Contents

Apperceptive agnosia

The Origin

Visual agnosia was first recognized by Lisseauer in 1889. She realized that there were two different types of visual agnosia: associative and apperceptive. She suggested that there were two ways in which object recognition could be impaired following brain damage. It could damage object representations themselves which prevent recognition because of list visual memory representation (associative agnosia). It could also occur because of damage to perceptual processing. This prevents recognition of because of poor input to otherwise intact representations (apperceptive agnosia)^[1] . Liesseuer noted that apperceptive agnosia caused geometric and volumetric property deficits. Lastly she recognized that it occurs because of damage in the right parietal posterior lesion groups^[5] .

Effects of Apperceptive Agnosia

Apperceptive visual agnosia results in profound difficulties on a patient's ability to recognize visually presented information.^[6] Apperceptive agnosia affects the perceptual processing of individuals. Impairments of elements such as color and motion makes it difficult to interpret shape or the spatial arrangements of objects.^[7] Deficits in apperceptive agnosics cannot be linked to deficits in acuity. Additionally, patients have an intact ability to attend to cued stimuli.^[3] They maintain the ability to maintain fixation, reach for moving targets, and write as well. Those with apperceptive agnosia, however, have difficultly copying geometric shapes and letters. In some cases individuals are able trace letters and shapes with their finger but they are unable to use the technique as a strategy to name objects.^[6]

Deficits in apperceptive agnosics seem to be differential based on categories. Apperceptive agnosia has been noted to affect both broad and specific deficits. Specific deficits includes impairments in the recognition of body parts, buildings, manipulated objects, animals, and places. Broad deficits includes living and man made things. Picture naming is impaired in visual apperceptive agnosia but recognition of objects can be achieved through accessing other modalities. For example an object can be recognized through touch. Also when it is spoken about, individuals with apperceptive agnosia are able to define the object. The continuing of the ability of patients to recognize the object through use of different sensory modalities shows that deficits arise because of a break down in the interaction between visual systems and semantic memory^[8] .

Location of Brain Damage

Each patient that suffers from apperceptive agnosia does not have brain damage in the exact same area. However, brain damage in proximity to the occipital lobe is largely correlated with the patterns of deficit seen in apperceptive agnosics. For example patient JB suffered extensive damage to the parietal-occipital areas to the left cerebral hemisphere leading to his deficit in the ability to name distinguish between structurally similar object.^[8]

Visually presented object recognition is largely mediated by a hierarchical occipitotemporal pathway. This pathway facilitates the distinction between regions allowing the processing of the visual features of objects. In addition the occipitoparietal pathway is sometimes damaged in apperceptive agnosia patients. Damage to this region leads to impairments in localization of visual stimuli.^[9]

Theories of Causation

No two apperceptive agnosic patients are the same, but case studies have been used to make theories on what causes the object recognition deficits. While it is established that semantics plays a large role in apperceptive agnosia deficits, it is not agreed upon how semantics alter recognition processes. One theory proposes that semantic memories are divided into differential semantic categories. Brain damage leads to apperceptive agnosia because there is damage to a particular semantic category. Another theory proposes that there are no different categories but there are different areas of the brain that stores different types of features. Living things are thought to be identified by their perceptual features and man-made objects are identified by their functional features. In this theory, damage to one particular area might cause a loss of ability to differentiate living things or non-living things depending on the area of damage. Yet another theory suggests that the pattern of deficit arise from independent impairments to a particular input modality and a single non perceptual semantic system that is organized by category. Deficits are largely due to semantics, however many categories are related perceptually as well. Objects that are biologically similar are likely to have physical resemblance to each other as well. Perceptual confusion arises because of structural similarity contributes or accounts for some modality specific deficit.

Object processing is said to occur by two processes. There is first a stage of object perception. In this step there is mapping of visual description from the stimulus to a set of stored structural descriptions onto a set of structural descriptions of familiar objects. In the second stage, there is object identification. In this step the structural description is mapped onto the semantic representations giving rise to a full specification of the object. Researchers differ in their believe of how perceptual knowledge has an effect. Some believe that the loss of perceptual attributes should always accompany structural similarity. Others observe that perceptual and structural information often accompany each other but they believe that the information can occur independently from each other. Based on patient information it seems that objects belonging to a category with many structurally similar neighbours would be vulnerable to this semantic access impairment.^[8]

Case Studies

No two apperceptive agnosics are the same so it is beneficial to look at individuals who suffer from apperceptive agnosia to see the range of impairments that can occur and the range of functioning that can remain.

