In this chapter a history of the description and explanations of aphasia will be given. This review will survey the first mention of the symptoms of aphasia (although it was not called ‘aphasia’ at the time), picking up descriptions through the ages until the first attempt to connect the faculty of language to a particular area in the brain at the turn of the 18 th century. From 1861, the pace of aphasia research increased. We offer a summary of the seminal work by Paul Broca, Carl Wernicke and Ludwig Lichtheim and then the move from their localizationist approach to the holistic view of John Hughlings Jackson, Henry Head and others. We make links between the neuro-anatomic localization of language in the nineteenth century and work that continued through the twentieth century, with reference to the American neurologist
Norman Geschwind and the Russian psychologist Alexander
Romanovich Luria. The final stage we consider is the experimental stage, where investigations are based on theoretical hypothese. We take the theoretical accounts of Roman Jakobson as a starting point of a new era, and we end by offering a brief overview of work in the twentieth century, until the 1980s. Selected aphasia investigation from the late twentieth century until the present day
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are reviewed under ‘current issue’ with which the chapter concludes. .
1
Introduction
The present knowledge of aphasia is the result of a long evolution, of which the start is hard to establish. From the moment that language became a faculty of human beings, there must have been patients who, due to strokes or traumatic brain injury, were unable to use their language as before. There are few early records of language impairments until the 19 th
century that the medical world showed interest for the phenomena of aphasia in general and the relation between language and, more specifically, the brain.
For most aphasiologists, scientific descriptions of aphasia are considered to date from
1861 when the Parisian surgeon Paul Broca related acquired speech disorders to a specific area in the brain. In 1874, the German neurologist Carl Wernicke described other phenomena, which were caused by lesions in other brain areas. Although there was a significant increase in the interest in the study of aphasia in the second half of the nineteenth century due to the publications of Broca and Wernicke, it is not correct to judge the previous descriptions of aphasia as uninteresting, bizarre or ‘prehistoric’, since the pronouncements of Broca, Wernicke and their contemporaries are, of course, the result of a historical development.
The overview has been divided into four periods:
1 Parts of this chapter are translations from Prins & Bastiaanse (1997). These are used with permission of the publisher (Bohn Stafleu Van Loghum). We would like to thank Ron Prins for his contribution to this chapter.
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(1) the early history, from the ancient Egypts until 1800, during which time aphasia symptoms were occasionally described and in which aphasia was generally not acknowledged to be a discrete syndrome syndrome;
(2) the period 1800-1860, in which the first attempts were made to develop a theory on the relation between language and the brain;
(3) the period 1861-1905, during which different types of aphasia were related to lesions in specific brain areas and were explained by ‘association’ models;
(4) the period 1906-1956, during which the anatomical-clinical correlations were replaced by a more psychological approach, some of which interpreted aphasia as a general cognitive impairment.
(5)
The ‘modern’ period 1956-1980, during which the linguistic aspects of aphasia were the main focus of research.
The contemporary views on aphasia will be discussed in the next chapter. This division in periods is quite arbitrary, of course: the history of aphasiology neither has a clear beginning, nor a clear ending. However, we chose the year 1956 as the beginning of the modern period, because in that year, Roman Jakobson published a remarkable paper in which the classical division of aphasia in a motor and a sensory type was defined in linguistic terminology (Jakobson, 1946). Jakobson’s study marks the beginning of the modern, (psycho)linguistic approach to aphasia, which is characterized by attempts to describe the different aphasia symptoms in linguistic terms and to explain them by experimental studies and psycholinguistic models.
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Early history
The oldest reference to aphasia we know comes from the so-called ‘Edwin Smith
Surgical Papyrus’ which was written around 1700 B.C., but which is presumed to be a thousand years older. In this papyrus (deciphered by Breasted in 1930) the Egyptian surgeons related ‘speechlessness’ to skull injuries.
If thou examinest a man having a wound in his temple penetrating to the bone [and] perforating his temple bone […] if thou ask him concerning his malady and he speak not to thee; while copious tears fall from both his eyes [...] [this is] an ailment not to be treated [...]
(Breasted, 1930, p. 284; italics by the present authors)
The first reference to aphasic symptoms in classical history can be found in the ‘Corpus
Hippocraticum’ (around 400 B.C.). In these writings several references are made to speech impairments in relation to strokes and epilepsy. Also, medical doctors from the
Hippacrates school knew that ‘speechlessness’ could be the result of brain lesions and that it was often accompanied by a paralysis of the tongue and the right side of the body
(Chadwick & Mann, 1950). During the first centuries A.D. some references to aphasic symptoms can be found in the Roman literature. Valerius Maximus (around 30 A.D.) decribed a ‘very learned man from Athens’ whose head was hit by a stone and who consequently suffered from a loss of his ‘memories for letters’.
Galenus (103-200 A.C.) is worth mentioning, because he was the first one to localize thinking, perceiving and movement in the brain. The material substrate of the higher
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cortical functions was seated, according to him, in the ventricles. Figure 1 contains an early illustration of this claim.
Figure 1 The three cerebral ventricles as presented in the
Philosophica from Gregor Reisch, published in 1504. The frontal ventricle, that is connected to the sense-organs, is the seat of perception (‘sensus communis’), fantasy (‘fantasia’) and imagination (‘imaginativa’); the middle ventricle is the seat of thought (‘cogitatia’) and judgment (‘estimatia’) and the posterior ventricle is the seat of memory (‘memorativa’).
