Apperceptive Visual Agnosia Research Articles

Ventral Variant Posterior Cortical Atrophy with Occipito-temporal Accumulation of Tau Proteins/Astrocyte Gliosis.

A 73-year-old woman with posterior cortical atrophy (PCA) presented with progressive apperceptive visual agnosia, alexia, agraphia, ventral simultanagnosia, prosopagnosia, and allocentric (stimulus-centered) left-sided hemispatial neglect. All of these symptoms were attributed to damage to the bilateral occipito-temporal cortices, consistent with ventral variant PCA. While the Pittsburgh compound B uptake was extensively distributed throughout the occipito-parietal (dorsal) and occipito-temporal (ventral) areas, the THK5351 (ligand binding to tau aggregates/astrocyte gliosis) accumulation was limited to the ventral area. These findings suggest that local accumulation of tau proteins and/or astrocyte gliosis over the occipito-temporal cortices can result in ventral variant PCA.

Patterns of Apperceptive and Associative Visual Agnosia amongst patients with Neurological disorders in a teaching hospital in Nigeria

Patterns of Apperceptive and Associative Visual Agnosia amongst patients with Neurological disorders in a teaching hospital in Nigeria

Apperceptive and associative visual object agnosia in patients with acute ischemic stroke

Visual object agnosia (VOA) is a loss of the ability to recognize visible objects in patients with the intact primary visual functions and in the absence of dementia. The apperceptive and associative variants of VOA are marked out. The apperceptive VOA is thought to be due to «pre-semantic» impairment of visual information processing. The associative VOA is caused by the loss of access to knowledge about the objects, and its semantic subtype is due to the disintegration of this knowledge itself. It is important to diagnose VOA and its variants in time to provide individualized approaches to medical rehabilitation of patients. Case reports of apperceptive and associative VOA in acute ischemic stroke are presented in this paper. These case reports indicate the possibility of the development of apperceptive and associative VOA in unilateral acute ischemic brain lesion. The variants of VOA can be recognized only by a detailed neuropsychological examination.

Asymmetric Bálint’s syndrome with multimodal agnosia, bilateral agraphesthesia, and ineffective kinesthetic reading due to subcortical hemorrhage in the left parieto-occipito-temporal area

ABSTRACT We report a patient with asymmetric Bálint’s syndrome (predominantly right-sided oculomotor apraxia and simultanagnosia and optic ataxia for the right hemispace), and multimodal agnosia (apperceptive visual agnosia and bilateral associative tactile agnosia) with accompanying right hemianopia, bilateral agraphesthesia, hemispatial neglect, global alexia with unavailable kinesthetic reading, and lexical agraphia for kanji (Japanese morphograms), after hemorrhage in the left parieto-occipito-temporal area. The coexistence of tactile agnosia, bilateral agraphesthesia, and ineffective kinesthetic reading suggests that tactile-kinesthetic information can be interrupted because of damage to the fiber connection from the parietal lobe to the occipito-temporal area, leading to these tactually related cognitive impairments.

Making Memories: The Development of Long-Term Visual Knowledge in Children with Visual Agnosia

There are few reports about the effects of perinatal acquired brain lesions on the development of visual perception. These studies demonstrate nonseverely impaired visual-spatial abilities and preserved visual memory. Longitudinal data analyzing the effects of compromised perceptions on long-term visual knowledge in agnosics are limited to lesions having occurred in adulthood. The study of children with focal lesions of the visual pathways provides a unique opportunity to assess the development of visual memory when perceptual input is degraded. We assessed visual recognition and visual memory in three children with lesions to the visual cortex having occurred in early infancy. We then explored the time course of visual memory impairment in two of them at 2 years and 3.7 years from the initial assessment. All children exhibited apperceptive visual agnosia and visual memory impairment. We observed a longitudinal improvement of visual memory modulated by the structural properties of objects. Our findings indicate that processing of degraded perceptions from birth results in impoverished memories. The dynamic interaction between perception and memory during development might modulate the long-term construction of visual representations, resulting in less severe impairment.

