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

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intellectual and language capabilities. The deficit of recognition is not limited to the naming of objects but is equally obvious in nonverbal testing, such as matching, copying, or discriminating between even simple visual stimuli. (Therefore, patients having problems with comparing the size of simple geometrical objects (e.g. Taylor and Warrington, 1973) can be considered as borderline to apperceptive agnosia, if their visual fields are intact.) These patients, suffering from apperceptive agnosias, are so severely handicapped that they often appear as blind to a casual observer. They perceive local colours and lines, but these do not constitute surfaces and objects (may be not unlike the situation in patients who achieve vision late in life by remedy of an inborn optical problem of the eyes; see Gregory and Wallace 1963; Fine et al. 2002). Hence they cannot bind together contours across breaks, e.g. caused by small occluding objects (see Grüsser and Landis 1991; Farah 1990), trace dotted lines, or avoid being distracted by scratches on a painting. Straight lines are better recognized than curved ones, while interrupted lines are worst (e.g. Goldstein and Gelb 1918; cf. also Corkin 1979; Mooney 1957; Russo and Vignolo 1967), indicating that the problem of binding together isolated contours can arise on different levels of processing. Real objects yield better results than photographs or line drawings, possibly due to the fact that patients rely partly on noncontour information such as colour or texture, hence on the ‘area’-system. Usually, the patients recognize objects based on haptic or auditory sensory information while not recognizing the same objects based on visual signals (Goldstein and Gelb 1918; Brown 1975; Rubens 1979; Adler 1944; Alexander and Albert 1983; Efron 1968; Benson and Greenberg 1969; Campion and Latto 1985; Campion 1987; Landis et al. 1982) and visual imagery seems to be preserved (Servos and Goodale 1995). Patients may develop a strategy of tracing contours by handor eye-movements and to recognize shapes from these trajectories.

Some patients seem to suffer from apperceptive agnosia only for stationary images, another indication for partly separated processing of motion information (see Chapter 5, this volume). It is no wonder that the patients suffering from an apperceptive agnosia in Lissauer’s (1890) terminology are unable to copy even simple drawings, as is described in detail in Chapter 10, this volume. This failure indicates that conscious perception does not have direct access to the neuronal representation of the outer world in the primary visual cortex since there a retinotopically ordered representation of the image exists, the copying of which should result in an acceptable copy of the ‘real’ object—at least during steady fixation.

The cause underlying these deficits is damage to the occipital and parietal cortex (sparing primary visual cortex), usually diffuse rather than focal, possibly affecting the white matter more than the grey matter of the brain (Landis et al. 1982).

Failure of object identification in associative agnosias: theory

Once the contours are grouped together to form surfaces and object-representations, the next step is to recognize these object representations. In patients suffering from associative agnosias, this step of analysis is selectively impaired. Konorski (1967) discriminated nine different object categories that together cover the entire field of

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object recognition and that have been described as being selectively impaired in neuropsychological patients: (1) small, manipulable objects; (2) large objects (e.g. furniture); (3) non-manipulable objects (e.g. houses); (4) facial identity; (5) emotional facial expression; (6) animals and animated objects; (7) letters and signs; (8) handwriting; (9) limb-positions. For all of these visual objects, isolating individual objects and discriminating them from the background, i.e. achieving figure–ground discrimination, is only a first step of object identification. The ultimate goal is not just to know that there are three separate objects, but also to know what these objects are.

Let’s assume the first two steps of visual analysis have been successfully solved: all relevant boundaries between objects have been identified, and those corresponding to different objects have been bound together, forming stable objector at least surfacerepresentations. (As mentioned above, this is a very difficult task without top-down information about possible ways of grouping, i.e. without stored templates of objects, so it may fail even though the neuronal mechanisms at the lower level are still intact.) But let’s assume that we have never before seen the object. It follows that we would not know what it is used for, what material it is made from, whether or not it is fragile, and so on—and, of course, we would not know its name. Familiar things are quite another matter: we have all this information stored in our brain. When looking at familiar objects the task is to find, on the basis of the current representation of an object we are looking at, the corresponding stored representation containing all this information. This may be easy for everyday objects, but is difficult for others that we know less well (what exact type of bird or of flower is it we are looking at?) as well as for objects seen from an unfamiliar perspective (cf. Warrington 1985).

