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A Disorder of Lightness Discrimination in a Case of Visual Form Agnosia
NOTE A DISORDER OF LIGHTNESS DISCRIMINATION IN A CASE OF VISUAL FORM AGNOSIA A.D. Milner1 and C.A. Heywood 2 CPsychological Laboratory, University of St. Andrews; 2 Dept of Experimental Psychology, University of Oxford)
INTRODUCTION
A subgroup of brain-damaged patients who suffer from a visual object-recognition disorder have been found to perform poorly even on a simple task of shape discrimination (Efron, 1969; Warrington, 1986). Such cases of "visual form agnosia" (Benson and Greenberg, 1969) are consequently distinguished from patients who suffer from "higher" varieties of visual agnosia (Humphreys and Riddoch, 1987; Warrington, 1985). In one recent account (Warrington, 1985), the disorder has in fact been classified as "pseudoagnosic", along with those patients whose poor recognition can be attributed to specific sensory deficits. We report here some of our findings in a patient whose visual deficits are very similar to such previously-described cases of visual form agnosia (e.g. Efron, 1969; Campion and Latto, 1985). BRIEF CASE REPORT
Our subject (DF), aged 34, whom we shall describe in detail elsewhere (Milner et al., manuscript in preparation) had suffered an episode of carbon monoxide poisoning 8 months prior to the tests we shall describe. DF presented with severe visual incapacity, including an inability to recognize objects, constructional apraxia, and restricted gaze; she also suffered from poor memory, acalculia, and a reduced spontaneity of speech and action. However she was neither dysphasic nor demented; there was no neglect; and there was no evidence of tactile agnosia. Sensory tests revealed adequate visual acuity (the contrast sensitivity function for sinusoidal gratings showed normal detection at 10-20 cpd- the highest spatial frequencies tested- though there was impairment at lower frequencies); preserved central visual fields (though an upper right quadrant scotoma was evident beyond 30° eccentricity); and clear though impaired stereopsis, motion perception, and colour vision (but in each case DF was unable to identify the shape that lay in depth, moved, or was differentiated by colour, respectively). Measurements of the PlOO evoked potential to a reversing chessboard pattern were of normal latency and amplitude. DF performed poorly on Efron's (1969) test of discrimination between squares and rectangles matched for area, whether asked to name them singly or make same/ different simultaneous comparisons. Scores only exceeded chance at side-ratios of 2:1 or greater (naming) or 6:1 (matching), and did not reach 90% even at the easiest ratio (6:1). LIGHTNESS AND COLOUR TESTS
We tested DF on the same tests of discrimination between hues and between achromatic greys as used by Heywood, Wilson and Cowey (1987); in all cases the stimulus materials consisted of samples derived from the Munsell series, within which adjacent Cortex, (1989) 25, 489-494
A.D. Milner and C.A. Heywood
490
OF: hues
Fig. 1 -
OF: greys
The Farnsworth-Munsell Test results for patient DF.
Fig. 2- The mean ordering-error scores for the 4 sub-series of the 100-Hue test, with the mean score for the equivalent achromatic series. DF's data are shown alongside those of the achromatopsic patient CB (Heywood eta!., 1987). The error bars in each case refer to the standard error of the mean. Farnsworth-Munsell test results
r---------------------, DF
r---------------------, CB
15
15
~
0
()
UJ
10
5
0
5
85~21 22-4243-6364-84
1-22
85-2122-4243-6364-84
1-22
HUES
GREYS
HUES
GREYS 0
Visual form agnosia
491 Fig. 3 - Performance in "oddity" tests with Munsell stimuli.
ODDITY TESTING HUES
100 80 60 40 u
20
Q)
.._ .._ 0
2
u
3
4
5
6
?P.
