Cases reported "Agnosia"

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1/52. Tactile morphagnosia secondary to spatial deficits.

    A 73-year old man showed visual and tactile agnosia following bilateral haemorrhagic stroke. Tactile agnosia was present in both hands, as shown by his impaired recognition of objects, geometrical shapes, letters and nonsense shapes. Basic somatosensory functions and the appreciation of substance qualities (hylognosis) were preserved. The patient's inability to identify the stimulus shape (morphagnosia) was associated with a striking impairment in detecting the orientation of a line or a rod in two- and three-dimensional space. This spatial deficit was thought to underlie morphagnosia, since in the tactile modality form recognition is built upon the integration of the successive changes of orientation in space made by the hand as it explores the stimulus. Indirect support for this hypothesis was provided by the location of the lesions, which could not account for the severe impairment of both hands. Only those located in the right hemisphere encroached upon the posterior parietal cortex, which is the region assumed to be specialised in shape recognition. The left hemisphere damage spared the corresponding area and could not, therefore, be held responsible for the right hand tactile agnosia. We submit that tactile agnosia can result from the disruption of two discrete mechanisms and has different features. It may arise from a parietal lesion damaging the high level processing of somatosensory information that culminates in the structured description of the object. In this case, tactile recognition is impaired in the hand contralateral to the side of the lesion. Alternatively, it may be caused by a profound derangement of spatial skills, particularly those involved in detecting the orientation in space of lines, segments and complex patterns. This deficit results in morphagnosia, which affects both hands to the same degree.
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2/52. Auditory agnosia and auditory spatial deficits following left hemispheric lesions: evidence for distinct processing pathways.

    Auditory recognition and auditory spatial functions were studied in four patients with circumscribed left hemispheric lesions. Patient FD was severely deficient in recognition of environmental sounds but normal in auditory localisation and auditory motion perception. The lesion included the left superior, middle and inferior temporal gyri and lateral auditory areas (as identified in previous anatomical studies), but spared Heschl's gyrus, the acoustic radiation and the thalamus. Patient SD had the same profile as FD, with deficient recognition of environmental sounds but normal auditory localisation and motion perception. The lesion comprised the postero-inferior part of the frontal convexity and the anterior third of the temporal lobe; data from non-human primates indicate that the latter are interconnected with lateral auditory areas. Patient MA was deficient in recognition of environmental sounds, auditory localisation and auditory motion perception, confirming that auditory spatial functions can be disturbed by left unilateral damage; the lesion involved the supratemporal region as well as the temporal, postero-inferior frontal and antero-inferior parietal convexities. Patient CZ was severely deficient in auditory motion perception and partially deficient in auditory localisation, but normal in recognition of environmental sounds; the lesion involved large parts of the parieto-frontal convexity and the supratemporal region. We propose that auditory information is processed in the human auditory cortex along two distinct pathways, one lateral devoted to auditory recognition and one medial and posterior devoted to auditory spatial functions.
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3/52. Massive impairment in executive functions with partial preservation of other cognitive functions: the case of a young patient with severe degeneration of the prefrontal cortex.

    Historical bases for the special role of the prefrontal cortex are outlined and the case of a 27-year-old woman with massive bilateral prefrontal damage of unknown etiology is then described. frontal lobe degeneration was repeatedly examined with magnetic resonance imaging and fluoro-deoxy-D-glucose-positron emission tomography and was found to include both orbital and dorsolateral aspects of the frontal lobes. While the degeneration initially measured was limited to portions of the orbital, medial and dorsolateral parts of both frontal lobes, with right-sided predominance, a second brain scan 15 months later revealed massive shrinkage of both frontal lobes, together with additional involvement of the posterior association cortices. The patient had completed her high-school education and had superior verbal long-term memory, normal short-term memory, and normal priming, but manifested grossly deficient scores in various frontal lobe-sensitive tests. Though a number of neurological examinations were performed, no plausible cause for the damage was established.
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4/52. Neural fate of seen and unseen faces in visuospatial neglect: a combined event-related functional MRI and event-related potential study.