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This idea was elaborated on by Nemesius (4 th
century A.C.), who attributed a function to each of the three ventricles 2 : the frontal ventricle was the seat of perception, the middle one the seat of the intellect and the posterior one the seat of memory. These ideas of
Galenus and Nemesis were generally accepted through the 16 th
century.
In the medical literature of the Renaissance, only short descriptions of aphasia and the relation to the brain can be found. In his work ‘Epistilarum Medicinalium’, Nicolas
Massa (1558) described the case of a handsome young man who was wounded because a lance injured his head; as a consequence he could not speak for eight days.
Since the doctors declared that they had seen no bone [in the wound] I concluded that the reason of the loss of voice was that part of the bone was lodged in the brain. I took an instrument from a certain surgeon who was in attendance and extracted the bone from the wound, whereupon the patient began to speak at once, saying: “Praise God, I am cured.” This drew much applause from the doctors, nobles, and attendants who were present. [Benton & Joynt, 1960, p. 208]
Johan Schenk von Grafenberg (1585), in his ‘Observationes medicae de capite humano’, contributed considerably to aphasiology, since he noticed that the inability to speak did not result from a paralyzed tongue. The fact that aphasia is not the result of a tongue
2 There are four cerebral ventricles, of course, but Nemesius looked upon the two symmetrical anterior (i.e. lateral) ventricles as being one and the same.
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paralysis would be ‘rediscovered’ several times in the next few centuries; even in the middle of the nineteenth centuries, people tried to cure aphasia by putting leeches on the tongue.
From the seventeenth century on, an increasing number of clinical description can be found that are more extensive and precise than those in earlier centuries. Johann Schmidt
(1676) described a case of aphasia with alexia (‘De oblivione lectionis ex apoplexia salva scriptione’). After a stroke, the patient was paralyzed on the right side of the body and produced verbal paraphasias. After some time, both the speech problems and the hemiplegia disappeared, whereas the alexia, despite help and lessons, did not improve.
Peter Rommel (1683), who was a ‘Stadtphysicus’ from Ulm, Germany, described a female patient with a severe aphasia and a right-sided hemiplegia. He called her language problems ‘aphonia rare’. The unusual thing of this case, was, according to Rommel, that the patient lost her speech, except the words ‘yes’ and ‘no’, and was able to recite
Biblical texts and prayers fluently.
In the eighteenth century there are several descriptions of aphasic symptoms, but also the first attempts to formulate theories. In his handbook, Johann A.P. Gresner (1770) published a long chapter on ‘die Sprachamnesie’. He described symptoms such as jargon aphasia, agraphia, speech automatisms and a differential deficit in reading Latin as opposed to German, none of which had been previously described. He also devoted considerable attention to the psychological mechanisms underlying aphasia. According to
Gesner, aphasia is not the result of a general intellectual or memory impairment, but a specific deficit in verbal memory. This deficit results in an inability to associate images or abstract ideas with the accompanying verbal symbols. The result of this deficit in the
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relation between concepts on the one hand and conventional linguistic signs on the other is that, under normal circumstances, the patient does not speak. However, if the idea that the patient has in his head is very lively and he feels a strong need to express this idea, this may result in a wrong association between word and idea, which is shown by neologisms and paraphasias. So if the patient uses the wrong words, this is not due to a deficit in thoughts, but of the fact that he ‘forgot’ his language. However, the words that are lost in memory, are still serving thoughts.
The period 1800-1860.
Franz-Joseph Gall
In the early years of the nineteenth centuries a renewal in thinking about the localization of cognitive functions took place. Scholars broke with the medieval ideas on the relation between body and soul. Undoubtedly, the instigator of this development was the
Viennese neuro-anatomist Franz-Joseph Gall (1758-1828), who, around the turn of the century, presented a new theory on the functions of the brain. He did this in his lectures, which were forbidden in 1801 by the Roman Catholic church. He then left Vienna and went to Paris, where he elaborated his ideas with the help of many of his followers.
According to his theory, the brain was no longer an undividable unit, but it existed of a large number of separate organs, each with their own form and function. Gall assumed that there were as many brain organs as there were mental functions.
Gall performed important anatomical research: he made the division between the white and the grey matter in the brain and described several important nerve fibers. However, his ideas on the localization of mental functions were not based on neuropathological
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(post-mortem) studies, but on ‘frenology’. In frenology, the mental functions were directly related to the form of the skull, by palpation. This form of ‘cranioscopy’ was based on the idea that strongly developed mental functions caused hypertrophy in the particular brain area, resulting in bumps at the outside of the skull. Gall located sensitivity of language in the part of the brain directly behind the eyes, because he noticed that people who were good in reciting long poems had protruding eyes. Also, a hysterical, nymphomaniac woman, with large bumps at the back of her head, made him assume that the sexual drive was seated in the cerebellum.
By systematically palpating the skulls of gifted people, criminals and mentally diseased
Gall finally designed a chart, on which 41 different areas could be related to an equal number of mental functions (parental love, destructiveness, language). His scheme is given in Figure 2.
Figure 2: The 41 mental functions localized by
Gall, given in Mattieu Williams (1894).
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The pseudo-scientific theory of phrenology was popular for around thirty years, but went rapidly into oblivion, mainly because of Flourens’ (1842; see next section) criticisms.
However, Gall’s idea that the seat of language ability was located in the cortical parts of the frontal areas, was accepted by others and remained the subject of heated discussions until 1861.