For objects we have never seen before, we somewhat resemble patients suffering from associative agnosia: we can copy the object’s image well enough, contour by contour, as shown in Chapter 10, this volume, but we do not know what we are copying here. (Admittedly, we may have an idea due to similar objects we saw in the past.) In reality, the task is even more difficult for the patient since we still have the neuronal machinery in place that guides the search for relevant contours in the image and that steers the binding of elements, e.g. in analogy to other, similar objects we have encountered before. The patient, on the other hand, having lost the ability to store representations of visual objects or to access this storage, may not have a single blueprint of a visual object at hand and hence lacks the concept of a visual object. All image analysis in this patient and hence both contour detection and binding has to be driven in a strictly ‘bottom–up’ way, i.e. entirely on the basis of sensory information. That type of analysis is much more difficult and prone to error than a process guided by top–down influence, i.e. by a concept of what the object looks like.

I would propose that associative agnosias are failures of a patient’s ability to find a stored representation matching the representation of the visual object at hand (cf. Hécaen and Angelergues 1963; Critchley 1964; Gloning et al. 1968; Damasio 1985; Damasio et al. 1990a). As mentioned in the introduction to this chapter, we still do not know exactly how visual information is analysed in the healthy brain. But a growing

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body of evidence suggests the use of distributed processing in neuronal networks with strong feedback connections (e.g. Palm 1982; Chapter 2, this volume; the subsection ‘Visual information-processing in the cortex’). These types of networks are relatively tolerant to defects of single elements, as well as of noise in the input, and can complete stimuli that are incomplete. Feeding the raw primal contour information into this network would lead to an output corresponding to the most similar object representation stored so far—the processes of object formation and object recognition would not be separated but take place simultaneously, in the same network, and would moreover incorporate visual memory.

One may wonder why this type of associative neuronal network still needs the stage of contour extraction and binding of features and does not analyse the ‘raw’ retinal image on a point-by-point basis, as supplied by the optic nerve. A plausible answer evolved from research in artificial intelligence. The network only works reliably if similar objects produce similar inputs to the network. This requirement is not met by a pixel-by-pixel input directly representing the retinal activation. Processes such as contour extraction and contour binding are a necessary prerequisite for object formation and identification. The excitation of individual photoreceptors signalling an object depends strongly on the level of illuminance, on wavelength composition of the illuminant, on the distance of the object, its position in the visual field, and its orientation to name just some parameters. All these accidental features that are irrelevant for object recognition have to be eliminated as completely as possible. To concentrate on the form of the object, by extracting its outer borders, is obviously a good way to achieve the goal of constancy: coding the object in similar ways irrespective of the above-mentioned accidental parameters.

In summary, associative agnosias are characterized by a failure to associate the representation of a presently displayed object with a stored representation of this object, and by a lack of top–down control in pattern analysis. Will this view be consistent with the results of patient studies? The next subsection will bring the answer!

Associative agnosias: patient studies

Associative agnosias in a strict sense are characterized by four criteria: (1) no (absolute) scotomata—or else, as is the case in most agnosic patients, scotomata that will not, by themselves, prevent object recognition. (The extended lesions required for agnosias, unfortunately, are most often associated with visual field defects.); (2) difficulty or inability to recognize visually presented objects as evidenced not only in naming, but also in nonverbal tests; (3) preserved ability to separate figure and ground (hence no pronounced problems in navigating through the environment) and preserved ability to copy and match stimuli. This feature is in strong contrast with apperceptive agnosias; (4) Preserved ability to recognize and name objects or people through other sense modalities such as audition, touch, or smell, and intact intelligence (Rubens and Benson 1971; Albert et al. 1975; Bauer 1982; Hécaen and de Ajuriaguerra 1956; Levine 1978; Levine and Calvanio 1989; Mack and Boller 1977; Macrae and Trolle 1956;

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McCarthy and Warrington 1986; Pillon et al. 1981; Ratcliff and Newcombe 1982; Riddoch and Humphreys 1987a,b; Wapner et al. 1978; Lissauer 1890; Bender and Feldman 1972; de Renzi 1986b; Heidenhain 1927; Hécaen et al. 1974; Kertesz 1979; Humphreys and Riddoch 1987a, b; cf. also Davidoff and Wilson 1985).

