Ординатура / Офтальмология / Английские материалы / The Neuropsychology of Vision_Fahle, Greenlee_2003

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hemisphere (Rees et al. 2000; Vuilleumier et al. 2000, cf. also de Haan et al. 1987a, b for a behavioural correlate in prosopagnosia).

The evidence presented in this section clearly proves that stimuli presented in the neglected part of the outer world nevertheless activate not only the primary visual cortex, but also extrastriate and ventral temporal areas. These neglected stimuli are at least partly analysed and categorized, but do not reach awareness, even if patients take them into account, e.g. in enumeration tasks. This is a fundamental difference to agnosias. Preserved analysis in the ventral stream (see Chapter 5, this volume) without awareness supports in principle the notion of two parallel streams of cortical processing only one of which is linked to awareness (cf. Milner and Goodale 1995; Goodale et al. 1991; Goodale and Milner 1992; Ettlinger 1990; Newcombe et al. 1987; Ratcliff 1982). Some of the details of this dichotomy are still under debate, since the simplistic dichotomy between conscious ventral processing and unconscious dorsal processing would only apply if neglect were, indeed, a defect caused by damage primarily of the parietal lobe.

Tests for detecting spatial neglect in patients

A number of clinical tests have been developed to diagnose neglect and to discriminate it from purely sensory disorders such as scotomata. A very widely used test consists of asking the patients to search for short lines on a sheet of paper and to cross them all with pencil strokes (cf. Lezak 1995). Neglect patients tend to cross only those targets displayed on their ipsilesional side. A somewhat more difficult task is to search for a specific shape, say, a star or circle, among squares, stars, and rhombi, and to cross only the circles, or to search for a specific letter. In the first task, patients have ‘just’ to detect that there are stimuli on their neglected side, while in the second type they must discriminate between different shapes. Patients may not be able to perform this discrimination even though they may be partly aware of the presence of these objects.

Another class of tests requires the patients to bisect, by a pencil mark, a line presented on a sheet of paper. When bisecting a horizontal line, patients suffering from neglect often deviate towards the ipsilesional side, sometimes dramatically (e.g. Ferber and Karnath 2001). Hence, they do not take into account most of the line length presented on their contralesional, neglected side. In a third type of test the patients are asked to describe and/or copy a picture. Usually, they will exclusively or predominantly describe the ipsilesional part of the picture, and likewise omit parts of the contralesional part when copying it. The same holds true when the patient draws the object from memory, another indication that neglect is not exclusively or predominantly a defect in processing of sensory information (see Bisiach and Luzzatti 1978; see also ‘Spatial neglect in allocentric, object-centred coordinates and for remembered landscapes’).

Localization of lesions

Typically, the lesions in patients suffering from neglect involve the parietal cortex, with much more severe symptoms in patients suffering from right-sided cortical lesions than in those suffering from lesions of the left hemisphere. Typically, the lesions are

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located in the inferior parietal lobe, particularly in the angular and supramarginal gyri, i.e. Brodmann’s areas 39 and 40, as well as the frontal lobe and/or the basal ganglia (Heilman and Valenstein 1972; Heilman et al. 1993; Leibovitch et al. 1998; Husain and Kennard 1996; Perenin 1997; Vallar 1993, 1998; Vallar and Perani 1986; cf. also Colombo et al. 1976). However, this view has been disputed recently with the claim that it is the temporal, not the parietal cortex that is responsible for spatial awareness (Karnath et al. 2001; cf. Driver 1996; Samuelsson et al. 1997). In the following, I will continue to ascribe neglect to injury of the parietal lobe, but this may have to be changed or extended to the temporal lobe in a later edition of this book. As with other neuropsychological syndromes, fibre-of passage damage may contribute to the symptoms, here through damage to fibre bundles running in the white matter beneath the parieto-temporo-occipital junction causing a disconnection syndrome (Leibovitch et al. 1998; Gaffan and Hornak 1997; Samuelsson et al. 1997).

It is difficult to more precisely specify the brain defect causing neglect by analogy to lesion studies in monkeys (cf. Chapter 5, this volume) since neglect deficits in monkeys are less persistent and less severe than in humans (for a recent review on this somewhat controversial problem, see Wardak et al. 2002). The parietal cortex of monkeys contains neurons not only with the usual contralateral but also with ipsilateral receptive fields (contrary to striate and extrastriate occipital cortex). The representation is strongest for regions close to the midline, i.e. close to the part of the outer world mainly represented by this side of cortex, and diminishes with distance from the midline, i.e. towards the periphery (Andersen et al. 1990; cf. also Pouget and Sejnovski 1997; Rizzolatti and Berti 1990). This graded representation is reminiscent of the spatially graded nature of neglect (see ‘Graduation of spatial neglect and extinction of stimuli’) and leads to less severe symptoms after unilateral (one-sided) cortical lesions.

