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Dr. Bob is Robert Hsiung, MD,
bob@dr-bob.orgShown: posts 1 to 5 of 5. This is the beginning of the thread.
Posted by alexandra_k on December 21, 2004, at 1:09:07
Physiological Findings and Delusions of Misidentification
The Capgras and Frégoli delusions are different kinds of delusions of mis-identification. In the Capgras delusion the subject seems to be mis-identifying someone they were previously close to such as a husband, wife, or child by maintaining that they have been replaced by an impostor, robot, or clone. In the Frégoli delusion the subject would seem to be mis-identifying strangers for people who are familiar to them when they maintain that people they know are disguising themselves as strangers and are following them around. It would seem plausible to consider that delusions of mis-identification may arise from a difficulty with processing perceptual information that would normally enable subjects to recognize people they know.
Interestingly, it has been found that subjects who have developed the Capgras delusion in response to cerebral trauma do process information regarding faces who are familiar to them differently from non-delusional controls, though perhaps in an unexpected way. While non-delusional subjects produce a heightened skin galvanization response to familiar faces as opposed to the faces of strangers, subjects with the Capgras delusion have been found to lack such a response, or to display a response that is significantly diminished compared to the responses of non delusional controls (Bruyer, 1991; Young and de Haan, 1992 and Young, 1994 in Stone and Young, 1997 p. 337).Subjects with the neurological condition of prosopagnosia have been found to display the usual heightened skin galvanization response to familiar faces. They are able to report that the faces seem familiar to them as normal subjects do, but they are unable to identify the face, or recall biographical information pertaining to the face that they have been shown. Ellis and Young (1990) consider these findings to provide some support for their thesis that there are two dissociable pathways involved in face recognition; a perceptual pathway, and an affective one. They maintain that these two pathways should be a part of a cognitive model of face recognition and they also consider these pathways to be realized in the brain on the dorsal and ventral routes. Breen et al., (2000) have critiqued the notion that the two cognitive pathways are realized on the dorsal and ventral routes, but they also maintain that the dual mode cognitive model could be realized on a single neural pathway. This does not seem to disrupt the cognitive model of face recognition; it just calls into question issues around how the model is realized on the neural wetware of the brain.
Ellis and Young (1990) link the perceptual pathway to the subject’s ability to recall and verbalize information pertaining to the face of the person they have been shown, such as biographical information, and the person’s name. This is the pathway that is damaged in subjects with prosopagnosia. Ellis and Young, (1990) do not explicitly consider the function of the affective pathway, except to postulate that its malfunction is responsible for the production of the anomalous experience that features in the Capgras delusion.
It still needs to be explained how such a lack of normal affective response to familiar faces is relevant to an explanation of the Capgras delusion. Although normal subjects are not typically aware of producing a heightened skin galvanization response to familiar faces and not to strangers it is thought that the lack of normal response would trigger consciously experienced ‘alarm bells’ that would serve to signal to the subject that something is wrong. It would seem plausible to consider that prior to head injury the delusional subject would have produced the greatest affective response to people who were close to them such as a wife, husband, or child. Post head trauma the difference between the response that should have occurred and the response that does occur would thus be the most anomalous for their loved ones. These findings would also seem relevant to an explanation of the Frégoli delusion if, for example, it was found that subjects with this delusion produced a heightened skin galvanization response to strangers. While this has not been empirically tested it would seem to be a plausible hypothesis in light of the findings of the physiological responses of subjects with the Capgras delusion. If it was found that subjects with the Frégoli delusion do produce a heightened response to at least some strangers then this would seem to go some of the way towards explaining why they say that strangers are people who are familiar to them.
Posted by smokeymadison on December 21, 2004, at 16:54:20
In reply to 1.4, posted by alexandra_k on December 21, 2004, at 1:09:07
Ellis and Young (1990) consider these findings to provide some support for their thesis that there are two dissociable pathways involved in face recognition; a perceptual pathway, and an affective one.
Related to my post for the prevoius thread, is there any evidence that it is the affective pathway that is messed up in these delusional subjects?
Ellis and Young, (1990) do not explicitly consider the function of the affective pathway, except to postulate that its malfunction is responsible for the production of the anomalous experience that features in the Capgras delusion.
