Associative Visual Agnosia Research Articles

Clinical and structural disconnectome evaluation in a case of optic aphasia

Optic Aphasia (OA) and Associative Visual Agnosia (AVA) are neuropsychological disorders characterized by impaired naming on visual presentation. From a cognitive point of view, while stimulus identification is largely unimpaired in OA (where access to semantic knowledge is still possible), in AVA it is not. OA has been linked with right hemianopia and disconnection of the occipital right-hemisphere (RH) visual processing from the left hemisphere (LH) language areas.In this paper, we describe the case of AA, an 81-year-old housewife suffering from a deficit in naming visually presented stimuli after left occipital lesion and damage to the interhemispheric splenial pathway. AA has been tested through a set of tasks assessing different levels of visual object processing. We discuss behavioral performance as well as the pattern of lesion and disconnection in relation to a neurocognitive model adapted from Luzzatti and colleagues (1998). Despite the complexity of the neuropsychological picture, behavioral data suggest that semantic access from visual input is possible, while a lesion-based structural disconnectome investigation demonstrated the splenial involvement.Altogether, neuropsychological and neuroanatomical findings support the assumption of visuo-verbal callosal disconnection compatible with a diagnosis of OA.

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.

Structural alterations and their underlying substrates in correlations with “what” stream visual pathways in progression stages of Alzheimer's disease: Associative visual objective agnosia (AVOA)

Introduction Visual agnosia is a promptly noticed neurological deficit in Alzheimer's disease (AD), affects the inferior temporal lobe, which leads an inability to perceive objects. The interconnection between the two cortices in visual ventral stream, the visual cortex (BA 17, 18, 19) and inferior temporal lobe (BA 20) explain how we perceive and recognize the objects, called associative object visual perception. We Team Neuron, focused on correlating the neural structural connectivity with associative visual agnosia in Alzheimer's patients using ;“Diffusion Tensor Imaging Tractography;”. The study involves fifty DTI datasets, both the sexes of Control and disease progression stages of AD, with age ranges from 50 to 90 years. Results On observation, the females displayed with progressive increase in the (number and volume) fibers among the cognitive declining stages of AD. But, the males, noticed with a bi-modal variation (number and volume) of fibers, within the disease progression stages of AD. Conclusion Although the statistical analysis was insignificant, it was noticed that the males are predominantly affected than females. The current observations, propose an insight to understand the bi-modal distribution of fibers in the male and progressive increase of fibers in the female, from the control to disease progression stages of AD. However, these findings need to be confirmed with functional and effective connectivity analysis for further understandings.

Perception of High-Level Content and the Argument from Associative Agnosia

Visual Associative agnosia is a rare perceptual impairment generally resulting from lesions in the infero temporal cortex. Patients suffering from associative agnosia are able to make accurate copies of line drawings, but they are unable to visually recognize objects - including those represented in line drawings - as belonging to familiar high-level kinds. The Rich Content View claims that visual experience can represent high-level kind properties. The phenomenon of associative agnosia appears to present us with a strong case for the Rich Content View. There are reasons for thinking that the experiences of an agnosic patient differ from those of a healthy subject. Given that there is a phenomenal contrast between the experiences of an associative agnosic and those of a healthy perceiver, one may argue that this contrast is due to differences in abilities to represent high-level kinds. I claim that there is indeed a phenomenal contrast between the visual experiences of an agnosic and those of a healthy perceiver. However, the explanation of this contrast that best fits the empirical data is compatible with the view that visual experience does not represent high-level kinds.

Is the Right Anterior Temporal Variant of Prosopagnosia a Form of ‘Associative Prosopagnosia’ or a Form of ‘Multimodal Person Recognition Disorder’?

