Covert facial recognition

Joachim Bodamer created the term prosopagnosia in 1947, which is a disorder where individuals have an inability to recognize faces of people. Individuals with this disorder do not have the ability to overtly recognize faces, but discoveries have been made showing that people with this disorder have the ability to covertly recognize faces. Covert facial recognition is the unconscious recognition of familiar faces by people with prosopagnosia. The individuals who express this phenomenon are unaware that they are recognizing the faces of people they have seen before.[1]

There are two types of prosopagnosia, congenital and acquired. Congenital prosopagnosia is an inability to recognize faces without a history of brain damage; while acquired prosopagnosia is caused by damage to the right occipital-temporal region of the brain. In the 1950s it was theorized that the right cerebral hemisphere was involved in facial recognition and in the 1960s this theory was supported by many experiments.[2]

Although the ability for overt facial recognition is inhibited in patients with prosopagnosia, there have been many studies done which show that some of these individuals may have the ability to recognize familiar faces covertly. These experiments have used behavioral and physiological measures in order to demonstrate covert facial recognition. A common physiological measure that is used is the measure of autonomic activity by using skin-conductance responses (SCR) which show a larger response in individuals with prosopagnosia who are shown pictures of familiar faces compared to pictures of unfamiliar faces.[2]

Theories and reasoning

Many theories reside in the topic of cognitive facial recognition. First, the theory of contradiction between prosopagnosia and covert recognition. Prosopagnosia is the inability to recognize faces but is believed to stem from damage to the ventral route of the visual system. Whereas covert recognition is shown in people that lost their ability to recognize faces, implying an intact ventral limbic structure projecting to the amygdala.[3]

Theory two states that it cannot be observed in developmental cases of prosopagnosia, which was proposed by Grueter. Developmental prosopagnosia is a severe face processing impairment without brain damage and visual or thinking dysfunction but can sometimes run in families (some indications that there may be a genetic reason for the disorder). This theory is thought to rely on the activation of face representations created during the time of normal processing.[4]

Contradicting the last theory, the affective valence in developmental prosopagnosia theory states that individuals may be processing faces on affective dimensions, feelings and emotions, rather than familiarity dimensions, previous occasions and when they met.[3]

Next is the dual-route models theory, proposed by Bauer, and states covert recognition can be seen in people that endured a time of normal face processing before actually getting the condition. With this, there are two different types of covert recognition: behavioral and physiological. Behavioral covert recognition is measured by reaction time and occurs within a cognitive pathway consisting of face recognition units (FRUs), personality identity units (PINs) and semantic information units. Physiological covert recognition is measured by SCR and is the second route that mediates reactions to familiar faces. This theory can be explained by the disconnection of FRUs or that it may be that the face recognition system is intact but has been disconnected from a higher system enabling their conscious awareness.[3]

The parallel distributing process is a theory that proposes it would be easier to relearn previous known faces rather than to learn new ones. This process has three steps: the distributed information is represented, memory and knowledge for some things are not stored explicitly but are connected between nodes, learning can occur with gradual changes to the connections. Damaged networks are less effective by zeroing the weight of the connection. Each connection is embedded and is still faintly there, making it easier to relearn.[5]

Other theories include one proposed by Bauer, states that neurological routes mediate overt recognition. His theory went with Bruce and Young’s theory that when using these three sequential stages in order, each stage will affect the next with overt mediation. The three stages are familiarity, occupation and name retrieval.[6]

Experiments

One of the very first studies into the diversion of pathways of overt and covert facial processing was done by Bauer in 1984.[6] This study has been the basis for most of the other studies and literature that has been conducted on the topic of prosopagnosia and covert processing. Three other larger studies were performed. Event-related potential studies were done with 20 subjects who were clear of psychological disorders. This was a face study using 315 faces and a string of characters. In each trial 30 of the faces were familiar and 90 novel faces were shown. Then, the 315 faces were shown and subjects were asked which were familiar. The faces were shown again from the first trial but without a string of letters. This resulted in higher load results for overt recognition with longer reaction time. High load tasks led to the ability to recall far fewer faces when the task was performed.[7]

The second study was directly into covert facial recognition in prosopagnosia. In this study faces were taken from a set of 166 faces, hair and background were removed. In the first task, 36 pictures were shown, half actors and have politicians. When the face was shown the subject was asked if it was a politician or actor. Both the control and prosopagnosia patients were able to identify which faces were which therefore reaction time was compared. The second task was to say which of the faces were famous in a set of forty famous and forty non-famous. Prosopagnosia subjects had little ability to make this distinction. Further, the third task also showed forty famous faces but instead of a random string written names were used. The faces remained until one was decided upon to match the name. The covert recognition was only present in two tasks. This was not on the first task which was meant to prime and lead to the fact that the prime may be the impairment of prosopagnosia.[2] SCR tests are often used to test covert facial processing but none of the experiments displayed significant results[8]

Facial recognition in disorders

There are several problems that may damage the ability to properly perceive faces, many of these don’t have effects on both the covert and overt recognition of faces. Many of these problems only have an effect on the overt recognition of faces and leave the covert recognition intact.

