CHAPTER ONE
Windows on the mind
Brian Butterworth
Institute of Cognitive Neuroscience, University College London
Case studies of neurological patients have been of central importance to neuropsychology for the past 150 years. Indeed for most of that time they were the only way of studying the relationship between brain systems and those cortical functions that would not yield to animal models. However, one might ask why we need to look again at old neurological cases. In these old cases, the localisation of a lesion was often problematic because a long period might have elapsed between the behavioural tests and the examination of the patientâs brain, while nowadays we can assess damage with some precision at the time the tests are made. What is more, in the old cases behavioural studies were rarely placed in the context of what we would now consider the necessary normal controls, or proper standardisation.
Perhaps the most striking difference between the scientific context of the studies reported in this volume and the situation today is that we have access to functional neuro-imaging that enables us to identify the brain systems active when carrying out the kinds of tasks the investigators found so instructive. Functional neuro-imaging appears to be a direct window on the mind. It seems as though we can actually see the processes of cerebration as they happen. We may therefore ask whether these classic cases can tell us anything about the brain and the organisation of cognition that we cannot find out better from a well-designed functional imaging study?
The situation seems to be analogous to Galileoâs time, when astronomers began to use the telescope. This enabled them to see things previously invisibleâlike the moons of Jupiterâjust as PET and fMRI enable us to see human brain activity as it happens. Galileo did not have a proper theory of optics, and so he could only guess what it is was that projected on to the objective lens of his instrument. Similarly, we donât really have a good account of what we are observing in the fMRI camera: Is it neural spiking or is it local field potential? Recent evidence suggests the latter, but that still does not reveal how local field potentials and changes to them code mental representations and operations on them. What about the broad organisation of the mind? We know from brain imaging which brain areas are relatively active during a task, but can we tell which of these areas are necessary to carry out the task? Can we tell how these areas are functionally related? At the moment, the answer is no to both questions. For this, we still need the old âwindow on the mindâ; studies of individual people, each with their own particular mix of damaged and spared functions.
These case studies depend on âexperiments of natureâ that are âdesignedâ to identify at least which are the necessary prerequisites for normal functioning, and which are not. For example, we may ask whether all the mechanisms for identifying letters are also necessary for identifying numbers. Monsieur C, Dejerineâs alexic case (Chapter 5), shows that there is part of the mechanism that is specialised for letters and is not needed for numbers because this patient can identify numbers but not letters.
New technologies do not eliminate the need for careful and systematic observation of naturally occurring phenomena. Galileoâs telescopic investigations did not make Tycho Braheâs observations of the positions of the stars and planets useless. Indeed, they told Galileo where he should be looking. In fact, descriptions of experiments of nature are vital to a whole range of sciences, from astronomy to zoology. What else are the stars and galaxies but experiments of nature? We certainly cannot recreate them in the lab (though we are getting closer to recreating some of the processes that drive the activities of stars). The theory of evolution of course depended on the careful annotation of, for example, species of finches in the GalĂĄpagosâanother scientifically crucial experiment of nature.
Marshall and Halligan (Chapter 17) suggest that âone definition of a classic paper is that the questions it raises continue to be of concern 20 (or more) years laterâ. This does not mean that the classic study was recognised as such when it was first published. For example, Freudâs 1891 monograph on aphasia sold few copies and was rarely cited until Stengelâs English translation, even though it contained original and important criticisms of the well-known Wernicke-Lichtheim model of disorders of language. It also contained Freudâs first published discussion of slips of the tongue.
Some of the studies in this collection were recognised as of critical importance almost as soon as they were published, while the impact of others came much later, sometimes after the author was long gone. What is it that makes a paper have immediate impact, while others languish for decades before their importance is acknowledged? Two factors seem relevant. The first is what we would now call the âimpact factorâ of the means of publication: major journal versus obscure journal; major scientific language versus a scientifically minor language; major publishing house with good distribution versus small publishing house, and so on. Secondly, was the world ready for the findings? That is, did the findings contribute to the development of any well-known theory, preferably with influential supporters?
Some papers had impact in a way that the author intended, while for others the case would be interpreted very differently today. Wernickeâs cases presented by Wallesch, Herrmann, and Bartels (Chapter 2) are interesting precisely because a modern neuropsychologist is unlikely to class them as âconductionâ aphasic patientsâa term invented by Wernicke himself. A cardinal symptom of conduction aphasia for us is poor repetition, but Wernickeâs aphasia, at that time, seemed to be a failure to monitor and correct errors in oneâs own speech (a point, incidentally, that Freud drew attention to). Wernickeâs PhD thesis, which described these patients, quickly became widely read.
