Prosopagnosia without topographagnosia and object agnosia associated with a lesion confined to the right occipitotemporal region

A patient is presented who developed prosopagnosia with a recent occipitotemporal infarct in the distribution of the right posterior cerebral artery. H ve topographical agnosia or object agnosia. He regained the ability to recognize faces of familiar persons, whereas he remained unable to identify faces of persons whom he met after the of persons whom he met after the disease onset. This case demonstrate that prosopagnosia may occur as a deficit of matching a perceived face to a memory store of the face, and that the failure to recognize unfamiliar faces may be due to the inability to form memory stores of new faces. These deficits can occur in association with a lesion confined to the right occipitotemporal region.     

Real object use facilitates object recognition in semantic agnosia

In the present paper we show that, in patients with poor semantic representations, the naming of real objects can improve when naming takes place after patients have been asked to use the objects, compared with when they name the objects either from vision or from touch alone, or together. In addition, the patients were strongly affected by action when required to name objects that were used correctly or incorrectly by the examiner. The data suggest that actions can be cued directly from sensory-motor associations, and that patients can then name on the basis of the evoked action.     

Eye movements during object recognition in visual agnosia

This paper reports the first ever detailed study about eye movement patterns during single object recognition in visual agnosia. Eye movements were recorded in a patient with an integrative agnosic deficit during two recognition tasks: common object naming and novel object recognition memory. The patient showed normal directional biases in saccades and fixation dwell times in both tasks and was as likely as controls to fixate within object bounding contour regardless of recognition accuracy. In contrast, following initial saccades of similar amplitude to controls, the patient showed a bias for short saccades. In object naming, but not in recognition memory, the similarity of the spatial distributions of patient and control fixations was modulated by recognition accuracy. The study provides new evidence about how eye movements can be used to elucidate the functional impairments underlying object recognition deficits. We argue that the results reflect a breakdown in normal functional processes involved in the integration of shape information across object structure during the visual perception of shape.     

Superior voice recognition in a patient with acquired prosopagnosia and object agnosia

Anecdotally, it has been reported that individuals with acquired prosopagnosia compensate for their inability to recognize faces by using other person identity cues such as hair, gait or the voice. Are they therefore superior at the use of non-face cues, specifically voices, to person identity? Here, we empirically measure person and object identity recognition in a patient with acquired prosopagnosia and object agnosia. We quantify person identity (face and voice) and object identity (car and horn) recognition for visual, auditory, and bimodal (visual and auditory) stimuli. The patient is unable to recognize faces or cars, consistent with his prosopagnosia and object agnosia, respectively. He is perfectly able to recognize people's voices and car horns and bimodal stimuli. These data show a reverse shift in the typical weighting of visual over auditory information for audiovisual stimuli in a compromised visual recognition system. Moreover, the patient shows selectively superior voice recognition compared to the controls revealing that two different stimulus domains, persons and objects, may not be equally affected by sensory adaptation effects. This also implies that person and object identity recognition are processed in separate pathways. These data demonstrate that an individual with acquired prosopagnosia and object agnosia can compensate for the visual impairment and become quite skilled at using spared aspects of sensory processing. In the case of acquired prosopagnosia it is advantageous to develop a superior use of voices for person identity recognition in everyday life.     

The role of color in object recognition: Evidence from visual agnosia

Background: The diagnosis of the behavioural variant of frontotemporal dementia (bvFTD) can be challenging. At present there is a paucity of prospective work addressing the specificity of current diagnostic criteria for bvFTD with respect to long-term outcome (i.e., false positives versus true positives).

Methods: Here we report two individuals who met current clinical criteria for bvFTD and who underwent detailed long-term clinical and neuropsychological follow-up. In addition, both had serial volumetric MRI and functional metabolic (FDG-PET) imaging separated by 5 years.

Results: One case had a slow clinical decline as well as both progressive atrophy and hypometabolism in a frontotemporal distribution, consistent with a neurodegenerative FTD syndrome. However, the second developed neither atrophy nor hypometabolism and remained clinically stable, a decade from symptom onset.

Conclusion: We propose that these cases illustrate that while there may be a slow evolution in bvFTD, it is possible that some cases who meet current criteria may not have a neurodegenerative syndrome. If correct, this hypothesis has important implications for the current diagnostic criteria. A potential hierarchy for diagnostic certainty in bvFTD is suggested.     

The influence of misnaming on object recognition: a case of multimodal agnosia

We present a case of multimodal agnosia in the visual and tactile modality due to an infarction in the territory of the left posterior cerebral artery. The patient's ability to recognize objects fluctuated depending on his verbal activity. When he misnamed presented objects, he tended to use them and to draw them in keeping with the wrong name. We submit that the mechanism causing associative agnosia is more dynamic than it was hitherto considered. It originates from the rivalry between top-down central regulation and bottom-up peripheral flow.     

Apperceptive agnosia and face recognition

Abstract

Are faces and objects recognized by separate visual recognition systems or might a single system subserve the recognition of both classes of input? Recognition of faces and objects by a single system predicts that prosopagnosics, who selectively lose the ability to recognize faces due to brain damage, should also lose the ability to recognize objects. Contrary to this prediction, case studies of prosopagnosia have reported intact object recognition. Further support for separate visual recognition systems comes from the case of HH reported here. Following a stroke involving the left posterior cortex, HH has a severe apperceptive visual agnosia for visually presented objects and an alexia for words. Yet, he shows relatively spared visual face processing. Such a performance pattern completes a double dissociation between face and object processing when coupled with prosopaganosia. More importantly, HH is the first apperceptive visual object agnosic to demonstrate spared face processing. The severity of his object-processing deficit is such that from the earliest levels in the visual processing hierarchy, distinct neural substrates must be responsible for processing some objects and faces. These results are discussed as support for Farah's model (Visual agnosia: disorders of object recognition and what they tell us about normal vision. Cambridge, MA: MIT Press, 1990) of object, face and word recognition.     