Jean-Baptiste Bouillaud
One of the most prominent followers of Gall’s ideas about the ‘speech centre’ was Jean-
Baptiste Bouillaud (1797-1881). He published a paper in 1825, in which he presented the results of autopsies of thirteen stroke patients, of whom eight had aphasia and five did not.
His conclusion was that aphasia is always caused by a lesion in the frontal lobes.
Furthermore, Bouillaud stated that in aphasia, either the articulation or the memory of words is impaired and that both forms should be distinguished from the inability to move the tongue. The thus described deficits are, according to Bouillaud, caused by lesions in different sites in the brain.
The ideas from Gall and Bouillaud on the existence of different cerebral centres in general and a specific speech centre in the frontal lobes were heavily criticized, both for empirical and for theoretical reasons. The most important critique came from Pierre
Flourens (1794-1867), who argued that, although the cerebral hemispheres are indeed responsible for perception and intellectual functions, all motor functions, including the one for speech, are entirely controlled by the cerebellum. Further fractionating of the cerebrum and the cerebellum was, according to Flourens, impossible. This means that the
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brain functions as a homogeneous unit and the effect of lesions is only dependent on the size.
Bouillaud’s ideas on localization of language were also disputed by the findings of
Andral (1834), who reported that 16 of his 37 patients with anterior lesions did not suffer from aphasia, whereas he had found 14 cases of aphasia in patients of whom the autopsy showed that the frontal lobes were intact. Despite this criticism, Bouillaud was convinced he was right. In 1848, he presented a large number of new cases to support his theory on the localisation of language functions (see Hécaen & Dubois, 1969). During the discussion on these cases, Bouillaud promised 500 francs for each one who would show him a patient with frontal lobe damage, without having suffered from aphasia.
The period 1861-1905
Broca’s discovery of the ‘speech centre’
Paul Broca (1824-1880) was head of the surgery department of the hospital Bicêtre in
Paris and also the secretary of the Association for Anthropology.
Medical and political controversies
On February 21 st
, 1861, Gratiolet was giving a lecture for this association, in which he said the shape of the brain was establishing intelligence. Broca disputed this and said that the degree of intelligence was more related to the volume
. Aubertin, Bouillaud’s son-in-law and a fervent supporter of his ideas on localization, then said that this discussion was useless, because the brain does not function as a unit; the functions of the different lobes should
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be studied independently. The discussions following Gratiolet’s lecture were very heated, because the controversy on the possible localization of speech had a political background: the supporters of the theory on discrete localization of mental functions (such as Aubertin) belonged to the republicans and liberals, whereas the people with the holistic view (such as
Flourens and Gratiolet) were mostly conservatives. The ‘localisationists’ were considered as being materialistic, radical and atheistic, because division of the human mind in separate, localizable abilities would damage human’s dignity as a creature of God.
In 1861, a 51 year old aphasic patient was brought into the surgery department of Broca, because of an infection in his right leg. This patient, who was called Leborgne, was known in the hospital as ‘Monsieur Tan’, because the word ‘tan’, together with the swearword ‘sacré nom de Dieu’ was the only thing he could say. He was reported to understand everything that was said to him. Broca invited Aubertin to investigate his patient and the latter confirmed that the lesion responsible for the speech problems should be situated in the anterior lobes.
Mr. Tan died on April 17 th
, 1861. One day later, Broca presented the brain of his patient
(see figure 3) and the history of his illness to the Association for Anthropology. In
August 1861, he gave a more detailed description, including the complete autopsy report, and, following Bouillaud, he made a principle distinction between the language faculty (a general language faculty, which governs all modes to express thought) and speech faculty.
According to Broca, monsieur Tan suffered from the latter: he had not lost his memory of
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words, nor had he problems with the nerves or muscles used for articulation and voice.
However, monsieur Tan lost the ability to coordinate the movements that are typical for articulated language. Broca called this ‘aphemie’; nowadays, this would be called
‘apraxia of speech’.
Figure 3: The brain of Monsieur Leborgne.
The lesion responsible for the speech disorder was, according to Broca, localized in the posterior part of the third, and possibly the second, frontal gyrus and had the size of an egg.
A couple of months later, a second aphasic patient came to the surgery department. This patient, the 84 year old monsieur Lelong, suddenly lost his speech five months before and the only words he could produce were ‘un, deux, trois’ (‘one, two, three’) and his name.
According to Broca, he understood everything that was said to him. He died twelve days after admittance to Broca’s department and in November 1861 Broca presented the
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autopsy report. Again, there was a lesion in the third and, to a lesser degree, in the second frontal gyrus of the left hemisphere. Although Broca was very cautious not to draw conclusions, the idea of the importance of the third frontal gyrus was highlighted, and he, maybe involuntarily, became one of the important agents of the discrete cerebral organization. In 1863, having studied fifteen cases of ‘aphemie’ with a lesion in the third frontal gyrus, he can be safely considered to be a localisationist.
In the same year, he promoted a second claim. After observing that the lesion showed in the left hemisphere in all eighteen patients with aphasia he had, he observed that the claim for the left hemisphsere could only be established if it were shown that lesions in the right third frontal gyrus did not affect articulated language. Parrot (1863) presented such a case. Since Broca considered both hemispheres to be each others reflection, he considered this case to be an exception. Two years later, however, he declared that
‘aphemie’ was, in 95% of the cases, caused by a lesion in the left hemisphere and that this relates to the fact that the majority of the people are right-handed. Thus we see evidence of a cautious approach and an awareness of the importance of double dissociations.