Even though matching of objects as well as copying is intact, this does not mean that perception as such is normal, as is implied by Teuber’s (1968) famous definition of ‘a normal percept, stripped of its meaning’. This definition mirrors the view, of this time, of perception as a strictly feedforward hierarchical system. In a feedback system, however, where recognition is achieved through an interactive process involving different levels of processing, one would indeed expect simple ‘perception’ to be disturbed even if ‘only’ the process of object recognition is defective. Indeed, associative agnosics do suffer from serious impairments also of object perception (not just of object identification) such as impairments when copying or comparing drawings (Humphreys and Riddoch 1987a,b; cf. Levine and Calvanio 1989; Mendez 1988; Ratcliff and Newcombe 1982). Hence, the slavish line-by-line copying of associative agnostics is no surprise. The same is true for the fact that their speed of copying is far slower than that of normal observers, but differs little between ‘possible’ and ‘impossible’ (and hence unfamiliar) objects, while normal observers copy familiar objects much faster than unfamiliar ones. The performance of agnosic patients decreases markedly for tachistoscopic stimulus presentations as well as for photographs (compared to real objects) and especially for line drawings (probably due to lack of information from the ‘area’ system, for example about the colour and shading of objects; see subsections ‘Different levels and separate channels of visual information processing’ and ‘Neuronal mechanisms for contour and position detection’). They also experience great problems with binding together objects that are partly occluded or that are symbolized by (strongly) interrupted lines as in the Gollin-figures (Gollin 1960; we all probably use top–down information to solve this task) or in hidden figures (Corkin 1979). Additional— rather than incomplete—information, on the other hand, improves performance in some patients, e.g. aiding categorization by supplying (auditory) information about the context in which the objects normally occur (e.g. Duensing 1952, 1953; Rubens and Benson 1971; cf. also Taylor and Warrington 1971). Finally, at least some of the patients suffering from associative agnosia experience severe difficulties in reading since they have to analyse words in a letter-by-letter way (see the subsection ‘Alexia and optic aphasia’).

Farah (1990) differentiates between two types of agnosia: (1) agnosia for objects that have to be decomposed into parts and hence require fast serial processing while representation is easy since the parts are simple (e.g. words) and (2) agnosia for objects represented as complex entities, where representation is more difficult while no fast serial processing is required.

There has been some controversy about which type of cortical damage causes associative agnosias. Some authors favour as an explanation left-sided lesions of occipital/temporal cortex (Warrington 1985; Boudouresques et al. 1972; Feinberg et al. 1986; Pillon et al. 1981; Hécaen and de Ajuriaguerra 1956; McCarthy and Warrington

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1986 cf. also Bisiach et al. 1979b), while others postulate bilateral damage of the inferior temporo-occipital junction (Alexander and Albert 1983), or else of the right side (Boudouresques et al. 1979; Levine 1978), or find associative agnosias as the result of diffuse brain damage (Taylor and Warrington 1971).

Specific associative agnosias: prosopagnosia

Associative agnosias may relate to all types of objects, or else to certain types of objects only and to the discrimination between classes of objects or else between individuals. The best-known example for associative agnosia for a (more or less!) limited class of objects certainly is prosopagnosia (Bodamer 1947), the failure to recognize faces (e.g. Pallis 1955; Assal et al. 1984; Bornstein and Kidron 1959; Cole and Perez-Cruet 1964; De Renzi 1986a,c ; Kay and Levin 1982; Lhermitte and Pillon 1975; Nardelli et al. 1982; Shuttleworth et al. 1982; Beyn and Knyazeva 1962; Bornstein et al. 1969; Cohn et al. 1977; Warrington and James 1967; Newcombe 1979; Whiteley and Warrington 1977; Levine 1978; Kertesz 1979; Hécaen and Angelergues 1962, 1963; Benton and van Allen 1972; Benson et al. 1974; Benton 1980; Damasio et al. 1990b; Gloning et al. 1966; Hamsher et al. 1979; Landis et al. 1986, 1988; Mazzucchi and Biber 1983; Pevzner et al. 1962; Tranel et al. 1988; Sergent and Villemure 1989; Rondot et al. 1967). It seems not to be caused by the fact that faces are more complex and similar to each other than most other visual objects, i.e. just the most difficult to discriminate.