Prosopagnosia is a disorder which causes the inability to use overt facial recognition.[9] While people suffering from prosopagnosia often cannot identify whose face they are looking at they usually show signs of covert recognition. This can be seen in their ability to accurately guess information during forced choice tasks.[2] Patients who are unable to identify faces of people that they know are still able to accurately guess information on the owners of the faces such as their professions and names.[10] When asked how confident of their answers the patients were, they would often give low ratings of confidence despite their high accuracy during the tests.[2] This shows that they are unable to overtly recognize the face but they are still able to recall information on the owners despite the fact that they can’t identify the owner.[11]

While prosopagnosia patients are unable to overtly recognize faces, patients with Capgras delusion are unable to covertly recognize faces. People suffering from Capgras delusion are able to properly identify a face, but lack the covert recognition that is normally evoked by a familiar face. Before the delusion set in patients would normally have a sensation of familiarity and have a heightened response to faces that they recognize. Once the delusion has set in the patients no longer feel that the face they are looking at is familiar to them and they can’t access the feelings they normally held for the owner of the face despite the fact that they can properly identify who the face belongs to. This condition causes patients with Capgras delusion to believe that the person has been replaced with a look-alike imposter.[11]

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See also

References

  1. Simon, Stéphane R., Asaid Khateb, Alexandra Darque, François Lazeyras, Eugene Mayer, and Alan J. Pegna (2011). "When the Brain Remembers, but the Patient Doesn't: Converging FMRI and EEG Evidence for Covert Recognition in a Case of Prosopagnosia". Cortex. 47 (7): 825–838. doi:10.1016/j.cortex.2010.07.009. PMID 20850714. S2CID 1228865.CS1 maint: multiple names: authors list (link)
  2. Rivolta, Davide, Romina Palermo, Laura Schmalzl, and Max Coltheart (2012). "Covert Face Recognition in Congenital Prosopagnosia: A Group Study". Cortex. 48 (3): 344–352. doi:10.1016/j.cortex.2011.01.005. PMID 21329915. S2CID 20862714.CS1 maint: multiple names: authors list (link)
  3. Bate, S.; Cook, S.J. (2012). "Covert recognition relies on affective valence in developmental prosopagnosia: Evidence from skin conductance response". Neuropsychology. 26 (6): 670–674. doi:10.1037/a0029443. PMID 22823135.
  4. Farah, Martha J.; Randall C. O'reilly & Shaun P. Vecera. (1993). "Dissociated Overt and Covert Recognition as an Emergent Property of a Lesioned Neural Network" (PDF). Psychological Review. 100 (4): 571–588. doi:10.1037/0033-295x.100.4.571. PMID 8255950.
  5. Eimer, M.; A. Gosling & B. Duchaine (2012). "Electrophysiological Markers of Covert Face Recognition in Developmental Prosopagnosia". Brain. 135 (2): 542–554. doi:10.1093/brain/awr347. PMID 22271660.
  6. Young, A. W. (1992). "Face recognition impairments". Philosophical Transactions of the Royal Society of London. Series B: Biological Sciences. 335 (1273): 47–54. doi:10.1098/rstb.1992.0006. PMID 1348137.
  7. Rodriguez, Y.S.; Fuster, J.I. & Leon, M.A.B (2008). "Covert and Overt face processing in healthy subjects: an ERP study" (PDF). International Journal of Bioelectromagnetism. 10 (4): 246–260. Archived from the original (PDF) on 2016-06-17. Retrieved 2015-03-23.
  8. Valdés-Sosa, M.; Bobes, M. A.; Quiñones, I.; Garcia, L.; Valdes-Hernandez, P.; Iturria, Y.; Asencio, J. (2011). "Covert face recognition without the fusiform-temporal pathways". NeuroImage. 57 (3): 1162–1176. doi:10.1016/j.neuroimage.2011.04.057. PMID 21570471. S2CID 2295770.
  9. Groome, David (2014). An Introduction to Cognitive Psychology. 27 Church Road, Hove, East Sussex BN3 2FA: Psychology Press. pp. 126–134. ISBN 9781848720923.CS1 maint: location (link)
  10. Fox, C. & G. Iaria, J. Barton (2008). "Disconnection in Prosopagnosia and Face Processing". Cortex. 44 (8): 996–1009. doi:10.1016/j.cortex.2008.04.003. PMID 18597749.
  11. Young, Garry (2009). "In What Sense 'familiar'? Examining Experiential Differences within Pathologies of Facial Recognition". Consciousness and Cognition. 18 (3): 628–638. doi:10.1016/j.cortex.2008.04.003. PMID 18597749. S2CID 20517855.
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