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HAPTER

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PHASIA

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N INTRODUCTION

Aphasia is an acquired language disorder, caused by a focal brain lesion after the period of language development. In this chapter, we consider the types of brain damage that may result in aphasia, and introduce the relation between brain and language. We introduce claims for the loci of the language facility and other cognitive functions.

Example of aphasic speech 1

I had good conversations with the people and what did you do on

Sunday?

well … that was work with people … so that was doing what the people say that they should be doing … I think that I have it about now did you conduct a service on Sunday?

from 10-11 and I am still there how did you prepare for a service? yes it it yes you must good

… that is difficult … you should do it well so you should have done it

… so you looked into it … you looked out of it and it was something or it was nothing and that was about it

This is an example of the speech of a 45 year old clergy man who suffered a stroke and who is answering the interviewer’s question what did you have to do as a clergyman?

His speech

1 Throughout the book, examples of spontaneous speech are given. Notice that we do not give any punctuation, except … to indicate pauses. The reason is that it is often hard to indicate clause boundaries in aphasic speech.

Text of the interviewer is always in italics .

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problems were due to a stroke and this sample is typical of the man’s aphasic speech. He had hardly any other cognitive deficits and there were no signs of dementia. The stroke affected the language area in the brain, one of the consequences of which was problems finding the right words. As can be seen in the example, his grammar is more or less intact, but it is difficult to tell what he is trying to say. In other stroke victims, the grammar may be selectively impaired, as in the following example of a 48 year old woman.

Example of impaired grammar

Where did you buy a new house? in Groningen centre of Groningen middle of Groningen ah … beautiful place. Can you tell me something about the new house you bought? What does it look like? new housing estate … premium estate … beautiful house … oh dear yes beautiful house … err ... magnificent from the outside … windows very very lovely house

How big is it? room... ninety meters... no! nine meters… all thresholds gone…beautiful garden … lovely

This speaker omits articles and verbs and does not make grammatical sentences. Again, her speech problems are due to a stroke that affected an area of the brain which is involved in language processing.

Definition of aphasia

These language disorders are called aphasia , which comes from Greek: αφατος (aphatos), meaning ‘no speech’. Aphasia may be defined as: an acquired language disorder, caused by a focal brain lesion after the period of language development.

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First of all, aphasia is a language disorder. In this text we use ‘ language disorder’ to show that we mean a central deficit that affects both comprehension and production and both spoken and written language. In case of the clergyman whose speech sample was given above, this means that when he cannot find a word during a conversation, he is not able to write it down either, because his ability to find words in general is reduced due to his brain lesion. In case of the woman who lost her ability to build grammatical sentences, it is likely that she will not understand complex grammatical constructions; it will be difficult for her to tell who did what to whom in sentences like the boy is teased by the girl . Defining aphasia as a language disorder distinguishes it from articulation disorders. Brain damage may affect articulatory abilities, for example, because the facial musculature is paralysed. In these cases, speech problems will occur, but the patient will be able to write and to understand language, because the language system itself is intact. It is quite common, however, for a person with aphasia to suffer from concomitant articulation disorders.

Aphasia should also be distinguished from developmental language problems in children. In order to make this distinction, aphasia is defined as an acquired language disorder.

Developmental language disorders may have several origins: neurological damage that arise perinatally; specific genetic syndromes (as in Down’s syndrome), but often there is no known cause (as in Specific Language Impairments). The nature and the development in all these disorders may be very different from those in aphasia and therefore they are excluded from the definition of aphasia. If children acquire brain damage (e.g. due to a traumatic injury or a stroke) during the critical period of language development, language problems may arise. This is called childhood aphasia .

Language, in all its complexity, is stored in the brain and damage to the language area results in aphasia. Language problems in persons in whom no neurological damage can be demonstrated may resemble aphasic output, however. This is, for example, the case in

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schizophrenia; speech of a person suffering from schizophrenia may be very confused, with incorrect sentence structures and it may sound like the speech of the clergyman given above.

Our definition of aphasia therefore includes ‘brain damage’ as a cause for the language disorders. Thus, we distinguish aphasia from the distorted language production which has a psychiatric origin.