This deficit corresponds well to the fact that many neurons in inferotemporal cortex respond best to defined views of different faces (see Chapter 1, this volume). Face recognition may involve several, partially separable processes that could be disturbed independ- ently—such as identification of a face as distinct from other object categories versus identification of the facial expression of a person. Hence, even within prosopagnosia, there may be different subtypes: patients experiencing difficulties in recognizing either the identity of faces (Bruyer et al. 1983; Shuttleworth et al. 1982), or else the emotional expression (Kurucz and Feldmar 1979), or both (Etcoff 1984). Some patients lose the ability to discriminate individual animals (Newcombe 1979; Bornstein et al. 1969; Assal et al. 1984; Young 1988), or animal species (Bornstein 1963; Boudouresques et al. 1979; Damasio et al. 1982; Gomori and Hawryluk 1984; Lhermitte et al. 1972; Lhermitte and Pillon 1975; Pallis 1955), plants (Boudouresques et al. 1979; Gomori and Hawryluk 1984; Whiteley and Warrington 1977), or even to judge food (Damasio et al. 1982; Michel et al. 1986; Whiteley and Warrington 1977), clothing (Damasio et al. 1982; Shuttleworth et al. 1982), or discriminate makes of cars (Boudouresques et al. 1979; Damasio et al. 1982; Gomori and Hawryluk 1984; Lhermitte et al. 1972; Lhermitte and Pillon 1975; Newcombe 1979; Shuttleworth et al. 1982; cf. also Benton and van Allen 1968).

Objective measures such as event-related brain potentials (ERPs; see Chapter 3, this volume), the psychogalvanic skin response, or reaction times demonstrated better preservation of face recognition on the basis of matching tasks in some patients than would have to be expected (Bauer 1984; Tranel and Damasio 1985, 1988; Renault et al. 1989; Bauer and Verfaellie 1988; de Haan et al. 1987a, b; Bruyer et al. 1983; cf., however, Newcombe et al. 1989; and see also the discussion on discrimination without awareness

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in Chapter 9, this volume). Hence, similarly to neglect (see subsection ‘Evidence for preserved processing of visual input’), some object formation may take place unnoticed by the ‘owner’ of the brain in one form (memory-impaired) of prosopagnosia).

The defects underlying prosopagnosia always include the right hemisphere, and generally an additional left-sided defect of the parieto-occipital area, most often with a left superior quadrantanopia. (cf. Meadows 1974a,b; Torii and Tamai 1985; de Renzi et al. 1986.)

Alexia and optic aphasia

Alexia (or dyslexia), the inability to read other than in a letter-by-letter way with preserved writing and comprehension of spoken language, might be considered to be an agnosia for words—at least if it is not caused by visual field defects (e.g. Mesulam 1985; Damasio and Damasio 1983; Warrington and Shallice 1979; 1980). In patients, alexia is caused most often by concentric narrowing of the visual field, with a remaining central field diameter of less than approximately 3 , or else a reduction of visual acuity, rather than by defects of higher cortical areas. Therefore, perimetric testing (see the subsection ‘Visual field testing: perimetry’) is essential in all patients suffering from alexia. Even hemianopia, i.e. blindness in one visual hemifield (see the subsection ‘Complete failure to see: blindness and scotomata’), will produce strong disturbances of reading (see Zihl 1995).

More pertinent to the topic of agnosias is the ‘pure’ alexia caused by certain lesions of the left posterior cortex, as are most cases of object agnosia without prosopagnosia. Latency to decipher individual words increases linearly with word length in these patients (Bub et al. 1989). Since single letters can be analysed, this deficit may be closely related to simultanagnosia (Farah 1990; see the subsection on ‘Balint’s syndrome and simultanagnosia’).

As mentioned earlier (in the subsection ‘Associative agnosias: patient studies’), patients might be able to solve even the problem of matching representations of presently perceived objects with those encountered earlier in life but still be unable to tell the name of the object they are shown—while they can convey the identity of the object, e.g. by gesturing its use. But while, in the case of an associative agnosia, patients are unable to tell or gesture what the use of the object is, those patients able to solve the matching problem can tell us what the object is for—e.g. ‘something used for locking doors’ if they fail to find the word ‘key’. They are just unable to connect the stored representation with its name—as sometimes occurs to all of us when searching for a word or for the name of a person we meet and whom we have not seen in a while: we may know where the person lives, works, etc., but the name escapes us nevertheless. (This fact by itself is an indication that the names of objects might be stored in a part of the brain differing from the one analysing visual input—not an implausible assumption given the inability to understand language after lesions of Wernicke’s area in the superior temporal cortex, close to the auditory cortex.) To make sure that it is indeed the connection between the visual representation of an object and its name that is missing, for the above example, we can rattle a bunch of keys. If the patient then finds the correct noun, we can be sure that, indeed, only the connection between visual representations of objects and their names is missing—a syndrome called optic aphasia, or anomia, which is the inability to name objects.