Patients sometimes suffer from neglect-like symptoms without parietal damage, especially after lesions of frontal (Damasio et al. 1980b; Heilman and Valenstein 1972; Husain and Kennard 1996) or subcortical areas (Bogousslavsky et al. 1988; cf. also Rafal and Posner 1987; Vallar 1993; Vallar and Perani 1987; Watson and Heilman 1979; Hildebrandt et al. 2002). Hence, whatever the neuronal structures may be whose defects underlie neglect of the contralesional part of the world, they are part of an extended network involving both subcortical structures and different parts of cortex, such as frontal, cingulate, and—most notably—inferior parietal and/or superior temporal cortex.

Neuronal and neuropsychological mechanisms of spatial neglect: deficit of attention versus representation?

It seems fair to say that the neuronal and neuropsychological mechanisms causing spatial neglect are not completely understood. Broadly speaking, there are two views regarding the underlying cause that are not necessarily mutually exclusive: lack of attentional resources on the one side, and lack of (spatial) representation on the other. Let’s first deal with the hypothesis that neglect is caused by a failure to attend to stimuli that are processed and relatively precisely analysed in the visual system but fail to reach

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consciousness, since attention is engaged in the ipsilesional part of the world. This phenomenon is not restricted to neglect patients, but applies to (neurologically) healthy observers as well in situations of sensory overload (e.g. Gorea and Sagi 2000). Human observers are unable to consciously process all of the information collected by the sense organs and transmitted to the brain. Hence, a selection has to take place, and one of the processes underlying this selection process is related to attention. We do have a certain control over where to direct our attention, but no total control—salient stimuli will automatically attract attention. Thresholds for detecting an object depend, to a certain degree, on whether or not they are attended to. In the extreme case, when our attention is engaged completely in analysing a specific aspect of a scene, or of an object (hence we are highly concentrated on this object or task), we may fail to perceive another aspect or object in spite of its being signalled to our primary visual cortex (e.g. change-blindness: Rensink et al. 1997).

The effect of attention on the processing of a stimulus can be measured not just by behavioural and, more specifically, psychophysical methods, but also by more objective ones. On the single-cell level, the responses of neurons in macaque monkey cortex to a specific stimulus increase when the animal attends the stimulus. The increase is more pronounced in higher, parietal and frontal areas than in the primary visual cortex (Wurtz et al. 1982; McAdams and Maunsell 1999; Desimone and Duncan 1995; Moran and Desimone 1985; see Giesbrecht and Mangun 2002 for a recent review on top–down attentional control), and neurons in the lateral interparietal (LIP) area of monkey cortex only respond to the attended stimulus or behaviourally relevant ones while ignoring all others (Gottlieb et al. 1998; Snyder et al. 1997). A similar increase of responses appears both in evoked sum-responses to visual stimuli (Chapter 3, this volume), and in the level of cortical blood oxygenation as measured by fMRI (e.g. Kastner and Ungerleider 2000; Corbetta 1998; Corbetta and Shulman 1998; for PET and event-related potentials, cf. Nobre et al. 1997, 2000; Neville and Lawson 1987). These examples of ‘neglected’ stimuli in normal observers with their psychophysical, electrophysiological, and imaging correlates are similar to the symptoms of neglect in patients. Hence, the problems that patients experience in directing their attention to the contralesional side of the outer world might be related to difficulties in steering attention in the visual field. This difficulty comes in graded specifications, from less severe forms that allow patients to attend to the contralesional side if no competitive stimuli are presented to the ipsilateral side, to more severe forms where, even under these artificial conditions with only one stimulus present, patients are not aware of a stimulus presented to their neglected side. So it seems fair to say that whatever causes neglect does have a spatial component.

A few details may not fit smoothly into this otherwise tempting and elegant model. One is the difference between defects of the two hemispheres. Injuries of the right parietal brain cause far more severe symptoms than those of the left hemisphere. So should only the right brain be able to steer attention? In that case, we would also expect severe attentional problems in patients’ ipsilesional hemifield after right parietal injury. So we

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must conclude that right parietal lesions impair the ability to shift the ‘spotlight of attention’ into the left half of extrapersonal space, while it can be moved within the right half of this space. This, however, is a notion less intuitively convincing than the more general notion of a defect in directing attention.

