A Cognitive Neuropsychological Approach to Assessment and Intervention in Aphasia

A clinician's guide

Anne Whitworth, Janet Webster, David Howard

• Publisher: Psychology Press
• Year: 2014
• ISBN:
  9781317918707
• Edition: 2
• Topic: Psychology
• Subtopic: History & Theory in Psychology
• Index: Psychology

This is a second edition of the highly popular volume used by clinicians and students in the assessment and intervention of aphasia. It provides both a theoretical and practical reference to cognitive neuropsychological approaches for speech-language pathologists and therapists working with people with aphasia. Having evolved from the activity of a group of clinicians working with aphasia, it interprets the theoretical literature as it relates to aphasia, identifying available assessments and published intervention studies, and draws together a complex literature for the practicing clinician.

The opening section of the book outlines the cognitive neuropsychological approach, and explains how it can be applied to assessment and interpretation of language processing impairments. Part 2 describes the deficits which can arise from impairments at different stages of language processing, and also provides an accessible guide to the use of assessment tools in identifying underlying impairments. The final part of the book provides systematic summaries of therapies reported in the literature, followed by a comprehensive synopsis of the current themes and issues confronting clinicians when drawing on cognitive neuropsychological theory in planning and evaluating intervention.

This new edition has been updated and expanded to include the assessment and treatment of verbs as well as nouns, presenting recently published assessments and intervention studies. It also includes a principled discussion on how to conduct robust evaluations of intervention within the clinical and research settings.

The book has been written by clinicians with hands-on experience. Like its predecessor, it will remain an invaluable resource for clinicians and students of speech-language pathology and related disciplines, in working with people with aphasia.

Part 1Theory and principles

1A cognitive neuropsychological approach Theories and models

DOI: 10.4324/9781315852447-3

An historical perspective

Cognitive neuropsychology first emerged as a coherent discipline in the 1970s as a reaction to the then dominant approach in neuropsychology. This earlier approach to neuropsychology (the ‘classical approach’) sought to characterise the performance of people with aphasia by defining them in terms of their localisation of lesion (see Shallice, 1988, for further discussion of this approach). The aim here was to understand the psychological functions of parts of the cortex by investigating the patterns of deficits shown by individuals with lesions in these areas, and identify syndromes defined in terms of deficits that frequently co-occurred. Over the last 30 years, in the UK at least, cognitive neuropsychology has expanded to become the dominant approach in neuropsychology. Part of the reason is that it moved neuropsychology from being of interest only to those concerned with brain behaviour relationships to a major source of evidence on the nature of normal processing. Another reason is that good cognitive neuropsychology pays real attention to providing accounts that address how individual people with brain lesions behave, often using sophisticated experimental methods to investigate the determinants of their performance.

The origins of cognitive neuropsychology lay in two papers on people with reading disorders by Marshall and Newcombe (1966, 1973). There were two critical features. First, Marshall and Newcombe realised that individual people with reading disorders could show qualitatively different patterns of impairment that would have been obscured by treating them as a group. They described two people who made semantic errors in single-word reading (e.g. NEPHEW → ‘cousin’, CITY → ‘town’; a difficulty described as ‘deep dyslexia’), two people who made regularisation errors (e.g. LISTEN → ‘liston’, ISLAND → ‘izland’; ‘surface dyslexia’), and two people who made primarily visually related errors (e.g. EASEL → ‘aerial’, PAMPER → ‘paper’; ‘visual dyslexia’). The second feature was that the nature of the individual's problems could be understood in terms of an information-processing model developed to account for the performance of normal individuals, in this case the ‘dualroute’ model of reading. Three of the essential features of cognitive neuropsychology that were to define the approach were evident here: (1) the realisation that the performance of the individual, not the average of a group, was the important evidence; (2) that the nature of errors was informative; and (3) that the explanations of individuals’ performance were to be couched in terms of information models of normal language processing and not in terms of brain lesions.