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Optic aphasia is not a real agnosia, since recognition of objects is possible and can be indicated, e.g. by gesturing (Assal and Regli 1980; Coslett and Saffran 1989; Gil et al. 1985; Larrabee et al. 1985; Poeck 1984; Riddoch and Humphreys 1987b; Sittig 1927; Spreen et al. 1966). Unlike for agnostic patients, perception is relatively unimpaired by the visual quality of the stimuli (and hence is similar for real objects, photographs, and line drawings) (Gil et al. 1985; Larrabee et al. 1985; Lhermitte and Beauvois 1973; Poeck 1984; Riddoch and Humphreys 1987b). Patients are not impaired regarding visual perception in everyday life, while associative agnostics are handicapped, e.g. by not recognizing other people. Usually, the deficit is caused by posterior left hemisphere stroke (Lhermitte and Beauvois 1973).

Associative agnosias and especially optic aphasias represent failures of visual analysis on the very last steps in the sequence of processing. But, as we will see in the next section, even if the processing of single object-representations can be finished, patients may still be impaired in using the results of this analysis.

Balint’s syndrome and simultanagnosia

Defects of visual attention: Balint’s syndrome

Balint’s (1909) syndrome (see also Anton 1898, 1899; Holmes 1918a; Holmes and Horrax 1919; Michel et al. 1964; Friedman-Hill et al. 1995) is characterized by: (1) inability to perform directed voluntary saccades (eye movements) to targets in the periphery of the visual field (‘psychic paralysis of gaze’); (2) inability to grasp or point to visual targets and to follow a moving target by means of smooth-pursuit eye movements (‘optic ataxia’); and (3) inability to pay attention to more than one object at a time, while paying attention only to a central focus (and even the attended object may fade spontaneously over time). The patients behave as if blind—due to the bilateral narrowing of their field of attention and of the restriction of their exploratory space, similar to that in the simultanagnosias (see the next subsection). The underlying brain defect generally includes bilateral parieto-occipital cortex, possibly including destruction of underlying fibre tracts (Alexander and Albert 1983).

Failures to perceive more than one object at a time: simultanagnosia and spatial disorientation

Definition, symptoms, and tests

Patients suffering from simultanagnosia (Wolpert 1924) accurately perceive individual details or elements of a visual scene but are unable to combine these details to a meaningful entity. Hence, there are similarities to deficits in visual exploration, as stressed by some authors (Zihl and von Cramon 1986), and, in a way, to apperceptive agnosia, the failure to combine individual contours (rather than objects). Some authors use the term in a more literal sense, as the inability to perceive more than one object, or element, at any given time (Luria 1959). This symptom is usually part of Balint’s syndrome (Balint 1909; see the preceding subsection). Single objects and faces are

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Fig. 7.17 The telegraph boy. Patients suffering from simultanagnosia or Balint’s syndrome will only report the features they are presently looking at but will not be able to understand the contents of the scene.

readily identified and recognized but, in stimuli displaying several objects, only one object is recognized at a time (cf. Girotti et al. 1982; Rizzo and Hurtig 1987; Holmes 1918a,b; Holmes and Horrax 1919; Kase et al. 1977; Kosslyn et al. 1990; Luria 1959; Luria et al. 1963; Tyler 1968; Williams 1970; cf. also Godwin-Austen 1965).

A widely used test for simultanagnosia is the telegraph-boy picture (Fig. 7.17). Simultanagnosic patients only perceive parts of the picture without understanding the scene. For obvious reasons, these patients also suffer from severe reading problems (alexia; see the eponymous subsection) and report, for example, that words would

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pop out from the page and then disappear, being replaced by other portions of text. The patients are unable to count the number of objects presented simultaneously, but perceive a number of elements simultaneously if they are grouped together to form an object (Girotti et al. 1982; Godwin-Austen 1965; Holmes 1918a,b; Holmes and Horrax 1919; Williams 1970). The patients, similarly to those suffering from apperceptive agnosia, may be unable to identify stimuli, or may guess an object’s identity on the basis of one feature they recognized. Due to their limited analysis of the visual surround, restricting the region of space and the number of objects they attend to at any one time, the patients may act as if blind, walking into obstacles and groping for objects. Furthermore, the patients may not be able to localize objects even if they identified them. This symptom fits in very well with the localization of the lesion: the occipitoparietal cortex where the visual world is represented in partly egocentric coordinates and changes less across saccades (as opposed to a retinotopic coordinate system; see the subsection ‘Failures to achieve a stable representation of extrapersonal space’ and the next subsection).