There is a tradition of contrasting the hypothesis that neglect is due to a disturbance of attention with the view that (quite to the contrary) neglect is due to a disturbance of spatial representation of contralesional space (Battersby et al. 1956; Bisiach and Berti 1987; Bisiach et al. 1979a; Denny-Brown and Banker 1954; Hecaen 1972; Paterson and Zangwill 1944; Scheller and Seidemann 1931). It should be clear by now that neglect is not a defect of representation by neurons that are retinotopically organized. Neuronal defects on the retinotopic level lead to scotomata, the relative position of which moves with the eyes. On the other hand, the defect does not decrease a general ability such as that needed to direct attention but restricts this ability to a part of the outer world. Based on these facts, and on the results of electrophysiological and imaging techniques that find the strongest effects of attention in the parietal lobes rather than in the primary or secondary visual cortices, we can assume that neglect is caused by damage to those representations of the outer world that are organized in egocentric (and possibly partly in allocentric) coordinates and whose neurons show strong influences of attention. This hypothesis is supported by the fact that the neurons in the cortical regions involved in neglect do have these egoor allo-centric receptive fields and are, by nature, to a large extent, polysensory, i.e. they integrate information from several sense modalities. Hence, these neurons would account also for multimodal forms of neglect (Andersen et al. 1997; Vallar 1998).

The symptoms encountered in neglect patients suggest that the internal representations of extrapersonal space in the parietal lobe are the neuronal basis for the subjective perceptual experience of this space—or that, at least, they are an essential prerequisite for this experience (cf. Bisiach and Berti 1987; Robertson et al. 1997; Driver and Vuilleumier 2001 for similar views). This is to say that neglect is caused by loss of the neuronal representation of the contralesional part of the outer world on an abstraction level characterized, to a first approximation, by an egocentric rather than retinotopic representation. A strong reciprocal inhibition between object representations exists at this representational level which is partly under volitional control (top–down attention) and which has access to awareness (or underlies the subjective experience of awareness; cf. Driver & Vuilleumier 2001).

One may go on and speculate that one of the reasons for this winner-take-all mechanism of attentional control that allows only one object representation at a time to reach awareness is related to the fact that, at any time, most of us are only capable of generating conscious motor output related to a single object. But the principle of one single representation and the exclusion of alternative interpretations seems to be a more general principle of cortical information-processing, as evidenced, for example, in binocular rivalry (see e.g. Blake and Logothetis 2002; Fahle 1982) and bistable figures (such as the Necker-cube).

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the ‘negative’ scotomata and failures of visual analysis described—and even real hallucinations. The most common example is the ‘migraine ophthalmique’, consisting of vivid phosphenes that start at an arbitrary position in the visual field and proceed, over several minutes, to neighbouring locations until they stop, most often at the visual field border (for a review, see Lauber 1944, and for visual imaginery, Kosslyn 1980; Sergeant 1990). They are thought to be triggered by vascular processes and may have caused some of the reports of ‘burning bushes’ and ‘unidentified flying objects’ (UFOs).

Other examples of positive visual symptoms are the hallucinations experienced by some during high fever, alcohol withdrawal delirium, and productive schizophrenic episodes as well as the ones produced by transcranial magnetic stimulation (see Chapter 6, this volume). But, even after strokes involving the visual areas and leading to visual field defects, a certain percentage of patients start to experience visual hallucinations, as indicated by sporadic evidence in the literature and the shy reports of some of our own patients. Many patients probably are too reluctant to even mention these symptoms for fear of being considered ‘crazy’. The same is true for patients suffering from (age-related) macular degeneration who often experience rather vivid hallucinations for up to a year after loss of central acuity (Charles-Bonnet syndrome). Systematic investigation of these symptoms is sparse due to the difficulties involved in quantifying such subjective experiences (but compare Santhouse et al. 2000). I would like to discriminate between positive symptoms on the one hand and hallucinations on the other.

Positive symptoms or hallucinations can have quite different underlying causes— cerebral bleedings, trauma, tumours, vascular disorders, or possibly afferent (sensory) deprivation or epileptic foci. They are quite common although most often only reported subsequent to explicit questioning (Lenz 1909; Gloning et al. 1968; Becke 1904; Kölmel 1985; Vorster 1893; Lamy 1895; Laehr 1896). Wilbrand and Sänger (1904) discriminated between simple and complex positive symptoms. Simple positive symptoms consist, for example, of small or extended light flashes, simple features, or colour tinges, usually caused by disturbances of occipital cortex (Meadows 1974b; Pötzl 1928; Bodamer 1947; Gloning et al. 1962, 1968; Lenz 1905; Horrax and Putnam 1932; Kölmel 1984; Hughlings-Jackson 1889; Jackson 1932; Jaspers 1973; cf. also Critchley 1966; Kandinsky 1881). Complex positive symptoms consist in the perception of objects, complex patterns, humans, animals, or scenes and are the symptoms one normally associates with the noun ‘hallucination’. They are quite common after injuries of the occipital cortex, and always occur after the injury, while simple positive symptoms may precede the injury, as a warning sign of e.g. insufficient blood supply. Patients are always aware of the unreal nature of these perceptions, which they usually experience in defective (or blind) parts of their visual field, unlike psychotic patients, and hence the term pseudo-hallucinations might be better suited.

