Conduction Aphasia

Susan E. Kohn

• Publisher: Psychology Press
• Year: 2013
• ISBN:
  9781134756773
• Edition: 1
• Topic: Psychology
• Subtopic: History & Theory in Psychology
• Index: Psychology

Over the past decade, questions about the clinical classification and experimental examination of aphasic patients have been raised. Growing doubts about the validity and reliability of standard clinical diagnoses have been responsible, in part, for the explosion of case studies in the neurolinguistic literature. In turn, rejection of classical aphasia diagnoses has made it difficult to synthesize much of this literature, and no alternative method for selecting and comparing aphasic patients has emerged. This volume was motivated by a desire to take a fresh look at the benefits that aphasia diagnosis has for both clinical and experimental work. This is accomplished by exploring one classical aphasia syndrome from a multidisciplinary perspective; that is, by presenting information from the disciplines of neurology, speech-language pathology, and experimental neurolinguistics. Given this scope, it is hoped that this work will appeal to an equally broad range of readers.

Chapter 1

Introduction: On the Notion of “Aphasia Syndrome”

Susan E. Kohn

Katherine L. Smith

Braintree Hospital

BostonUniversity School of Medicine

In the late 1800s, theoretical discussion of the neurological localization of language functions found support in case descriptions of individuals with focal lesions and concomitant language difficulty (Lee, 1981). A diagnostic system for classifying aphasic patients emerged from this work, including such syndromes as Broca’s, Wernicke’s, conduction, and the transcortical aphasias (cf. Lichtheim, 1985; Wernicke, 1874/1977). Whereas the reliability and validity of this classical system is currently under debate, it still influences clinical and experimental work in cognitive neuropsychology.

During the 1940s, the methodology of experimental psychology was adopted, so that group studies were undertaken that averaged performance of aphasics with similar difficulties (Shallice, 1988). Although case studies began to reappear in the late 1960s, the group study approach dominated the literature until the early 1980s, when researchers became disillusioned with this methodology because of the heterogeneity typically present in experimental groups of aphasics (Marshall, 1986). As a result, the case study has once again gained popularity for neuropsychological research. Contemporary case studies are much more detailed and systematic than those undertaken by the early diagram makers, with greater emphasis placed on relating impaired performance to normal functioning (cf. Shallice, 1988).

The recent revival of the case study has prompted much discussion about the proper methodology for studying the cognitive and linguistic deficits of neurologically impaired adults. In addition to questioning the merit of the group study, the validity of the classical aphasia syndromes has come under attack. Both have been criticized for poor reliability (Badecker & Caramazza, 1985; Caramazza & McCloskey, 1988). Syndromes have also been criticized for not being able to classify enough aphasic patients (Lecours, Basso, Moraschini, & Nespoulous, 1984; Marshall, 1986).

Although there is continued support for group studies in cognitive neuropsychology (Caplan, 1988; Newcombe & Marshall, 1988; Poeck, 1983; Zurif, Gardner, & Brownell, 1989), there is growing discontent with the use of syndromes, especially the classical ones, for research purposes (and even for clinical purposes; Caplan, 1992). The rejection of the classical aphasia syndromes in the current literature is rather ironic, given the return to case studies (i.e., the methodology of the early diagram makers) and the fact that the cognitive models used to explain these modern cases reflect the spirit of the early diagram makers (Shallice, 1988). Both approaches consider language processing to be composed of separate abilities that can be independently impaired by neurological damage. There has been virtually no recent detailed discussion of the definition of aphasia syndrome by those who still appeal at some level to the classical framework.

Perhaps the “antisyndrome” literature paints too bleak a picture, because it fails to consider all the issues needed to properly define an aphasia syndrome. For example, a nonoptimal definition of “syndrome” is sometimes adopted (cf. Schwartz, 1984), and a questionable syndrome is often used to argue against the notion of “syndrome” (e.g., agrammatism; Badecker & Caramazza, 1985—see following).

Moreover, few alternatives to the use of syndromes in the clinical and research domain have been suggested. Both Ellis (1987) and Caramazza (Caramazza, 1986; Caramazza & McCloskey, 1988; McCloskey & Caramazza, 1988) proposed that intensive experimental study of individual aphasic patients provides sufficient information for relating deficits to impairment within a model of normal cognitive functioning. Shallice (1988) followed basically the same plan, adding that the experimental study of aphasic patients should include baseline testing to identify similar patients for replicating findings and should include attempts to recognize task-specific strategies. In the clinical domain, Caplan (1992) described a similar approach to patient assessment for treatment purposes.

Whereas cognitive models are important to the process of explaining neurolinguistic deficits, model-based evaluations of aphasia involve many of the same issues as evaluations that are guided by a classification system (e.g., identifying adaptive strategies to deficits; distinguishing deficits with similar behavioral manifestations; see later). We argue that the notion of syndrome is a useful construct for furthering both clinical and experimental work in cognitive neuropsychology. The field of aphasia is inherently eclectic, attracting researchers and clinicians from such fields as linguistics, neuropsychology, cognitive psychology, neurology, and speech pathology. With these different dis-ciplines come differences in terminology and methods for characterizing aphasic behavior. Work in these domains will be more fruitful if there is a common system of aphasia classification. This framework will promote better understanding of work outside one’s specialty and facilitate communication across the different domains. Because the focus of an aphasia evaluation will differ according to one’s discipline, such a classification system cannot be all inclusive but can provide guidance for furthering work in one’s discipline (cf. Poeck, 1983; see later).