Similarly, the implications of Warrington and Shalliceâs patient, JB, were quickly recognised, first and foremost because JB provided the double dissociation with amnesic patients whose short-term memory (STM) was spared. This should have driven a stake through the heart of single memory theories immediately, but many students of memory (especially in the United States) took no notice of neuropsychological findings in the 1970s. Martinâs chapter (Chapter 3) draws attention to the fact that JB appeared to have intact speech, and thus could be distinguished from the conduction aphasic patients first clearly characterised by Lichtheim, a follower of Wernicke. However, debates still rage over the correct interpretation of cases like JB and PV. Is there a subtle language deficit that affects span tasks, as Alan Allport has claimed (Allport, 1984)? Does STM deficit affect language understanding, as Vallar, Baddeley, and many others have maintained (Vallar & Baddeley, 1984)? I confess an interest in this latter debate, having argued that it does not, on the basis of subjects with very poor performance on span tasks but intact comprehension (Butterworth, Campbell, & Howard, 1986).
Sometimes, indeed, a study can be highly influential in ways that would have appalled the authors, at least at the time of writing. This seems to have been the case with Caramazza and Zurifâs study of aphasic comprehension. Caplan (Chapter 7) points out that the theory proposed turned out to be wrong, and the methodology flawed. In fact Caramazza himself would now disavow using groups of patients classified into syndromes to test cognitive hypotheses (Caramazza, 1986). Nevertheless, as Caplan notes: âIt is not unreasonable to argue that all the work that has gone on in the past 25 years on disorders of syntactic comprehension and the neural basis for this functional ability has its origin in this paperâ. All of us make mistakes doing science, but it takes a special talent to make what the philosopher Austin called âa ground-floor first-water mistakeâ.
Singer and Lowâs study of an acalculic patient (Chapter 4) described for the first time specific problems in transcoding from one form of numbers to another, a theme that was not taken up again for 50 years, but which is now seen to be separable from calculation. Even more dramatic is Wolffâs description of what we now recognise as deep dyslexia (Chapter 6): some 70 years elapsed between the publication of this case and Marshall and Newcombeâs (1973) classic paper outlining the theoretical basis of semantic errors in reading.
Ellis describes in detail (Chapter 16) three cases that for many years were thought to be within the remit of psychiatrists rather than neuropsychologists, but are now seen to reflect highly selective cognitive deficits with a potentially well-defined neuroanatomical basis.
Some papers are classics just because, as in other branches of science, the ingenuity of the experimenters throws new light on an old problem. One excellent example is Bisiach and Luzzattiâs now famous âPiazza del Duomoâ experiment (Chapter 17). Their method of asking unilateral neglect patients to imagine a scene from different points of view enabled them to demonstrate convincingly that the phenomenon was not due to a sensory deficit. There is still a debate as to how best to explain it, more than 20 years on.
In their Preface to the first volume of Classic Cases in Neuropsychology, the editors wrote: âEach chapter highlights the importance of the case for the development of neuropsychology ⊠authors were asked to take particular care to put right any misunderstandings or misconceptions about an historical case that may have influenced neuropsychological developmentâ. The authors in this volume have responded magnificently to the challenge of the previous volume. I am sure that all readersâneuropsychologists or notâwill find their understanding both of the history of neuropsychology and the nature of the relationship between brain and cognitive functions greatly enriched by this splendid set of studies.
REFERENCES
Allport, A. (1984). Auditory-verbal short-term memory and conduction aphasia. In H. Bouma & D.G. Bouwhuis (Eds.), Attention and performance X: Control of language processes. Hillsdale, NJ: Lawrence Erlbaum Associates Inc.
Butterworth, B., Campbell, R., & Howard, D. (1986). The uses of short-term memory: A case study. Quarterly Journal of Experimental Psychology, 38A, 705â738.
Caramazza, A. (1986). On drawing inferences about the structure of normal cognitive systems from the analysis of impaired performance: The case for single-patient studies. Brain & Cognition, 5, 41â66.
Marshall, J., & Newcombe, F. (1973). Patterns of paralexia: A psycholinguistic approach. Journal of Psycholinguistic Research, 2, 175â199.