JB

Patient JB was able to match spoken words to target pictures almost perfectly when the target was presented with three other dissimilar distractors from the same semantic category. However, when the distractors were similar to each other and from the same semantic category his functioning decreased significantly. His abilities show evidence that the problem may lay in an interaction between processes involved in specification of the object’s visual structural description and access to semantic systems.^[8]

ELM

Patient ELM has deficits in the ability to name drawings of living things even though her ability to name man-made things remain intact. The early visual processing of shapes appear to be intact as well. In addition, unlike many patients, the ability to identify overlapping drawings of man-made objects remained intact. ELM was able to match both living and non-living things viewed from different perspectives. ELM’s deficit lied in the fact that he was not able to distinguish between drawings that were real and plausibly unreal objects that were living; however, he was able to make the distinction when the objects were man made. His impairments resulted due to damage to structural description of living things. There were problems with integrating features of structurally similar shapes of objects belonging to the same semantic category. This inability might be because of the distance between associated objects. The ones that are semantically close to each other are harder to differentiate.^[8]

HJA

HJA had deficits in differentiating between living things. She also made errors while naming line drawings. Instead of naming the pictures HJA frequently gave feature-by-feature description of the object (e.g. instead of saying circle, she would say many little dots). In addition, she would separate parts of drawn object instead of saying the name of the whole (e.g. handle and hairs when referring to paintbrush). HJA has problems segmenting global shapes when elements are closely grouped together. However, unlike the other patients, HJA has no problem copying and identifying overlapping drawings. In addition, HJA was able to draw objects accurately from memory.^[8]

Populations Affected by Apperceptive Agnosia

There are a subset of groups that apperceptive agnosia is more wide spread.

Alzheimer’s Disease

Visual agnosia (both apperceptive and associative) can be found as prevalent in Alzheimer’s Disease (AD) patients. Visual agnosia may be present in early stages of AD and can often act as an indicator of AD.^[10] Apperceptive agnosia results from diffuse cortical pathology of AD. There is early involvement in the hippocampus and the entorhinal cortex followed by a spread to adjacent areas with neurofibulary tangles (NFT). Gradual extension of NFT throughout the occipital, parietal, and temporal regions devoted to vision occur resulting in visual agnosia.^[7]

Parallels to Apperceptive Agnosia

When referring to apperceptive agnosia visual and object agnosia are most commonly discussed. This occurs because apperceptive agnosia is most likely to present visual impairments. However, in addition to visual apperceptive agnosia there are also cases of apperceptive agnosia in other sensory areas.

Auditory Agnosia

There is a small group of people who have auditory apperceptive agnosia. Impairments in audition take place despite intact audiogram. In some cases the deficit is in the ability to recognize spoken words and in other cases unable to recognize environmental sounds. In all cases individuals are able to read, write, name objects, and converse intelligently. Similar to visual impairments, the deficit arise because of damage in the temporal lobe. In the case of auditory agnosia bilateral lesions are present in the right temporal gyrus.^[11]

In addition to verbal and nonverbal auditory agnosia, there are cases of auditory apperceptive agnosia where patients are unable to recognize music in the absence of sensory, intellectual, and verbal impairments. In these cases there may be a melodic or a memory basis established in the brain and damage to those areas lead to music agnosia. Agnosia occurs because of failure to re-encode melodic information properly. This associated with right-sided lesions interrupting the melodic route in the brain.^[12]

Tactile Agnosia

The majority of the population are able to recognize familiar objects with a few touches. There are subsets of individuals who are unable to recognize objects by touch because of a small cerebral infraction. The impairment is restricted to the hands even though sensation is not impaired. Tactile impairments result in the inability of shape representations specific to tactile modality. This is similar to visual apperceptive agnosia in that it is basic level processing that is impaired.^[2]

Prosopagnosia

Prosopagnosia is a type of visual apperceptive agnosia. Human activities relies heavily on the ability to distinguish faces from other objects.^[13] Individuals who suffer from prosopagnosia have the ability to tell that a face is a face, however, they are unable to distinguish between faces. They fail to distinguish differences in race and difference in gender. People with severe impairments are sometimes unable to recognize their own faces. Apperceptive prosopagnosia results because of the perceptual process underlying the discrimination of the external and internal face configuration.^[14] See more Prosopagnosia.

References

See also

• Agnosia
• Visual agnosia
• Associative agnosia
• Visual space

Further reading

• Fundamentals of Sensation and Perception, Michael Levine. Oxford University Press (3rd Edition). London, 2000.
• Visual Perception, Tom Cornsweet. Harcourt Publishing, London, 1970.