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Imagine a researcherrequesting you to copy a picture. It's a simple task. You move yourinstrument of illustration across a sheet of blank paper with ease,glancing from the given picture to your own sketch in progress. Whenyou are finished you observe a satisfactory replica and feel a senseof accomplishment and proficiency with the similarity you haveachieved between picture and sketch. Then the researcher querieswhether you can tell him what you have drawn. You search theinterconnected lines, the edges, and the shapes of your sketch butcannot answer what the picture represents. Finally, an explanation isgiven. You have just drawn a house- a simple triangle resting on topof a square. Your sense of accomplishment is quickly replaced with afeeling of despair.

Visual agnosia is aneurological disorder characterized by the inability to recognizefamiliar objects (Farah, 1990). Object recognition is the ability toplace an object in a category of meaning. Most cases of visualagnosia are brought about through cerebral vascular accidents ortraumatic brain injury typically inhibiting sufficient amounts ofoxygen from reaching vital body tissues (Zoltan, 1996). There are avast array of impaired abilities and deficits associated withindividuals diagnosed with visual agnosia. These impairments varyconsiderably from individual to individual (Farah, 1990). Somepatients cannot recognize pictures of things such as trees and birds,despite being able to describe such objects or recognize them throughother senses such as sound and touch. Other patients demonstrate aninability to recognize faces of friends and family members (Goodale,1995). The functional impairments experienced as a result of visualagnosia are detrimental to both the diagnosed individual and allthose who interact with the individual.

Unfortunately objectrecognition disorders such as agnosia comprise a neglected field ofstudy and the existing theories to explain this phenomenon are oftenvague and problematic (Farah, Monheit, & Wallace 1991). Visualagnosia is a very rare syndrome, and there are only a small number ofcases available to study. This research obstacle is furthercompounded by the variance of impairments in visual agnosics (Vecera& Gilds 1998).

In an attempt to groupsimilar cases of visual agnosia for more sufficient study, twoseparate categories have emerged: apperceptive agnosia andassociative agnosia. However, the different fields of study andvarious researchers involved in studying visual agnosia often havediscrepancies in defining these categories. Apperceptive agnosia istypically characterized by an inability to recognize familiar objectscaused by damage to early perceptual processes, and associativeagnosia is typically characterized by an inability to recognizefamiliar objects despite having no damage to early perceptualprocesses (Vecera & Gilds 1998). Many subcategories of visualagnosia exist as well, however, the subdivision of agnosias has beena matter of debate ( Farah 1999). Such examples would includeintegrative agnosia, prosopagnosia, optic aphasia, and simultagnosia.Integrative agnosia is classified by the inability to percieve partsas a whole (Sadja & Finkle 1995). Prosopagnosia is distinguishedby an impairment in the ability to percieve faces of known people(Zoltan 1996). Patients with optic aphasia have an impairment ofobject recognition in only specific objects (Farah 1999).Simultagnosia is characterized by the inability to percieve more thanone thing at a time and also an impairment in distinguishing betweentwo perceptual acts (Farah 1999).

Agnosia has been diagnosedin patients with all kinds of brain damage. Cases have been notedafter both unilateral and bilateral damage to both the right and lefthemispheres of the brain (Humohreys 1999). Patients with impairmentsto recognize faces usually have bilateral inferior lesions to thebrain and occasionally have unilateral right hemisphere lesions(Humphreys 1999). Patients who exhibit impairments with wordrecognition usually have unilateral left inferior lesions to thebrain. Those who exhibit impairments in both word recognition andface recognition usually exhibit bilateral lesions (Farah1999).

The earliest researchers ofagnosia theorized that visual agnosia was the result of reducedlow-level visual processing with impairments to mental abilities(Vecera & Gilds 1998). This theory is often termed thesensory-deficit account. As supporting evidence, researchers Benderand Feldman (1998) examined all hospital records of diagnosed visualagnosics within a twenty-year period and discovered that no case waswithout evidence of either reduced low-level visual processing ormental dysfunction (Vecera & Gilds1998). However this earlytheory was problematic because it did not identify a specificcognitive mechanism that could have been damaged; the theory alsofailed to explain the different patterns of behavior evident inapperceptive and associative agnosia (Farah et al. 1991).

