[Picture agnosia without alexia, visuospatial agnosia or object agnosia].
Explore the source record for details and available documents.
Agnosia↗
SEARCH · Search PubMed
Results for “AGNOSIA”
Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
Auditory agnosia restricted to environmental sounds following cortical deafness and generalized auditory agnosia.
We encountered a case of auditory agnosia restricted to environmental sounds, which was associated with the development of bilateral subcortical lesions after suffering a bilateral putaminal hemorrhage. The patient had a history of a putaminal hemorrhage on her left side without any major disability. Three years later, she suffered a putaminal hemorrhage on the other side. The clinical picture started with cortical deafness, then changed to generalized auditory agnosia for verbal and environmental sounds, and finally developed into auditory agnosia confined to the perception of environmental sounds. Her errors in a test of sound recognition were discriminative rather than associative in nature. Neuro-radiological examinations revealed bilateral subcortical lesions involving the fibers from the medial geniculate body to the temporal lobes after bilateral putaminal hemorrhage. This case suggested that the subcortical lesion involving bilateral acoustic radiation could cause either cortical deafness, auditory agnosia of all sounds, or auditory agnosia restricted to environmental sounds.
Agnosia↗
[Spatial agnosia and agnosia of physiognomies, sequelae of cortical blindness].
Explore the source record for details and available documents.
Agnosia↗
[A case of visual spatial agnosia--an abortive form of Bálint's syndrome with unilateral spatial agnosia].
Explore the source record for details and available documents.
Agnosia↗
[About a case of visual agnosia with prosopagnosia and colour agnosia].
Explore the source record for details and available documents.
Aged↗
Toe agnosia in Gerstmann syndrome.
The following case report presents a patient exhibiting Gerstmann syndrome accompanied by toe agnosia. A 72 year old right handed woman had a focal lesion in the angular gyrus of the left hemisphere which was caused by a glioblastoma multiforme. The first symptom she had complained of was severe headache. Standardised neuropsychological tests of intelligence, memory, attention, fluency, apraxia, and language functions as well as tests for the assessment of agraphia, acalculia, right-left disorientation, and digit agnosia were performed. The patient displayed all four symptoms of the Gerstmann syndrome--namely, agraphia, acalculia, right-left disorientation, and finger agnosia. The patient did not display aphasia, constructional apraxia, or any other neuropsychological impairment. In addition to the four symptoms of the Gerstmann syndrome an agnosia of the toes was found. Further studies should determine whether finger agnosia in Gerstmann syndrome is usually accompanied by toe agnosia. Finger agnosia in the context of this syndrome may be better named digit agnosia.
Aged↗
Neuroanatomic correlates of visual agnosia in Alzheimer's disease: a clinicopathologic study.
OBJECTIVE: To examine the neuroanatomic correlates of visual agnosia in AD. METHODS: 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. RESULTS: 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. CONCLUSIONS: 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.
Aged↗
What is it like to be a patient with apperceptive agnosia?
Neuropsychological deficits have been widely used to elucidate normal cognitive functioning. Can patients with such deficits also be used to understand conscious visual experience? In this paper, we ask what it would be like to be a patient with apperceptive agnosia (a deficit in object recognition). Philosophical analyses of such questions have suggested that subjectively experiencing what another person experiences would be impossible. Although such roadblocks into the conscious experience of others exist, the experimental study of both patients and neurologically normal subjects can be used to understand visual processing mechanisms. In order to understand the visual processes damaged in apperceptive agnosia, we first review this syndrome and present a case study of one such patient, patient J.W. We then review several theoretical accounts of apperceptive agnosia, and we conclude that studies of the patients themselves may not allow us to discriminate between the various explanations of the syndrome. To test these accounts, we have simulated apperceptive agnosia in neurologically normal subjects. The implications of our results for understanding both apperceptive agnosia and normal visual processing are discussed.
Adult↗
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.
Agnosia↗
Associative visual agnosia and alexia without prosopagnosia.
Disagreement over the neuroanatomical substrate of associative visual agnosia encompasses such basic issues as: (1) the necessity for bilateral lesions; (2) the intrahemispheric locus of damage; and (3) the roles of disconnection versus cortical damage. We examined three patients whose associative visual agnosia encompassed objects and printed words but spared faces. CAT scans revealed unilateral dominant occipitotemporal strokes. CAT scans of four previously reported cases with this same profile of associative agnosia were obtained. Dominant parahippocampal, fusiform and lingual gyri were the most extensively damaged cortical regions surveyed and were involved in all cases. Of white matter tracts surveyed, only temporal white matter including inferior longitudinal fasciculus was severely and universally involved. Splenium of the corpus callosum was frequently but not always involved. We conclude there is a form of associative visual agnosia with agnosia for objects and printed words but sparing face recognition which has a characteristic unilateral neuropathology. Damage or disconnection of dominant parahippocampal, fusiform and lingual gyri is the necessary and sufficient lesion.