Was Broca really the first?
There is some doubt on the question whether Broca is indeed the first scientist to locate language disorders in the left cerebral hemisphere. Gustave Dax, the son of Marc Dax (1770-1837), claims that in 1836 his father gave a lecture in
Montpellier, in which he explicitly claimed that language disorders are virtually always the results of a left hemisphere lesion. This lecture was
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presented for publication to the Medical Academy in Paris in 1863 by his son
Gustave, but was rejected. Two years later it was published in a shortened form in a popular medical journal. When the librarian of the Medical Faculty in Montpellier made enquiries among twenty doctors who were present at the conference in 1836, nobody remembered Marc Dax’s lecture. Hence, there was some doubt that Dax’s lecture was really presented.
Aphasia versus Aphemie
Armand Trousseau (1801-1867) is known in the history of aphasia because he was the first one to use the term ‘aphasia’ (Trousseau, 1864). It is less known that Trousseau’s definition of aphasia was different from Broca’s. He defined ‘aphemie’ as an articulation disorder occurring with spared language comprehension and intelligence. Trousseau described aphasic patients who did not only suffer from articulation disorders, but also encountered problem with reading, writing, drawing and gesturing. On the basis of these clinical observations, Trousseau concluded that aphasic patients always exhibit intellectual impairments. The aphasic patient has not only ‘forgotten’ how the words are articulated, but also and foremost, the words themselves. This loss of ‘formulas of thought’ is, according to Trousseau, always paired to a decrease of intellectual abilities.
The contribution of Carl Wernicke
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Carl Wernicke’s (1848-1905) now classic monography
Der aphasische
Symptomencomplex. Ein psychologische Studie auf anatomischer Basis was published in
1874. In this study, he described, for the first time, an aphasia syndrome in which patients could not understand spoken language, although hearing and intelligence remained unimpaired. These patients with ‘sensory’ aphasia (as Wernicke called this syndrome) spoke fluently, but made so many errors in the choice and order of the words that they became incomprehensible. Autopsy of two of the brains of these patients revealed an atrophy of the first and part of the second left temporal gyrus. Therefore, Wernicke assumed this area to be the sensory speech centre.
Wernicke contrasted this sensory aphasia, with that where the patient understands little or nothing, to the ‘motor aphasia’ described by Broca. In motor aphasia, the patient speaks little but can understand. According to Wernicke, the motor speech centre in the frontal lobe was a kind of store for the ‘motor images of words’, whereas the auditory images of words’ were stored in the sensory language centre in the temporal lobe. Both language centres were, according to Wernicke, connected through a bunch of fibers running through the insula and was later known as the arcuate fasciculus. Wernicke gave the following sketch (figure 4). Notice that although he assumed language was represented in the left hemisphere, his sketch is of a right hemisphere.
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Figure 4: Wernicke’s diagram of the psychologicalanatomical representation of language: a
1
= entrance of the auditory track in the brainstem; a = centre for auditory images of words; b = centre of motor images of words; b
1
= entrance of motor track in the brain stem;
F = frontal pole, O = occipital pole, C = central fissure,
S = Sylvian fissure.
A lesion to these fibers (a disconnection) resulted, again according to Wernicke, in a third aphasia type: conduction aphasia. Patients with conduction aphasia have, just like patients with a sensory aphasia, a fluent output, containing many errors, but they have no problems with understanding spoken language, and, hence, they notice their errors, unlike patients with sensory aphasia.
Wernicke described and localized two new aphasia types and importantly developed a psychologically based theory to explain the aphasic phenomena he observed. The starting point for this theory is that the speech process begins with the retrieval of auditory word images in the posterior language centre. These images are subsequently transferred, via
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the bundle of fibers, to the frontal (motor) speech centre, where the related articulatory programs are formed. According to Wernicke the posterior language centre also works as a kind of steering and correction mechanism.
On the basis of this simple anatomical schema, the major aphasia types could be explained. A lesion in the frontal speech centre disturbs the articulation process, but leaves comprehension intact (motor aphasia). A lesion in the posterior language centre disturbs language comprehension and results in phoneme and word substitutions in spoken language, of which the patient is unaware, because the steering and correction mechanisms do not function properly (sensory aphasia). Since the frontal speech centre is intact, the patient makes no articulatory errors and he speaks fluently. A lesion in the bunch of fibers between the posterior and frontal language centre results in a fluent aphasia, because the frontal speech centre is intact. However there are phoneme substitutions, because the posterior language centre cannot transmit the complete and correct language information as the connection is broken. Since the auditory word images in the posterior language centre are intact, the patient can understand what is said to him and is aware of his errors (conduction aphasia).
The associationists’ school: Lichtheim and other diagram makers
Wernicke’s anatomical-psychological model was enthusiastically received because of its explanatory nature and soon gave rise to the development of all kinds of diagrams, in which the distinct centres for speech, language comprehension, writing and reading were related in different ways.
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The supporters of this associationists’ school expected that with the help of these diagrams all important aphasia symptoms could be explained by assuming lesions in one or more of these language centres or in the connections between them. Equally, they claimed that, given the site of the lesion, valid predictions could be made about the aphasic symptomatology that would be the consequences. However, the associationists were more interested in their theories (diagrams) than in empirical findings, with the result that on the one hand, they postulated aphasic syndromes that did not occur, whereas on the one hand, certain clinical aphasia types were ignored, because the symptoms did not fit the diagrams (such as Broca’s aphasia).
