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Scientific Reports May 2017A wealth of evidence from behavioural, neuropsychological and neuroimaging research supports the view that face recognition is reliant upon a domain-specific network...
A wealth of evidence from behavioural, neuropsychological and neuroimaging research supports the view that face recognition is reliant upon a domain-specific network that does not process words. In contrast, the recent many-to-many model of visual recognition posits that brain areas involved in word and face recognition are functionally integrated. Developmental prosopagnosia (DP) is characterised by severe deficits in the recognition of faces, which the many-to-many model predicts should negatively affect word recognition. Alternatively, domain-specific accounts suggest that impairments in face and word processing need not go hand in hand. To test these possibilities, we ran a battery of 7 tasks examining word processing in a group of DP cases and controls. One of our prosopagnosia cases exhibited a severe reading impairment with delayed response times during reading aloud tasks, but not lexical decision tasks. Overall, however, we found no evidence of global word processing deficits in DP, consistent with a dissociation account for face and word processing.
Topics: Adult; Aged; Behavior; Female; Humans; Linguistics; Male; Middle Aged; Neuropsychological Tests; Prosopagnosia; Reading; Task Performance and Analysis; Visual Perception; Young Adult
PubMed: 28490791
DOI: 10.1038/s41598-017-01917-8 -
Neuropsychologia Feb 2019Traditionally, developmental prosopagnosia (DP) has been thought of as an apperceptive condition that hinders individuals' ability to encode face structure. However,...
Traditionally, developmental prosopagnosia (DP) has been thought of as an apperceptive condition that hinders individuals' ability to encode face structure. However, several authors have recently raised the possibility that many DPs may be able to form accurate percepts, but be unable to maintain those percepts over time. The present study sought to distinguish these possibilities. In our first experiment 16 DPs and 22 typical controls completed a delayed match-to-sample task with face and car stimuli, with a retention interval of 1-second (low demand) or 6-seconds (high demand). As expected, the participants with DP were worse than the controls at face matching, and were disproportionately impaired at matching faces relative to cars. However, the relative degree of impairment seen in the DPs did not interact with retention interval; they exhibited similar levels of impairment when matching faces with 1- and 6-second delays. Next, we compared the performance of 72 DPs and 54 typical controls on the Cambridge Face Perception Test (CFPT), a task that measures face perception ability in a way that minimises the memory demands. As expected, we found that the DPs were impaired at the group level. This difference was not attributable to a few individuals with an apperceptive profile; rather we found evidence that the distribution of CFPT scores seen in the DP sample was shifted relative to that of typical controls. Some heterogeneity is likely in any neurodevelopmental population, and DP is no different. Generally, however, these findings suggest that selective STFM impairment may be relatively uncommon in this population. Instead, deficits of perceptual encoding may play a larger role in DP than currently acknowledged.
Topics: Adult; Aged; Choice Behavior; Female; Humans; Male; Memory; Middle Aged; Pattern Recognition, Visual; Photic Stimulation; Prosopagnosia; Psychological Tests; Young Adult
PubMed: 30502377
DOI: 10.1016/j.neuropsychologia.2018.11.014 -
Brain : a Journal of Neurology Dec 2019Damage to the right fusiform face area can disrupt the ability to recognize faces, a classic example of how damage to a specialized brain region can disrupt a...
Damage to the right fusiform face area can disrupt the ability to recognize faces, a classic example of how damage to a specialized brain region can disrupt a specialized brain function. However, similar symptoms can arise from damage to other brain regions, and face recognition is now thought to depend on a distributed brain network. The extent of this network and which regions are critical for facial recognition remains unclear. Here, we derive this network empirically based on lesion locations causing clinically significant impairments in facial recognition. Cases of acquired prosopagnosia were identified through a systematic literature search and lesion locations were mapped to a common brain atlas. The network of brain regions connected to each lesion location was identified using resting state functional connectivity from healthy participants (n = 1000), a technique termed lesion network mapping. Lesion networks were overlapped to identify connections common to lesions causing prosopagnosia. Reproducibility was assessed using split-half replication. Specificity was assessed through comparison with non-specific control lesions (n = 135) and with control lesions associated with symptoms other than prosopagnosia (n = 155). Finally, we tested whether our facial recognition network derived from clinically evident cases of prosopagnosia could predict subclinical facial agnosia in an independent lesion cohort (n = 31). Our systematic literature search identified 44 lesions causing prosopagnosia, only 29 of which intersected the right fusiform face area. However, all 44 lesion locations fell within a single brain network defined by connectivity to the right fusiform face area. Less consistent connectivity was found to other face-selective regions. Surprisingly, all 44 lesion locations were also functionally connected, through negative correlation, with regions in the left frontal cortex. This connectivity pattern was highly reproducible and specific to lesions causing prosopagnosia. Positive connectivity to the right fusiform face area and negative connectivity to left frontal regions were independent predictors of prosopagnosia and predicted subclinical facial agnosia in an independent lesion cohort. We conclude that lesions causing prosopagnosia localize to a single functionally connected brain network defined by connectivity to the right fusiform face area and to left frontal regions. Implications of these findings for models of facial recognition deficits are discussed.