Aged↗
Auditory agnosia.
Auditory agnosia can be defined as the defective recognition of non-verbal sounds and noises. The clinical picture of this disorder is described and the scarcity of knowledge of auditory agnosia derived purely from single cases is discussed. Next, experimental studies on unselected series of brain-damaged patients, especially designed to clarify the relation of auditory agnosia to aphasia and to the hemispheric locus of the lesion are reported. The results consistently point to the existence of two types of auditory agnosia, a semantic-associative one, specifically associated with lesions of the left hemisphere and aphasia, and a discriminative one, specifically associated with lesions of the right hemisphere. The hypothesis is advanced that the semantic-associative variety of auditory agnosia is part of a wider cognitive disorder.
Agnosia↗
Ettlinger revisited: the relation between agnosia and sensory impairment.
The concept of agnosia as a higher order functional impairment, which can occur in the absence of low level visual perceptual deficits, continues to provoke debate. This controversy is complicated by the fact that, on close examination, agnosic patients do tend to have some perceptual difficulties. Thus the issue centres around the question as to whether these deficits play a causal part in the aetiology of agnosia or whether they are functionally independent, with both impairments resulting from the substantial cerebral lesions involved in agnosia. In 1956, Ettlinger published a study in which he compared the performance of patients with visual recognition deficits and patients with posterior brain lesions whose recognition abilities were intact. He argued that visual perceptual problems could not explain the recognition deficit in agnosia as he saw far worse perceptual impairments in patients who did not experience any problems in visual recognition. Although the logic of Ettlinger's argument is not disputed, some criticisms have arisen concerning the study, such as the fact that his experimental group did not include a truly object agnosic patient. In addition, Ettlinger's visual-sensory assessment can no longer be considered comprehensive in the light of present day knowledge of the cerebral visual apparatus. This study therefore investigated three (prosop)agnosic patients and five patients with unilateral brain lesions without recognition deficits on an extensive battery of visual sensory tests. The results support Ettlinger's original claim that (in some cases) agnosia cannot be explained as resulting from lower level visual impairments.
Adult↗
What processing is impaired in apperceptive agnosia? Evidence from normal subjects.
Visual agnosia is a neuropsychological syndrome characterized by a failure of object identification. Apperceptive agnosia, an object identification deficit caused by damage to early perceptual processes, has been explained by appealing to both damaged early sensory processes and to damaged preattentive grouping processes. Which of these two explanations best accounts for the behavior of these patients? We present results from two experiments designed to distinguish rival theoretical accounts of apperceptive agnosia. In our studies, we attempted to simulate apperceptive agnosia in neurologically intact subjects. Sensory-deficit accounts of the syndrome predict that degrading visual processing would make normal subjects perform like patients; grouping-deficit accounts predict that removing perceptual organization cues from visual displays would make normal subjects perform like patients. We were able to simulate the behavior of an apperceptive agnosic patient by removing perceptual organization cues, consistent with a grouping-deficit account of this syndrome. The implications for understanding both apperceptive agnosia and normal visual functioning are discussed.
Adult↗
[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.
Aged↗
[Visual object agnosia: current conceptions].
Visual agnosia for objects is a difficulty in recognizing objects presented visually. This difficulty can not be explained by a mental deterioration, a disorder of attention or a lack of familiarity with the object. Two criteria are essential but disputed: the absence of visual sensory difficulty necessary for adequate perception; possible recognition of the object by another sensory modality. An object is characterized by a triple representation: formal, semantic, lexical. The clinical, cognitive, pathophysiological analysis lead to distinguish 3 types of visual agnosia. 1) Aperceptive visual agnosia: patients see badly with morphological errors; the disorder concerns visual informations processing that is a necessary condition for identifying the formal representation of the object; the lesions are bilateral and involve the occipito-temporal cortex. 2) Associative visual agnosia: patients can copy, are not aphasic, but give erroneous verbal responses; the disorder concerns the links between formal representations and semantic, lexical representations; the lesions are unilateral and involve the left gyrus angularis connections. 3) Asemantic visual agnosia: patients have lost the meanings of objects and words; the disorder concerns semantic representations; the lesions are bilateral and involve the temporo-limbic cortex.
Agnosia↗
[The acquisition of language through finger spelling in a child with auditory agnosia (author's transl)].