The approach developed from an initial focus on reading disorders to encompass a variety of other domains. These include, in a vaguely chronological order, spelling disorders, memory impairments (including both long-and short-term memory), semantic disorders, disorders of word retrieval, disorders of object and picture recognition, word-comprehension impairments, disorders of action, executive disorders, sentence-processing impairments, number processing, and calculation. The initial focus, in terms of the people whose disorders were investigated, was on adults with acquired brain lesions, typically following stroke, head injury or, more rarely, brain infections such as herpes simplex encephalitis. The focus has now broadened to encompass developmental disorders, and those disorders found in progressive brain diseases, most prominently the dementias.

Methods have also shown a gradual change. While the early studies were in-depth investigations of single individuals, there has been an increasing use of case series designs where a series of people are investigated using the same set of tasks. The data are not, however, analysed in terms of groups, but rather the focus is on accounting for the patterns of performance of a group of people analysed individually. Here, both differences and similarities between individuals constitute the relevant evidence. Theoretical models have also evolved. While box and arrow models of cognitive architecture remain a major source of explanatory concepts, there has been increasing use of computational models, usually confined to specific domains such as reading, word retrieval or comprehension.

Finally, there has been, since 1987—when effective functional imaging of language was first developed — and particularly in the last 15 years, a resurgence of interest in localisation of cognitive functions in the brain. This has been fuelled by the development of imaging methods such as positron emission tomography (PET) and functional magnetic resonance imaging (fMRI) that can be used to measure changes in regional blood flow (reflecting local synaptic activity) in the brain while people are engaged in cognitive tasks. These methods have allowed people to explore how and where the information-processing modules are represented in the brain (e.g. Price et al., 2003; Price, 2012).

Cognitive neuropsychology as a working theoretical model

With the abandonment of theories that drew direct links between localising lesions in the brain and characterising deficits in speech and language, the replacement model drew on the components involved in processing information and the interconnections between such components. These were first illustrated in Morton and Patterson's (1980) version of the logogen model. Morton and Patterson (1980) revised and articulated earlier versions of the logogen model (which date back to Morton, 1969) to account for both the types of errors and the factors influencing reading performance (e.g. word imageability; part of speech) in people with deep dyslexia. This model was a quintessential ‘box and arrow’ processing diagram that specified a number of component processes (the boxes) and how they interrelate (the arrows). The model referred to in this book is illustrated in Figure 1.1 and is (loosely) based on Patterson and Shewell's (1987) adaptation of the earlier logogen models.

Figure 1.1 Language-processing model for single words, based on Patterson and Shewell's (1987) logogen model

While a model of this kind may appear complex, each of these components appears to be necessary to account for the processing of single words. As Coltheart, Rastle, Perry, Langdon and Ziegler (2001) argued: ‘All the complexities of the model are motivated. If any box or arrow were deleted from it, the result would be a system that would fail in at least one language-processing task at which humans succeed’ (p. 211).

If different modules and connections (boxes and arrows) in this model can be independently impaired, a very large number of possible patterns of performance may result from a lesion. Given this large number, one clearly cannot assume that any two people will necessarily have the same pattern of performance. The idea, therefore, that aphasia can be grouped into a limited number of identifiable and homogeneous ‘syndromes’ must necessarily fail. This does not, of course, mean that there will not be resemblances between the performances of different people with aphasia; to the extent that they have the same components damaged, this is precisely what we would predict. Nor does it mean that some combinations of symptoms do not appear more frequently than others. It simply means that one cannot group data from people with aphasia together as the differences between individuals are important (Shallice, 1988). Analysis of data from single individuals is the necessary consequence.