Selective impairment of living things and musical instruments on a verbal ‘Semantic Knowledge Questionnaire’ in a case of apperceptive visual agnosia

Semantic memory was investigated in a patient (MR) affected by a severe apperceptive visual agnosia, due to an ischemic cerebral lesion, bilaterally affecting the infero-mesial parts of the temporo-occipital cortices. The study was made by means of a Semantic Knowledge Questionnaire (Laiacona, Barbarotto, Trivelli, & Capitani, 1993), which takes separately into account four categories of living beings (animals, fruits, vegetables and body parts) and of artefacts (furniture, tools, vehicles and musical instruments), does not require a visual analysis and allows to distinguish errors concerning super-ordinate categorization, perceptual features and functional/encyclopedic knowledge. When the total number of errors obtained on all the categories of living and non-living beings was considered, a non-significant trend toward a higher number of errors in living stimuli was observed. This difference, however, became significant when body parts and musical instruments were excluded from the analysis. Furthermore, the number of errors obtained on the musical instruments was similar to that obtained on the living categories of animals, fruits and vegetables and significantly higher of that obtained in the other artefact categories. This difference was still significant when familiarity, frequency of use and prototypicality of each stimulus entered into a logistic regression analysis. On the other hand, a separate analysis of errors obtained on questions exploring super-ordinate categorization, perceptual features and functional/encyclopedic attributes showed that the differences between living and non-living stimuli and between musical instruments and other artefact categories were mainly due to errors obtained on questions exploring perceptual features.All these data are at variance with the ‘domains of knowledge’ hypothesis’, which assumes that the breakdown of different categories of living and non-living things respects the distinction between biological entities and artefacts and support the models assuming that ‘category-specific semantic disorders’ are the by-product of the differential weighting that visual-perceptual and functional (or action-related) attributes have in the construction of different biological and artefacts categories.

Visuo-Spatial Imagery Impairment in Posterior Cortical Atrophy: A Cognitive and SPECT Study

This study investigated the cognitive profile and the cerebral perfusion pattern in a highly educated 70 year old gentleman with posterior cortical atrophy (PCA). Visuo-perceptual abilities, spatial memory, spatial representation and navigation, visuo-spatial mental imagery, semantic and episodic-autobiographical memory were assessed. Regional cerebral blood flow (rCBF) was imaged with SPECT. Cognitive testing showed visual-perceptual impairment, apperceptive visual and landmark agnosia, topographical disorientation with way-finding deficits, impaired map learning and poor mental image generation. Semantic memory was normal, while episodic-autobiographical memory was impaired. Reduced rCBF was found mainly in the right hemisphere, in the precentral gyrus, posterior cingulate and middle temporal gyri, cuneus and precuneus, in the left superior temporal and lingual gyri and in the parahippocampus bilaterally. Hypoperfusion in occipito-parietal regions was associated with visuo-spatial deficits, whereas deficits in visuo-spatial mental imagery might reflect dysfunction related to hypoperfusion in the parahippocampus and precuneus, structures which are responsible for spatial and imagery processing. Dissociating performance between preserved semantic memory and poor episodic-autobiographical recall is consistent with a pattern of normal perfusion in frontal and anterior temporal regions but abnormal rCBF in the parahippocampi. The present findings indicate that PCA involves visuo-spatial imagery deficits and provide further validation to current neuro-cognitive models of spatial representation and topographical disorientation.

Visuo-spatial imagery impairment in posterior cortical atrophy: a cognitive and SPECT study.

This study investigated the cognitive profile and the cerebral perfusion pattern in a highly educated 70 year old gentleman with posterior cortical atrophy (PCA). Visuo-perceptual abilities, spatial memory, spatial representation and navigation, visuo-spatial mental imagery, semantic and episodic-autobiographical memory were assessed. Regional cerebral blood flow (rCBF) was imaged with SPECT. Cognitive testing showed visual-perceptual impairment, apperceptive visual and landmark agnosia, topographical disorientation with way-finding deficits, impaired map learning and poor mental image generation. Semantic memory was normal, while episodic-autobiographical memory was impaired. Reduced rCBF was found mainly in the right hemisphere, in the precentral gyrus, posterior cingulate and middle temporal gyri, cuneus and precuneus, in the left superior temporal and lingual gyri and in the parahippocampus bilaterally. Hypoperfusion in occipito-parietal regions was associated with visuo-spatial deficits, whereas deficits in visuo-spatial mental imagery might reflect dysfunction related to hypoperfusion in the parahippocampus and precuneus, structures which are responsible for spatial and imagery processing. Dissociating performance between preserved semantic memory and poor episodic-autobiographical recall is consistent with a pattern of normal perfusion in frontal and anterior temporal regions but abnormal rCBF in the parahippocampi. The present findings indicate that PCA involves visuo-spatial imagery deficits and provide further validation to current neuro-cognitive models of spatial representation and topographical disorientation.

Atrofia cortical posterior

Posterior cortical atrophy (PCA) is a neurodegenerative syndrome, usually due to Alzheimer's disease. The first symptoms are progressive impairment of visuo spatial (Balint's and Gertsmann's syndromes) or visuo perceptive (visual agnosia, alexia) function. Episodic memory and executive function are spared until later stages. We report two males aged 51 and 55years and three females aged 50, 54 and 56 years, with posterior cortical atrophy. Ophthalmologic study was normal in all. Presenting signs and symptoms were visual ataxia, simultagnosia, agraphia, acalculia, spatial disorientation and unilateral neglect (Balint's and Gerstmann's syndromes). Apperceptive visual agnosia, aphasia, apraxia and alexia were also observed. One female had cortical blindness. Structural images were inconclusive, but PET scan and SPECT disclosed functional impairments in occipitotemporal or occipitoparietal areas.

