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Dr. Annika Schoemann

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Sven Beckstette

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Dr. Ulrike Pompe-Alama

  "Soul Blindness—perception stripped off its meaning" 

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Soul Blindness—perception stripped off its meaning


Dr. Ulrike Pompe-Alama

Junior Professor for Philosophy of Simulation Institute of Philosophy, University Stuttgart



The concept of soul blindness [1] captures the paradox of having a perception while being unable to grasp its meaning—we perceive without recognizing.


It was H. Lissauer [2] who, already in 1890, distinguished between two forms of the disorder. The socalled apperceptive agnosias comprise deficits in the generation of a percept, leading to a kind of partial blindness, while associative agnosias comprise the cognitive inaccessibility of otherwise normal perception so that an object can neither be named nor described nor otherwise classified.


Visual agnosias grant us unique insight into the organization and inner workings of our mind and brain. Forms of apperceptive agnosia, for example, illustrate how the visual cortex divides and processes features of the visual world.


The default mode of perception presents our visual world as a coherent, colorful, detailed, focal collection of distinct objects in three-dimensional space. And sometimes there is motion. When you are wearing glasses, you immediately understand how easily this phenomenology can be disturbed. Luckily, a pair of lenses can remedy blurry vision due to poor eyesight. It gets much harder, though, when the cause for perceptual disturbances is not the eyes, but the brain.


In our brains, visual stimuli are processed by the primary visual cortex, which is located at the very back of the brain, in the occipital pole. Sensory data from the retina are projected into it and visual features like color, form, and motion are analysed in specialized areas (V3 for form, V4 for colour and V5 for motion, for example) to be re-integrated into a single percept. Apperceptive agnosias occur when one or more of these areas are injured or destroyed, with the effect that incoming information can be neither processed nor projected forward to other brain areas. In this case, the perception of some visual features can be impaired, while the perception of others remains intact. We can easily imagine the loss of colour vision (achromatopsia) but it is rather more difficult to imagine our visual phenomenology without forms. Patients with visual form agnosia perceive objects only as colored blobs without contours. Even more challenging is it to imagine the loss of the perception of movement (akinetopsia). Continuous movements, e.g. of approaching cars or fluids being poured into a cup, are registered in discrete steps, not unlike what one perceives when viewing a scene under a strobe light.


These low-level functions of the visual cortex form the basis for all further processing of visual information and are essentially involved in perception-driven cognition. Usually, our brain is able to compensate for the loss of these functions, e.g., due to a stroke, by virtue of its capacity to recruit neighbouring healthy cells to take over the tasks of the damaged areas. This, however, does not hold for the described impairments. The so-called plasticity of the brain does not affect primary functions such as the analysis of visual stimuli. Furthermore, information processing in the primary visual cortex is not only essential for our visual phenomenology, but also for memory of visual impressions. Sacks and Wasserman [3], for example, describe the case of a painter who gradually lost his memory for colors after having lost his color vision.


Associative agnosias reveal further complexities of our cerebral architecture. A patient’s perception as such is intact but they are unable to cognitively process and understand what they see. They are able to name and describe the visual features of objects, such as their color, form, texture or size and are even able to copy drawings but are not in a position to state the object’s name or its function [4].


Naming objects but also drawing objects from memory might be impossible if only the name of the object is pre sented to the patient. Equally, patients might be unable to verify statements about objects such as “an oyster has four legs” [5]. Here, we are facing Munk’s case of soul blindness. The eye sees but the mind cannot find meaning in it.


Names and functions of objects are parts of our semantic world knowledge. We normally associate this knowledge directly with the percept. This direct link, however, is disrupted in patients suffering from visual associative agnosia.


Quite often, the deficit is selective, which means that only objects belonging to a certain object category are affected, such as animals or tools [6], faces [7] (prosopagnosia), words (alexia), and the environment (including landmarks such as the Eiffel Tower) [8]. Finally, there is the phenomenon of simultanagnosia, where only one object at a time can be perceived, even though several objects are simultaneously presented.


Although practically each case is unique and varies from other cases, there are some typical classes of objects for which impairments occur. For example, patients’ deficits are confined to body parts [9] or objects that can typically be found indoors [10]. Most often, though, impairments are observed for either man-made objects (artefacts, tools) or animals, and fruits / vegetables [11]. Case M.D., for example, described by Hart et al. [12], was unable to name fruits and vegetables such as oranges or peaches, but was quickly able to name things like an abacus or a sphinx. Tests revealed that he was impaired in naming fruits and vegetables not only when they were presented visually, but also when he was allowed to touch them, or when he was given a verbal description.


The ability to access semantic knowledge via other moda-lities such as touch or sound is reported in many cases. Patients are thus able to recognize the item when they hear a typical sound or when the patient is allowed to handle it. Sirigu and colleagues [13] describe the case of a patient who is severely impaired in his recognition of common objects. The only way for him to access information about objects is to either describe or mime how the object is manipulated; yet, he fails to recognize the object’s proper function. Presented with a safety pin, for example, he would say: “You open it on one side, stick something on it, close it, and it stays in. I can tell you how it works, but I don‘t see its exact use. I don‘t think I have seen one like this before, it is not a very common object.”


