Hellspawn

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 perceive 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