The construct of associative prosopagnosia is strongly debated for two main reasons. The first is that, according to some authors, even patients with putative forms of associative visual agnosia necessarily present perceptual defects, that are the cause of their recognition impairment. The second is that in patients with right anterior temporal lobe (ATL) lesions (and sparing of the occipital and fusiform face areas), who can present a defect of familiar people recognition, with normal results on tests of face perception, the disorder is often multimodal, affecting voices (and to a lesser extent names) in addition to faces. The present review was prompted by the claim, recently advanced by some authors, that face recognition disorders observed in patients with right ATL lesions should be considered as an associative or amnestic form of prosopagnosia, because in them both face perception and retrieval of personal semantic knowledge from name are spared. In order to check this claim, we surveyed all the cases of patients who satisfied the criteria of associative prosopagnosia reported in the literature, to see if their defect was circumscribed to the visual modality or also affected other channels of people recognition. The review showed that in most patients the study had been limited to the visual modality, but that, when the other modalities of people recognition had been taken into account, the defect was often multimodal, affecting voice (and to a lesser extent name) in addition to face.

視覚失語に移行した連合型視覚失認の 1 例

視覚失語に移行した連合型視覚失認の 1 例

POD08 Abnormal saliency processing in a patient with visual form agnosia

BackgroundWhen we look at a visual scene our scanning eye movements are not random. We have previously compared the eye movements made by two patients with associative visual agnosia with...

A Case of Associative Visual Agnosia with Preserved Perception of Overlapping Figures

Lissauer (1890) の定義に相応しい，形態と意味の連合が障害された本来の連合型視覚失認が左一側性病変により生じたと考えられる例を報告した。症例は，25 歳の右利き男性で，図形の模写も錯綜図に含まれる物体をスムーズになぞることも可能であることから，物体の形態知覚は良好に保たれていると考えられた。物体認知に関する検査では，視覚を通じての呼称が著しく不良で，触覚や定義からの呼称はそれよりも有意に良好であった。絵カードのカテゴリー分類も困難であることから，視覚失語の可能性は否定された。頭部 CT では，左半球の側脳室三角部～後角の周辺領域，脳梁膨大部の後方領域に出血巣を認めた。本例では視空間の探索行動の乏しさがみられたが，固視した単一の物体の視覚認知への影響は少ないと考えられた。本論文では，形態知覚が保たれた本来の連合型視覚失認が左一側性病巣で生じる場合のメカニズムについて，視覚失語との対比を含めて論じた。

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.

Associative Visual Agnosia: A Case Study

We report a case of massive associative visual agnosia. In the light of current theories of identification and semantic knowledge organization, a deficit involving both levels of structural description system and visual semantics must be assumed to explain the case. We suggest, in line with a previous case study [1], an alternative account in the framework of (non abstractive) episodic models of memory [4].

Could dynamic attractors explain associative prosopagnosia?

Prosopagnosia is one of the many forms of visual associative agnosia, in which familiar faces lose their distinctive association. In the case of prosopagnosia, the ability to recognize familiar faces is lost, due to lesions in the medial occipitotemporal region. In "associative" prosopagnosia, the perceptual system seems adequate to allow for recognition, yet recognition cannot take place. Our hypothesis is that a possible cause of associative prosopagnosia might be the occurrence of Dynamic attractors in the brain's auto-associative circuits. We present a biologically plausible model composed of two stages: Pre-processing and face recognition. In the first stage, the face image is passed through Gabor filters which model the kind of visual processing carried out by the simple and complex cells of the primary visual cortex of higher mammals and the resulting features are fed into a Pseudo-inverse associative neural network for the recognition task. Next, we damage the network by reducing self-connections below a certain threshold in order to create dynamic attractors and hence hinder the networks ability to recognize familiar faces (faces already learned). Results obtained from simulations show that the resulting network responses are very similar to those of associative prosopagnosic patients. We conclude that the problems concerning associative prosopagnosia may partly be explained through the concepts of dynamic attractors. Although there is no known cure for prosopagnosia, we believe that the focus of any treatment should be to help the individual with prosopagnosia develop compensatory strategies for remembering faces. Adults with prosopagnosia as a result of stroke or brain trauma can be retrained to use other clues to identify faces. And a cure for children born with prosopagnosia might eventually rely on reinforcement techniques that reward them for paying attention to faces during early childhood. Reinforcement learning from examples of patterns to be classified using habituation and association would create lower dimensional local basins in the brain, which would form a global attractor landscape with one basin for each face. These local basins would eventually constitute dynamical memories that solve difficult problems in classifying and recognizing faces.

