Short Description or Definition

Visual agnosia is a neurological deficit that results in impairments in the perception and recognition of complex visual stimuli such as common objects or faces, while low-level visual processes and the memory systems remain intact. The primary cause of these deficits is damage in the lateral part of the occipital lobes and/or in the ventral portion of the temporal lobes.

Categorization

Visual agnosias can be divided into two main types: apperceptive visual agnosias and associative visual agnosias. This distinction was first put forth by Lissauer (1980), who suggested a pathological difference between (1) the inability to correctly perceive an object as a coherent whole because of perceptual deficits and (2) the inability to ascribe meaning to an object despite an accurate perception of that object because of deficits in accessing the stored object representations. He dubbed the former as “apperceptive” and the latter as “associative.”

Neuropsychology and Psychology of Visual Agnosia

The earliest documented cases of visual agnosia date back to the late 1800s. Lissauer was the first scientist to formally report a patient with visual agnosia. He suggested that the ability to recognize objects could be affected by brain damage independently from low-level visual perception. Moreover, he proposed that the visual recognition of objects consisted of two separate stages: the apperceptive stage and the associative stage. During the apperceptive stage, a sensory representation of an object is created, while during the associative stage, knowledge connected to that sensory representation is retrieved so that a visual stimulus can be recognized (Lissauer 1980). The idea of two distinct processing stages led Lissauer to propose that brain injury could affect either of the two processes independently, giving rise to distinct symptomologies and two different forms of agnosia (Lissauer). This distinction is still used as the general framework for understanding agnosias in modern neuropsychology.

Apperceptive visual agnosias include different types of perceptual impairments that cause the misperception of objects despite intact low-level visual processes (Farah 1990). For example, patients diagnosed with apperceptive agnosia may demonstrate difficulties in grouping sets of local features that represent full objects or the components of a visual scene (Farah and Feinberg 2006). Apperceptive agnosias are most commonly caused by large lesions encompassing the lateral portion of the occipital lobes and extending into the temporal lobes. Common causes of these types of lesions are stroke, anoxia, and carbon monoxide poisoning (c.f. Ghadiali 2004). Because of the heterogeneity of deficits found in apperceptive agnosia patients, Farah (1990, 2004) has proposed several subtypes: a narrow definition of apperceptive agnosia, ventral simultagnosia, and a perceptual categorization deficit.

According to Farah (1990, 2004), pure apperceptive agnosia is a deficit in general shape perception and discrimination. Apperceptive agnosic patients show reasonably intact performance on tasks measuring visual acuity, color vision, and motion detection, while they are greatly impaired on tasks requiring them to recognize, match, and copy visual stimuli as simple as Xs and Os or as complex as common objects (Farah 1990). These patients will usually exhibit large diffuse lesions in the occipital lobes.

Ventral simultagnosia was first defined as the inability to process more than one object or more than one part of a complex object, at any one time (Wolpert 1924, as reported in Farah 1990). In contrast to pure apperceptive agnosics, these patients can recognize objects and use shape information, but they report not “seeing” more than any one element at the time, regardless of where the objects are in the visual field (i.e., it is not specific to a side of space, as in spatial neglect). For example, when presented with complex visual scenes, these patients are able to recognize individual objects in a scene, but cannot make sense of a scene as a whole. It has been suggested that simultagnosia is a by-product of a reduction in visual attention, resulting in a functionally reduced visual field (Michael and Henaff 2004). Simultagnosia generally arises from large bilateral lesions extending from the occipital lobes to the temporal or parietal lobes (Farah 1990, 2004).

Finally, “perceptual category deficits” comprise a third subtype of apperceptive agnosia (Warrington and colleagues, as reported in Farah 1990). Patients exhibiting this impairment have difficulties in recognizing objects in unconventional views, despite being able to do so when the objects are presented in their canonical orientation. The few case studies of patients with this sort of deficit report lesions to the “right posterior quadrant of the brain, especially the right posterior inferior parietal lobe” (Farah 1990, 2004). More recently, Mulder et al. (1995) observed patients with similar deficit with a similar left-lateralized lesion, suggesting that the side of the lesion might not be diagnostic of this deficit.

Unlike the majority of patients with apperceptive agnosias, patients with associative visual agnosia can “see” and perceive objects and their parts, but they cannot assign meaning to them. These deficits are usually associated with damage to the inferior-temporal occipital junction and the ventral temporal cortex. The lesions can be caused by traumatic brain injury, infarction of the posterior cerebral artery, and less frequently by tumors, hemorrhages, and demyelination (Ghadiali 2004).

