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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.

Adult↗
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.

Adult↗
PubMed2001

[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.

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PubMed1989

[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↗
PubMed1982

[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↗
PubMed1994

[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.

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PubMedDate not supplied

[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↗
PubMed1995

[A case of integrative visual agnosia].

We report a 78-year-old right-handed man with integrative visual agnosia (Humphreys et al.) that was associated with bilateral medial occipito-temporal infarction. The patient showed superior altitudinal hemianopsia, alexia, prosopagnosia, cerebral achromatopsia, and object agnosia. Elementary perception and information processing supposed to be executed by the stream to the parietal lobe were intact, since he was able to perceive the position and speed of moving object (catching the flying ball). He could not categorize neither real objects nor line drawings by sight. However, copying and matching of them was accurate, suggesting that his agnosia was an associative type (Lissauer). Detailed neuropsychological examinations revealed that his agnosia was due to a disturbance in integrating local form features into a perceptual whole. In addition, this patient showed difficulty in retrieval of objects from memory. However, it is unlikely that this disturbance itself was a cause of this particular form of agnosia.

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PubMed1997

[Visual agnosia induced by cerebrovascular disease].

Visual objects can be classified into some categories such as faces, landscapes, objects and letters. Visual agnosia specific to one of these categories can occur. This type of visual agnosia occurs at the occipitotemporal lobe lesion where the visual cognitive center exists, and is often induced by vascular disease of the posterior cerebral artery. In this study we categorized the symptoms of visual agnosia and presented the natures of these symptoms of patients, and then investigated the lesions responsible for the symptoms. In addition, we clarified the current most important issue for each symptom. Based on our results, we discussed the visual cognitive functions of the occipitotemporal lobe. The results indicate that visual cognitive dysfunction with respect to faces, landscapes, objects and letters corresponds to prosopagnosia, agnosia for streets, associative object agnosia and pure alexia, respectively. Investigation of the relationship between the symptoms of the above conditions and the responsible regions shows that the right medial-posterior region, right medial-anterior region, both lateral regions (left side is superior) and the left medial region are important in the visual cognition of faces, landscapes, objects and letters, respectively. Thus, it is speculated that the visual cognitive functions occur independently at different regions of the occipitotemporal lobe for each visual category.

Agnosia↗
PubMed1997

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.

Journal Article↗
PubMed1999

Mirror agnosia and mirror ataxia constitute different parietal lobe disorders.

We describe two new clinical syndromes, mirror agnosia and mirror ataxia, both characterized by the deficit of reaching for an object through a mirror in association with a lesion of either parietal lobe. Clinical investigation of 13 patients demonstrated that the impairments affected both sides of the body. In mirror agnosia, the patients always reached toward the virtual object in the mirror and they were not capable of changing their behavior even after presentation of the position of the object in real visual space. In mirror ataxia (resembling optic ataxia) although some patients initially tended to reach for the virtual object in the mirror, they soon learned to guide their arms toward the real object, all of them producing many directional errors. Both patient groups performed poorly on mental rotation, but only the patients with mirror agnosia were impaired in line orientation. Only 1 of the patients suffered from neglect and 3 from apraxia. Magnetic resonance imaging showed that in mirror agnosia the common zone of lesion overlap was scattered around the posterior angular gyrus/superior temporal gyrus and in mirror ataxia around the postcentral sulcus. We propose that both these clinical syndromes may represent different types of dissociation of retinotopic space and body scheme, or likewise, of allocentric and egocentric space normally adjusted in the parietal lobe.

Adult↗
PubMed1994

Apperceptive visual agnosia: a case study.

A man with an infarction of his inferior temporal and occipital association cortex bilaterally, which spared primary visual cortex, had impaired visual recognition of objects, faces, colors, words, and gestures. Analysis of visual function indicated that the recognition failures resulted from an agnosia, rather than elemental visual impairment. Whereas his impairment of gesture recognition appeared to be related to an associative agnosia, his inability to recognize objects was related to an apperceptive agnosia. There may be four subtypes of apperceptive agnosia: one where the internal object representations or structural descriptions are impaired, another where an adequate percept cannot be derived, a third where the internal referent and percept are dissociated, and a fourth where both levels are impaired. Our patient demonstrated a failure to relate individual elements to the whole, a failure to integrate multiple elements, and a reliance on global perception. He had normal object imagery. These results suggest that, whereas internal representations were intact, he was unable to form adequate perceptual representations.