Optic Aphasia: A Case Study

Optic aphasia is a rare syndrome in which patients are unable to name visually presented objects but have no difficulty in naming those objects on tactile or verbal presentation. We report a 79-year-old man who exhibited anomic aphasia after a left posterior cerebral artery territory infarction. His naming ability was intact on tactile and verbal semantic presentation. The results of the systematic assessment of visual processing of objects and letters indicated that he had optic aphasia with mixed features of visual associative agnosia. Interestingly, although he had difficulty reading Hanja (an ideogram), he could point to Hanja letters on verbal description of their meaning, suggesting that the processes of recognizing objects and Hanja share a common mechanism.

Electrophysiological correlates of associative visual agnosia lesioned in the ventral pathway

Visual agnosia has been well studied by anatomical, neuropsychological and neuroimaging studies. However, functional changes in the brain have been rarely assessed by electrophysiological methods. We carried out electrophysiological examinations on a 23-year-old man with associative visual agnosia, prosopagnosia and cerebral achromatopsia to evaluate the higher brain dysfunctions of visual recognition. Electrophysiological methods consisted of achromatic, chromatic and category-specific visual evoked potentials (CS-VEPs), and event-related potentials (ERPs) with color and motion discrimination tasks. Brain magnetic resonance imaging revealed large white matter lesions in the bilateral temporo-occipital lobes involving the lingual and fusiform gyri (V4) and inferior longitudinal fasciculi due to multiple sclerosis. Examinations including CS-VEPs demonstrated dysfunctions of face and object perception while sparing semantic word perception after primary visual cortex (V1) in the ventral pathway. ERPs showed abnormal color perception in the ventral pathway with normal motion perception in the dorsal pathway. These electrophysiological findings were consistent with lesions in the ventral pathway that were detected by clinical and neuroimaging findings. Therefore, CS-VEPs and ERPs with color and motion discrimination tasks are useful methods for assessing the functional changes of visual recognition such as visual agnosia.

Evidence for perceptual deficits in associative visual (prosop)agnosia: a single-case study

Associative visual agnosia is classically defined as normal visual perception stripped of its meaning [Archiv für Psychiatrie und Nervenkrankheiten 21 (1890) 22/English translation: Cognitive Neuropsychol. 5 (1988) 155]: these patients cannot access to their stored visual memories to categorize the objects nonetheless perceived correctly. However, according to an influential theory of visual agnosia [Farah, Visual Agnosia: Disorders of Object Recognition and What They Tell Us about Normal Vision, MIT Press, Cambridge, MA, 1990], visual associative agnosics necessarily present perceptual deficits that are the cause of their impairment at object recognition Here we report a detailed investigation of a patient with bilateral occipito-temporal lesions strongly impaired at object and face recognition. NS presents normal drawing copy, and normal performance at object and face matching tasks as used in classical neuropsychological tests. However, when tested with several computer tasks using carefully controlled visual stimuli and taking both his accuracy rate and response times into account, NS was found to have abnormal performances at high-level visual processing of objects and faces. Albeit presenting a different pattern of deficits than previously described in integrative agnosic patients such as HJA and LH, his deficits were characterized by an inability to integrate individual parts into a whole percept, as suggested by his failure at processing structurally impossible three-dimensional (3D) objects, an absence of face inversion effects and an advantage at detecting and matching single parts. Taken together, these observations question the idea of separate visual representations for object/face perception and object/face knowledge derived from investigations of visual associative (prosop)agnosia, and they raise some methodological issues in the analysis of single-case studies of (prosop)agnosic patients.

