A case of visual agnosia for picture with right occipital lobe infarction]

We report a 74-year-old right-handed man with visual agnosia for picture due to right occipital lobe infarction. The patient had a remarkable impairment in visual recognition for standardized pictures made by Snodgrass and Vanderwart, in addition to left hemianopsia, left visuospatial neglect, and mild prosopagnosia. The visual agnosia for picture was generally recognized as a mild-type of the visual object agnosia, which was extremely rare in the patients with right occipital lesion. We discussed the mechanism of the visual agnosia in the right occipital lesion. Therefore, it raises the possibility that the broad impairment of the right occipital artery territory including parahippocampal gyrus as well as corpus callosum can cause the visual agnosia for picture.     

Associative visual agnosia without alexia.

A brain-damaged man was unable to appreciate the nature of objects and meaningful nonverbal symbols presented visually, although he could see, draw, describe, and match these stimuli. He had no difficulty understanding visually presented words. Auditory and tactile recognition of both verbal and nonverbal stimuli were normal. Our findings provide evidence that two neuropsychologic mechanisms were responsible for this disorder. One was an interhemispheric visual-verbal disconnection; the other was a specific categorization defect for visual, nonverba, meaningful stimuli. Neither mechanism alone was sufficient; both were necessary.     

A case of visual agnosia for objects (author's transl)]

Following an ischemic accident in the territory of the left posterior cerebral artery, a 71 year-old woman had a severe disorder of visual recognition of objects while she quickly identified them by touch. Visual recognition of pictures, written symbols, colours and, to a lesser degree, faces was also impaired. A careful examination showed that the patient's defect could not be accounted for by general intellectual impairment, language disorder, visual acuity, or pattern discrimination deficit. These findings are consistent with the classical concept of associative agnosia: the pathophysiology of the syndrome is discussed.     

A case of visual agnosia showing a disorder of pre-semantic visual classification

A case (J.R.) of associative visual agnosia (loss of meaning for visually presented objects without any serious sensory disorder) is reported. When asked to match a given name to sample the patient made both visual and semantic errors. Whereas semantic errors were reduced by priming, visual errors were intractable. It is argued that there is a disorder at the stage of pre-semantic abstraction, similar to that postulated elsewhere for some cases of deep dyslexia, contributing to the agnosia.     

Slowly progressive visual agnosia or apraxia without dementia

Two patients manifested a progressive impairment of visuoperceptive abilities and one patient a progressive generalized apraxia, in the absence of dementia and oral language disorders. The disease started in the presenium and the follow-up was of five, two and half and two years, respectively. The relation of these clinical pictures to cases of generalized dementia and to cases with isolated, progressive aphasia is discussed.     

Associative visual agnosia: a case study

This report describes a case of associative visual agnosia caused by a left sided, cortico-subcortical, inferior temporo-occipital infarction. Performance on visual perceptual tests was normal, while it was defective on visual classification tasks. Visual agnosia was interpreted as a visuo-verbal disconnection plus a categorization deficit for visual meaningful common stimuli. The left occipito-temporal lesion disrupted the visual classification process and prevented access of visual information to language areas and limbic system. The absence of right hemispheric lesion accounted for the normal recognition of familiar faces and other unique individual stimuli such as familiar places, whose recognition occurs through contextual evocation.     

A case of SSPE presenting visual disturbance and serial MRI study]

A case of subacute sclerosing panencephalitis (SSPE) was reported. The patient was a 16-year-old boy and he initially developed visual disturbance. His neurologic symptoms were myoclonus, dementia, and visual disturbance which was rare as an initial symptom in SSPE. Fundoscopy revealed bilateral pole chorioretinitis and macular degeneration. Serial MRI study demonstrated the lesions in the brain and right eye ball. The distribution varied as time went on. T2-weighted MR images showed the lesions more clearly than T1-weighted MR images. In this case dementia was marked but the lesions in the cerebrum on the MR images were considerably smaller than expected. Although MR image is useful to show the lesions, the discrepancy between clinical signs and MR images may be present in the early stage in SSPE.     