The neuropsychological and neuroradiological correlates of slowly progressive visual agnosia

The case of a 64-year-old woman affected by slowly progressive visual agnosia is reported aiming to describe specific cognitive-brain relationships. Longitudinal clinical and neuropsychological assessment, combined with magnetic resonance imaging (MRI), spectroscopy, and positron emission tomography (PET) were used. Sequential neuropsychological evaluations performed during a period of 9 years since disease onset showed the appearance of apperceptive and associative visual agnosia, alexia without agraphia, agraphia, finger agnosia, and prosopoagnosia, but excluded dementia. MRI showed moderate diffuse cortical atrophy, with predominant atrophy in the left posterior cortical areas (temporal, parietal, and lateral occipital cortical gyri). 18FDG-PET showed marked bilateral posterior cortical hypometabolism; proton magnetic resonance spectroscopic imaging disclosed severe focal N-acetyl-aspartate depletion in the left temporoparietal and lateral occipital cortical areas. In conclusion, selective metabolic alterations and neuronal loss in the left temporoparietooccipital cortex may determine progressive visual agnosia in the absence of dementia.

What are we seeing?

Posterior cortical atrophy (PCA) is a dementing syndrome that presents with signs and symptoms of cortical visual dysfunction.1 The clinical features of PCA reflect dysfunction of both the ventral/occipito-temporal visual processing pathway causing apperceptive visual agnosia, alexia, and prosopagnosia and dorsal/occipito-parietal pathway causing Balint syndrome (simultanagnosia, optic ataxia and ocular apraxia), transcortical sensory aphasia, apraxia, and some or all of the elements of Gerstmann syndrome (agraphia, acalculia, finger agnosia, right-left disorientation).2,3 Frontal lobe functions and memory are relatively preserved until later in the course of the disease. In this issue of Neurology , McMonagle et al.4 describe the cognitive profile of 19 patients with PCA and compare this to the profile of 11 patients with typical amnestic Alzheimer disease …

Posterior Cortical Atrophy: Clinical Characteristics and Differences Compared to Alzheimer’s Disease

Background: Predominant and progressive complex visual disorders are often due to posterior cortical atrophy (PCA), a rare early-onset dementing syndrome presenting with visual complaints. In clinicopathological studies, PCA is most commonly considered a form of Alzheimer’s disease (AD); no prior study has evaluated clinical differences between PCA and AD. Methods: This study identified 15 patients who presented with progressive complex visual disorders and predominant occipitoparietal hypoperfusion on SPECT. These patients were retrospectively compared on clinical variables with 30 patients with clinically probable AD matched for gender, age and duration of illness. Results: The PCA patients presented with alexia, elements of Balint’s syndrome, apperceptive visual agnosia, dressing apraxia and environmental disorientation along with elements of Gerstmann’s syndrome. Compared to the AD patients, the 15 PCA patients (mean age of onset 58 years, range 51–64) had significantly better verbal fluency, less memory difficulty, more depression and greater insight into their illness but similar familial and apolipoprotein E risk factors. In the PCA patients, MRI often showed occipitoparietal atrophy without detectable mesiotemporal atrophy. Conclusions: PCA is a distinct clinical syndrome and not just AD with prominent visual deficits. Compared to AD controls, PCA patients have better language and memory but more insight and depression and more posterior atrophy on MRI. These results indicate clinical criteria for the diagnosis of PCA and recommend specific interventions such as visual aids and antidepressant medications. Similar risk factors and course suggest that PCA is most commonly an early-onset posteriorly shifted AD variant.

Apperceptive agnosia and face recognition

Are faces and objects recognized by separate visual recognition systems or might a single system subserve the recognition of both classes of input? Recognition of faces and objects by a single system predicts that prosopagnosics, who selectively lose the ability to recognize faces due to brain damage, should also lose the ability to recognize objects. Contrary to this prediction, case studies of prosopagnosia have reported intact object recognition. Further support for separate visual recognition systems comes from the case of HH reported here. Following a stroke involving the left posterior cortex, HH has a severe apperceptive visual agnosia for visually presented objects and an alexia for words. Yet, he shows relatively spared visual face processing. Such a performance pattern completes a double dissociation between face and object processing when coupled with prosopaganosia. More importantly, HH is the first apperceptive visual object agnosic to demonstrate spared face processing. The severity of his object-processing deficit is such that from the earliest levels in the visual processing hierarchy, distinct neural substrates must be responsible for processing some objects and faces. These results are discussed as support for Farah's model (Visual agnosia: disorders of object recognition and what they tell us about normal vision. Cambridge, MA: MIT Press, 1990) of object, face and word recognition.