Similar to apperceptive visual agnosias, several subtypes of the general syndrome have been identified on the basis of the different kinds of selective impairments observed across the patient population. Patients afflicted with associative visual agnosia can present either an impairment in recognizing many different categories of objects, or they can present recognition impairments that are either specific to a single object category (i.e., faces or letters) or that seem to affect general subcategories of objects much more so than others (i.e., man-made objects or living things).

The general form of associative agnosia can be defined as an impairment in recognizing, naming, matching, and at times, but not in all cases, drawing objects from many different categories, despite intact recognition using modalities other than vision and normal low-level visual perception (Farah 1990, 2004). These deficits are restricted to the visual modality, as these patients can recognize objects if presented to them via a different sensory modality. This general impairment is usually caused by large bilateral lesions encompassing portions of both the occipital and temporal lobes (Farah and Feinberg 2006).

There have been many case studies reporting patients who show difficulties in recognizing specific object categories (De Renzi and di Pellegrino 1998). Such case studies have given rise to a taxonomy of category-specific visual agnosias. The most prominent of these selective impairments has been termed “prosopagnosia” (Bodamer 1943), in reference to a deficit in visual recognition that is mostly or entirely specific to faces. Prosopagnosic patients are unable to recognize familiar people, including family members, from their faces, and have difficulty in learning and remembering new faces. The lesions found in these patients are either right-lateralized or bilateral and include either or both lateral occipital areas and ventral temporal lobe areas. There have also been reports of selective impairments specific to visual letter and visual word recognition. In contrast to patients suffering from face recognition deficits, these patients show left-lateralized lesions in occipitotemporal areas. Farah and colleagues have found that the maximum overlap across patients with letter and word deficits is a lesion site in the left parahippocampal gyrus, fusiform gyrus, and lingual gyrus (Farah and Feinberg 2006). Finally, there are several case studies reporting patients with impaired visual recognition for objects in categories that are associated by their meaning or function rather than by visual similarity. For example, Warrington and Shallice (1984) described a double dissociation between patients showing a deficit in recognizing living things, but normal recognition of nonliving things, and patients showing a deficit in recognizing nonliving things, but normal recognition of living things.

Across the literature, there are many instances in which patients show more than one of these object-selective impairments. For example, there are patients who show deficits on face recognition and word recognition but have relatively spared object recognition. Alternatively, some patients show impaired word and object recognition but relatively spared face recognition. Such co-occurrences are consistent with a systematic pattern of lesion sites, such that a single selective impairment usually results from unilateral lesions, while two or more impaired categories are usually the result of bilateral lesions (Farah and Feinberg 2006).

The nature of associative agnosia is still somewhat controversial in that it is unclear whether the deficit is a disorder of perception, a disorder of semantic memory, or possibly a disorder across both domains. One account has proposed that “pure” associative agnosias are the result of damaged stored visual representations in the absence of perceptual deficits, such that when a new stimulus is processed by an intact visual system, there is no stored representation available for matching it with the sensory input (Riddoch and Humphreys 2003). However, Farah and colleagues have proposed that perceptual-level deficits may exist in such patients, because they typically exhibit very slow, feature-by-feature strategies in processing visual stimuli, even when they successfully perform a task. Such findings hint that both perception and memory are functioning abnormally in these patients (Farah and Feinberg 2006).

Evaluation

Case studies of visual agnosic patients employ a variety of tasks to determine the specificity of the deficit encountered. Some of the most widely used tests used are the Birmingham Object Recognition Test (BORB; Riddoch and Humphreys 1993), the Visual and Space Perception Battery (VOSP; Warrington and James 1991), the Graded Naming Test (McKenna 1997), and the Pyramid and Palm Trees Test (Howard and Patterson 1992).

The BORB is the most comprehensive of these measures, as it is intended to diagnose any visual object recognition impairment, including both the apperceptive and associative types of visual agnosia. The BORB contains behavioral tests to measure low-level visual perception, object perception, and retrieval of semantic knowledge about objects. The VOSP contains a series of tests designed to assess object and space perception. The Graded Naming Test is designed to measure patients’ ability to name objects taken from many different categories from line drawing representations. The Pyramid and Palm Trees Test is designed to assess object recognition in patients who may also have verbal impairments.

Treatment

There is no direct treatment for visual agnosias. However, patients can benefit from rehabilitation teaching them alternative strategies to compensate for their specific deficits and also from repetitive training to attempt to recover some of the impaired functions (Ghadiali 2004).

Cross-References