Including the presence of brain damage in the definition is not enough, however, it should be focal brain damage. Focal refers to one specific focus of damage that causes the language disorders which is in contrast to diffuse damage, where there is damage spread across a larger area of the brain. The latter happens in certain types of dementia (for example, of the

Alzheimer type) or when there are multiple lesions which often result in dementia as well such as ‘vascular dementia’ or ‘multi infarct dementia’. Most types of dementia eventually result in speech and / or language problems, but these are different in both nature and course from the language disorders caused by focal brain damage. Unlike aphasia, language disorders in dementia are progressive, that is they worsen whereas aphasia often lessens over time. Thus language disorders associated with dementia are not included in our definition of aphasia although some researchers refer to the language disorders in dementia as ‘aphasia in dementia’.

Finally, we only speak of aphasia if the language disorder is acquired after the period of language development. Of course, people learn new words every day, so language development basically never stops, but there is convincing evidence that grammar is more or less fully matured some time before puberty. Younger children may develop language disorders, due to stroke, which happens very rarely, but more frequently due to diseases that affect the brain, such as meningitis and encephalitis. It may also arise due to specific syndromes, such as the Landau Kleffner syndrome. The main cause of acquired brain damage resulting in language problems in children is, however, injury due to an external cause, for

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example, a traffic accident. The language problems of these children are referred to as childhood aphasia . Both the symptoms and the outcomes of the condition are different from the problems that arise in adult aphasia; therefore, acquired language problems due to brain damage in children are excluded in the definition of aphasia.

Causes of aphasia

Why does brain damage result in aphasia? Brain cells only function properly if sufficient essential nutrients (e.g. glucisis, oxygen) are provided and these are transported to and from the brain by the blood. In case of a lack of these nutrients, the cells become hypo-ischemic and brain cells ‘die’. This is known as necrosis. Until recently, it has been thought that brain cells, unlike cells of, for example, the skin do not regenerate and that, therefore, brain damage is irreversible. It was thought, therefore, that once a person becomes aphasic, the condition is permanent. Nevertheless, it is now known that the situation is not quite as cut and dried. First, during the first few months after the occurrence of the brain damage, significant improvement and even complete recovery in functioning are possible. Some cells that fail to function because of a lack of oxygen nutrients may ‘regenerate’ especially if stimulated. Further, the view that once a brain is damaged it cannot regenerate in any way is now thought not to be correct. Following recent animal brain research, it is has been demonstrated that there can be some level of regeneration within the brain, what is known as plasticity in the adult brain.

Although this type of research is in its infancy, the outlook seems to be brighter than has previously been the standard view. These findings provide an explanation for the changes seen in people with aphasia, changes that appear to run contrary to the predictions that follow the view that there can be no regeneration in the brain. Second, there are other explanations for improvement after brain damage and these are more widely known and accepted. When the brain gets damaged, swelling known as oedema often occurs, because of the wound in the

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brain. This is comparable to swelling of a knee after an injury. The swelling causes the pressure to increase within the brain, as the brain is within a confined and non-expandable space. Because of the this swelling, some cells die, but others may receive too little nutrients to function, but enough to survive. As the swelling diminishes after the immediate acute stage, the pressure on the brain diminishes, and this allows the non-functioning brain cells to start to re-function. There is also some evidence that during the first half year post-onset, certain connections between the cells may regenerate during the first few weeks or months. This explains why spontaneous recovery of cognitive and physical functions takes place during the first six months after the onset of brain damage.

There are four possible ways to acquire focal brain damage. Each of them may result in aphasia, depending on the site of the lesion. We will first present the causes of focal brain damage and then discuss the relation between the brain on the one hand and language and other cognitive functions on the other.

Causes of focal brain lesions

By far the most common cause of aphasia is a stroke, or, in medical terms, a cerebro vascular accident or C.V.A.

This term is loaned from Latin: cerebrum translates as ‘brain’ and vascular derives from the Latin vasulum meaning ‘vessel’) thus the term means an ‘accident in the vessels of the brain’. This can happen in three different ways.

The first is a hemorrhage , a rupture in one of the arteries supplying the brain: the blood flows out the artery (see figure 1), with the consequence that the area that is supplied by the damaged artery receives insufficiently oxygen and other vital elements and ceases to function.