A child with auditory agnosia for verbal and nonverbal sounds was reported. He was born without difficulty and his early development was normal. At the age of 14 months, he suffered from herpes simplex encephalitis and fell in a trance. Soon after he recovered from the illness, he found not to pay any attention to sounds and not to speak any words. He was referred to Teikyo University hospital at 2.5 years of age for the hearing measurement. The average threshold of conditioned orientation reflex audiometry at 500, 1000 and 2000 Hz were 85 dB, while the threshold of auditory brain stem response was 15 dB which is normal. CT scan demonstrated bilateral lesions of superior temporal gyrus. Neurological examination revealed nothing particular except the troubles with hearing and speech. He was made a diagnosis of auditory agnosia. The speech therapy was started at two years old. During the first three years, he was taught how to communicate with gestures and lip reading. However, it was difficult for him to understand the meaning of gestures and lip reading. During these years he could acquire lip reading of simple words. As to environmental sounds, he could respond the telephone-bell and the organ at three years and seven months old, but could not discriminate other sounds. At five years old, finger spelling for his language education was introduced. He appeared to have learned finger spelling more easily and could read and write several letters through finger spelling within a month. One year after introduction of finger spelling, he acquired about 60 words (54 nouns and 6 verbs) and could read words and two-words sentences. However, the speed of his acquisition of language was very slow for his age. Now, he can understand mother's simple instructions and communicate with his mother and his speech therapist through finger spelling, but his responses toward environmental sounds are not stable yet. The course of this patient suggests that language acquisition of children with auditory agnosia might be different from that of deaf children. The prognosis of auditory agnosia in children is controversial. In this patient, the development of language is not good as well as in most previous reports, perhaps because of extensive lesions of language area. The patients with auditory agnosia is frequently mistaken for deaf or mentally retarded children. We emphasize that the early diagnosis and early speech therapy with visual communication are needed for these children.
Agnosia↗
[Multimodal or multisensorial agnosia?].
A 75 year-old right handed woman had persistent right homonymous hemianopia and alexia without agraphia caused by a haemorrhagic stroke of the left occipito-temporal region. Six months later she suffered sudden onset visual and auditory agnosia, following a second haematoma, contralateral to the first one, in the right occipito-temporal region including the lingual and fusiform gyri. None of the disorders concerned semantic representation, so that an asemantic agnosia was excluded. Her performance in naming and recognition tests, in both visual and auditory modalities, demonstrated a wide range of responses and errors. The pattern of visual symptoms suggested "associative visual agnosia narrow sense" (Farah, 1990); auditory agnosia concerned only the non verbal stimuli. These findings were discussed in terms of anatomical mechanisms subserving perceptual, semantical, visuo and auditory-verbal representation. In this case, visual and auditory, agnosia appears to be independent.
Aged↗
[Tactile agnosia and dysfunction of the primary somatosensory area. Data of the study by somatosensory evoked potentials in patients with deficits of tactile object recognition].
The question as to whether a failure of recognition unrelated to impaired sensory processing or to disorder of naming can occur in the somato-sensory modality has been eagerly debated in the french neurology. Taking as an argument the fact that he had never observed a tactile agnosia in the absence of subtle sensory deficits Dejerine denied the localizing value of tactile agnosia (or asterognosis). Conversely Delay, 20 years later, identified tactile performances such as discrimination of texture and shapes, which he considered as a specific neocortical function, that were lost in parietal syndromes with astereognosis and preserved elementary sensations. He also coined the term "tactile asymbolia" to qualify the patients with astereognosis in whom these performances are preserved. When referring to the definition of agnosias only "tactile asymbolia" should be considered as a "true" tactile agnosia. The recording of early somatosensory evoked potentials (SEPs) now offers the possibility of assessing non invasively the function of the primary somatosensory cortex (in particular area 3b). We have recorded SEPs to median nerve or finger stimulation in 309 subjects with a focal hemispheric lesion presenting with a somatosensory deficit of any type. We could confirm that asterognosis referable to impaired discrimination of textures and/or shapes in the absence of impaired elementary sensation is quite rare since it was observed in only 12 of our patients (3.9%). Moreover early cortical SEPs reflecting the activity of the primary somatosensory area (N20 or/and P27) were clearly abnormal in all of them. A single patient of this group of 12 could be considered as a case of tactile asymbolia but his early cortical SEPs were abnormal. The only condition combining a failure of tactile recognition of objects with normal early SEPs is represented by the "tactile anomia" observed in callosal dysconnexions. Thus, in our patients unable to identify objects by palpation in spite of preserved elementary sensation, we were unable to identify a case of pure tactile agnosia. These results are to be confronted with the recent observation by Caselli (1991, 1993) that tactile object recognition is partially, but selectively, impaired in inferior parietal lesions supposed to disconnect the ventrolateral associative somatosensory cortex from its limbic targets.
Adult↗