A case of abulia without memory disturbance due to infarction of the bilateral genua of the internal capsules]

A 68-year-old right handed man with treated hypertension presented with acute-onset somnolence without hemiparesis, dysarthria or sensory disturbance. Although he became laconic and his verbal responses were only in short terms, his replies were accurate and judgmental. A cranial MRI in axial, coronal, and sagittal section revealed small hemorrhagic infarcts essentially limited to the bilateral capsular genua without involvement of the inferior thalamic peduncles. A 123I-IMP single photon emission CT disclosed remarkable hypoperfusion in the bilateral frontal cortex. After a week of somnolence, he gradually became wakeful, but was still abulic. Neuropsychological examinations revealed no memory disturbance. We consider that disconnection of the thalamo-frontal projection at the genua of the internal capsules caused somnolence, apathy, and abulia in our case. The hitherto reported cases of the genu infarcts that showed memory disturbance had the lesion involving both the inferior thalamic peduncle and its nearby mamillothalamic tract. In contrast, our case without memory disturbance had infarcts confined to the genua apparently sparing the two tracts, implicating that memory function may be preserved when such structures are intact.     

Symptoms and lesion localization in visual agnosia]

There are two cortical visual processing streams, the ventral and dorsal stream. The ventral visual stream plays the major role in constructing our perceptual representation of the visual world and the objects within it. Disturbance of visual processing at any stage of the ventral stream could result in impairment of visual recognition. Thus we need systematic investigations to diagnose visual agnosia and its type. Two types of category-selective visual agnosia, prosopagnosia and landmark agnosia, are different from others in that patients could recognize a face as a face and buildings as buildings, but could not identify an individual person or building. Neuronal bases of prosopagnosia and landmark agnosia are distinct. Importance of the right fusiform gyrus for face recognition was confirmed by both clinical and neuroimaging studies. Landmark agnosia is related to lesions in the right parahippocampal gyrus. Enlarged lesions including both the right fusiform and parahippocampal gyri can result in prosopagnosia and landmark agnosia at the same time. Category non-selective visual agnosia is related to bilateral occipito-temporal lesions, which is in agreement with the results of neuroimaging studies that revealed activation of the bilateral occipito-temporal during object recognition tasks.     

A disorder of lightness discrimination in a case of visual form agnosia

Benson and Greenberg (1969) described an "agnosic" patient whose severe visual recognition disorder could be accounted for in terms of a deficit in the perception of shape. We report here on a recent case of this disorder (visual form agnosia), and have found that she performs very poorly on tasks of discriminating shades of grey, although she is able to discriminate between hues. This sensory deficit helps to explain some of her perceptual difficulties; it also provides further evidence for parallel feature-processing in the human brain complementary to and consistent with recent physiological data on the visual cortex in animals.     

A case of associative visual agnosia: neuropsychological findings and theoretical considerations

A 61-year-old right-handed man fell downstairs and was found unconscious. There was no abnormality in the general physical examinations. Neurological examinations revealed a quadrantanopia. Neuropsychological examination revealed an impairment in recent verbal memory, alexia, agraphia, object agnosia, color naming difficulty, prosopagnosia, and visuospatial constructional disability. CT scan demonstrated subcortical hematomas in the temporo-occipital regions of both hemispheres. MRI demonstrated extensive low-intensity lesions in the lingual, fusiform and posterior inferior temporal gyri on both hemispheres. Both inferior longitudinal fasciculi were also affected. His neuropsychological deficits seem best described as a typical form of associative visual agnosia. From the results of neuroradiological findings, the authors emphasize that associative visual agnosia might be produced by an intrahemispheric disconnection between the visual cortices and the temporal lobes which are supposed to be the storage site of the engrams of visual memories. Moreover, the neuropsychological findings suggest that the visuo-constructional ability to convert the two-dimensional input to the three-dimensional construction and the capacity of three-dimensional imagination were severely impaired in our patient. It was considered that these neuropsychological features play an important role in the recognition difficulties of associative visual agnosia.     

A case of associative visual agnosia: Neuropsychological findings and theoretical considerations

Abstract

A 61-year-old right-handed man fell downstairs and was found unconscious. There was no abnormality in the general physical examinations. Neurological examinations revealed a quadrantanopia. Neuropsychological examination revealed an impairment in recent verbal memory, alexia, agraphia, object agnosia, color naming difficulty, prosopagnosia, and visuospatial constructional disability. CT scan demonstrated subcortical hematomas in the temporo-occipital regions of both hemispheres. MRI demonstrated extensive low-intensity lesions in the lingual, fusiform and posterior inferior temporal gyri on both hemispheres. Both inferior longitudinal fasciculi were also affected. His neuropsychological deficits seem best described as a typical form of associative visual agnosia. From the results of neuroradiological findings, the authors emphasize that associative visual agnosia might be produced by an intrahemispheric disconnection between the visual cortices and the temporal lobes which are supposed to be the storage site of the engrams of visual memories. Moreover, the neuropsychological findings suggest that the visuo-constructional ability to convert the two-dimensional input to the three-dimensional construction and the capacity of three-dimensional imagination were severely impaired in our patient. It was considered that these neuropsychological features play an important role in the recognition difficulties of associative visual agnosia.     