Another more recentexplanation is the "peppery mask" account. It is theorized thatpatients with visual agnosia have a presence of random visual noisebecause of obstructing air bubbles circulating in the blood or thepresence of blood clots present in an intact blood vessel (Farah etal. 1991). As a result, random areas of dimmed vision areas arescattered throughout the visual field in varying size and severityand thus the visual agnosic sees the world through a peppered maskthat degrades their visual processing (Vecera & Gilds 1998).However, while the peppery mask account explains the degradedlow-level visual processing, the theory offers no explanation for thevarious grouping disorders that tend to appear in visual agnosics.The serious difficulty encountered in the peppery mask account isthat the presence of detrimental random visual noise peppering thevisual field would seem to increase reliance upon perception of thewhole picture despite the broken pieces. However, visual agnosicsseem to perceive the parts without being able to identify the whole(Sajda & Finkle 1995).

To seek understanding andexplanation of perceptual grouping disorders, researchers formulatedthe grouping-deficit account. This account hypothesizes that patientswith visual agnosia have impairments in preattentive perceptualgrouping processes (Vecera & Gilds 1998). Such impairments wouldbe difficulty in organizing segments of information into the totalityof the information it represents. The main limitation imposed on thegrouping-deficit account is that little data has been formulated frompatients that examines lower-level grouping processes (Farah 1990).Furthermore, the existing research on these lower-level groupingprocesses was not directed at differentiating the group-deficitaccount from the peppery mask account (Vecera & Gilds 1998).

Currently, researchers aretaking new approaches in determining which account of visual agnosiabest explains the syndrome. Through experimentation, researchers havebeen attempting to simulate visual agnosia in subjects with normalvision. In an experiment by Vecera & Gilds (1998), researcherscovered different displays with a peppery mask to simulate thepeppery mask condition in subjects with normal vision. Normalsubjects were expected to simulate the behavior of a visual agnosicpatient when looking through the manipulated mask. However, themanipulation of a peppery mask did not lead to different patterns ofbehavior when compared to the patterns of behavior measured fromunmasked displays (Vecera & Gilds 1998). These researchersconducted another experiment to explore the grouping-deficit account.They removed nonaccidental properties from displayed objects, such asparallelism and cotermination and various aids used to organize orgroup the visual field. When these properties were removed, objectrecognition and grouping was difficult, if not impossible (Vecera& Gilds, 1998).

The working theories ofexplanation yield very few treatment implications. In an effort tooptimize the life of a visual agnosic, two main approaches ofrehabilitation are suggested to individuals with visual agnosia. Inutilizing a remedial approach, an example of a suggested exercise isfor patients to identify objects that are a necessity forindependence and practice identifying these objects (Zoltan 1996).Second, as an adaptive approach, Zoltan suggested that patients beprovided with labels for objects of necessity. By utilizing bothapproaches patients can increase their ability to recognize objectsand maximize independence.

Given the vast differencesof impairments between patients with visual agnosia, the lack of anagreement on the definition of categories of visual agnosia, and thefailure to formulate a proficient explanation of the cognitivemechanisms behind the hidden perceptual processes that are involvedin the syndrome of visual agnosia it can be concluded that furtherresearch is desperately needed. Nevertheless, the current researchdata yield significant pieces of a puzzle that show encouraging signsof fitting together to enhance our understanding and advancement ofknowledge surrounding object recognition disorders.

Farah, M.J. VisualAgnosia: Disorders of Object Recognition and What they tell us aboutNormal Vision. The MIT Press: Massachusettes, 1990.155p.

Farah, M.J., Monheit, M.A.& Wallace, M.A. (1991) Unconscious Perception of ExtinguishedVisual Stimuli: Reassessing the Evidence. Neuropsychologia,29, 949-958.

Farah, M.J. Relations Amongthe 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. CaseStudies in the Neuropsychology of Vision. The Psychology Press:UK, 1999.

Sajda P. & Finkle, L.H.(1995) Intermediate Visual Representations and the Construction ofSurface 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 CognitiveNeuroscience, 10 (5), p.568

Zoltan, B. Vision,Perception, & Cognition: A Manuel for the Evaluation andTreatment of the Neurologically Impaired Adult. SlackIncorporated: New Jersey, 1996. 109-111.