Chapter 027. Aphasia, Memory Loss, and Other Focal Cerebral Disorders (Part 11)

The Occipitotemporal Network for Face and Object Recognition: Prosopagnosia and Object Agnosia Perceptual information about faces and objects is initially encoded in primary (striate) visual cortex and adjacent (upstream) peristriate visual association areas. This information is subsequently relayed first to the downstream visual association areas of occipitotemporal cortex and then to other heteromodal and paralimbic areas of the cerebral cortex. Bilateral lesions in the fusiform and lingual gyri of the occipitotemporal cortex disrupt this process and interfere with the ability of otherwise intact perceptual information to activate the distributed multimodal associations that lead to the recognition of faces and...
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Chapter 027. Aphasia, Memory Loss, and Other Focal Cerebral Disorders (Part 11) Chapter 027. Aphasia, Memory Loss, and Other Focal Cerebral Disorders (Part 11) The Occipitotemporal Network for Face and Object Recognition:Prosopagnosia and Object Agnosia Perceptual information about faces and objects is initially encoded inprimary (striate) visual cortex and adjacent (upstream) peristriate visualassociation areas. This information is subsequently relayed first to the downstreamvisual association areas of occipitotemporal cortex and then to other heteromodaland paralimbic areas of the cerebral cortex. Bilateral lesions in the fusiform andlingual gyri of the occipitotemporal cortex disrupt this process and interfere withthe ability of otherwise intact perceptual information to activate the distributedmultimodal associations that lead to the recognition of faces and objects. Theresultant face and object recognition deficits are known as prosopagnosia andvisual object agnosia. The patient with prosopagnosia cannot recognize familiar faces, including,sometimes, the reflection of his or her own face in the mirror. This is not aperceptual deficit since prosopagnosic patients can easily tell if two faces areidentical or not. Furthermore, a prosopagnosic patient who cannot recognize afamiliar face by visual inspection alone can use auditory cues to reach appropriaterecognition if allowed to listen to the persons voice. The deficit in prosopagnosiais therefore modality-specific and reflects the existence of a lesion that preventsthe activation of otherwise intact multimodal templates by relevant visual input.Damasio has pointed out that the deficit in prosopagnosia is not limited to therecognition of faces but that it can also extend to the recognition of individualmembers of larger generic object groups. For example, prosopagnosic patientscharacteristically have no difficulty with the generic identification of a face as aface or of a car as a car, but they cannot recognize the identity of an individualface or the make of an individual car. This reflects a visual recognition deficit forproprietary features that characterize individual members of an object class. Whenrecognition problems become more generalized and extend to the genericidentification of common objects, the condition is known as visual object agnosia.In contrast to prosopagnosic patients, those with object agnosia cannot recognize aface as a face or a car as a car. It is important to distinguish visual object agnosia from anomia. The patientwith anomia cannot name the object but can describe its use. In contrast, thepatient with visual agnosia is unable either to name a visually presented object orto describe its use. The characteristic lesions in prosopagnosia and visual objectagnosia consist of bilateral infarctions in the territory of the posterior cerebralarteries. Associated deficits can include visual field defects (especially superiorquadrantanopias) or a centrally based color blindness known as achromatopsia.Rarely, the responsible lesion is unilateral. In such cases, prosopagnosia isassociated with lesions in the right hemisphere and object agnosia with lesions inthe left. The Limbic Network for Memory: Amnesias Limbic and paralimbic areas (such as the hippocampus, amygdala, andentorhinal cortex), the anterior and medial nuclei of the thalamus, the medial andbasal parts of the striatum, and the hypothalamus collectively constitute adistributed network known as the limbic system. The behavioral affiliations of thisnetwork include the coordination of emotion, motivation, autonomic tone, andendocrine function. An additional area of specialization for the limbic network,and the one which is of most relevance to clinical practice, is that of declarative(conscious) memory for recent episodes and experiences. A disturbance in thisfunction is known as an amnestic state. In the absence of deficits in motivation,attention, language, or visuospatial function, the clinical diagnosis of a persistentglobal amnestic state is always associated with bilateral damage to the limbicnetwork, usually within the hippocampo-entorhinal complex or the thalamus. Although the limbic network is the site of damage for amnestic states, it isalmost certainly not the storage site for memories. Memories are stored in widelydistributed form throughout the cerebral cortex. The role attributed to the limbicnetwork is to bind these distributed fragments into coherent events andexperiences that can sustain conscious recall. Damage to the limbic network doesnot necessarily destroy memories but interferes with their conscious (declarative)recall in coherent form. The individual fragments of information remain preserv ...