As an illustration, a summary of the famous diagram of Ludwig Lichtheim is presented, that, despite severe criticism, still has some validity and, in a slightly different version can be seen as the anatomical basis for the aphasia classification of the Boston school
(Goodglass & Kaplan, 1972, 1983, 2000). Also, the similarities with the modern day cognitive-neuropsychological flowcharts are striking.
Lichtheim’s diagram (see Figure 5) has five cortical memory centres, that form the basis for speech (M = Broca’s area), language comprehension (A = Wernicke’s area), reading
(O), writing (E) and conceptual representations (B). The five language centres are connected with each other and with subcortical areas in the following way. M and A have a direct connection with the conceptual representations (i.e. meaning of words), O and E do not. This implies that written language (both reading and writing) is always dependent on oral language; a-A is the connection that sends the auditory-verbal information and Mm the connection that connects the articulation centre to the lower motor centres.
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Figure 5: Lichtheim’s language model
Lichtheim, using this diagram, distinguished seven aphasia types: (1) cortical motor aphasia; (2) cortical sensory aphasia; (3) conduction aphasia; (4) transcortical motor aphasia; (5) subcortical motor aphasia; (6) transcortical sensory aphasia; (7) subcortical sensory aphasia or word deafness. The numbers 1-7 correspond to the lesion site as indicated in the right diagram of Figure 3.
The cognitive theory of aphasia by John Hughlings Jackson
Wernicke’s strict localization theory was generally accepted until early twentieth century.
One of the first critics of the ‘diagram makers’ was John Hughlings Jackson (1833-1911), who published a large number of papers between 1864 and 1882 (collected in Jackson,
1932). In these papers he promoted a view of aphasia that was radically different from the common theories of that time.
Jackson defined aphasia as a ‘propositionalizing disability’, meaning the inability to provide propositions or information. This inability was not restricted to speech, but also to symbols in general. Thus, aphasic patients who cannot provide oral information are usually also unable to express their ideas in gestures. Speech, writing and gesturing are,
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according to Jackson, all dependent on ‘inner speech’, that is, making propositions. He distinguished ‘propositional speech’ from ‘automatic speech’. He based this on his observation that automatic speech maybe preserved, whereas propositional speech is no longer possible (cf. Monsieur Tan, Broca’s first patient, who was only able to say ‘tan tan, sacre mon Dieux’). Since language and thought are connected, the aphasic patient is always ‘lame in thinking’; hence, aphasia should be considered to be a cognitive disorder.
Jackson’s ideas on the relation between language and thought resulted in a principal rejection of the associationists’ localisation theory of Wernicke and his followers.
Jackson stated that in language it is the propositions, that is the sentencesthat are important not the words. Therefore, it is not justified to explain the different types of aphasia in terms of the loss of static word images that are stored in separate memory storages. Language use, according to Jackson, is too complex a function to localize in a few separate parts of the cortex. As early as 1874, contemporary to the publication of
Wernicke’s monography, Jackson stated: ‘to locate the damage which destroys speech and to locate speech are two different things’ (Jackson, 1932, p 129).
The period 1906-1956
Pierre Marie, the iconoclast
In 1906, the Parisian medical doctor Pierre Marie (1853-1940) published three articles with the title ‘Revision de la question de l’aphasie’. These publications caused the foundations of the ingenuous building of the diagram makers shake. In these articles, the first of which had the provocative title ‘La troisième circonvolution frontale gauche ne joue aucun rôle special dans la function du langage’ (‘the left third frontal gyrus does not
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play any role in the function of language’), Marie argued that there were a few known cases of patients who had a lesion in Broca’s area, but no motor aphasia, whereas there were many cases of aphasia, in which Broca’s area was intact. These findings had been verified at post-mortem. Marie took it one step further by stating that motor aphasia was in fact a mixture of a cortical articulation disorder (‘anarthrie’, now known as ‘dysarthria’) and sensory aphasia as described by Wernicke. The latter he considered the only real form of aphasia: ‘l’aphasie est une’: lit. ‘the aphasia is one’. Marie, however, disagreed about the ‘sensory’ character of this aphasia type. According to him, aphasia was a kind of intellectual impairment that manifested itself mainly in the use of abilities that have been taught.
Psychological approaches to aphasia
Although the holistic and cognitive ideas on aphasia by Pierre Marie were heavily criticized by his contemporaries, especially by Déjérine, they formed the foundation for a more psychologically oriented approach to aphasia, which became more prominent in the first half of the twentieth century. An important representative of this approach is Arnold
Pick (1851-1924), who published a study on aphasia in 1913, in which he put aphasia in a language-psychological context. Just like Jackson, to whom he dedicated his study, Pick denied the existence of word images as psychological units. Central in Pick’s study was the description of a sentence production model in which he tried to explain different forms of agrammatism (i.c. in aphasic patients, young children and individuals with severe learning difficulties or psychosis). This model describes sentence production as a four stage process: (1) creation of a global, intuitive thought, non-verbal and
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undifferentiated; (2) development of a structured thought in the form of a nonverbal proposition; (3) creation of a grammatical sentence scheme, in which prosodic and affective elements are included; (4) word selection.
According to Pick, the agrammatism of aphasic patients can be considered as a regression from conventional syntax (stage 3) to syntax of thoughts (stage 2) and the typical telegraphic speech of these patients is the consequence of an economy principle of the damaged cerebral organ, resulting in omission of redundant elements (i.e. free standing and bound grammatical morphemes). Agrammatism, is, in Pick’s words ‘Notsprache’, a condition in which the patient adapts to his deficit. Pick’s ideas can be seen as the predecessor of the adaptation theory as formulated by Kolk (Kolk & Heeschen, 1990; see next chapter).