Additionally, the blood that leaks out of the artery into the confined space within the skull increases the intracranial pressure. The leaked blood puts pressure on the tissue surrounding

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the artery and prevents that area from functioning. Thus the surrounding tissue is damaged as well.

Figure 1: Illustration of how a hemorrhage affects the supply of nutrients in the brain.

The second kind of C.V.A. is an infarction . There are two possible causes of an infarct. First there is thrombosis . Thrombosis is defined as a blood clot in the vein. When blood reaches open air, it will clot, which prevents us from bleeding to death after a cut in the finger. In damaged arteries, however, blood clotting may appear because the inner tissue of the artery is affected. When these clots grow, they will partially or entirely block the artery. As a consequence, the area behind the clot is insufficiently supplied with oxygen and glucose and therefore ceases to function (see figure 2).

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Figure 2: Illustration of how thrombosis may block the bloodstream.

A great risk of a thrombosis, even if it is not situated in the brain itself, but in the heart or the carotid artery in the neck, is that parts of it may tear off and flow with the blood into smaller arteries, which they may (partially or totally) block. Again, the area behind the blockage will cease to function (see figure 3). A blood clot that tears off is called an embolus.

Figure 3: Illustration of how an embolus may block the bloodstream.

The second most frequent cause of aphasia is traumatic brain injury (T.B.I.) , also called a brain contusion.

The term ‘traumatic’ refers to the fact that the damage arise from an outside cause, which, in peace time, is most commonly a traffic accident. It may also be caused by falling from a scaffolding, violence, gun shots et cetera. This explains why aphasia due to traumatic brain injury is more often seen in younger people, whereas aphasia due to stroke is usually found in the elderly.

Within T.B.I., a distinction is made between open and closed head injury , referring to whether or not the skull is damaged. Open injuries bring risks of complications of infection that add to the severity of the condition. In T.B.I., the lesion may be large and diffuse rather than focal or

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there are multiple lesions. As a consequence, aphasia due to traumatic brain injury is usually accompanied by other severe and often more prominent cognitive disorders, such as memory and behavioural problems. One exception to the large lesions in T.B.I. is the small and highly well-circumscribed lesion caused by a gunshot. These small lesions have contributed significantly to our knowledge of aphasia and the representation of language in the brain in the 20th century. Many soldiers who acquired head wounds due to gunshots or metal splinters in several wars, especially the first and second world wars, have been extensively studied by scientists in the Soviet Union, the UK and the United States of America (for example by

Luria, Head and Geschwind, whose contributions will be discussed in the chapter on the history of aphasiology).

The third type of brain damage that may cause aphasia is a tumour . Whether this tumour is malignant or benignant is immaterial as far as the aphasia is concerned. A tumour is needs space and as said above, the brain is protected by an inflexible skull, leaving no extra space in the brain. Hence, when a tumour grows, it will press on healthy tissue. If this tissue is involved in language, then aphasia will be the result.

The final and less common cause of aphasia is an infection in the brain, such as meningitis or encephalitis. This rarely occurs and the descriptions of aphasia after an infection are restricted to a number of case studies.

In summary, there are several reasons why brain areas involved in language processing may be damaged. The most common one is a stroke or cerebro vascular accident (C.V.A.), of which there are three different forms: haemorrhage, thrombosis and emboli. The second cause

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is traumatic brain injury (T.B.I.), which mainly occurs in younger people. Relatively seldom aphasia is caused by a brain tumour or a brain infection.

Language and the brain

The brain consists of two more or less symmetrical halves, each consisting of the cerebrum

(the larger part), the cerebellum and the brain stem. Each half is called a hemisphere (Greek: hÄ“misphaírion, meaning ‘half ball’), see figure 4 for a lateral view of the cerebrum and cerebellum of the left hemisphere. The large part with the convolutions is the cerebrum, the striped part in the lower right corner is the cerebellum.

Figure 4: Lateral view of the left hemisphere.

