[Neuropsychological analysis of the frontal syndrome].
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Biomedical subjects
Publications and source records attributed to J L Signoret.
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Prosopagnosia is a neurologically based deficit characterized by the inability to recognize faces of known individuals in the absence of severe intellectual, perceptual, and memory impairments. The nature of the underlying disturbance was investigated in three patients in an attempt to identify the structural and functional levels at which the processing of faces breaks down, the relation between prosopagnosia and associated deficits, and the specificity of the prosopagnosic disturbance. The breakdown of face processing resulted from unilateral damage in different cerebral structures of the right hemisphere in the three patients, and it involved different functional levels of face processing, but all three patients displayed perceptual impairments of unequal severity. In one patient (R.M.), the deficit encompassed all perceptual operations on faces, including matching identical views of the same faces, but it did not extend to all categories of objects characterized by a close similarity among their instances; the second patient (P.M.) exhibited a less severe perceptual impairment but was unable to derive the configurational properties from a facial representation and to extract its physiognomic invariants; the third patient (P.C.) had not lost the capacity to differentiate faces on the basis of their configurations but could not associate a facial representation with its pertinent memories. Associated deficits were present in each patient but differed depending on the anatomofunctional locus of the breakdown, although all patients were impaired at recognizing noncanonical views of objects that they readily recognized when shown from a conventional viewpoint. However, performance dissociation within patients and double dissociation between patients suggest that these associated deficits are not necessary concomitants of prosopagnosia.
Prosopagnosia is an acquired neurological impairment characterized by an inability to experience a feeling of familiarity at the view of faces of known individuals and to identify these individuals. The inability of prosopagnosic patients to recognize faces does not entail that perceived faces go unprocessed in their brains, and there are indications that cognitive operations are still performed whereby a perceived face reactivates pertinent memories, but either these operations cannot be completed or their outcome fails to reach consciousness. A series of experiments were conducted on three severe prosopagnosic patients in an attempt to understand better this phenomenon known as covert face recognition, the conditions for its occurrence, and its functional locus. The capacity of the patients implicitly to access pertinent knowledge related to overtly unrecognized faces was inversely related to the severity of their perceptual deficit, suggesting that some preserved ability to extract the physiognomic invariants of a face is a necessary condition for the occurrence of the phenomenon. However, the results indicated that covert recognition does not take place at a perceptual or structural level although it is initiated at such a level, that it may have more than one underlying mechanism, and that it is achieved through the reactivation of specific information related to the individual's identity. Under special conditions that restricted the relevant knowledge that needed to be activated, transient overt recognition of faces was experienced by one of the prosopagnosic patients.
This study involved twleve parkinsonian patients exposed to abnormal movements provoked by L-DOPA. Including six patients with "mid-dose" dyskinesias and six others with "onset and end of dose" dyskinesias, Correlation between the circumstances of onset of abnormal movements and plasma concentrations of DOPA and O-methyl-DOPA, after administration of a dose of L-DOPA + IDC, gave the following results: 1) mid-dose dyskinesias appeared with the highest plasma concentrations of DOPA, at the maximum therapeutic effect; 2) onset and end of dose occurred during rise and fall in plasma levels of DOPA, coinciding with the relief and the reappearance of parkinsonian symptoms respectively; 3) no correlation could be established between plasma concentrations of O-methyl-DOPA and the duration of the period of clinical remission or of abnormal movements. These biochemical data, completed by the neuropharmacological study of one patient with onset and end of dose abnormal movements suggest the predominant role of a disturbance in central dopaminergic mechanisms in the genesis of abnormal movements, whatever their nature.