Five types of visual illusion are generally discriminated (e.g. Zihl and von Cramon 1986). The first is palinopsia or visual perseveration (Robinson and Watt 1947; Critchley 1951; Pötzl 1954; Bender et al. 1968). Patients perceive an object for several

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seconds or even minutes after the object has disappeared, or after they have performed a saccade to a new visual field position. Hence, this illusion is a kind of cortical afterimage (but without contrast reversal!). The underlying cause is always a bilateral defect, caused by infarctions or tumours (Critchley 1951; Bender et al. 1968) or else cortical hypoxia (Adler 1944). This type of illusion is always associated with other visual illusions or positive symptoms (Kinsbourne and Warrington 1963; Brust and Behrens 1977; Kömpf et al. 1983).

The second type of illusion is visual allesthesia, the illusory transportation of stimuli to (a mirror-symmetric part of) the contralateral visual half field—or, more rarely, in vertical direction into the corresponding quadrant of the visual field (Beyer 1895; Herrman and Pötzl 1928; Jacobs 1980; Gloning et al. 1968). The third type of illusion is metamorphopsia, i.e. short-lived but repeatedly occurring qualitative changes of perception, usually experienced as deformations in the form of objects, and often associated with changes in perceived orientation (Klopp 1951, 1955; Pichler 1957; Critchley 1966). Metamorphopsias are often associated with other illusions (Kömpf et al. 1983; Gloning et al. 1968; Hecaen and Angelergues 1963; Hoff and Pötzl 1935a).

The fourth type of illusion is visual dysmetropsia, i.e. a change in the perceived distance of objects, usually combined with a change of perceived size. Macropsia means that objects appear as larger; micropsia that they appear as smaller. Both are usually experienced in the contralesional hemifield (if at all) after defects in the temporooccipital cortex, and sometimes in migraine attacks (Gloning et al. 1968). The last illusion to be mentioned is polyopsia, or polyopia. It differs from diplopia caused, for example, by eye muscle disorders in that it persists even monocularly, after closure of one eye (Mingazzini 1908; Pötzl 1928; Hoff and Pötzl 1935b; Gloning et al. 1968; Kömpf et al. 1983; Bender 1945; Meadows 1973). Typically, several representations of an object are arranged around the real position of this object. The symptoms are usually caused by bilateral lesions of occipital cortex (Gloning et al. 1968).

Some types of epilepsy, especially of the temporal lobes, can lead to short visual hallucinations, as can electrical stimulation of the cortex during brain operations (Penfield 1947, 1965, 1972). Surprisingly, some patients undergoing electrical stimulation reported seeing objects and even scenes without any feelings of strangeness. These reports are consistent with the generally accepted belief that our feelings and thoughts rely on the electrical activity in neuronal ensembles of the central nervous system. Still, it is surprising that such a coarse manipulation as injecting a current into a circumscribed brain region leads to well-structured hallucinations.

These observations in humans are supported by better-controlled experiments in monkeys. As a first step, Salzman et al. (1990) identified cells in monkey area MT or V5 in the middle temporal lobe (see Fig. 7.5) sensitive for detecting one direction of stimulus motion. The monkey was trained to discriminate between different directions of stimulus motion and to indicate the corresponding direction after each stimulus presentation. Injection of small electrical currents during the presentation of these moving stimuli significantly changed the response behaviour of the monkey in favour of the

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direction signalled by the neurons stimulated electrically. Control experiments ruled out any direct influence of these cells and of this electrical stimulation on motor centres of the brain. This is to say that, obviously, injection of current, leading to rather unspecific stimulation probably of both excitatory and inhibitory neurons in a small part of cortex, cannot be distinguished by the cortex—and by its owner—from excitation through the correct channels, namely, the optic nerves, but changes perception of the outer world (not just the motor response). This result was corroborated by additional experiments in which the monkeys were required to make exactly this discrimination between purely visual stimuli and those accompanied by electrical cortical stimulation, and failed to distinguish between the two situations.

To conclude, analysis of visual signals can fail on very different levels of processing, from the retina to higher levels of cortical processing, producing a variety of different symptoms from blindness to disorders of contour or form perception, and from neglect of part of the world to production of perceptions without correlates in the outer world. Knowledge of the normal functioning of the (visual) brain helps us to understand these symptoms and syndromes, and the study of patients suffering from visual disturbances sheds some light on the processes underlying normal perception in healthy observers.

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