Two other famous representatives of the ‘psychological school’ are Henry Head (1861-
1940) and Kurt Goldstein (1878-1965). Head defined aphasia as a ‘disorder in the symbolic formulation and expression (Head, 1926) and stated that just as there was no centre for walking, there was no centre for speech, writing or reading. Furthermore, he stressed the importance of detailed and objective descriptions of aphasic deficits. He was the first one to develop an assessment battery with verbal and non-verbal tasks. His main study (Head, 1926), which consisted of 400 pages of clinical protocols, has been immensely influential in the quantitative approaches to aphasia research.
Goldstein is generally considered to be a very important representative of the cognitive approach to aphasia. His main studies (e.g. Goldstein, 1948) are characterized by an attempt to explain aphasia within the framework of Gestaltpsychology . According to
Goldstein, the basic disorder in aphasia is the inability to differentiate between ‘figure’
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and ‘background’, resulting in a patient’s inability to abstract (‘loss of categorical attitude’). This inability to abstract manifests itself in language in word-finding problems in spontaneous speech and naming disorders, and therefore is most prominent in ‘anomic aphasia’.
Localisation is not dead
Although the psychological approach to aphasia was the most common one in the first half of the twentieth century, the anatomical-clinical approach was not refuted by everyone. The strict localisationists’ ideas were followed in extremis by some researchers (Henschen, Nielsen, Kleist). Karl Kleist
(1887-1962) described in his book Gehirnpathologie (Brain Pathology,
1934), separate centres for both expressive and receptive use of phonemes, words, word meanings and sentences (so eight language centres in total). A large number of other cognitive functions (for example, singing, counting, recognition of colours and objects) were, according to Kleist connected to discrete cortical regions. His listing of distinct centres arose from detailed studies of 250 soldiers of the First World War with traumatic brain injury
However, the localisationists’ view did not meet with many supporters during this period and most aphasiologists thought that the higher cortical functions in general, and language in particular, were much too complex to localize in distinct brain areas.
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The interest in localization of aphasia and the anatomical basis of language increased again since the 1960s. This historic switch is mainly due to the clinical-anatomical studies of Norman Geschwind and to the work of the Russian neuropsychologist Luria
(see below).
Modern theories
In the second half of the twentieth century, many developments in the field of aphasiology, both in fundamental research and in clinical practice. We put the boundary of the modern time, rather arbitrarily, in the late 1950s, to correspond to the starting point of experimental studies. In the 1970s there is a strong influence of linguistics and for the first time, phonological production deficits and syntactic comprehension deficits are subject of research.
The 1950s and 1960s: the rise of experimental aphasiology
We have chosen 1956 as the start of a new period. In this year, Roman Jakobson (1896-
1982) published his famous study in which he characterized the two seminal types of aphasia, motor (Broca’s) aphasia and sensory (Wernicke’s) aphasia in linguistic terms.
For his linguistic analysis, Jakobson assumed two processes, which are normally operating in synthesis, selection and combination
. According to Jakobson, Broca’s aphasia can be seen as a combination deficit that mainly affects speech and is predominantly manifested in the chaining of phonemes within words and words within sentences. According to his analysis, telegraphic speech of Broca patients was a deficit in the serial organization at the sentence level. Wernicke’s aphasia, he suggested, was a
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selection deficit, due to which the patient has problems with the choice of the correct phonemes and words, resulting in phoneme and word substitutions (phonemic and verbal paraphasias). Apart from this, Wernicke patients have problems with comprehension of spoken language, because they are unable to distinguish words that are closely related phonemically or semantically. Jakobson’s second claim linked language dissolution to language development. He predicted that grammatical elements would be lost in aphasia in the reverse order that they developed in children.
Although Jakobson’s linguistic analysis of aphasia is too simplistic and too general, his idea that aphasia is primarily a linguistic disorder that can only be described with the help of linguistic principles, was the start of a series of experiments in which attempts were made to interpret the various aphasic symptoms and link them to linguistic theories.
Goodglass & Hunt (1958), for example, tested Jakobson’s hypothesis. In aphasia, the inflectional
–s
in finite verbs (‘John dreams’) should be lost sooner that the possessive
–s
(‘John’s dream), whereas the plural –s
(‘the dreams’) should last longest, since the opposite pattern had been found in language acquisition. In the first case, the
–s
indicates the relationship between constituents, i.e. subject and finite verb, in the second case, it signals the relationship within a constituent, whereas the plural –s does not has any relationship, it only has a semantic function. This linguistic hypothesis was supported by the group study (with 24 aphasic patients, not selected for aphasia type) of Goodglass and
Hunt, both for production and for comprehension.
Fluency
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Jakobson’s theory provided a stimulating framework for experimental research on the influence of linguistic variables on the language performance of aphasic patients. Goodglass et al. (1964) found, for example, that with an objective language variable, called ‘Phrase Length
Ratio’ (which is the number of word groups of five or more words, divided by the number of word groups of one or two words) fluent and non-fluent aphasic speakers could be distinguished. Additionally, the
Phrase Length Ratio turned out to be a suitable criterion to distinguish the three main aphasia types, because all patients previously diagnosed as having Broca’s aphasia belonged to the non-fluent group, whereas the patients diagnosed with either Wernicke’s and anomic aphasia were characterized as fluent. Benson (1967) used ten spontaneous speech characteristics (e.g. speech rate, melody, utterance length, paraphasias) to classify patients as fluent or nonfluent. He stated that more than two-thirds of the patients could reliably be classified as fluent or non-fluent with these variables. This psycholinguistic division correlated with a neuroanatomical one: non-fluent aphasia turned out to be caused by anterior lesions (in the frontal lobe), whereas fluent aphasia was the result of posterior damage (in the temporal and / parietal lobe).
