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

MAGNETIC STIMULATION IN STUDIES OF VISION AND ATTENTION 173

Stimulation to the parietal cortex reduced the ability to detect stimuli. Being able to reproduce neglect is an important step in modelling the phenomenon and one wonders whether a reaction time approach might increase the sensitivity of this particular assay. At the other end of the clinical scale, Olivieri et al. (1999) have reversed rather than reproduced a neuropsychological phenomenon. They studied patients with right or left hemisphere brain lesions and gave TMS to frontal or parietal cortex of the intact hemisphere 40 ms after the subjects were presented with unilateral or bilateral tactile stimuli to be detected. Those patients with right hemisphere lesions showed a reduction in extinction when TMS was given over the left frontal region, thus supporting the interpretation of Kinsbourne (1977) and Seyal et al. (1995).

Looking forward

The use of TMS has many applications in the vision sciences that await the attentions of researchers. The effects of learning and plasticity are good paradigms for investigating cortical change and the potential for combining TMS with other neuroimaging techniques will widen the scope of its utility in the study of vision.

Acknowledgements

The authors’ works are supported by the Medical Research Council, the Dr Hadwen Humane Research Trust, and the Royal Society.

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Part 5

Psychophysics: patient studies

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Chapter 7

Failures of visual analysis: scotoma, agnosia, and neglect

Manfred Fahle

Introduction

This chapter covers different types of failure to analyse the visual world, starting with the complete loss of vision, blindness, as well as blindness for circumscribed parts of the visual field, scotomata. These disturbances of visual perception can be adequately assessed by different perimetric methods. But vision is disturbed in some patients even though they are able to detect bright points—the method used to assess the visual field in clinical tests (perimetry). These patients will show normal results in perimetry in spite of severe problems of visual perception.

‘Vision’ is not just one single unified capacity, but has many components, partly subserved by different cortical areas. The number of separate and functionally distinct visual cortical areas may be above 40 or even 50. Defects of different areas may lead to specific symptoms characterized by relatively distinct deficits of visual perception, e.g. difficulties in discriminating colours, perceiving motion, seeing depth, or discriminating retinal image motion due to eye movements from motion due to object movements.

The second part of the chapter presents some syndromes characterized by difficulties in perceiving of and discriminating between different domains or submodalities of vision, while leaving most others intact, such as acquired inability to assess visual motion, or acquired colour blindness caused by cerebral damage (achromatopsia, see also Chapter 8, this volume).

On a more complex level of image analysis, the features detected in the different submodalities have to be bound together to segregate figures from their surround and to create object representations. I will argue that this process of object synthesis is heavily influenced by prior learning and experience and involves not only button-up processing governed by the sensory input but also top–down influences from ‘higher’ processing levels, making it difficult to find intact low-level analysis even if exclusively higher-level centres have been damaged.

Finally, the visual object representations formed in the cortex have to be matched with stored representations of objects in order to identify the class and possibly the identity of the object perceived. Problems in object formation are traditionally called agnosias, and a short survey of the different types will be given in the third part (see also Chapter 10,

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this volume). The individual steps of visual analysis may not be separated from each other as clearly as outlined above, due to the reflexive nature of cortical pattern analysis, with strong feedback from higher stages of analysis on earlier stages, but the deficits are still sufficiently different to justify—and to require—a distinction between these syndromes.

The chapter ends with an overview of the most astonishing examples—in my view— of failed visual perception: simultanagnosia; neglect; and Balint’s syndrome. These syndromes share the phenomenon that conscious perception of objects in (parts of) the peripheral visual field is absent in spite of intact stimulation of the primary visual cortex by these objects.

It would be a great advantage if precise knowledge about the normal function of the visual system and about visual perception could supply us with a sound framework to classify all the different symptoms encountered in patients and to precisely infer structural brain defects from behavioural symptoms, and vice versa. As it stands, such a detailed knowledge of the exact operations taking place during analysis of visual scenes is still fragmentary in spite of recent advances in neurobiological research. These advances, many of which are outlined in the first part of this book (see especially Chapters 1, 2, and 5), indeed help to understand the sometimes puzzling symptoms encountered in neuropsychological patients. I will try to fill in some gaps of knowledge by means of speculation in the following section to produce a consistent taxonomy of symptoms encountered in visual neuropsychology. Hopefully, the resulting picture will be at least consistent and plausible to some readers. Overall, the chapter will combine the theoretical background with clinical findings and with a description of at least some of the methods used to diagnose patients suffering from failures of visual analysis.

Blindness, scotomata, and visual information processing

Complete failure to see: blindness and scotomata

Certainly the most severe and fundamental disturbance of visual perception is blindness, the complete lack of subjective perception and of responsiveness to visual stimu- lation—hence an apparent failure of visual analysis. Blindness may occur not only for the entire visual field, but also parts of the field may become blind while others still elicit a perception. Hence, testing visual acuity, the resolution limit at the centre of the visual field, is not at all sufficient to assess visual function in patients suffering from lesions of the visual system. The entire visual field has to be tested. Circumscribed areas of ‘blindness’ are called scotomata. They can be the result of lesions on the level of the retina, optic nerve, lateral geniculate nucleus (LGN), optic radiation, or visual cortex.

On the retinal level radiation coming from visual objects is transformed to activate neurons and some early image processing is achieved such as enhancement of luminanceand hue-contrasts. Lesions on this level result in scotomata of just the affected eye. Defects in the right and left retinae usually subtend over noncorresponding visual field

FAILURES OF VISUAL ANALYSIS: SCOTOMA, AGNOSIA, AND NEGLECT 181

Fig. 7.1 Visual field defects (scotomata) caused by lesions at different levels of the visual system. Retinal lesions produce unilateral, incongruent scotomata in the affected eyes (and hemifields), and so do optic nerve defects (A). Lesions of the chiasm (B), optic tract, lateral geniculate nucleus (LGN), and optic radiation (D, E, F) produce lesions only in the contralesional hemifield that are roughly congruent, i.e. cover the same area when tested monocularly. The same is true for the primary, or striate, visual cortex, area 17. Lesions of extrastriate cortical areas often create blindness in one quadrant while the other one is spared, due to the fact that the representations of the upper and lower visual field are

separated in extrastriate cortical areas (cf. Fig. 7.7). From Fahle (2003b). (See Plate 1, colour plate section.)

portions of both eyes. These scotomata, for example, result from increased intraocular pressure (glaucoma) or from deficits in blood supply to the retina or optic nerve.

Lesions of the optic nerve peripheral to the partial crossing-over of fibres at the optic chiasm (Fig. 7.1) usually cause visual field defects for only one eye, while those beyond the chiasm, i.e. in the optic tract, lead to corresponding, or congruent scotomata in both eyes. The same is true for lesions located in the LGN, the optic radiation, and the visual cortex. Figure 7.1 summarizes the effects of lesions of the visual system on the visual fields of the patients. It should be noted that lesions of the optic tract and optic radiation generally produce scotomata less congruent in the two eyes than lesions of (primary) visual cortex do, since fibres from the two eyes seem to finally converge to form a retinotopic map only in the cortex (Walsh and Hoyt, 1969; see, however, Teuber et al. 1960). Hence fibres from corresponding locations of both retinae may not necessarily run very close to each other in the optic radiation.

The cortical representation of the fovea is located at the posterior pole of the brain, i.e. in the occipital cortex. The representation of the horizontal meridian, i.e. the horizontal line in the visual field through the fixation point, is represented in the depth of the calcarine fissure (Fig. 7.2) which runs through the medial bank of the occipital