By Candace N. Palmer
Stephen F. Austin State University Spring 2002
Imagine a researcher requesting you to copy a picture. It's a simple task. You move your instrument of illustration across a sheet of blank paper with ease, glancing from the given picture to your own sketch in progress. When you are finished you observe a satisfactory replica and feel a sense of accomplishment and proficiency with the similarity you have achieved between picture and sketch. Then the researcher queries whether you can tell him what you have drawn. You search the interconnected lines, the edges, and the shapes of your sketch but cannot answer what the picture represents. Finally, an explanation is given. You have just drawn a house- a simple triangle resting on top of a square. Your sense of accomplishment is quickly replaced with a feeling of despair.
Visual agnosia is a neurological disorder characterized by the inability to recognize familiar objects (Farah, 1990). Object recognition is the ability to place an object in a category of meaning. Most cases of visual agnosia are brought about through cerebral vascular accidents or traumatic brain injury typically inhibiting sufficient amounts of oxygen from reaching vital body tissues (Zoltan, 1996). There are a vast array of impaired abilities and deficits associated with individuals diagnosed with visual agnosia. These impairments vary considerably from individual to individual (Farah, 1990). Some patients cannot recognize pictures of things such as trees and birds, despite being able to describe such objects or recognize them through other senses such as sound and touch. Other patients demonstrate an inability to recognize faces of friends and family members (Goodale, 1995). The functional impairments experienced as a result of visual agnosia are detrimental to both the diagnosed individual and all those who interact with the individual.
Unfortunately object recognition disorders such as agnosia comprise a neglected field of study and the existing theories to explain this phenomenon are often vague and problematic (Farah, Monheit, & Wallace 1991). Visual agnosia is a very rare syndrome, and there are only a small number of cases available to study. This research obstacle is further compounded by the variance of impairments in visual agnosics (Vecera & Gilds 1998).
In an attempt to group similar cases of visual agnosia for more sufficient study, two separate categories have emerged: apperceptive agnosia and associative agnosia. However, the different fields of study and various researchers involved in studying visual agnosia often have discrepancies in defining these categories. Apperceptive agnosia is typically characterized by an inability to recognize familiar objects caused by damage to early perceptual processes, and associative agnosia is typically characterized by an inability to recognize familiar objects despite having no damage to early perceptual processes (Vecera & Gilds 1998). Many subcategories of visual agnosia exist as well, however, the subdivision of agnosias has been a matter of debate ( Farah 1999). Such examples would include integrative agnosia, prosopagnosia, optic aphasia, and simultagnosia. Integrative agnosia is classified by the inability to percieve parts as a whole (Sadja & Finkle 1995). Prosopagnosia is distinguished by an impairment in the ability to percieve faces of known people (Zoltan 1996). Patients with optic aphasia have an impairment of object recognition in only specific objects (Farah 1999). Simultagnosia is characterized by the inability to percieve more than one thing at a time and also an impairment in distinguishing between two perceptual acts (Farah 1999).
Agnosia has been diagnosed in patients with all kinds of brain damage. Cases have been noted after both unilateral and bilateral damage to both the right and left hemispheres of the brain (Humohreys 1999). Patients with impairments to recognize faces usually have bilateral inferior lesions to the brain and occasionally have unilateral right hemisphere lesions (Humphreys 1999). Patients who exhibit impairments with word recognition usually have unilateral left inferior lesions to the brain. Those who exhibit impairments in both word recognition and face recognition usually exhibit bilateral lesions (Farah 1999).
The earliest researchers of agnosia theorized that visual agnosia was the result of reduced low-level visual processing with impairments to mental abilities (Vecera & Gilds 1998). This theory is often termed the sensory-deficit account. As supporting evidence, researchers Bender and Feldman (1998) examined all hospital records of diagnosed visual agnosics within a twenty-year period and discovered that no case was without evidence of either reduced low-level visual processing or mental dysfunction (Vecera & Gilds1998). However this early theory was problematic because it did not identify a specific cognitive mechanism that could have been damaged; the theory also failed to explain the different patterns of behavior evident in apperceptive and associative agnosia (Farah et al. 1991).