8
9
10
GREYS
100
/ o,,',,, -----o _,,/ o----- o-----o----- o
80
c~_____ //
60
/
40
7
steps
//
0
I
0
20 2
3
4
5
6
7
8
steps
9
10
stimulus items are subjectively equally-spaced. First, the standard Farnsworth-Munsell 100-Hues Test, was used. The test requires the subject to arrange in sequence four separate sets of small hue samples (matched for reflectance and saturation), adjacent values of which differ in equal JND steps. The charts in Figure I present the ordering errors (calculated by the standard scoring procedure) in polar fashion around the colour circle. This task was performed sub-normally by DF (Figure I a), but nonetheless far better than by the previously-tested achromatopsic patient CB (Heywood et al., I987). By contrast, DF performed the comparable test using the achromatic series (shades of grey) very poorly, as shown in Figure I b. The results of the two patients are contrasted quantitatively in Figure 2. Secondly, we tested DF on a less cognitively-demanding "oddity" task, using two sets of II Munsell "swatches" (7.5 em X 5 em) differing in hue (a red-orange and a greenyellow series), and a comparable series of achromatic swatches. The subject was required on each trial to indicate which of three swatches (two alike, one different) was the "odd man out". The three stimuli for a given trial were selected from an li-swatch series constructed in 1.25 JND steps of hue, or the equivalent along the grey-scale. For each task (two hue sets and the grey set), there were 110 test trials. Figure 3 shows the data for DF as
A.D. Milner and C.A. Heywood
492
reds-oranges
9
rho:0.94
•
~
<(
•
(/)
z
~1
(/)
w a:
•
•
yellows-greens
9
•
rho:0.97
•
z5
a: w
•
5
•
•
•
• 5
9 Achromatic
9
•
•
•
•
•
•
•
•
• •
5
9
rho:0.25
•
•
5
•
•
•
• I
5 STIMULUS RANK
I
9
Fig. 4 - Rank-ordering by DF of Munsell "swatches" differing either in hue only or in reflectance only.
compared with those of the achroma top sic patient CB. Chance performance would be 33% correct. (N .B. Since all stimuli were presented equally-often with all others, the data for the larger step-differences are based on relatively few pairings, and are accordingly less reliable). DF's performance was uniformly above-chance when comparing hues (though it should be noted that normal subjects are virtually error-free on the task), but had an extremely high threshold with the achromatic stimuli. Following oddity testing, DF was asked to place the swatches in rank order; in each case the two extreme values were given to her and she was asked to arrange the remaining 9 stimuli between them. She produced near-correct sequences for the two hue series, but a virtually random one for the grey series (Figure 4). The Spearman rank correlation coefficients for the two hue series were significant at the p< .01 level, whilst that for the grey series was non-significant. DISCUSSION
Clearly DF has a very severe deficit in discrimination along the grey scale under the present testing conditions (i.e. in a relatively low spatial-frequency range), in doubledissociation with the achromatopsic patient CB (Heywood et al., 1987), who performed comparatively well on such tasks. [Likewise, the pattern of impairment in optic neuritis is the opposite one of poorer chromatic than luminance-based discrimination (Mullan and Plant, 1986) as well as typically the presence of a slowed PIOO]. Although DF's deficit was not absolute (e.g. her Farnsworth-Munsell achromatic performance was still better than chance), such a loss of discrimination must nonetheless render her vision heavily reliant upon chromatic distinctions. In an extreme case this could be compared to a normal
Visual form agnosia
493
observer having to face a near-equiluminant visual world. Equiluminant displays cause severe difficulties in seeing stable contours; real and apparent motion; depth and solidity (through a variety of channels); the linking of features; and even figure/ground relationships (Gregory, 1977; Livingstone and Rubel, 1987; Troscianko, 1987). These are all powerful precursors to the object-recognition process. Certainly the observed deficit in achromatic discrimination offers an explanation of DF's subjective difficulties in segregating visible objects and in seeing clear contours. It may thereby also provide a partial explanation of her recognition difficulties. However, it is not possible to account fully for the range and severity of DF's visual form agnosia in these terms. Along with previous reports (Zihl, von Cramon and Mai, 1983; Warrington, 1986; Heywood et al., 1987), the present observations confirm that there must be a high degree of independence in the human brain between the systems processing different elementary stimulus features. They should be considered together with an earlier description of a patient who had a wavelength-contingent acuity loss without agnosia (Rovamo, Hyvarinen and Hari, 1982), and are consistent with recent work on the physiology and anatomy of these systems in the monkey (Livingstone and Rubel, 1988; Maunsell and Newsome, 1987; Zeki and Shipp, 