The cerebrum consists of two ‘layers’ the cortex and the subcortex. The outside layer, which can be seen in figure 4, is the cortical area, consisting of over 10 11 neurons and this area is associated with the storage and representation of cognitive functions, including language. It is organised in convolutions, or gyri (singular: gyrus). Beneath the cortex lie the subcortical areas, which contain several structures and the pathways that connect the different parts of the cortex. A picture of the brain in which the cortical and subcortical areas can clearly be

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distinguished is given in figure 5. The cut is made form back to forth, the front of the brain is up, the back down. This is called a dorsal view.

Figure 5: Dorsal view of the brain.

In the large majority (95-98%) of right-handed people, language is represented in the left hemisphere; in around 50% of the left-handed people language is represented in the right hemisphere, dependent on the left-handedness in the family. In a small percentage of the lefthanded people is represented in both hemispheres. In almost 50% of the left-handers is represented in the left hemisphere, just like in most right-handers. Thus, aphasia is usually caused by a lesion in the left hemisphere (also called the dominant hemisphere ). When a right-handed individual acquires aphasia due to a lesion in the right hemisphere, this is called crossed aphasia , which is very rare and virtually only reported in individuals who come from families in which there are many left-handers.

Aphasia is most often caused by cortical lesions; aphasia due to subcortical damage is rare, but it does occur. This is called subcortical aphasia, which will be discussed in chapter 3.

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The cerebellum plays an important part in co-ordinating motor functions, among which articulation (co-ordination of the muscles of the face and throat, the larynx and pharynx et cetera) and writing (for which co-ordination of eyes and hand is needed). It has recently been shon that the cerebellum might play a role in the language network (Stowe et al., ??; Mariën,

??), but, as far as we know now, cerebellar lesions do not cause aphasia.

The left hemisphere and some cognitive functions

The cortical areas of both hemispheres may be divided in four parts: the frontal, the temporal, the occipital and the parietal lobes. Here, we will focus on the left hemisphere, because this one is most important for language functions. Some other functions that are important in relation to language will also be discussed. In Figure 6, the four areas are shown.

Figure 6: The four lobes of the left hemisphere.

The frontal lobe is bordered by two fissures or ‘sulci’, the Rolandic or central sulcus and the

Sylvian or lateral sulcus. The frontal lobe has many important functions, such as attention and the initiation of activities, but we will focus on the two functions that are most important in relation to aphasia, that is, motor skills and language. Lying anterior to the central sulcus is a gyrus known as the motor strip . On this motor strip, the motor skills of the contralateral side

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of the body are represented so, in figure 7, the representation of the right side of the body is shown. For each body part, the size of representation is related to the extent of motor agility associated with parts of the body. As can be seen in figure 7, there is little space for the trunk, not highly developed in human being with respect to movement skills, compared to the hand which is capable of a range of complex movements. It can also be seen that the mouth, lips and other parts that are important for speech have relatively large areas of representation. This is, of course, because of the agility and range of complex movements needed for articulation.

Lesions that affect the motor strip have serious consequences for the individual: not only may the contralateral side of the body be paralysed, but movements required for articulate speech may be affected as well. Therefore, people with aphasia often suffer from a paralysis of the right side of the body and articulation disorders as well.

Figure 7: Representation of the motor functions in the brain.

The second important function that is located in the left frontal lobe is language. The lower parts, of foot, of the third left frontal gyrus is also called Broca’s area (see figure 8). Paul

Broca was a nineteenth century French surgeon who was the first to publish claims about the

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localisation of (spoken) language in the left frontal lobe. We will return to this in chapter 9 on the history of aphasiology. Broca’s area plays an important part in the representation of grammar: if a patient has a lesion in or around Broca’s area, it is likely that s/he will have problems with grammar This does not mean, which is important to stress, that grammar is located in Broca’s area. Presumably, as we know now from recent neuro-imaging studies, grammar is not represented in one particular part of the brain. We do know, however, that

Broca’s area and its vicinity need to be intact for normally functioning of many grammatical operations. When these areas are damaged, the person will speak agrammatically . An example is the speech sample of the woman that was presented at the beginning of this chapter. Usually, comprehension of grammatically complex sentences (for example, passive sentences such as ‘the boy that is chased by the girl’) is impaired as well, which is not surprising, considering that aphasia is a central language disorder.