Interestingly, although he is able to appropriately describe the mechanical properties of the safety pin, he cannot identify it as a safety pin. In response to the picture of a jackhammer, for example, he would mime the vibration and look down at his hands miming the appropriate holding posture, remarking, “It makes a lot of noise“. When the experimenter asked what the object might be used for he said, “Probably to make holes …”. After a pause he added, “in the wall … when you want to hang a picture”. Here, the correct function was recognized and even information about the object’s specific sound was accessed; yet the object’s proper function was attributed to the wrong context. Similarly, an iron was supposed to be used for spreading glue evenly. Again, the action was mimed correctly, indicating an understanding of the object‘s functional properties, without correctly identifying the object and recogniz-
ing its proper function.


The diversity and selectivity of associative agnosias confronts us with the issue of how object-related knowledge is structured and organized in the brain. Two competing accounts are available so far. According to the first, objects belonging to a specific category are processed and stored in specifically dedicated neuronal modules. Thus, there is a specific face-recognition area or an area responsible for processing living things and one for man-made objects, etc. [14]. The other account holds that such a specialization is not feasible, and that gradually overlapping features of visually similar objects create specialized areas, which can be trained by increased exposition to classes of stimuli [15].


Most cases of visual agnosia can be traced back to acquired lesions, such as strokes or head traumata. Some forms of prosopagnosia, however, seem to be present from birth (it is estimated that 2 % of the population suffer from a congenital form of face blindness) and seem to have a genetic, heritable component. In other cases, visual agnosia can be caused by neurodegenerative diseases such as Alzheimer’s disease or are caused by a severe global decrease in brain matter, e.g. due to alcoholism [16].


For the patient, the impairment can cause considerable distress and impose a significant challenge to daily activities. It is vital, therefore, to try and listen to the reported specificity of the individual case in order to be able to understand and classify it. The important but also exciting aspect of agnosias is that each case offers unique and deep insight into the complex interplay of perception, memory and cognition and thereby into the marvels of the human mind.


[1]     First mentioned by H. Munk, Ueber die Functionen der Grosshirnrinde Gesammelte Mittheilungen aus den Jahren 1877–80, Berlin 1881 One year later, in 1891, S. Freud coined the term “isual agnosia,” which is still used today.

[2]     H. Lissauer, Ein Fall von Seelenblindheit nebst einem Beitrag zur Theorie derselben. Archiv für Psychiatrie und Nervenkrankheiten, Vol. 21,1890, pp. 222–270.

[3]     O. Sacks, R. Wasserman, “The Case of the Colorblind Painter,” The New York Review of Books 34, No. 19, 1987, pp. 25–33.

[4]     E. Capitani, M. Laiacona, B. Mahon, A. Caramazza, “What are the facts of semantic category-specific deficits? A critical review of the clinical evidence,” Cognitive Neuropsychology 20, 2003, pp. 213–261.

[5]     G. Sartori, R. Job, “The oyster with four legs: a neuropsychological study on the interaction of visual and semantic information,” Cognitive Neuropsychology 5, 1988, pp. 105–132.

[6]     E. K. Warrington, “The selective impairment of semantic memory,” Quarterly Journal of Experimental Psychology 27, 1975, pp. 635–657.

[7]     For an interesting account of face blindness see O. Sacks, The Mind’s Eye, New York 2010.

[8]     This variant leads to people getting easily lost, cf. G. K. Aguirre, “Topographical Disorientation: A Disorder of Way-finding Ability,” in Neurological Foundations of Cognitive Neuroscience, ed. by M. D’Esposito, Cambridge, MA 2003.

[9]     M. Dennis, “Dissociated naming and locating of body parts after left anterior temporal lobe resection: An experimental case study,” Brain and Language 3, 1976, pp. 147–163. See also C. Sacchett, G. W. Humphreys, “Calling a squirrel a squirrel but a canoe a wigwam: A category-specific deficit for artifactual objects and body parts,” Cognitive Neuropsychology 9, 1992, pp. 73–86.

[10]    A. Yamadori, M. L. Albert, “Word category aphasia,” Cortex 9, 1973, pp. 83–89.

[11]    A. Caramazza, J. R.  Shelton, “Domain-specific knowledge systems in the brain: The animate-inanimate distinction,” Journal of Cognitive Neuroscience 10, 1988, pp. 1–34.

[12]    J. Hart, R. S. Berndt, A. C. Caramazza, “Category-specific naming deficit following cerebral infarction,” Nature 316, 1985, pp. 439–440.

[13]    A. Sirigu, J.-R. Duhamel, M. Poncet, M., “The role of sensorimotor experience in object recognition. A case of multimodal agnosia,” Brain 114, 1991, pp. 2555–2573 (the two quotations following in the running text are from p. 2555 and p. 2556).

[14]    M. J. Farah, J. L. McClelland, “A computational model of semantic memory impairment: Modality-specific and emergent category specificity,” Journal of Experimental Psychology: General 120, 1991, pp. 339–357.

[15]    I. Gauthier, M. J. Tarr, M.J., “Unraveling mechanisms for expert object recognition: bridging brain activity and behavior,” Journal for Experimental Psychology: Human Perception and Performance 28, 2002, pp. 431–446.

[16]    I. Biran, M. D. Coslet, “Visual Agnosia,” Current Neurology and Neuroscience Reports 3, 2003, pp. 508–512.

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