1988). There is a spectrally broad-band system with low spatial resolution identifiable with the magnocellular retino-geniculo-striate pathway, and a separate parvocellular system which seems to carry the "colour" and "detail" information into the striate cortex. At this point a divergence within the parvocellular stream between systems specialized for carrying wavelength and orientation information respectively appears to occur (Livingstone and Rubel, 1984). An initial hypothesis which might explain many of DF's visual deficits is that her principal visual pathology relates to the magnocellular channel. It is possible that this is selectively vulnerable where it is physically most separate from the parvocellular system, namely in the lateral geniculate nucleus or even in the optic tract (Reese and Cowey, 1988). A major puzzle, however, would be why form discrimination is lost if there has been a survival of both branches of the parvocellular stream, i.e. the orientation-selective high-spatial-frequency channel as well as the colourselective channel. A possibility which we are now examining is whether there is "covert" knowledge of form in DF, which is inaccessible to her awareness (Milner, 1989). ABSTRACT
Benson and Greenberg (1969) described an "agnosic" patient whose severe visual recognition disorder could be accounted for in terms of a deficit in the perception of shape. We report here on a recent case of this disorder (visual form agnosia), and have found that she performs very poorly on tasks of discriminating shades of grey, although she is able to discriminate between hues. This sensory deficit helps to explain some of her perceptual difficulties; it also provides further evidence for parallel feature-processing in the human brain complementary to and consistent with recent physiological data on the visual cortex in animals. Acknowledgements. The authors are grateful to Prof. A. Cowey and Drs. E. DeHaan and D.l. Perrett for their helpful comments on an early draft of this paper. REFERENCES
D.F., and GREENBERG, J.P. Visual form agnosia. A specific defect in visual discrimination. Archives of Neurology, 20: 82-89, 1969. CAMPION, J., and LATIO, R. Apperceptive agnosia due to carbon monoxide poisoning. An interpretation based on critical band masking from disseminated lesions. Behavioural Brain Research, 15: 227-240, 1985. EFRON, R. What is perception? Boston Studies in the Philosophy of Science, 4: 137-173, 1969. GREGORY, R.L. Vision with isoluminant colour contrast: 1. A projection technique and observations. Perception, 6: 113-119, 1977. BENSON,
494
A.D. Milner and CA. Heywood
HEYWOOD, C.A., WILSON, B., and CowEY, A. A case study of cortical colour "blindness" witb relatively intact achromatic discrimination. Journal of Neurology, Neurosurgery and Psychiatry, 50: 22-29, 1987. HUMPHREYS, G.W., and R!DDOCH, M.J. The fractionation of visual agnosia. In G.W. Humphreys and M.J. Riddoch (Eds.), Visual Object Processing: A Cognitive Neuropsychological Approach. Hove: Erlbaum, 1987, Ch. 10, pp. 281-306. LIVINGSTONE, M.S., and HUBEL, D.H. Anatomy and physiology of a color system in the primate visual cortex. Journal of Neuroscience, 4: 309-356, 1984. LIVINGSTONE, M.S., and HUBEL, D.H. Psychophysical evidence for separate channels for tbe perception of form, color, movement, and depth. Journal of Neuroscience, 7: 3416-3468, 1987. LIVINGSTONE, M., and HUBEL, D. Segregation of form, color, movement, and depth: anatomy, physiology, and perception. Science, 240: 740-749, 1988. MAUNSELL, J.H.R., and NEWSOME, W.T. Visual processing in monkey extrastriate cortex. Annual Review of Neuroscience, 10: 363-401, 1987. MILNER, A.D. Implicit knowledge in visual form agnosia: a preliminary study. Paper presented to Experimental Psychology Society: Swansea, April 1989. MULLAN, K.T., and PLANT, G.T. Colour and luminance vision in human optic neuritis. Brain, 109: 1-13, 1986. REESE, B.E., and COWEY, A. Segregation of functionally distinct axons in the monkey's optic tract. Nature, 331: 350-351, 1988. RoVAMO, J., HYVJi.RINEN, L., and HARI, R. Human vision without luminance-contrast system: selective recovery of the red-green colour-contrast system from acquired blindness. Documenta Ophthalmologica Proceedings Series, 33: 457-466, 1982. TROSCIANKO, T. Perception of random-dot symmetry and apparent movement at and near isoluminance. Vision Research, 27: 547-554, 1987. WARRINGTON, E.K. Agnosia: the impairment of object recognition. In J.A.M. Frederiks (Ed.), Handbook of Clinical Neurology, 1(45). Amsterdam: Elsevier, 1985, Ch. 23, pp. 333-349. WARRINGTON, E.K. Visual deficits associated with occipital lesions in man. Experimental Brain Research, Supplementum Series, 11: 247-261, 1986. ZEKI, S., and SHIPP, S. The functional logic of cortical connections. Nature, 335: 311-317, 1988. ZIHL, J., von CRAMON, D., and MAr, N. Selective disturbance of movement vision after bilateral brain damage. Brain, 106: 313-340, 1983. Dr. A.D. Milner, Psychological Laboratory, The University, St. Andrews, Fibe KY16 9JU, Scotland.