This chapter begins by considering the nature of the syndrome at a level that is appropriate for assessing neuropsychological deficits. To facilitate an understanding of our proposals with respect to aphasia classification, illustrative examples involve language breakdown. Once a definition of syndrome is developed, several issues that are important for creating an aphasia classification system are examined. The chapter ends with a topic that can be considered properly once the definition of aphasia syndrome has been discussed—the applications of an aphasia classification system.

The opinions that follow are not necessarily held by the other authors in this volume. However, the issues raised are critical for the general purpose of this book—developing an optimal definition of conduction aphasia that is relevant for both clinical and experimental work.

DEFINING “SYMPTOM”

All definitions of syndrome involve the identification of behavioral features, or symptoms, that in some way cluster to form a “symptom-complex.” The standard medical definition of a symptom involves a patient’s subjective report of behavioral changes. However, such a definition is not appropriate in neuropsychology, because patients can be unaware of their deficits (e.g., anosognosia). With aphasia, there is another common complication in that patients’ language difficulties can interfere with their ability to articulate their problems. Identification of symptoms due to neuropsychological deficits will always have to be determined, or at least verified, by behavioral testing.

Brown (1988) offered a conception of symptom that is more relevant for the current context. He referred to “an error or positive symptom” as “a moment in flow prematurely displayed.” He believes that symptoms are “submerged levels processed normally distal to the point of damage,” and that “pathology disrupts the subsurface stage and exposes the normal processing at the disrupted segment” (pp. 10–11). For example, the phonemic paraphasias of conduction aphasics reflect breakdown at a phonemic level of planning that is part of the normal speech production system (see Buckingham, this volume, for details).

Kolk and Heeschen (1990) made an important distinction with respect to neuropsychological symptoms. In addition to the type of behavior described by Brown, which they referred to as “impairment symptoms,” they recognized the existence of “behavioral abnormalities that are the result of a patient adapting to impairment” (p. 221). They referred to these behaviors as “adaptation symptoms.” We discuss later the distinctions between behaviors that are direct reflections of a functional deficit versus adaptive strategies to this deficit that is critical for developing a valid understanding of aphasia syndromes.

A distinction must also be made between behaviors that exist acutely and those that emerge during recovery (Kertesz, 1983; Marshall, 1986). Errors in aphasia diagnosis are made because syndrome definitions rarely include information about the evolution of symptoms (Schwartz, 1984). When attempts are made to recognize changes over time, a change in aphasia diagnosis is usually made. For example, when the comprehension difficulties of a Wernicke’s aphasic diminish, but repetition difficulties remain severe, the diagnosis is often changed to conduction aphasia (e.g., Basso, Capitani, & Zanobio, 1982; Naeser & Hayward, 1978). However, this change in diagnosis does not clarify the nature of the aphasia. If syndromes differ with respect to their associated underlying deficits (see later), then a change in diagnosis implies that the deficit has changed. It is unlikely that the so-called Wernicke’s-to-conduction aphasic has actually suffered one deficit acutely and another one after the aphasia begins to resolve. (This situation should be distinguished from one in which a deficit is masked acutely yet becomes evident later on; e.g., dysarthria obscuring phonemic paraphasias.) It would be less confusing to call such a patient, for example, a resolving Wernicke’s aphasic, given that the source of impaired repetition differs between Wernicke’s and conduction aphasia (see chapters 3 and 7, this volume, for further discussion).

The effects of symptom evolution are also usually ignored in experimental investigations of aphasia (but see Crary & Kertesz, 1988; Green, 1969; Kohn & Smith, 1991; Panzeri, Semenza, & Butterworth, 1987). As Caramazza and Badecker (1989) pointed out, we are not certain of the impact of this issue on our understanding of neuropsychological phenomena; it could be considerable.

A symptom is often described at a level where more than one underlying functional deficit could be responsible, and, consequently, it could be associated with more than one syndrome (Kertesz, 1990). For example, Broca’s, Wernicke’s, and conduction aphasics produce phonemic paraphasias. Only statistical analysis can identify variables that distinguish among these syndromes, such as the effects of target length and the phonemic accuracy of paraphasias (Kohn, 1985, 1988).

The fact that a given symptom can result from different underlying deficits is one motivation behind Shallice’s (1988) “critical-variable approach” for investigating neuropsychological deficits. He argued that different sources of a particular symptom can be distinguished by comparing patients who perform at a similar level on a task and yet are affected by different task variables. For example, two patients might score similarly on a test of oral reading; yet one patient produces more errors as words decrease in frequency, whereas the other patient produces more errors as words increase in length.