In 1970, Goodglass et al. published a study on the relation between aphasia type (Broca’s,
Wernicke’s anomic and conduction aphasia) and the nature of the comprehension disorder. Broca patients encountered most problems when they had to point to pictures
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after a series of auditorily presented words (e.g. chair – cat – clock – fork – lamp );
Wernicke patients’ main problem was judging whether a sentence was grammatical or not (‘I want you home on time’ versus ‘I want you home to time’), whereas for patients with anomic aphasia comprehension of single words was most difficult. Such qualitative difference were not found, however, in a sentence comprehension study by Parisi &
Pizzamiglio (1970), focused on morphosyntactic sentence structure. Although Wernicke patients scored lower on their test than Broca patients, the complexity hierarchy was the same for both aphasia types.
The second half of the twentieth century saw a renewed interest in aphasia classification as well as an explosion in experimental research in aphasiology. Apart from establishing the dichotomy in fluent and non-fluent aphasia, new classification schemes were published that were clearly different from the classical aphasia typology which were discussed in Chapter 3. Some researchers, such as Schuell et al. (1964) and Bay (1964), interpreted aphasia as a unitary syndrome, following Pierre Marie. They assumed that there is only one form of aphasia and that the various classical aphasia types should be considered as a mixture of ‘real’ aphasia and several non-linguistic concomitant impairments, such as visual and senso / motor deficits (Schuell) or auditory and cognitive deficits (Bay). The unitary account of aphasia has, however, been largely left behind.
Alexander Romanovich Luria (1902-1977)
Research in aphasia was also occurring in the Soviet Union. Alexander
Romanovich Luria and his collaborators contributed considerably to the
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theory on aphasia. Luria’s ideas were mainly based on clinical research on more than 800 trauma patients from the Second World War. Virtually all patients were young soldiers and almost half of them had aphasia, caused by gunshots or grenade splinters. The injuries resulted in small lesions and relatively pure forms of aphasia. Luria (1966; 1970) described six aphasia types, each of which is related to a lesion in a specific brain area. His classification system is based on a combination of psycholinguistic and neuro-anatomical characteristics. His work has been influential in many
Scandinavian countries, Russia and countries of the former Soviet Union.
The 1970s: the influence of linguistics
In the 1970s, there was a considerable amount of research investigating performance at phoneme, word and sentence level.
At the phoneme level, Blumstein (1973) published a study of phonemic paraphasias in the spontaneous speech of patients with Broca’s, Wernicke’s and conduction aphasia. Her results revealed that these three patient groups demonstrated a similar pattern of phonemic errors, that could be described in terms of distinctive features.
Most of the substitution errors were changes by only one feature, for example, [voice]. This means that a /p/ was substituted by a [b] more often than by a nasal. This study was the start of research to phonological and articulatory deficits in aphasia.
At the word level, Norman Geschwind (1926-1984) was an important contributor to our knowledge on aphasia. He worked within the Wernicke – Lichtheim framework.
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Geschwind (1972) described the anatomical basis of object naming. According the
Geschwind, at least six different stages can be distinguished in naming an object (e.g. an apple), both from a neuro-anatomical and from a psycholinguistic point of view:
(1) The target stimulus (the visual image of the apple) is projected on the primary visual cortex, where the specific visual processing takes place.
(2) The visual pattern is transferred to the visual association cortex where the perceptual analysis and synthesis (that is, object recognition) happens.
(3) A connection (association) is made between the visual image of the apple and the auditory form ‘apple’, stored in Wernicke’s area. This association is made in the angular gyrus that contains the ‘rules’ for recoding visual perception into auditory perception and the other way around. The angular gyrus can be considered, both from an anatomical and from a functional point of view, as a transfer area between the temporal, occipital and parietal lobe, in which processing takes place of auditory, visual and tactile-kinesthetic information respectively. The angular gyrus, due to its location, enables synthesis of these three kinds of sensory information and is specifically important for establishing visual – auditory associations, which are fundamental for naming.
(4)
The auditory form of the word ‘apple’, is (in abstract form, of course) transferred to Broca’s area via the arcuate fasciculus, that connects Wernicke’s and Broca’s areas.
(5) In Broca’s area, the articulation program for the word ‘apple’ is activated.
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(6) On the basis of this articulatory program the muscles of the articulation organs
(tongue, lips etc.) are activated via the primary motor cortex and the word ‘apple’ is pronounced.
This model can explain a large number of aphasic symptoms in a relatively simple way.
For example, a lesion in Wernicke’s area will result in an inability understand the name of objects, because the corresponding auditory form is not present and, hence, the perceived series of phonemes cannot be connected to it. A lesion in Broca’s area should not result in comprehension problems at the word level, because the auditory patterns in
Wernicke’s area are intact. The Broca patient will have articulation problems, because the articulation patterns are no longer available. Geschwind did not only describe the process of word comprehension and production, he also modeled reading disorders.