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.     

Visual agnosia without alexia

A 41-year-old man presented with bilateral posterior cerebral artery infarcts. He had visual object agnosia and prosopagnosia with preservation of reading abilities. There was also defective visual memory, topographic orientation, and color perception, as well as simultanagnosia. From the clinical facts and CT findings, it was postulated that bilateral visual-limbic disconnection accounted for the patient's visual agnosia and related disturbances.     

Prosopagnosia without hemianopsia after unilateral right occipitotemporal lesion

Three atypical features were noted in a patient with prosopagnosia due to a right occipital hematoma: prosopagnosia was unassociated with achromatopsia, spatial disorientation or left visual field alexia; the right visual field was normal and the left field only slightly impaired; the lesion was apparently unilateral.     

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.     

Prosopagnosia and disturbance of color recognition during recovery from cortical blindness]

Neuropsychologic findings during recovery from cortical blindness are described in four right-handed patients (two female, two male) aged 53 to 70 years. The lesions were due to occlusion of both posterior cerebral arteries (Case 1) and vascular spasm following subarachnoidal hemorrhage (Case 3) or angiography (Cases 2 and 4). Complete blindness lasted for 3 months until death in Case 1, 4 weeks in case 2, and 1 to 2 days in Cases 3 and 4. Confusional states and visual hallucinations were pronounced in three cases. Anosognosia (Anton's syndrome) was most pronounced in a patient with occlusion of both posterior cerebral arteries and less obvious in the remaining patients. During the recovery phase, symptoms of right hemisphere involvement were prominent with left-sided hemianopsia and diminished optokinetic nystagmus to the left, prosopagnosia in two cases, and dysmorphopsia with altered physiognomic recognition in one case. Transient disturbances of color recognition occurred in three patients. The observations are discussed with reference to clinical and neuropathologic findings of the literature.     

Non-conscious face recognition in patients with face agnosia

Four patients with face agnosia, a condition in which there is a failure to recognize previously known faces or faces that ought to have been learned without difficulty, were studied with an experimental paradigm in which both overt (verbal self-report) and covert (electrodermal skin conductance response) probes of recognition were used. The results showed a striking dissociation between the two indices: (1) all 4 patients generated more frequent and significantly larger-amplitude skin conductance responses to familiar faces, as compared to unfamiliar ones. This outcome contrasts with the finding that (2) none of the patients was able to give discriminatory verbal ratings of familiar versus unfamiliar faces. The positive electrodermal discrimination is interpreted as an index of the rich co-activation of records that is produced when familiar facial stimuli successfully trigger the reassembly of previously acquired representations of the physical structure of faces. The results of this co-activation, however, are unavailable to consciousness. This is seen as the consequence of lesion-related disruption of linkages between face records, on the one hand, and non-face records that contain information uniquely and unequivocally apposite to the possessor of a particular face.     

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.     

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.     

Prosopagnosia without apparent cause: overview and diagnosis of six cases

We compared six cases of congenital prosopagnosia to unimpaired participants using standardized test batteries, tailor-made experimental paradigms, and clinical questionnaires. Every prosopagnosic participant displayed deficits in recognizing famous faces and retaining novel faces over short periods of time. Other aspects of face perception such as judgment of emotional expression, speech reading and memory for faces and names were impaired to a lesser degree or only in single cases. No evidence was found for general visual deficits or social dysfunctions. Two of our six cases are first order relatives, and a further three report first-order relatives suffering from prosopagnosic symptoms. The results are in line with the idea of a genetic component to congenital prosopagnosia.     

Hippocampal histone acetylation regulates object recognition and the estradiol-induced enhancement of object recognition

Histone acetylation has recently been implicated in learning and memory processes, yet necessity of histone acetylation for such processes has not been demonstrated using pharmacological inhibitors of histone acetyltransferases (HATs). As such, the present study tested whether garcinol, a potent HAT inhibitor in vitro, could impair hippocampal memory consolidation and block the memory-enhancing effects of the modulatory hormone 17β-estradiol E2. We first showed that bilateral infusion of garcinol (0.1, 1, or 10 μg/side) into the dorsal hippocampus (DH) immediately after training impaired object recognition memory consolidation in ovariectomized female mice. A behaviorally effective dose of garcinol (10 μg/side) also significantly decreased DH HAT activity. We next examined whether DH infusion of a behaviorally subeffective dose of garcinol (1 ng/side) could block the effects of DH E2 infusion on object recognition and epigenetic processes. Immediately after training, ovariectomized female mice received bilateral DH infusions of vehicle, E2 (5 μg/side), garcinol (1 ng/side), or E2 plus garcinol. Forty-eight hours later, garcinol blocked the memory-enhancing effects of E2. Garcinol also reversed the E2-induced increase in DH histone H3 acetylation, HAT activity, and levels of the de novo methyltransferase DNMT3B, as well as the E2-induced decrease in levels of the memory repressor protein histone deacetylase 2. Collectively, these findings suggest that histone acetylation is critical for object recognition memory consolidation and the beneficial effects of E2 on object recognition. Importantly, this work demonstrates that the role of histone acetylation in memory processes can be studied using a HAT inhibitor.