5, so that a patient in whom that process is damaged will experience problems with all these tasks. Unfortunately, deficits can also tend to co-occur for reasons that are of neurological importance, but of less interest specifically to the cognitive neuropsychologist.

It could be, for example, that tasks 1, 3, 4, and 5 have no overlap in terms of the cognitive processes required for their execution, but that four discrete sets of cognitive processes are mediated by four adjacent areas of the brain. If this is so, then a brain injury which damages one of those areas will tend also to damage the others, so that deficits on the four tasks which depend on those four regions will tend to be associated. This point as applied to language disorders was well expressed by Lord Brain (1964, p.7) in the following passage:

… let us consider two aspects of language which we will merely call a and b to indicate that we habitually distinguish them in our own minds and give them different labels. Let us further suppose that they are both depressed [i.e., impaired] in a particular aphasic patient. There are several possible explanations of this. The primary disturbance may involve a, and the disturbance of b may be secondary to this, or conversely, we may implicate some general function c and say that both a and b are particular examples of disorder c. These are all functional or dynamic [cognitive] interpretations. But there is also the possibility that there is no functional relationship between a and b. They are involved together merely because their pathways, though separate in terms of neurones, run close enough together to be damaged by the same lesion.

Associations which occur for anatomical reasons rather than cognitive-psychological reasons will be encountered on several occasions in this book. They are revealed in their true colours when the exceptional patient is discovered whose lesion affects some but not all of the anatomically adjacent regions and which, therefore, affects some but not all of the cognitive tasks mediated by those regions. In sum, theoretical arguments based...