Implicit integration in a case of integrative visual agnosia

We present a case (SE) with integrative visual agnosia following ischemic stroke affecting the right dorsal and the left ventral pathways of the visual system. Despite his inability to identify global hierarchical letters [Navon, D. (1977). Forest before trees: The precedence of global features in visual perception. Cognitive Psychology, 9, 353-383], and his dense object agnosia, SE showed normal global-to-local interference when responding to local letters in Navon hierarchical stimuli and significant picture-word identity priming in a semantic decision task for words. Since priming was absent if these features were scrambled, it stands to reason that these effects were not due to priming by distinctive features. The contrast between priming effects induced by coherent and scrambled stimuli is consistent with implicit but not explicit integration of features into a unified whole. We went on to show that possible/impossible object decisions were facilitated by words in a word-picture priming task, suggesting that prompts could activate perceptually integrated images in a backward fashion. We conclude that the absence of SE's ability to identify visual objects except through tedious serial construction reflects a deficit in accessing an integrated visual representation through bottom-up visual processing alone. However, top-down generated images can help activate these visual representations through semantic links.     

Chronic subdural hematoma presenting visual disturbance: a case report]

The authors reported a rare case of chronic subdural hematoma presenting bilateral visual impairment caused by papilledema. A 49-year-old man was admitted to our department due to left blurred vision. On admission, ophthalmological examination revealed visual acuity disturbance on the left eye, bilateral nasal visual field defect and papilledema. CT scan and MRI demonstrated bilateral subdural hematoma. No remarkable findings were detected on cerebral angiography. After evacuation of bilateral subdural hematomas, his visual symptoms recovered. In this report, we discuss the mechanism of visual impairment caused by chronic subdural hematoma.     

A case of slowly progressive aphasia accompanied with auditory agnosia]

A 68-year-old right-handed woman was admitted to our hospital because of difficulty to speak and understand conversation over 10 years. She was able to make herself by writing. No change in her personality or behavioral abnormality was observed so that she could live without help. Although her WAIS score and auditory brain stem response were normal, she could not understand the speech or distinguish the sound. She also spoke plenty of words fluently, resulting in undifferentiated jargon. She did not make any effort in speaking. Her speech was, however, unclear and hard to understand. Brain MRI scan disclosed a moderate atrophy of bilateral temporal lobe and enlargement of Sylvius fissure. A three-dimension reconstructed brain surface image showed enlargement of the perisylvian fissure, and atrophy of the gyrus frontalis inferior, operculum, gyrus temporal superior, bilaterally. Reduced cerebral blood flow was demonstrated on 99mTc-ECD SPECT in the left thalamus and bilateral fronto-temporal lobe. A diagnosis of slowly progressive aphasia with auditory agnosia was made. Our case suggests that bilateral disturbance of neuronal network between the primary auditory area and the secondary auditory area is responsible to the consequence of auditory agnosia.     

Number processing and calculation in a case of visual agnosia

We describe the performance of a brain-damaged subject who suffered from visual agnosia leading to major difficulties in generating and exploiting visual representations from long-term memory. His performance in a physical judgement task in which he was required to answer questions about the visual shapes of Arabic numerals reflected his agnosic problems. However, he showed no impairment in usual number processing and calculation tasks. This case shows that, despite some commonalities in number and object processing, actual numerical processes are not affected by visual agnosia and can be preserved even when fine visual processes are impaired.     

When is a view unusual? A single case study of orientation-dependent visual agnosia

Several hypotheses have been proposed to explain why some neurological patients fail to recognise objects from unusual views: that it results from difficulty identifying an object's principal axis when it is foreshortened, identifying an object when landmark features are occluded, or an inability to rotate mental images. It was possible to test these hypotheses by examining the recognition abilities of a single case (A.S.), by using stimuli that were “unsusual” only because of picture-plane misorientation. A.S. showed a recognition deficit in which his accuracy was proportional to the extent of misorientation from the normal upright for the object—although both principal axis and feature information remain visible after picture-plane rotation. Furthermore, A.S. performed with normal accuracy, and normal pattern of reaction time performance, on tasks of mental rotation. These findings suggest that none of these traditional accounts can adequately explain why this patient was unable to recognise objects from unusual views. These findings are discussed the light of recent suggestions of the basis of this type of disorder.