    To compare neural activity produced by visual events that escape or reach conscious awareness, we used event-related MRI and evoked potentials in a patient who had neglect and extinction after focal right parietal damage, but intact visual fields. This neurological disorder entails a loss of awareness for stimuli in the field contralateral to a brain lesion when stimuli are simultaneously presented on the ipsilateral side, even though early visual areas may be intact, and single contralateral stimuli may still be perceived. Functional MRI and event-related potential study were performed during a task where faces or shapes appeared in the right, left, or both fields. Unilateral stimuli produced normal responses in V1 and extrastriate areas. In bilateral events, left faces that were not perceived still activated right V1 and inferior temporal cortex and evoked nonsignificantly reduced N1 potentials, with preserved face-specific negative potentials at 170 ms. When left faces were perceived, the same stimuli produced greater activity in a distributed network of areas including right V1 and cuneus, bilateral fusiform gyri, and left parietal cortex. Also, effective connectivity between visual, parietal, and frontal areas increased during perception of faces. These results suggest that activity can occur in V1 and ventral temporal cortex without awareness, whereas coupling with dorsal parietal and frontal areas may be critical for such activity to afford conscious perception.
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5/52. Monocular and binocular distance cues: insights from visual form agnosia I (of III).

    The human nervous system constructs a Euclidean representation of near (personal) space by combining multiple sources of information (cues). We investigated the cues used for the representation of personal space in a patient with visual form agnosia (DF). Our results indicated that DF relies predominantly on binocular vergence information when determining the distance of a target despite the presence of other (retinal) cues. Notably, DF was able to construct an Euclidean representation of personal space from vergence alone. This finding supports previous assertions that vergence provides the nervous system with veridical information for the construction of personal space. The results from the current study, together with those of others, suggest that: (i) the ventral stream is responsible for extracting depth and distance information from "monocular" retinal cues (i.e. from shading, texture, perspective) and (ii) the dorsal stream has access to binocular information (from horizontal image disparities and vergence). These results also indicate that DF was not able to use size information to gauge target distance, suggesting that intact temporal cortex is necessary for "learned size" to influence distance processing. Our findings further suggest that in neurologically intact humans, object information extracted in the ventral pathway is combined with the products of dorsal stream processing for guiding prehension. Finally, we studied the "size-distance paradox" in visual form agnosia in order to explore the cognitive use of size information. The results of this experiment were consistent with a previous suggestion that the paradox is a cognitive phenomenon.
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6/52. Dissociated active and passive tactile shape recognition: a case study of pure tactile apraxia.

    Disorders of tactile object recognition (TOR) may result from primary motor or sensory deficits or higher cognitive impairment of tactile shape representations or semantic memory. Studies with healthy participants suggest the existence of exploratory motor procedures directly linked to the extraction of specific properties of objects. A pure deficit of these procedures without concomitant gnostic disorders has never been described in a brain-damaged patient. Here, we present a patient with a right hemispheric infarction who, in spite of intact sensorimotor functions, had impaired TOR with the left hand. Recognition of 2D shapes and objects was severely deficient under the condition of spontaneous exploration. Tactile exploration of shapes was disorganized and exploratory procedures, such as the contour-following strategy, which is necessary to identify the precise shape of an object, were severely disturbed. However, recognition of 2D shapes under manually or verbally guided exploration and the recognition of shapes traced on the skin were intact, indicating a dissociation in shape recognition between active and passive touch. Functional MRI during sensory stimulation of the left hand showed preserved activation of the spared primary sensory cortex in the right hemisphere. We interpret the deficit of our patient as a pure tactile apraxia without tactile agnosia, i.e. a specific inability to use tactile feedback to generate the exploratory procedures necessary for tactile shape recognition.
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7/52. Transient visuospatial disorder from angiographic contrast.

