Filosofia della mente e scienze cognitive - Lezione ottobre 2016 Capgras delusion was first identified by French psychiatrist Joseph Capgras. In a 1923 paper, he wrote about a patient, "Madame M," who for 10 years had been "transforming everyone in her entourage, even those closest to her, such as her husband and daughter, into various and numerous doubles."

Cognitive Neuropsychology Defining the field and its approach: using theories of normal performance to account for effects of brain injury using effects of brain injury to test theories of normal performance Example: Prosopoagnosia Vs Capgras delusion

3 PROSOPAGNOSIA ‘Prosopagnosia’ is the term used to describe the complete inability to recognize previously familiar faces  voice recognition remains, however

4 A monothematic delusion

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is characterized by the firm and sometimes dangerous belief that some people are no longer who they were: instead they have been replaced by doubles, impostors, robots, aliens and so forth. 6

Capgras Syndrome Demonstrates implausibility but cannot change feeling

Ellis and Young suggested that, despite their obvious differences, there might be a link between prosopagnosia and Capgras delusion.  They posited the idea that the two conditions might be mirror images of one- another. 8

It is known that autonomic responses to faces, as measured by changes in the skin conductance response (SCR), are larger when faces are familiar than when they are not. 9

Skin conductance response has been used to demonstrate the fact that, despite the absence of overt, conscious face recognition, at some level patients with prosopagnosia can discriminate the faces of people they know  i.e., they show the normal elevated SCRs to previously familiar faces compared with faces never encountered before the brain damage that caused the prosopagnosia. 10

 Thus, prosopagnosic patients are unable to recognize familiar faces but they still show autonomic affective responses, as indicated by increased skin conductance, to familiar faces.  By contrast, people with Capgras delusion do not show differential autonomic activity to familiar compared with unknown faces! 11

Hypothesis: the Capgras delusion arises from an affective deficit in face processing.  Skin conductance responses were measured in Capgras patients who were shown familiar and unfamiliar faces.  As predicted by the hypothesis, the increased response to familiar faces that is found in normal subjects was absent or greatly reduced in these patients. 12

13 (a)Mean skin conductance responses (SCRs) to familiar faces (yellow bars) and unfamiliar faces (red bars) for three groups of subjects. The normal subjects and non-delusional psychiatric controls show larger responses to familiar compared with unfamiliar faces. Capgras patients do not show this differential response. (b)Comparison of SCRs to a repeated tone. This demonstrates that the lack of a familiar face differential for Capgras patients cannot be attributed to a general lack of SCR responsivity. Both Capgras patients (blue symbols) and normal controls (red) show a pattern of habituation as the tone is repeated. Ellis et al. (1997)

When a patient with Capgras delusion sees his wife, he will still be able to know that the woman he is looking at looks just like his wife, because of the intactness of his face recognition system.  it is the system subserving the autonomic response that is disrupted in Capgras patients. 14

The occurrence of autonomic face discrimination in the absence of overt recognition implies that there are two distinct and independent routes to recognition:  one (the identification detector), termed the ventral route, involving structures along the longitudinal fasciculus between visual cortex and limbic system;  and the other, the dorsal route (capable of detecting the ‘significance’ of a face) passing from visual cortex through the superior temporal sulcus, inferior parietal lobe and cingulate gyrus to the limbic system (primarily the amygdala). 15

16 Normal face processing.  The yellow route shows the covert dorsal route via the IPL (inferior parietal lobule) and the STS (superior temporal sulcus).  The red route is the overt ventral route to recognition.

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18 In prosopagnosia the overt ventral route is damaged, hence face recognition is compromised.

19 the damage is postulated to be in the covert dorsal route

20 Neuroanatomical account of face processing (a)Normal face processing. The yellow route shows the covert dorsal route via the IPL (inferior parietal lobule) and the STS (superior temporal sulcus). The red route is the overt ventral route to recognition. (b)In prosopagnosia the overt ventral route is damaged, hence face recognition is compromised. (c)This account can also be applied to explain Capgras delusion, where the damage is postulated to be in the covert dorsal route.

Bauer’s model is inconsistent with the modal, single route model of face recognition

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The system subserving this autonomic response that is disrupted in Capgras patients.  As a result, these patients have an experience analogous to seeing an identical twin of one’s best beloved.  The visual match is there, but not the emotional response. 23

Brendan Maher: ‘‘A delusion is a hypothesis designed to explain unusual perceptual phenomena’’ (Maher 1974, p. 103).  There is an unusual phenomenon related to the sight of a spouse’s (or other familiar person’s) face in Capgras delusion (the unexpected absence of autonomic response), and the abductive inference “That’s not my spouse” provides an explanation of this unusual phenomenon. 24

If this were the complete explanation of the delusion, then anyone who suffered any form of brain damage that prevented familiar faces from evoking responses of the autonomic nervous system would suffer from Capgras delusion, and that is not the case. E.g., patients with damage to ventromedial regions of frontal cortex are like Capgras patients in that they too show no greater autonomic responding to familiar than unfamiliar faces; but these patients are not delusional. 25

26 This model also suggests how the two routes of recognition must be brought together in order for a delusion to occur. An abnormality at location marked ‘ A ’ will lead to a loss of overt face recognition and, therefore, is an account for prosopagnosia. An abnormality at location marked ‘ B ’ will lead to a loss of the affective response and the autonomic reaction to a face, and will therefore also lead to a conflict in the integrative device and is an account for Capgras delusion. An abnormality at location ‘ C ’ will lead to a loss of differential skin conductance responses for familiar and unfamiliar faces but will not lead to delusions; hence, this is an account for the performance of fronto-ventromedial lesioned subjects. One difference between this model and the Breen et al. model is that the person identity nodes and the affective response module are not directly connected. Connection between these modules would imply that damage at A or B could be circumvented. An adaptation of the Breen et al. model of face recognition and misidentification syndromes.

There must be an additional cognitive deficit in the Capgras patients (a “second factor”): some form of impairment of belief evaluation processes.  It appears that in Capgras the facial recognition system, getting only one sort of appropriate information, sends this on to more central systems which are also in trouble. 27 Stone, T. & Young A. (1997). Delusions & brain injury: The philosophy and psychology of belief. Mind and Language 12,