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PubMed2003

Visual agnosia.

The visual agnosias are an intriguing class of clinical phenomena that have important implications for current theories of high-level vision. Visual agnosia is defined as impaired object recognition that cannot be attributed to visual loss, language impairment, or a general mental decline. At least in some instances, agnostic patients generate an adequate internal representation of the stimulus but fail to recognize it. In this review, we begin by describing the classic works related to the visual agnosias, followed by a description of the major clinical variants and their occurrence in degenerative disorders. In keeping with the theme of this issue, we then discuss recent contributions to this domain. Finally, we present evidence from functional imaging studies to support the clinical distinction between the various types of visual agnosias.

Agnosia↗
PubMed2004

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.

Agnosia↗
PubMed1998

Bilateral tactile agnosia: a case report.

This study reports a 64-year-old right-handed male who manifested bilateral tactile recognition deficits. They were diagnosed as bilateral tactile agnosia, since the patient showed difficulty in semantic association of objects despite preserved hylognosis and morphognosis. The patient had a bilateral lesion in the subcortical region of the angular gyrus. The case reported by Endo et al. (1992) had a right hand tactile agnosia due to a subcortical lesion in the left angular gyrus. Our findings support Endo's hypothesis that tactile agnosia occurs when the somatosensory association cortex is disconnected from the semantic memory store located in the inferior temporal lobe by a subcortical lesion of the angular gyrus. We suggest that the extent of the lesion in the tactual-semantic pathway is related to the severity of tactile agnosia and the types of the tactile naming errors.

Agnosia↗
PubMed1979

Visual agnosia: the dual deficit of perception and recognition.

This case of visual agnosia is of special interest because of its causation by trauma, of the unusually long follow-up (10 1/2 years), and the evidence for dual deficits of recognition and perception. Although most of the findings were characteristic of associative visual agnosia with preserved perceptual function, the poor copying, contrasted to better spontaneous drawing, suggested apperceptive agnosia as well. Prosopagnosia, alexia without agraphia, Balint's syndrome, visual static agnosia and simultanagnosia were also observed. The patient had persisting amnestic syndrome, but no dementia or aphasia. The responses to visual stimulation were perseverations, form confusions and confabulations. Visual evoked potentials were severely, bilaterally abnormal and computerized tomographic localization showed bilateral lesions also. The stages of recognition are analysed through this case of visual verbal disconnection and the importance of memory in perception is highlighted.

Adult↗
PubMed2003

Agnosia for scenes in topographagnosia.

Topographagnosia is most commonly attributed to an agnosia for landmarks. In order to define the nature of this agnosia, we studied a patient with isolated topographic disorientation (TD) after a stroke in the right medial occipitotemporal region. The patient got lost in familiar environments but could readily read and draw maps, describe familiar routes, and provide correct directions. He had normal perceptual test performance and met criteria for topographagnosia rather than for other forms of topographic disorientation. Two ecologically valid route tests assessed the nature of his agnosia. On a familiar route, he could recognize major landmarks. He could not, however, recognize route configurations made up of combinations of visual features each lacking individual distinctiveness. On a test of route learning, he learned landmarks that differed in minor details and could use them to orient himself along a route. He had difficulty, however, recognizing and learning scenes lacking salient landmarks. This agnosia for scenes was worse for semantically-related environments, but improved with semantic knowledge such as street names. In addition, the patient lacked overt prosopagnosia but tended toward semantic errors in the recognition of famous faces. Together these findings suggest that this patient's inability to recognize a route resulted from an inability of intact perceptual units for scenes, composed of specific visual configurations of individually indefinite features, from accessing stored representations.

Aged↗
PubMed1989

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.

Agnosia↗