Topics: Brain; Brain Mapping; Humans; Image Processing, Computer-Assisted; Magnetic Resonance Imaging; Nerve Net; Prosopagnosia; Reproducibility of Results
PubMed: 31740940
DOI: 10.1093/brain/awz332 -
Journal of Vision Aug 2019Despite extensive investigation, the causes and nature of developmental prosopagnosia (DP)-a severe face identification impairment in the absence of acquired brain...
Despite extensive investigation, the causes and nature of developmental prosopagnosia (DP)-a severe face identification impairment in the absence of acquired brain injury-remain poorly understood. Drawing on previous work showing that individuals identified as being neurotypical (NT) show robust individual differences in where they fixate on faces, and recognize faces best when the faces are presented at this location, we defined and tested four novel hypotheses for how atypical face-looking behavior and/or retinotopic face encoding could impair face recognition in DP: (a) fixating regions of poor information, (b) inconsistent saccadic targeting, (c) weak retinotopic tuning, and (d) fixating locations not matched to the individual's own face tuning. We found no support for the first three hypotheses, with NTs and DPs consistently fixating similar locations and showing similar retinotopic tuning of their face perception performance. However, in testing the fourth hypothesis, we found preliminary evidence for two distinct phenotypes of DP: (a) Subjects characterized by impaired face memory, typical face perception, and a preference to look high on the face, and (b) Subjects characterized by profound impairments to both face memory and perception and a preference to look very low on the face. Further, while all NTs and upper-looking DPs performed best when faces were presented near their preferred fixation location, this was not true for lower-looking DPs. These results suggest that face recognition deficits in a substantial proportion of people with DP may arise not from aberrant face gaze or compromised retinotopic tuning, but from the suboptimal matching of gaze to tuning.
Topics: Adult; Attention; Eye Movements; Facial Recognition; Female; Humans; Male; Middle Aged; Prosopagnosia; Saccades
PubMed: 31426085
DOI: 10.1167/19.9.7 -
Current Neurology and Neuroscience... May 2019Functional imaging studies, intracranial recordings, and lesion-deficit correlations in neurological patients have produced unique insights into the cognitive mechanisms... (Review)
Review
PURPOSE OF REVIEW
Functional imaging studies, intracranial recordings, and lesion-deficit correlations in neurological patients have produced unique insights into the cognitive mechanisms and neural substrates of face recognition. In this review, we highlight recent advances in the field and integrate data from these complementary lines of research to propose a functional neuroanatomical model of face identity recognition.
RECENT FINDINGS
Rather than being localized to a single specialized cortical region, face recognition is supported by a distributed neural network. Core components of the network include face-selective visual areas in the ventral occipito-temporal cortex, whereas the extended network is comprised of anterior temporal lobe structures involved in the retrieval of multimodal identity-specific knowledge about familiar individuals, the amygdala responsible for generating emotional responses to faces, and prefrontal regions that provide top-down executive control of the recognition process. Damage to different network components results in neuropsychological disorders of face identity processing manifested either as impaired recognition of familiar faces (prosopagnosia, person recognition disorders) or as false recognition/misidentification of unfamiliar faces. Face identity recognition requires the coordinated activity of a large-scale neural network. Neurological damage can compromise the structural/functional integrity of specific network nodes or their connections and give rise to face recognition disorders with distinct clinical features and underlying cognitive mechanisms determined primarily by the location of the lesion.
Topics: Facial Recognition; Humans; Magnetic Resonance Imaging; Male; Prosopagnosia; Temporal Lobe
PubMed: 31144153
DOI: 10.1007/s11910-019-0960-9 -
PeerJ 2023Developmental prosopagnosia is a relatively common visuo-cognitive condition, characterised by impaired facial identity recognition. Impairment severity appears to...
Developmental prosopagnosia is a relatively common visuo-cognitive condition, characterised by impaired facial identity recognition. Impairment severity appears to reside on a continuum, however, it is unknown whether instances of milder deficits reflect the successful use of spontaneous (typical) face recognition strategies, or the application of extraneous compensatory cues to recognition. Here, we explore this issue in two studies. First, 23 adults with developmental prosopagnosia were asked about their use of spontaneous versus compensatory face recognition techniques in everyday life, using a series of closed- and open-ended questions. Second, the same participants performed a computerised famous face recognition task where they were asked to provide reasons why they could make any successful identifications. Findings from both studies suggest that people with developmental prosopagnosia can successfully, and quite frequently, use compensatory strategies to recognition, and that these cues support the majority of instances of preserved familiar face recognition. In contrast, 16 of the 23 participants were able to spontaneously recognise familiar faces on at least some occasions, but there were vast individual differences in frequencies of success. These findings have important implications for our conceptualisation of the condition, as well as for diagnostic practice.