Figure 8: Broca’s area in the foot of the third frontal gyrus.

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The temporal lobe is bordered by the Sylvian fissure; the border at the posterior side is less clearly defined. The function of the temporal lobe that is most important in relation to aphasia is auditory analysis. The middle parts of both upper (superior) temporal lobes (also know as

Heschl’s gyri) analyse ánd recognise incoming sounds. When a bell rings, the brain

‘understands ’ what is heard. This is done bilaterally, that is, by both hemispheres. When there is damage in Heschl’s gyrus in one hemisphere, people do not necessarily notice, since the other hemisphere can still do the work. If, however, there are bilateral lesions in Heschl’s gyri, then the patient is no longer able to recognise sounds. Fortunately, this does not happen very often. The patient with bilateral damage to Heschl’s gyri will hear the bell, but not be able to distinguish it from the telephone and he will not be able to discriminate between a barking dog and a meowing cat. In the most severe case, the patient will act like somebody who is deaf, although hearing itself is not impaired.

Adjacent to Heschl’s gyrus in the left hemisphere is the posterior part of the superior temporal gyrus, also known as Wernicke’s area (see figure 9), called after the nineteenth century

German medical doctor Carl Wernicke, who has been equally influential in the history of aphasiology as Paul Broca. Wernicke’s area plays an important role in the representation of language. It is the place where word forms are stored and, therefore, extremely important for both comprehension and production of language. If this area is damaged, as we will see later, both comprehension and production of spoken words will be compromised, leading to one of the most severe forms of aphasia.

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Figure 9: Wernicke’s area in the posterior part of the superior temporal gyrus.

The posterior lobes of the cortex are known as the occipital lobes, the most important function of which is vision. The eyes project the images to the occipital lobes, so that we can interpret what we see. Contrary to hearing, there is no double representation for vision: what we see in our right visual field is recognised by the left occipital lobe and vice versa. In figure 10 this can be seen.

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Figure 10: The division of the right and left visual field.

Damage to the right occipital lobe will thus result in a loss of the left visual field and damage to the left occipital lobe to a loss of the right visual field. Depending on the nature of the impairment this is called hemianopia , in which case the patient compensates for his disorder by turning his head, or visual neglect in which case the patient neglects the impaired side.

Surprisingly, hemianopia usually occurs in right visual field disorders (so with a left-sided lesion, as most common in aphasia) and visual neglect usually occurs for the left visual field

(and in damage to the right occipital lobe). The consequences of a visual neglect may be striking: patients only eat from one half of the plate and may ask for more food despite having food still on the plate. When asked to draw a clock (see figure 11), they draw all digits at the right side and when asked to write or read, they ignore the left side of the paper (see figure

12).

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Figure 11: A clock drawn by a person with left visual neglect.

Figure 12: Text written by a person with left visual neglect.

Although hemianopia or visual neglect are not directly related to spoken language use (they do, of course, impact on written language skills), it is important to realise that they may seriously interfere with language testing . Visual field deficits may interfere when pictures are used as test materials as the visual deficit (rather than the language deficit) may prevent the patient from correctly interpreting the pictures or the visual deficit may interfer the patient’s ability to scan an array of pictures. Further, the presence of such impairments has serious implications for treatment.

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Finally, there is the parietal lobe that is bordered by the Rolandic or central sulcus on the front; the parietal lobes is not clearly bordered from the occipital and temporal lobes. There are two functions that are important in relation to aphasia. The first is awareness of space and time, which means that the parietal lobe registers where we are, how to find our way, what season, month, day or time it is et cetera. A lesion to the parietal lobe (in which functions cannot be exactly localised so far), may thus result in an inability to find one’s way, even in very familiar places and / or to tell what season, day, or time it is. A second important function is the so-called praxis , which refers to sequencing of motor skills involved in many daily activities that people learn during life and that are performed automatically, once acquired. Examples are tying one’s shoes laces, dressing and undressing, and writing. These motor skills are very hard for children to learn. Other skills that are necessary for actions to be performed are stored in the parietal lobe, such as sequences of movements required for learnt tasks such as making a cup of tea, preparing filter coffee or lighting a candle. In these types of task, various specific objects and actions have to be manoeuvred in a certain sequence in order to complete the task. .The ability to execute such patterns can be damaged by parietal brain damage, even though the motor skills themselves remain intact. The disorder is called apraxia. If the apraxia is severe, even if the person concerned is not paralysed, has no memory problems and his language is intact, he may still be unable to live independently. It is possible that such problems may accompany aphasia if there has been damage involving the parietal lobe and in these cases, both assessment and treatment of aphasia becomes more difficult.