One possible response to such symptom-deficit ambiguity is to describe symptoms at a detailed enough level that such ambiguities are avoided. In the preceding example, then, the symptom would not be “impaired oral reading,” but, rather, “reading difficulty that is affected by word length.” However, increasing the specificity of symptoms creates other problems. The number of symptoms would likely escalate to an unwieldy number for a viable classification system. In addition, the identification of highly specific symptoms requires a level of analysis that could not always be accomplished by a simple bedside exam, rendering the classification system less desirable for neurological assessment. For these reasons, symptoms should be described at a more general level, using patterns of symptom co-occurrence to distinguish deficits (see following).

In addition to the qualitative issues surrounding the definition of symptom, there are quantitative issues concerning the methodology for determining when an individual is displaying a particular symptom. We cannot expect symptoms to occur during all relevant contexts, given that performance disrupted by a neuropsychological deficit can vary from one moment to the next. As Brown (1979/1988) observed, syndromes “are not stable entities but rather refer to the qualitative mean of performance” (p. 43).

Typically, problems frequently displayed by an individual are the ones that are given the status of a symptom. For example, verbal paraphasias are often numerous in Wernicke’s aphasics, but not in conduction aphasics. As a result, this error type is identified as a symptom in Wernicke’s, but not conduction, aphasia (Goodglass & Kaplan, 1983).

It is difficult to specify how frequently a behavior must be displayed by an individual in order to constitute a symptom. In the case of an aphasic, every observed abnormality cannot be considered to be symptomatic of a syndrome. There are distal effects of language deficits on other components of the language system that surface only on occasion (e.g., semantic paraphasias in the conversation of conduction aphasics). Only if an infrequent behavior is consistently associated with one deficit should it be considered a symptom; its occurrence would then always have a clear relationship to a syndrome.

Summary

Although the methods needed for the precise identification of a symptom require further study, the concept of a symptom is clear enough to proceed in the next section with a discussion of the role it plays in defining a syndrome. In the present context, we consider a symptom to involve a frequently occurring impaired behavior, distinguishing between behaviors that directly reflect deficits versus those that involve adaptive strategies to deficits, and between behaviors that appear acutely versus those that emerge later postonset.

DEFINING “SYNDROME”

Critiquing Past Definitions

Usually, a syndrome label in neuropsychology is used clinically and experimentally without a precise definition of the syndrome with respect to the distribution of its symptoms. There are two basic approaches to symptom distribution: Either the members of a symptom-complex represent a statistical phenomenon or they represent a fixed set (see later).

The definition of syndrome that appears to be used most frequently is the weaker of the two basic approaches identified previously. This definition equates a syndrome with a set of symptoms that reliably, or statistically, co-occur (e.g., Benson, 1979; Marshall, 1982, 1986; Poeck, 1983). In this way, all symptoms are treated equally, so that no single symptom need be present to render a diagnosis. Caramazza (1984) referred to this approach as the psychologically weak sense of syndrome, Newcombe and Marshall (1988) referred to it as a “variable” definition of syndrome, and Schwartz (1984) referred to it as a polytypic syndrome based on “family resemblance.”

The polytypic syndrome has a fundamental weakness. The fact that any one of the diagnostic features may or may not be present implies that there may not be a unitary reason for the co-occurrence of the corresponding symptoms. How can a particular language deficit(s) exist for an aphasia syndrome, if any symptom need not occur for diagnosis (Caramazza, 1984)?

This problem with a polytypic syndrome has contributed to the view that the classical aphasia syndromes are atheoretical and necessarily heterogeneous (cf. Caramazza, 1984). However, the classical syndromes as originally conceived were not of this psychologically weak sense. Only through recent usage has the sense of the syndrome been so weakened and made less precise (Schwartz, 1984). For example, Wernicke initially conceived of conduction aphasia as a disconnection between Wernicke’s and Broca’s area (i.e., between acoustic and motor word forms) and considered the route between these two areas to play an indirect regulatory role in speech production (Wernicke, 1874/1977). Consequently, his initial description of the syndrome emphasized the hesitant paraphasic speech of these aphasics. Given the reliance of repetition on this temporofrontal route, it is not surprising that Lichtheim (1885), and later Wernicke (1906/1977), added impaired repetition to the list of expected symptoms. Over the years, the status of repetition has become central to the diagnosis of conduction aphasia, presumably because it is easy to assess. This change in orientation has distorted the understanding of this syndrome (see following, and chapter 7, this volume).

The polytypic syndrome also presents problems in reliability with respect to providing a patient with a diagnosis tha...

Table of contents

• Cover
• Halftitle
• Title
• Copyright
• Contents
• Preface
• 1 Introduction: On the Notion of “Aphasia Syndrome”
• 2 Early Concepts of Conduction Aphasia
• 3 Diagnosis of Conduction Aphasia
• 4 CT Scan Lesion Sites Associated with Conduction Aphasia
• 5 Phonological Production Deficits in Conduction Aphasia
• 6 Issues Arising Regarding the Nature and Consequences of Reproduction Conduction Aphasia
• 7 Conclusions: Toward a Working Definition of Conduction Aphasia
• Author Index
• Subject Index