Topics: Adult; Humans; Cues; Facial Recognition; Prosopagnosia; Recognition, Psychology; Male; Female; Middle Aged
PubMed: 37483961
DOI: 10.7717/peerj.15497 -
Graefe's Archive For Clinical and... Mar 2015
Topics: Humans; Prosopagnosia
PubMed: 25550096
DOI: 10.1007/s00417-014-2890-1 -
Cognitive and Behavioral Neurology :... Jun 2016Whipple disease is a rare, chronic multisystem infectious disease. The central nervous system (CNS) is secondarily involved in 43% of patients; 5% of patients have...
Whipple disease is a rare, chronic multisystem infectious disease. The central nervous system (CNS) is secondarily involved in 43% of patients; 5% of patients have isolated or primary CNS involvement. The most frequent CNS symptoms are cognitive changes. Prosopagnosia is an inability to recognize familiar faces, in a person who does not have vision impairments or cognitive alterations. This relatively rare condition is usually related to vascular, traumatic, degenerative, or infectious lesions. We report a 54-year-old woman who presented subacutely with fever, headache, and seizures that led to a diagnosis of infectious meningoencephalitis. She improved temporarily on broad-spectrum antibiotics, but then developed a chronically evolving cognitive impairment with associative prosopagnosia as the major complaint. She had a history of sporadic abdominal pain and mild sacroiliac arthralgia. After a negative duodenal biopsy, we confirmed primary CNS Whipple disease by polymerase chain reaction and brain biopsy. We treated the patient with ceftriaxone for 15 days and then co-trimoxazole for 2 years. At 8-year follow-up, she had no further impairments, but continuing prosopagnosia. To our knowledge, this is the first description of isolated prosopagnosia in a patient with primary CNS Whipple disease. Because CNS Whipple disease can lead to serious, irreversible lesions if not promptly treated, clinicians must suspect the diagnosis, treat with long-term antibiotics, and follow patients carefully to prevent recurrence.
Topics: Anti-Bacterial Agents; Ceftriaxone; Cognition Disorders; Female; Humans; Middle Aged; Prosopagnosia; Whipple Disease
PubMed: 27336807
DOI: 10.1097/WNN.0000000000000091 -
Journal of Neuropsychology Sep 2018The sudden inability to recognize individual faces following brain damage was first reported in a scientific journal 150 years ago and termed 'prosopagnosia' 70 years...
The sudden inability to recognize individual faces following brain damage was first reported in a scientific journal 150 years ago and termed 'prosopagnosia' 70 years ago. While the term originally identified a face-selective neurological condition, it is now obscured by a sequence of imprecisions. First, prosopagnosia is routinely used to define symptoms of individual face recognition (IFR) difficulties in the context of visual object agnosia or other neurological conditions, or even in the normal population. Second, this over-expansive definition has lent support to a long-standing within-category recognition account of prosopagnosia, that is, that the impairment of IFR reflects a general impairment in recognizing within-category objects. However, stringent experimental studies of classical cases of prosopagnosia following brain damage show that their core impairment is not in recognizing physically similar exemplars within non-face object categories. Instead, the impairment presents specifically for recognizing exemplars of the category of faces. Moreover, compared to typical observers, the impairment appears even more severe for recognizing individual faces against physically dissimilar than similar distractors. Here, I argue that we need to limit accordingly our definition of prosopagnosia to a clinical (i.e., neurological) condition in which there is no basic-level object recognition impairment. Other criteria for prosopagnosia are proposed, with the hope that this conservative definition enables the study of human IFR processes in isolation, and supports progress in understanding the nature of these processes.
Topics: Adult; Female; Humans; Agnosia; Brain; History, 19th Century; History, 20th Century; Magnetic Resonance Imaging; Pattern Recognition, Visual; Photic Stimulation; Prosopagnosia; Recognition, Psychology
PubMed: 29845731
DOI: 10.1111/jnp.12162 -
Journal of Neurology May 2008
Topics: Face; Humans; Male; Mental Processes; Migraine with Aura; Neurologic Examination; Orientation; Pattern Recognition, Visual; Photic Stimulation; Prosopagnosia; Visual Cortex; Visual Perception
PubMed: 18344052
DOI: 10.1007/s00415-008-0809-7