Vallar, G., & Baddeley, A.D. (1984). Phonological short-term store, phonological processing and sentence comprehension: A neuropsychological case study. Cognitive Neuropsychology, 1, 121â141.
PART ONE
Language, calculation, memory
CHAPTER TWO
Wernickeâs cases of conduction aphasia
Claus-W. Wallesch and Claudius Bartels
Department of Neurology, Otto-von-Guericke University of Magdeburg, Germany
Manfred Herrmann
Department of Neuropsychology/Behavioral Neurobiology, University of Bremen, Germany
INTRODUCTION
In 1874, the 26-year-old psychiatrist-in-training, Carl Wernicke, published his MD thesis Der aphasische Symptomencomplex. This slim volume has probably become the most frequently quoted German medical thesis. Wernicke derived a model of language processing from the newly developed fibre anatomy of his time, which emphasised a role for the forebrain association fibres in the representation of cognitive processes, especially semantic representations. Wernicke attempted, as the subtitle of his thesis suggests, âa psychological study with an anatomical foundationâ. Based on the literature, Wernicke localises Brocaâs area in the foot of the third frontal convolution and hypothesises its function as a centre for speech movement concepts. From physiological data and conjecture, he assumes the presence of another language centre in the first temporal convolution, which he viewed as the cortical target of the acoustic nerve. Thus, Wernicke considered the temporal area to be a centre for auditory word images. It has to be noted that although Wernicke demonstrated the localisation and connections of these centres on a right hemisphere, he was aware of the left hemisphere dominance for language (p. 7). Even more curiously, Wernickeâs diagram shows a monkeyâs brain.
In 1874, Wernicke explicitly did not localise more central language processes: âThe forebrain surface is a mosaic of such simple elements, which are characterised by their anatomical connections with the bodyâs surface. All that exceeds these most simple functions, the integration of sensations to a concept, thinking, consciousness, is a function of the fibre masses, which connect areas on the forebrain surface with each other. These have been termed âassociation fibresâ by Meynert.â (p. 4).
Using anatomical preparations, Wernicke (1874, pp. 17â19) described association fibres between the perisylvian structures that he assumed to provide connections between the sensory and the motor speech areas. He considered these especially important for language development by imitation (p. 13). In proficient speakers, lesion of these association fibres should result in the following (pp. 26â27; translation by Köhler et al., 1998):
The patient comprehends all. ⊠He can say everything, but the choice of correct words is impaired in a similar manner as just described [with aphasia resulting from lesion of the sensory language centreâthe authors]. The auditory word image (âKlangbildâ) is preserved and can be accessed from those associations that form the word concept, but it cannot determine the correct choice of motor concepts (Bewegungsvorstellungen). ⊠Therefore, words are confused. ⊠However, here another form of correction is possible, which is little used in the normal speech process but which can completely exchange the unconscious by the conscious route. ⊠Hearing is intact and the auditory perception is transmitted to the centre for auditory word images. The spoken word is perceived and found correct or wrong. If attentive, the patient knows that he spoke wrongly. ⊠The patient will be able to practise what he wants to say by previous silent articulation; and if he is a strong-willed and attentive person, he will be able to compensate his deficit by conscious, laborious and time-consuming correction.
In the context of this passage, it has to be kept in mind that the concept of the phoneme was developed after the publication of Wernickeâs thesis (Köhler, Bartels, Herrmann, Dittmann, & Wallesch, 1998). The linguistic unit Wernickeâs production model was based upon was the syllable.
TWO CASES OF CONDUCTION APHASIA DESCRIBED BY WERNICKE
Altogether, Wernicke presents 10 cases in his thesis (see Table 2.1). Not surprisingly, attempts to classify the aphasia syndromes of Wernickeâs patients according to modern criteria (e.g. Wallesch & Kertesz, 1993) give different results from Wernickeâs interpretation. The case of Peter would probably not be considered as aphasia today, as all symptoms that are described can be accounted for by dysarthria and confusional state, and anarthria or mutism in the last days before death. Wernicke could not accept motor aphasia in the case of Itzigsohn, as the symptoms included agraphia and a comprehension deficit for prepositions. Seidel is analysed as a prototypical transcortical motor aphasia; Wernicke only uses a different name (âinsularâ aphasia). However, the same term is also used for Salmonsky...