    BACKGROUND: The blood-brain barrier may be permeable under the clinical settings of uncontrolled hypertension, renal insufficiency, immunosuppressive drugs, and intravascular radiographic contrast. Some reversible neurological complications after angiography are caused by cortical penetration of contrast media detected on brain computed tomographic (CT) scans. OBJECTIVES: To describe the first report of a transient visuospatial disorder having elements of Balint syndrome, and caused by angiographic contrast penetration of the bilateral parieto-occipital cortex; and to review cases published between 1980 and 2001 of cortical contrast penetration, documented by CT. RESULTS: Simultanagnosia, optic ataxia, and ocular apraxia occurred in a 74-year-old woman who received nonionic contrast media during a failed renal angioplasty. Contrast noted in the bilateral parieto-occipital cortex on the initial CT scan disappeared after 4 days with clinical resolution. CONCLUSIONS: Angiographic contrast tends to breach the blood-brain barrier of the vertebrobasilar circulation, penetrating the occipital cortex and leading to transient, localizable syndromes of cortical blindness or abnormal visuospatial processing.
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8/52. Posterior alien hand syndrome after a right thalamic infarct.

    The alien hand syndrome, as originally defined, should be reserved for cases in which the hand feels foreign "together with" observable involuntary motor activity. These involuntary movements are unusual during or after acute stroke. Three varieties of alien hand syndrome have been reported, involving lesions of the corpus callosum alone, the corpus callosum plus dominant medial frontal cortex, and posterior cortical and subcortical areas. A patient with posterior alien hand syndrome of vascular aetiology is reported. Imaging studies disclosed an isolated infarction of the right thalamus sparing other cerebral regions.
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9/52. Tactile agnosia and tactile aphasia: symptomatological and anatomical differences.

    Two patients with tactile naming disorders are reported. Case 1 (right hand tactile agnosia due to bilateral cerebral infarction) differentiated tactile qualities of objects normally, but could neither name nor categorize the objects. Case 2 (bilateral tactile aphasia after operation of an epidural left parietal haematoma) had as severe a tactile naming disturbance as Case 1, but could categorize objects normally, demonstrating that tactile recognition was preserved. Case 1 may be the first case of tactile agnosia clearly differentiated from tactile aphasia. CT scans of Case 1 revealed lesions in the left angular gyrus, and in the right parietal, temporal, and occipital lobes. Case 2 had lesions in the left angular gyrus and of posterior callosal radiations. Our findings suggest that tactile agnosia appears when the somatosensory association cortex is disconnected by a subcortical lesion of the angular gyrus from the semantic memory store located in the inferior temporal lobe, while tactile aphasia represents a tactual-verbal disconnection.
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10/52. Ventral occipital lesions impair object recognition but not object-directed grasping: an fMRI study.

    D.F., a patient with severe visual form agnosia, has been the subject of extensive research during the past decade. The fact that she could process visual input accurately for the purposes of guiding action despite being unable to perform visual discriminations on the same visual input inspired a novel interpretation of the functions of the two main cortical visual pathways or 'streams'. Within this theoretical context, the authors proposed that D.F. had suffered severe bilateral damage to her occipitotemporal visual system (the 'ventral stream'), while retaining the use of her occipitoparietal visual system (the 'dorsal stream'). The present paper reports a direct test of this idea, which was initially derived from purely behavioural data, before the advent of modern functional neuroimaging. We used functional MRI to examine activation in her ventral and dorsal streams during object recognition and object-directed grasping tasks. We found that D.F. showed no difference in activation when presented with line drawings of common objects compared with scrambled line drawings in the lateral occipital cortex (LO) of the ventral stream, an area that responded differentially to these stimuli in healthy individuals. Moreover, high-resolution anatomical MRI showed that her lesion corresponded bilaterally with the location of LO in healthy participants. The lack of activation with line drawings in D.F. mirrors her poor performance in identifying the objects depicted in the drawings. With coloured and greyscale pictures, stimuli that she can identify more often, D.F. did show some ventral-stream activation. These activations were, however, more widely distributed than those seen in control participants and did not include LO. In contrast to the absent or abnormal activation observed during these perceptual tasks, D.F. showed robust activation in the expected dorsal stream regions during object grasping, despite considerable atrophy in some regions of the parietal lobes. In particular, an area in the anterior intraparietal sulcus was activated more for grasping an object than for just reaching to that object, for both D.F. and controls. In conclusion, we have been able to confirm directly that D.F.'s visual form agnosia is associated with extensive damage to the ventral stream, and that her spared visuomotor skills are associated with visual processing in the dorsal stream.
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