Using this kind of model to explain patterns of performance with people with aphasia involves making several assumptions, described and defended in detail by, among others, Caramazza (1986), Shallice (1988) and Coltheart (2001). Coltheart (2001) describes four assumptions:

1. Functional modularity. Some, at least, of the components of the cognitive system are modular, meaning that they operate independently, or relatively independently, of other components.
2. Anatomical modularity. Some, at least, of the modules of the cognitive system are localised in different parts of the brain. As a result, brain lesions can result in selective information-processing deficits, either by destroying the tissue responsible for particular modules or by disconnecting them. Functional modularity does not necessarily entail anatomical modularity.
3. Universality of cognitive systems. This simplifying assumption is that all normal people have the same cognitive systems. This is a plausible assumption for language processing, for example, but is clearly not directly applicable in domains of which some people have no experience, for example music. Note that it is not claimed here that all people will have equal experience and facility in all aspects of their cognitive system, rather that different people do not have radically different cognitive architectures for the same processes.
4. Subtractivity. The result of a brain lesion is to destroy, damage or impair one or more components of the normal cognitive system. Damage does not result in new information-processing systems. On the other hand, a person with brain damage may rely on different sources of information to perform a task, but these use processing systems that were available pre-morbidly. For example, a person with a severe face recognition impairment (prosopagnosia) may come to rely on a person's dress or voice to recognise them. While normal individuals may not rely on these strategies to recognise people, they can do so when necessary.

Models like that in Figure 1.1 are, in this form, radically underspecified. The diagram says nothing about how the processing in the boxes is achieved. Each of the cognitive modules will necessarily have structure and may comprise a whole set of component processes. For example, Figure 1.1 has a box called ‘phonological assembly’. Levelt, Roelofs and Meyer (1999) argue that there are a number of separable processes involved in phonological assembly, including separate spell out of both the segmental and metrical structure. There is evidence that there can be separable impairments of these component processes (Nickels & Howard, 2000).

A working assumption is that any of the modules in the diagram can be lost or damaged as a result of cortical lesions. An individual with aphasia might have damage to one or several modules or the mappings between them. Because of the functional architecture of the brain, some patterns of deficits will be more frequent than others, but because lesions vary both in their precise cortical locations and in the cutting of sub-cortical white matter fibre tracts, identical patterns of deficit in any two people are unlikely. One objective in assessment can be to identify which of the modules and mappings (boxes and arrows) are damaged and which are intact, yielding a concise explanation of the pattern of performance across a range of tasks and materials.

In Chapters 4–8 we describe, in outline only, the nature of the processing in many of the components of the model. We are aware, of course, that we are not putting forward a complete, or even necessarily accurate, model of language processing even just for single words. Our fundamental claim, in the context of this book, is much more modest. It is that the model in Figure 1.1 provides a usable working model of language processing. It provides a level of description that can be used to guide a process of assessment that can identify levels of breakdown and intact and impaired processes in people with aphasia.

Competing models

There are many models of single-word processing that can be, and have been, used to account for patterns of language breakdown as well as normal processing. Many of these are task-specific, dealing, for example, with spoken word production (e.g. Foygel & Dell, 2000; Levelt et al., 1999; Rapp & Goldrick, 2000, Oppenheim, Dell & Schwartz, 2010), spoken language comprehension (e.g. Marslen-Wilson, 1987), or semantic representation (e.g. Tyler, Moss, Durrant-Peatfield & Levy, 2000). Evaluation of such models is beyond the scope of what this book aims to achieve. However, while these models do attempt to provide detailed accounts of representations and processes involved in particular tasks, they provide little information on how different tasks relate to each other. For example, the phonological assembly module in the lexical model of Figure 1.1 is a common output process shared by picture naming, word reading and word repetition. Impairment at this level should result in qualitatively similar patterns of impairment across all three tasks (some quantitative differences may be due to the differing nature of the input to the module). This is the pattern found in many people with phonological deficits in speech production (e.g. Caplan, Vanier & Baker, 1986; Franklin, Buerk & Howard, 2002).

Some models do, however, highlight the shared nature of processes and aim to account for patterns of performance across different tasks. In 1979, motivated by patterns of cross-modal repetition priming, Morton had revised the original 1969 logogen model that had a single lexicon for spoken word recognition, spoken word production, written word recognition and written ...