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At least 19 recordsLinked to original sources
PubMed2000

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↗
PubMed2003

Music agnosia and auditory agnosia. Dissociations in stroke patients.

A review and an experimental study were carried out in search of dissociations between the recognition of music (music agnosia) and that of environmental sounds (auditory agnosia) in stroke patients. The review focused on 45 adequately studied cases published since 1883. The experimental study consisted of administering standard tests of music and environmental sound recognition to 40 unselected patients with unilateral stroke. Among case reports, music was selectively impaired more frequently than environmental sounds, whereas the reverse occurred in the experimental study. In this, right hemisphere lesions tended either to disrupt the apperception of environmental sounds, sparing music entirely, or to disrupt both environmental sounds and melody, sparing rhythm, whereas left hemisphere lesions tended to spare melody and to disrupt rhythm, either selectively or in association with the semantic identification of environmental sounds.

Adult↗
PubMed1997

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.

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PubMed1999

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.

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PubMed2004

Clinical management of agnosia.

Agnosia is a neurological recognition deficit that affects a single modality. Visual agnosias include pure object agnosia, prosopagnosia, akinetopsia, and pure alexia. Auditory agnosias include pure word deafness, phonagnosia, and pure sound agnosia. New neuroimaging tools have permitted scientists to better understand the loci of lesions that cause various agnosias and from that knowledge to develop theories about the processing networks that contribute to perception and recognition in each modality. These research data, in turn, inform the rehabilitation process. By utilizing current knowledge about neuroprocessing networks, clinical professionals can differentially diagnose agnosias from aphasia and other cognitive deficits. Practical approaches to treatment of agnosia will follow once the diagnosis is established.

Agnosia↗
PubMedDate not supplied

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.

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PubMed1985

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↗
PubMed1994

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.

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PubMed1982

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.

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PubMed1995

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.

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PubMed1998

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.

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