An important contribution
A study of Goodglass & Baker (1976) investigating the representation of semantic fields was very important. Their idea was that semantic fields are composed of seven different, associative categories. For an ‘orange’, for example, this is filled in as follows: super-ordinate : fruit; attribute : juicy; contrast co-ordinate : apple; function associate : eat; functional context : dessert; sound-alike word: arrange; identity : the name of the object itself.
The focus of this study was on the relation between the semantic structure of words on the one hand and language comprehension and naming on the other.
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Goodglass and Baker tested control subjects and aphasic patients with poor and relatively spared comprehension. The participants were presented a picture that they had to name; then the written word appeared underneath the picture, while they heard fourteen other words. Half of the auditorily presented words belonged to one of the seven associative categories, the other half were unrelated. The subject had to indicate whether there was a relation between the target word and the heard word by pushing a button and reaction times were measured. Patients with poor language comprehension were worse in naming the pictures than those with good comprehension.
Also patients with poor comprehension did not only make more errors in the second part and had slower reaction time, but the incorrect reactions and the order of the reaction times for the various associative categories were also deviant from those of the control subjects and the aphasic patients with good comprehension. Aphasic patients with poor comprehension reacted quicker on co-ordinates that the other subjects and slower on functional context and words with an associative function. The authors concluded that patients with poor comprehension often know what a certain object is, but that know less about it than before: the semantic fields of the objects are more restricted.
Due to this restriction of the semantic fields, these patients have poorer comprehension. Hence, in patients with poor comprehension there is an underlying semantic disorder, because the semantic fields are restricted.
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Zurif et al.’s (1972) paper on sentence level comprehension has been very influential.
They were the first to point to the nature of syntactic comprehension deficits in patients with Broca’s aphasia. In 1976, a second paper was published by Caramazza & Zurif. The results of these studies showed a parallel between the production and comprehension deficits in Broca’s aphasia: their spoken output is characterized by syntactic problems
(telegraphic speech) ánd their comprehension of syntactic relations is affected.
Caramazza & Zurif (1976) tested comprehension of sentences like ‘the girl that the boy is pushing is blond’. Broca patients had obvious problems with these sentences: they performed at chance level, not knowing who pushed whom. Caramazza & Zurif concluded that in these patients the syntactic knowledge was lost. Although other researchers (e.g. Parisi & Pizzamiglio, 1970) had earlier pointed to the comprehension problems at the sentence level in Broca’s aphasia, Caramazza & Zurif were the first to give a structural explanation of these comprehension problems.
Caramazza and Zurif showed that Wernicke patients also have problems understanding the meaning of word order; however, they made lexical semantic errors as well (they pointed, for example, to a picture on which the boy kicks the girl, instead of pushes. The papers of Zurif and colleagues’ research of grammatical comprehension problems were influential, but 30 years late, there is still no consensus on the underlying cause of this deficit in Broca’s aphasia.
After their innovative work, Caramazza’s and Zurif’s ways diverted, with each of them exploiting a major division in methodological approaches to aphasia research within aphasiology. Caramazza became an advocate of the so-called ‘case studies’ approach, a methodology that is supported by cognitive neuropsychologists, also called ‘radical
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cognitivists’. His focus is on lexical semantic deficits, in the tradition of Geschwind
(1972; 1974). Zurif remained convinced that group studies reveal important information about the organisation of language in the brain. This issue on case versus group studies continues today and will be discussed further in the next chapter on current issues .
Suggested further reading
About the history of aphasia:
Eling, P. (1994) Reader in the History of Aphasia: From Franz Gall to Norman
Geschwind.
Amsterdam: John Benjamins. An edited volume of the mentioned period.
Finger, S. (2000). Minds behind the Brain. A History of the Pioneers and their
Discoveries . Oxford/New York: Oxford University Press.
Code, Ch. & Tesak, J. (2007) Milestones in the History of Aphasia.
London: Psychology
Press.
On the early history:
Benton A.L., & Joynt, R.J. (1960). Early descriptions of aphasia. Archives of Neurology,
3 , 205–222. From the 400 B.C. till 1800.
Buckingham, H. (2006) A pre-history of the problem of Broca’s aphasia. Aphasiology, 20,
792-810.
Prins, R.S. & & Bastiaanse, R. (2006) Early history of aphasia. Aphasiology, 20, 761-792.
From 1700 B.C. till 1861.
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The original French papers of, for example, Bouillaud and Broca have been reprinted in:
Hécaen, H., & Dubois, J. (1969). La Naissance de la Neuropsychologie du Langage
1825–1865 (Textes et Documents).
Paris: Flammarion.
On neuropsychology:
Geschwind, N. (1974). Selected Papers on Language and the Brain.
Dordrecht, Boston:
D. Reidel Publishing Compagny.
Luria, A.R. (1966). Higher Cortical Functions in Man.
London: Tavistock Publications.
In Musée Dupuytren in Paris, the brains that Paul Broca examined can still be seen.
Among them are the brains of monsieur Leborgne and Monsieur Lelong. In 1984, the brain of Monsieur Leborgne was CT-scanned and the results are published in:
Signoret, J.–L., Castaigne, P. Lhermitte, F. Abelanet, R., & Lavorel, P. (1984).
Rediscovery of Leborgne's brain: Anatomical description with CT–scan. Brain and Language, 22 , 303–319.
In 2000, an MRI-scan was made of the brain of Monsieur Leborgne, the results of this have been published in:
Dronkers, N.F. (2000) The pursuit of brain-language relationships. Brain and Language,
71 , 59-61.
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