There are several types of apraxia, which are not directly related to language, but there is one kind that is particularly important in relation to aphasia. As said, praxis refers to all sequences of motor skills that have to be programmed. One of these skills is speaking: this is an extremely complex motor skill, in which many different organs are involved, but that is fully

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automatized. Parietal damage may disrupt this process and we then speak of verbal apraxia or apraxia of speech ( AOS) . A person with verbal apraxia is not longer able to programme articulation. Pure verbal apraxia is rare, but it often accompanies aphasia; it will be extensively discussed in chapter 2. It should be noted, however, that it is not sure whether pure apraxia of speech is due to parietal damage.

Posterior to the Rolandic sulcus, in the parietal lobe, opposite to the motor strip lies the socalled sensory strip . Comparable to the motor strip, here the sensory images of the contralateral side of the body are represented: large areas for highly sensitive parts of the body and small part for the less sensitive parts. When a one-to-one ratio is made and the areas on the sensory strip are projected to the body an odd creature will appear, as shown in figure 13.

Such a man is called a homunculus .

Figure 13: The homunculus, in which the sensitive areas are presented relative to the size the occupy in the brain.

A lesion in the sensory strip will result in a reduced sensitivity in the contralateral body part.

If the motor strip is not affected, the patient will be able to move the contralateral extremities, but may not feel them, which may result in a unilateral neglect . In that case one side of the body is ignored; sometimes the patient does not even use this side, even though there are no motor restrictions. This mainly happens with right side brain lesions, just as in visual neglect.

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Since brain lesions, especially the ones following strokes, are usually large, aphasia is often accompanied by one or more motor or cognitive disorders, such as hemianopia, right-sided paralysis apraxia and articulation impairments. A typical lesion that will cause aphasia is drawn in figure 14. Such a lesion will probably cause aphasia with articulation disorders and a right-sided paresis. Small lesions do occur, though, resulting in relatively pure syndromes.

Figure 14: A typical brain lesion resulting in aphasia.

Most recent developments in localisation of language functions in the brain

Paul Broca (1824-1880) localised language in the brain based on neuro-anatomical evidence.

We will come back to this in the history chapter. His method was post-mortem examination, the only possible way to verify the lesion site and to localise language functions in the brain, until the 1950s. Two important developments in neurological investigations have to do with the possibility to study the brain in vivo, that is, when the patient is alive and conscious. An important study was done in 1959, by Penfield and Roberts, who used electric stimulation during brain surgery. Individuals with epilepsy underwent surgery to remove the epileptic focus while being conscious, which is not as bad as it sounds, since the brain is insensitive.

During surgery, several tests were presented to the patients and at the same time small parts of the brains were electrically stimulated, resulting in non-functioning. This was done to identify the language areas, to avoid that languages areas would be removed. For example, Wernicke’s

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area was stimulated during naming of pictures. As a result, the patient was no longer able to name the pictures. In this way, several language functions were tested and the results were compared to those of the post-mortem studies that had been done up to that date. The results did not always overlap. There are some objections to localisation studies like this. It may be argued, for example, that cognitive functions, such as language, may be organised differently in epileptic patients, as a result of multiple seizures.

Another main contribution was provided by neuro-imaging. The first new technique was

Computer Tomography scanning, CT-scanning for short, which is non-invasive and therefore not demanding to the patient. This has been used in clinical practise since 1971 (but the first brain scans took about 9 hours). With this technique, different tissues and materials in the brain show differently on the scan. For example, bone is white, healthy brain tissue is grey and fluid is black. Tissue that doesn’t use (sufficient) oxygen, is also black. Because the brain is scanned centimetre by centimetre, it is possible to localise exactly which areas use oxygen normally and which do not (see figure 15 and 16), thus allowing localisation of damaged tissue.