A hypothesis about the neuronal mechanisms in simultanagnosia

It should be kept in mind that humans change fixation more than once per second— hence the representation of the visual world changes position at the same frequency in the primary visual cortex. Hence, a more ‘durable’ representation is required that is at least partially stable over eye movements. This representation should also be able to synthesize, over subsequent eye movements, a reasonably detailed representation of the visual world. Single-cell recordings in the parietal lobe of monkeys indeed revealed neurons coding objects in partly heador world-centred rather than retina-centred coordinates (cf. Andersen et al. 1997; Chapter 5, this volume; cf. also the subsection ‘Failure to achieve a stable representation of extrapersonal space’). It fits in well with this view of visual information-processing that the parietal cortex is part of the dorsal processing stream that is often called the ‘where’ system.

I would like to propose that a defect in the egocentric representation would not only cause the inability to localize objects across eye movements, but may also cause the ‘main’ symptom of simultanagnosia—loss of the ability to store object representations across eye movements. As a consequence of the inability to store representation even for short periods the patient is unable to create a body-centred representation of the world (see the subsection ‘Failures to achieve a stable representation of extrapersonal space’ and Karnath et al. 2002; cf. Robertson et al. 1997). Intuitively, it also fits in very well that moving objects pose greater problems for these patients than stationary ones. If only a retinotopic representation is left, cortical object representations will undergo massive distortions if the object moves from the centre to the periphery. The finding that simultanagnosic patients are better able to perceive several objects if these are close together (hence do not require eye movements to be perceived in sufficient detail) would be compatible with this hypothesis. However, there are indications that not only eye movements, but also shifts of attention may lead to an extinction of the newly attended object and to an extinction of the previous concept (Luria 1959).

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Many of the above arguments would also apply to the Balint syndrome (see eponymous section).

Visual disorientation in simultanagnosia

Another symptom of these patients is their visual disorientation, the inability to keep track of the position of a previous stimulus while analysing a new object and to code spatial relations between objects. The visual system codes spatial relations within objects differently from relations between objects. Therefore, simultanagnosic patients can preserve the ability to identify single objects, unlike those patients suffering from apperceptive agnosia.

The inability to code spatial relations is also apparent in the copies that simultanagnosic patients produce of drawings, which have an ‘exploded’ look even though the patient easily recognized the object (quite different from associative agnosiacs who produce exact copies without object recognition). As in the case of neglect patients, there has been some debate whether the deficit in simultanagnosia is primarily one of attention or of representation, but this seems more a semantic than a genuine discrepancy as we will see in the section on neglect (cf. Posner et al. 1984; Bisiach et al. 1979a; Shallice 1989; Farah 1990). The inability to keep track of previous positions will inevitably lead to problems of visual exploration and to a piecemeal type of perception (cf. Zihl and von Cramon 1986; Pötzl 1928; Newcombe et al. 1987).

Different subtypes of simultanagnosia

Some authors doubt the existence of an isolated deterioration in the detection of a whole (scene) with intact detection of its details, as postulated in simultanagnosia (Bay 1950; Weigl 1964; Rubens 1979), and some discriminate between two types of simultanagnosia: (1) dorsal simultanagnosia, a deficit in the spatial system that leads to the inability to attend to more than one item at a time (while single multipart objects, e.g. words, can still be perceived); (2) ventral simultanagnosia: inability to recognize more than one object at a time (however, since the attentional system is intact, patients have no problems in navigation; Farah 1990).

A subgroup of simultanagnosic patients, called ‘ventral simultanagnosics’ by Farah (1990), as opposed to the ‘dorsal simultanagnosics’ described above, suffer from lesions in the left inferior temporo-occipital region. By and large, symptoms of the two patient groups of ventral and dorsal simultanagnosias are very similar (Bauer 1993; de Renzi 1982; Frederiks 1969; Kertesz 1987; Williams 1970). But an important difference is that the patients suffering from ventral simultanagnosia due to unilateral lesions, fail to recognize multiple objects (as the bilateral parieto-occipital patients with the dorsal simultanagnosia do), but are able to see multiple objects and hence can count and manipulate objects and walk around without running into obstacles. This group of simultanagnosic patients seems still to possess an egocentric map of the outer world, but to have problems with moving ‘attention’ (or conscious analysis) from one object to the next. Reading is possible in a letter-by-letter way—synthesizing words by sequential analysis of letters.