INTRODUCTION
A subgroup of brain-damaged patients who suffer from a visual object-recognition disorder have been found to perform poorly even on a simple task of shape discrimination (Efron, 1969; Warrington, 1986). Such cases of "visual form agnosia" (Benson and Greenberg, 1969) are consequently distinguished from patients who suffer from "higher" varieties of visual agnosia (Humphreys and Riddoch, 1987; Warrington, 1985). In one recent account (Warrington, 1985), the disorder has in fact been classified as "pseudoagnosic", along with those patients whose poor recognition can be attributed to specific sensory deficits. We report here some of our findings in a patient whose visual deficits are very similar to such previously-described cases of visual form agnosia (e.g. Efron, 1969; Campion and Latto, 1985). BRIEF CASE REPORT
Our subject (DF), aged 34, whom we shall describe in detail elsewhere (Milner et al., manuscript in preparation) had suffered an episode of carbon monoxide poisoning 8 months prior to the tests we shall describe. DF presented with severe visual incapacity, including an inability to recognize objects, constructional apraxia, and restricted gaze; she also suffered from poor memory, acalculia, and a reduced spontaneity of speech and action. However she was neither dysphasic nor demented; there was no neglect; and there was no evidence of tactile agnosia. Sensory tests revealed adequate visual acuity (the contrast sensitivity function for sinusoidal gratings showed normal detection at 10-20 cpd- the highest spatial frequencies tested- though there was impairment at lower frequencies); preserved central visual fields (though an upper right quadrant scotoma was evident beyond 30° eccentricity); and clear though impaired stereopsis, motion perception, and colour vision (but in each case DF was unable to identify the shape that lay in depth, moved, or was differentiated by colour, respectively). Measurements of the PlOO evoked potential to a reversing chessboard pattern were of normal latency and amplitude. DF performed poorly on Efron's (1969) test of discrimination between squares and rectangles matched for area, whether asked to name them singly or make same/ different simultaneous comparisons. Scores only exceeded chance at side-ratios of 2:1 or greater (naming) or 6:1 (matching), and did not reach 90% even at the easiest ratio (6:1). LIGHTNESS AND COLOUR TESTS
We tested DF on the same tests of discrimination between hues and between achromatic greys as used by Heywood, Wilson and Cowey (1987); in all cases the stimulus materials consisted of samples derived from the Munsell series, within which adjacent Cortex, (1989) 25, 489-494
A.D. Milner and C.A. Heywood
490
OF: hues
Fig. 1 -
OF: greys
The Farnsworth-Munsell Test results for patient DF.
Fig. 2- The mean ordering-error scores for the 4 sub-series of the 100-Hue test, with the mean score for the equivalent achromatic series. DF's data are shown alongside those of the achromatopsic patient CB (Heywood eta!., 1987). The error bars in each case refer to the standard error of the mean. Farnsworth-Munsell test results
r---------------------, DF
r---------------------, CB
15
15
~
0
()
UJ
10
5
0
5
85~21 22-4243-6364-84
1-22
85-2122-4243-6364-84
1-22
HUES
GREYS
HUES
GREYS 0
Visual form agnosia
491 Fig. 3 - Performance in "oddity" tests with Munsell stimuli.
ODDITY TESTING HUES
100 80 60 40 u
20
Q)
.._ .._ 0
2
u
3
4
5
6
?P.