Figure 15: Picture of a slice through the normal brain.

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Figure 16: Picture of slices through a lesioned brain.

By using CT-scanning, a comparison between loss of function and lesion site is possible while the patient is alive. It is also possible to relate improvement of cognitive functions to changes in lesion size by rescanning the brain: tissue that was not functioning just after the injury, might have become active after the oedema decreases. The main gain of CT-scanning in relation to aphasia, is that the lesion site and size can be seen when the patient is alive. CTscanning has also shown that lesions limited to the parietal lobe may cause aphasia (although this is rare), and that, especially in the acute phase, subcortical lesions may result in aphasia.

Further developments became available in the 1980s: Positron Emission Tomography or PETscanning has made it possible to study the working brain: by injecting a subject with radioactive water or having him / her inhale radio-active gas, brain activity can be visualized.

Those brain areas that are active use more oxygen than other, as can be seen in figure 17 where the red areas indicate the most activity.

Figure 17: An example of PET-scanning: the coloured areas use relatively much oxygen.

Usually the so-called subtraction method is used in PET-scanning. For figure 17, the areas that are active during listening to the names of means of transport and household objects have

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been subtracted from the areas that are active when subjects listen to the names of animals and vegetables. So, the red areas in figure 17 are active when people listen to the names of animals and vegetables, but not when they listen to the names of means of transport and household objects, implying that the red areas play a role in the representation of the names of living things.

There are some drawbacks to PET-scanning, one of which is the involvement of radioactivity. This is the reason that in experimental investigations into the relation between language and the brain, a new technique is increasingly used: functional Magnetic Resonance

Imaging or fMRI. The idea is similar to PET-scanning, but instead of measuring brain activity by means of radio-activity, magnetic fields are used, which makes it more friendly to the subjects. A big disadvantage of fMRI for investigating language functions is that it is very noisy, making it difficult to study spoken language production and comprehension so far.

Another problem is that fMRI is highly sensitive to movement. Using overt speech is therefore hardly possible: articulation requires too much movement to acquire reliable results.

However, some progress has been made here: nowadays overt speech studies are possible, but only at the word level. Neuro imaging methods will further be discussed in the chapter on current issues.

Summary

Aphasia has been [can be-RSP] defined as a language disorder in adults, due to focal brain damage. This brain damage may be caused by a cerebro vascular accident (C.V.A.), traumatic brain injury (T.B.I.), a tumour or an infection. In most people, the left hemisphere is dominant for language, although in left-handers, the right hemisphere may be. Both hemispheres can be divided into four lobes. For the left hemisphere, the frontal and temporal lobes are important

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in relation to aphasia, because the main language centres, Broca’s and Wernicke’s area are situated in these two lobes.

Further reading

Calvin & Ojemann (1994)

Conversations with Neil’s Brain: The Neural Nature of Thought and Language.

Reading: Adinson-Wesley. This book describes the awake surgery of a virtual person Neil, who is epileptic. All kinds of language and memory tests are assessed during surgery. A highly interesting and highly readable book that teaches a lot on how higher cortical functions are represented in the brain.

Sachs, O. (1985) The Man w ho Mistook His Wife for a Hat and other Clinical Tales.

Summit:

Simon and Schuster. A collection of popularly described case studies of people with cognitive disorders.

Luria, A.R. (1972) The Man with the Shattered World . Cambridge , MA: Harvard University

Press. A novel, based on the diary of Zazetsky, a WWII soldier who was shot in the head. He had many perceptual problems, which have been beautifully described in this book.

Janet Lees (1993) Children with Acquired Aphasias. London: Whurr Publishers. (Second edition 2005).

Websites:

On brain anatomy: neuroanatomy interactive atlas on http://www9.biostr.washington.edu/

Many pictures and 3D movies on the brain.

On cognition and the brain: http://faculty.washington.edu/chudler/neurok.html This page is called neuroscience for kids , but is very informative for adults as well.

Informative websites for aphasic patients and their environment: www.aphasiainternational.com www.aphasia.org

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References

Penfield, W., & Roberts, L. (1959). Speech and Brain Mechanisms . Princeton, NJ: Princeton

University Press.

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