Neuroanatomic correlates of visual agnosia in Alzheimer's disease: a clinicopathologic study.

To examine the neuroanatomic correlates of visual agnosia in AD. The authors performed an anterograde clinicopathologic study of 23 patients with clinically and neuropathologically confirmed AD in a 305-bed acute care geriatric hospital and a 165-bed acute care psychiatric hospital. The presence of apperceptive visual agnosia was assessed using the Ghent's overlapping figure test and the Gottschaldt's hidden figure test. Associative visual agnosia was examined using the conceptual items of the Columbia Mental Maturity Test. Correlations between neurofibrillary tangle (NFT) and senile plaque (SP) densities and visual agnosia were studied using forward stepwise logistic regression. A statistically significant relation was found between NFT densities in Brodmann's areas 18, 19, and 37, and associative visual agnosia, whereas NFT densities in the areas studied did not correlate with the presence of apperceptive visual agnosia. Senile plaque counts did not correlate with any of the neuropsychological parameters. These results support the existence of a dichotomy between associative and apperceptive agnosia, and show that only the former is related to the damage of secondary and high-order visual association areas in AD. In addition, the results suggest that SP densities do not represent a valuable pathologic correlate of visual agnosia in this disorder.

Severe apperceptive visual agnosia in left unilateral pathology: An unusual deficit in the absence of bilateral brain disease

Severe apperceptive visual agnosia in left unilateral pathology: An unusual deficit in the absence of bilateral brain disease

Severe apperceptive visual agnosia in left unilateral pathology: An unusual deficit in the absence of bilateral brain disease

Severe apperceptive visual agnosia in left unilateral pathology: An unusual deficit in the absence of bilateral brain disease

Consciousness of perception after brain damage.

Disturbances of visual perception after brain damage provide clues to understanding consciousness and the brain. In this article we review six visual disorders in which perception and consciousness are dissociated as a result of brain damage: blindsight, implicit shape perception in apperceptive visual agnosia, covert recognition of faces in prosopagnosia, unconscious perception in neglect and extinction, implicit reading in pure alexia, and implicit object recognition in associative visual agnosia. We consider these six disorders from the standpoint of three main schools of thought concerning consciousness and the brain, namely a localized system for consciousness, consciousness as a state of integration, and consciousness as a property of graded representation. The findings suggest that these syndromes do not share a single mechanism and that it is conceivable that more than one explanation will be necessary both within and across syndromes. We conclude on the basis of the current evidence that it is unlikely that any single brain system is necessary for conscious awareness of perception that does not play a role in perception as well.

Cognitive stages in visual recognition: Visual agnosia

The clinical spectrum of visual agnosia includes a variety of cognitive deficits and the incidence and relationship of these remain problematic. The syndromes of apperceptive and associative visual agnosia overlap most often but the occasional well documented dissociation is of great interest. Experimental evidence concerning these entities is scant and at times controversial but suggests several levels of processing that may be impaired independently. In this article, I shall address myself to these syndromes and attempt to describe the cognitive stages in visual recognition with respect to their intact and defective state, so as to provide an explanation of how the visual system functions cognitively.

Apperceptive agnosia due to carbon monoxide poisoning. An interpretation based on critical band masking from disseminated lesions

Apperceptive visual agnosia is normally held to be a specific deficit in ‘apperception’ - a hypothetical postsensory stage in visual processing. This paper describes the investigation of a patient diagnosed as suffering from a classical apperceptive agnosia resulting from carbon monoxide poisoning. Controlled behavioural testing confirmed the apparent agnosia but revealed that he could be trained to make a number of visual discriminations which had not been apparent from routine clinical examination and that he suffered a number of subtle sensory impairments which likewise had not hitherto been apparent. Evoked potential recording to grating patterns showed a complex pattern of brain responses involving interactions between spatial frequency, orientation and hemisphere recorded from. The data suggested that the agnosia was caused by sensory impairments rather than a deficit in apperception. We proposed that the impairments were caused by loss of certain spatial frequency and orientation information but rejected an interpretation based on the concept of processing channels in favour of one based on object contour masking by a peppery field defect caused by disseminated lesions. This interpretation received some support from fine grain static perimetry, contrast sensitivity function measurement and orientation discrimination in the two hemifields. Qualitatively similar results were obtained in normal subjects whose field was artificially masked. The results have implications for theories of visual agnosia and for theories of vision based on the concept of processing channels.