8
9
10
GREYS
100
/ o,,',,, -----o _,,/ o----- o-----o----- o
80
c~_____ //
60
/
40
7
steps
//
0
I
0
20 2
3
4
5
6
7
8
steps
9
10
stimulus items are subjectively equally-spaced. First, the standard Farnsworth-Munsell 100-Hues Test, was used. The test requires the subject to arrange in sequence four separate sets of small hue samples (matched for reflectance and saturation), adjacent values of which differ in equal JND steps. The charts in Figure I present the ordering errors (calculated by the standard scoring procedure) in polar fashion around the colour circle. This task was performed sub-normally by DF (Figure I a), but nonetheless far better than by the previously-tested achromatopsic patient CB (Heywood et al., I987). By contrast, DF performed the comparable test using the achromatic series (shades of grey) very poorly, as shown in Figure I b. The results of the two patients are contrasted quantitatively in Figure 2. Secondly, we tested DF on a less cognitively-demanding "oddity" task, using two sets of II Munsell "swatches" (7.5 em X 5 em) differing in hue (a red-orange and a greenyellow series), and a comparable series of achromatic swatches. The subject was required on each trial to indicate which of three swatches (two alike, one different) was the "odd man out". The three stimuli for a given trial were selected from an li-swatch series constructed in 1.25 JND steps of hue, or the equivalent along the grey-scale. For each task (two hue sets and the grey set), there were 110 test trials. Figure 3 shows the data for DF as
A.D. Milner and C.A. Heywood
492
reds-oranges
9
rho:0.94
•
~
<(
•
(/)
z
~1
(/)
w a:
•
•
yellows-greens
9
•
rho:0.97
•
z5
a: w
•
5
•
•
•
• 5
9 Achromatic
9
•
•
•
•
•
•
•
•
• •
5
9
rho:0.25
•
•
5
•
•
•
• I
5 STIMULUS RANK
I
9
Fig. 4 - Rank-ordering by DF of Munsell "swatches" differing either in hue only or in reflectance only.
compared with those of the achroma top sic patient CB. Chance performance would be 33% correct. (N .B. Since all stimuli were presented equally-often with all others, the data for the larger step-differences are based on relatively few pairings, and are accordingly less reliable). DF's performance was uniformly above-chance when comparing hues (though it should be noted that normal subjects are virtually error-free on the task), but had an extremely high threshold with the achromatic stimuli. Following oddity testing, DF was asked to place the swatches in rank order; in each case the two extreme values were given to her and she was asked to arrange the remaining 9 stimuli between them. She produced near-correct sequences for the two hue series, but a virtually random one for the grey series (Figure 4). The Spearman rank correlation coefficients for the two hue series were significant at the p< .01 level, whilst that for the grey series was non-significant. DISCUSSION
Clearly DF has a very severe deficit in discrimination along the grey scale under the present testing conditions (i.e. in a relatively low spatial-frequency range), in doubledissociation with the achromatopsic patient CB (Heywood et al., 1987), who performed comparatively well on such tasks. [Likewise, the pattern of impairment in optic neuritis is the opposite one of poorer chromatic than luminance-based discrimination (Mullan and Plant, 1986) as well as typically the presence of a slowed PIOO]. Although DF's deficit was not absolute (e.g. her Farnsworth-Munsell achromatic performance was still better than chance), such a loss of discrimination must nonetheless render her vision heavily reliant upon chromatic distinctions. In an extreme case this could be compared to a normal
Visual form agnosia
493
observer having to face a near-equiluminant visual world. Equiluminant displays cause severe difficulties in seeing stable contours; real and apparent motion; depth and solidity (through a variety of channels); the linking of features; and even figure/ground relationships (Gregory, 1977; Livingstone and Rubel, 1987; Troscianko, 1987). These are all powerful precursors to the object-recognition process. Certainly the observed deficit in achromatic discrimination offers an explanation of DF's subjective difficulties in segregating visible objects and in seeing clear contours. It may thereby also provide a partial explanation of her recognition difficulties. However, it is not possible to account fully for the range and severity of DF's visual form agnosia in these terms. Along with previous reports (Zihl, von Cramon and Mai, 1983; Warrington, 1986; Heywood et al., 1987), the present observations confirm that there must be a high degree of independence in the human brain between the systems processing different elementary stimulus features. They should be considered together with an earlier description of a patient who had a wavelength-contingent acuity loss without agnosia (Rovamo, Hyvarinen and Hari, 1982), and are consistent with recent work on the physiology and anatomy of these systems in the monkey (Livingstone and Rubel, 1988; Maunsell and Newsome, 1987; Zeki and Shipp, 