Another more recent explanation is the "peppery mask" account. It is theorized that patients with visual agnosia have a presence of random visual noise because of obstructing air bubbles circulating in the blood or the presence of blood clots present in an intact blood vessel (Farah et al. 1991). As a result, random areas of dimmed vision areas are scattered throughout the visual field in varying size and severity and thus the visual agnosic sees the world through a peppered mask that degrades their visual processing (Vecera & Gilds 1998). However, while the peppery mask account explains the degraded low-level visual processing, the theory offers no explanation for the various grouping disorders that tend to appear in visual agnosics. The serious difficulty encountered in the peppery mask account is that the presence of detrimental random visual noise peppering the visual field would seem to increase reliance upon perception of the whole picture despite the broken pieces. However, visual agnosics seem to perceive the parts without being able to identify the whole (Sajda & Finkle 1995).
To seek understanding and explanation of perceptual grouping disorders, researchers formulated the grouping-deficit account. This account hypothesizes that patients with visual agnosia have impairments in preattentive perceptual grouping processes (Vecera & Gilds 1998). Such impairments would be difficulty in organizing segments of information into the totality of the information it represents. The main limitation imposed on the grouping-deficit account is that little data has been formulated from patients that examines lower-level grouping processes (Farah 1990). Furthermore, the existing research on these lower-level grouping processes was not directed at differentiating the group-deficit account from the peppery mask account (Vecera & Gilds 1998).
Currently, researchers are taking new approaches in determining which account of visual agnosia best explains the syndrome. Through experimentation, researchers have been attempting to simulate visual agnosia in subjects with normal vision. In an experiment by Vecera & Gilds (1998), researchers covered different displays with a peppery mask to simulate the peppery mask condition in subjects with normal vision. Normal subjects were expected to simulate the behavior of a visual agnosic patient when looking through the manipulated mask. However, the manipulation of a peppery mask did not lead to different patterns of behavior when compared to the patterns of behavior measured from unmasked displays (Vecera & Gilds 1998). These researchers conducted another experiment to explore the grouping-deficit account. They removed nonaccidental properties from displayed objects, such as parallelism and cotermination and various aids used to organize or group the visual field. When these properties were removed, object recognition and grouping was difficult, if not impossible (Vecera & Gilds, 1998).
The working theories of explanation yield very few treatment implications. In an effort to optimize the life of a visual agnosic, two main approaches of rehabilitation are suggested to individuals with visual agnosia. In utilizing a remedial approach, an example of a suggested exercise is for patients to identify objects that are a necessity for independence and practice identifying these objects (Zoltan 1996). Second, as an adaptive approach, Zoltan suggested that patients be provided with labels for objects of necessity. By utilizing both approaches patients can increase their ability to recognize objects and maximize independence.
Given the vast differences of impairments between patients with visual agnosia, the lack of an agreement on the definition of categories of visual agnosia, and the failure to formulate a proficient explanation of the cognitive mechanisms behind the hidden perceptual processes that are involved in the syndrome of visual agnosia it can be concluded that further research is desperately needed. Nevertheless, the current research data yield significant pieces of a puzzle that show encouraging signs of fitting together to enhance our understanding and advancement of knowledge surrounding object recognition disorders.
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Farah, M.J., Monheit, M.A. & Wallace, M.A. (1991) Unconscious Perception of Extinguished Visual Stimuli: Reassessing the Evidence. Neuropsychologia, 29, 949-958.
Farah, M.J. Relations Among the Agnosias. Case Studies in the Neuropsychology of Vision. The Psychology Press: UK, 1999. (9) 181.
Goodale, M.A. (1995) Perceiving the World and Grasping It: Is there a difference? Lancet, 343, 930.
Humphreys, G.W. Case Studies in the Neuropsychology of Vision. The Psychology Press: UK, 1999.
Sajda P. & Finkle, L.H. (1995) Intermediate Visual Representations and the Construction of Surface Perception. Journal of Cognitive Neuroscience, 7, 267-291.
Vecera, S.P. & Gilds, K.S. (1998) What Processing is Impaired in Apperceptive Agnosia: Evidence from Normal Subjects. Journal of Cognitive Neuroscience, 10 (5), p.568
Zoltan, B. Vision, Perception, & Cognition: A Manuel for the Evaluation and Treatment of the Neurologically Impaired Adult. Slack Incorporated: New Jersey, 1996. 109-111.