A Case Study of Visual Agnosia without Perceptual Processing or Structural Descriptions Impairment

We report a new case of visual associative agnosia. Our patient (DJ) was impaired in several tasks assessing visual processing of real objects, colour pictures, and line drawings. The deficit was present both with naming and gesturing responses. Object processing in other modalities (verbal, auditory nonverbal, and tactile) was intact. Semantic processing was impaired in the visual but not in the verbal modality. Picture-word matching was better than single picture identification. DJ's visual perceptual processing, was intact in several tasks such as visual attributes discrimination, shape discrimination, illusory contours perception, segmentation, embedded figures processing and matching objects under different viewpoints. Most importantly, we show that there was no impairment of stored structural descriptions and that the patient was able to build new visual representations. These results are considered in the context of Farah's (1990, 1991) proposals about visual associative agnosia.

The cognitive impairments due to the occipito-parietal brain injury after gunshot: a successful neurorehabiliation case study

Objective : The presented case study describes the beneficial results of the neuropsychological rehabilitation of a gunshot victim, even with late initialization of the therapy--over 1 year after head trauma. Design : A case study of DE, a victim with bilateral damage of the parietal-occipital regions of the brain due to a gunshot. Methods : Neuropsychological rehabilitation, first preceded by an initial neuropsychological examination (standard psychological tests: WAIS-R, RAVLT, Rey's CFT, BVRT and clinical experiments tailored to DE's condition), was initiated 1 year after trauma. The rehabilitation programme consisted of computer-based tasks, paper-and-pencil exercises, and occupational therapy. The patient's progress was assessed as improvement in performance in standardized tests and computer-based tasks. Results : DE was diagnosed with complex cognitive deficits syndrome, including visual associative agnosia, apraxia, visuospatial and constructive disorders and linguistic defects. After 1 year of rehabilitation the patient's functioning significantly improved as measured by psychological tests and computer-based tasks ( p < 0.05) as well as the evaluation of the patient's quality of life. Conclusions : The case study demonstrates beneficial effects of neurorehabilitation even initialized at the so-called 'late stage' after a brain injury.

Visual object processing in schizophrenia: evidence for an associative agnosic deficit

Early studies suggested visual form perception impairment in schizophrenia. To re-examine this claim and characterise the deficit neuropsychologically, 41 schizophrenic patients were administered tests sensitive to different levels of visual object perception and recognition. Intellectually well-preserved patients were examined separately on these and additional tests. Single case analysis was also applied to four patients showing varying degrees of general intellectual impairment. As a group, the patients showed little impairment on tests of early visual object perception, but greater impairment on higher-level visual processing tests, in particular object recognition and naming. This held true for patients with preserved general intellectual function. Single case analysis suggested that patients with schizophrenia have a selective deficit affecting object recognition and identification, with a pattern similar to visual associative agnosia in neurological patients.

Atrofia cortical posterior

Posterior cortical atrophy (PCA) is a dementing syndrome characterized by an early alteration of higher visual functions. Patients usually develop a perceptive visual agnosia related to Balint syndrome. Verification showed Alzheimer s disease (AD) in most PCA observations (13/14 cases), and it can be concluded that there is a posterior variant of AD with prominent visual symptomatology. However, most PCA cases have not been verified and the nature of the disorder remains unknown in these observations. An early and severe unilateral occipital horn dilatation was found in one out of every six cases with non verified PCA. To the best of our knowledge, this image has not been described in AD and these observations could be of different nature. On the other hand, some non verified PCA cases have occasionally manifested as an associative visual agnosia. The nature of this type of associative disorder is unknown, but it could be similar to the nature of semantic dementia, a non Alzheimer s syndrome related to unspecific lesions of temporal lobes.