1988). There is a spectrally broad-band system with low spatial resolution identifiable with the magnocellular retino-geniculo-striate pathway, and a separate parvocellular system which seems to carry the "colour" and "detail" information into the striate cortex. At this point a divergence within the parvocellular stream between systems specialized for carrying wavelength and orientation information respectively appears to occur (Livingstone and Rubel, 1984). An initial hypothesis which might explain many of DF's visual deficits is that her principal visual pathology relates to the magnocellular channel. It is possible that this is selectively vulnerable where it is physically most separate from the parvocellular system, namely in the lateral geniculate nucleus or even in the optic tract (Reese and Cowey, 1988). A major puzzle, however, would be why form discrimination is lost if there has been a survival of both branches of the parvocellular stream, i.e. the orientation-selective high-spatial-frequency channel as well as the colourselective channel. A possibility which we are now examining is whether there is "covert" knowledge of form in DF, which is inaccessible to her awareness (Milner, 1989). ABSTRACT
Benson and Greenberg (1969) described an "agnosic" patient whose severe visual recognition disorder could be accounted for in terms of a deficit in the perception of shape. We report here on a recent case of this disorder (visual form agnosia), and have found that she performs very poorly on tasks of discriminating shades of grey, although she is able to discriminate between hues. This sensory deficit helps to explain some of her perceptual difficulties; it also provides further evidence for parallel feature-processing in the human brain complementary to and consistent with recent physiological data on the visual cortex in animals. Acknowledgements. The authors are grateful to Prof. A. Cowey and Drs. E. DeHaan and D.l. Perrett for their helpful comments on an early draft of this paper. REFERENCES
D.F., and GREENBERG, J.P. Visual form agnosia. A specific defect in visual discrimination. Archives of Neurology, 20: 82-89, 1969. CAMPION, J., and LATIO, R. Apperceptive agnosia due to carbon monoxide poisoning. An interpretation based on critical band masking from disseminated lesions. Behavioural Brain Research, 15: 227-240, 1985. EFRON, R. What is perception? Boston Studies in the Philosophy of Science, 4: 137-173, 1969. GREGORY, R.L. Vision with isoluminant colour contrast: 1. A projection technique and observations. Perception, 6: 113-119, 1977. BENSON,
494
A.D. Milner and CA. Heywood
HEYWOOD, C.A., WILSON, B., and CowEY, A. A case study of cortical colour "blindness" witb relatively intact achromatic discrimination. Journal of Neurology, Neurosurgery and Psychiatry, 50: 22-29, 1987. HUMPHREYS, G.W., and R!DDOCH, M.J. The fractionation of visual agnosia. In G.W. Humphreys and M.J. Riddoch (Eds.), Visual Object Processing: A Cognitive Neuropsychological Approach. Hove: Erlbaum, 1987, Ch. 10, pp. 281-306. LIVINGSTONE, M.S., and HUBEL, D.H. Anatomy and physiology of a color system in the primate visual cortex. Journal of Neuroscience, 4: 309-356, 1984. LIVINGSTONE, M.S., and HUBEL, D.H. Psychophysical evidence for separate channels for tbe perception of form, color, movement, and depth. Journal of Neuroscience, 7: 3416-3468, 1987. LIVINGSTONE, M., and HUBEL, D. Segregation of form, color, movement, and depth: anatomy, physiology, and perception. Science, 240: 740-749, 1988. MAUNSELL, J.H.R., and NEWSOME, W.T. Visual processing in monkey extrastriate cortex. Annual Review of Neuroscience, 10: 363-401, 1987. MILNER, A.D. Implicit knowledge in visual form agnosia: a preliminary study. Paper presented to Experimental Psychology Society: Swansea, April 1989. MULLAN, K.T., and PLANT, G.T. Colour and luminance vision in human optic neuritis. Brain, 109: 1-13, 1986. REESE, B.E., and COWEY, A. Segregation of functionally distinct axons in the monkey's optic tract. Nature, 331: 350-351, 1988. RoVAMO, J., HYVJi.RINEN, L., and HARI, R. Human vision without luminance-contrast system: selective recovery of the red-green colour-contrast system from acquired blindness. Documenta Ophthalmologica Proceedings Series, 33: 457-466, 1982. TROSCIANKO, T. Perception of random-dot symmetry and apparent movement at and near isoluminance. Vision Research, 27: 547-554, 1987. WARRINGTON, E.K. Agnosia: the impairment of object recognition. In J.A.M. Frederiks (Ed.), Handbook of Clinical Neurology, 1(45). Amsterdam: Elsevier, 1985, Ch. 23, pp. 333-349. WARRINGTON, E.K. Visual deficits associated with occipital lesions in man. Experimental Brain Research, Supplementum Series, 11: 247-261, 1986. ZEKI, S., and SHIPP, S. The functional logic of cortical connections. Nature, 335: 311-317, 1988. ZIHL, J., von CRAMON, D., and MAr, N. Selective disturbance of movement vision after bilateral brain damage. Brain, 106: 313-340, 1983. Dr. A.D. Milner, Psychological Laboratory, The University, St. Andrews, Fibe KY16 9JU, Scotland.