OK, so they speculate that it is the AFFECTIVE pathway that is messed up. why do they postulate this? is it possible that extreme emotion caused the pathway to misfunction and cause the delusion? i am still considering the notion that extreme emotion is the start for some to a delusion. when i say for some, i mean that not everyone in severe emotional distress becomes delusional, but for those who are delusional, it started with extreme emotion.
this is all very interesting for me. i did a literature review a while back on whether being manic or depressed and having OCD would lower the "delusional threshold" and result in mere obsessions becoming delusions. i didn't find much, actually. i am somewhat familiar with research in face recognition b/c my cognitive psychology prof was doing research on it at the time and included a lot of it in the class lectures.
SM
Posted by alexandra_k on December 21, 2004, at 18:00:06
In reply to Re: 1.4, posted by smokeymadison on December 21, 2004, at 16:54:20
>is there any evidence that it is the affective pathway that is messed up in these delusional subjects?
The 'affective pathway' is just the name they have given to the pathway that produces the affective (skin galvanisation) response. Subjects with cerebral injury and the Capgras delusion do not produce the affective response, therefore there is a breakdown in their affective pathway.
(At this stage the positing of an affective pathway has a hint of circularity about it)
Ok. Nows the time to fess up, they really are focused on Capgras and Fregoli delusions that occur in response to cerebral injury. There is a (fairly) localised site of damage, which leads to a (fairly) specific deficit (the lack of affective response) and that seems to produce a fairly specific delusional belief. I like this because I am interested in the relationship between neurological, cognitive, and intentional (common sense) explanation - though its relevance for delusions that occur for other reasons (e.g., Schizophrenia) remains unclear... It is unclear whether subjects who develop the Capgras delusion within the context of schizophrenia will be found to have a similar lack of affective response.
> i mean that not everyone in severe emotional distress becomes delusional, but for those who are delusional, it started with extreme emotion.This sounds like a two-factor model though. What I want to consider is whether there is something different about the anomalous experiences (or emotional distresses, if you like) of subjects who do and do not develop delusions. In the Cotard delusion the delusion seems to result from a LOSS of emotion if you will, and thus it doesn't seem to be extreme distress that is so relevant. That being said, Maher thinks that the difference between delusional and nondelusional subjects is a function of the intensity and duration of the anomalous experience. Maybe you have sympathy with this line?
I have a little list of delusions that I have compiled...
1)Cotard 'I am dead'
2)Capgras 'My wife has been replaced by an impostor'
3)Fregoli 'People I know are disguising themselves as strangers and are following me around'
4)Unilateral Neglect 'Thats not my arm - It's yours!'
5)Reduplicative Paramnesia 'My husband died long ago - but he is also a current patient on this ward'
6)Mirrored Self Mis-Identification 'There is a person in the mirror who follows me around'
7)Thought Insertion 'Someone elses thoughts are being inserted in my mind'
8)Alien Control 'Someone else is initiating my actions'
9)Thought Withdrawal 'Someone is taking thoughts from my mind'
10)Thought Broadcast 'Other people can hear my thoughts'
11)Reference 'The tables signified that the world was coming to an end'
12)Grandeur 'I am god'
13)Persecution / Paranoid 'The FBI are out to get me'
14)Jealousy 'My partner is cheating on me'
15)Erotomania 'Winston Peters is in love with me'
16)Somatic 'I don't have any internal organs'.Now most theorists attempt to explain 7-16 which typically occur in schizophrenic delusions. The recent neurological findings of subjects with cerebral injury, however has led to theorists working within the framework of cognitive neuro psychology to have a go at 2-6. I think it is fair to say that most accept the explanation of 1 that I have already given. An explanation of 2-3 can be fairly easily adapted to explain 7-8, though it would be much nicer if we could get an explanation of 9-10 to flow out of this I need to think about this much more...
Anyways. my point is that typically explanations of delusion were psychodynamic. Psychodynamic explanations cannot hope to account for delusion in the case of cerebral injury, though, and have poor prospects for explaining why damage to the right hemisphere seems to be implicated.
Psychologists have thus started from the top of the list while psychiatrists have started from the bottom. it is unclear whether an account within one framework can be applied to all. Maybe neurological delusions will need a different kind of explanation to psychiatric ones.
But Freud didn't get to be famous by limiting his speculations to what he wanted to do with his own mother... we should at least try...
Posted by smokeymadison on December 21, 2004, at 20:20:03
In reply to Re: 1.4 » smokeymadison, posted by alexandra_k on December 21, 2004, at 18:00:06
>>In the Cotard delusion the delusion seems to result from a LOSS of emotion if you will, and thus it doesn't seem to be extreme distress that is so relevant.
yes, but what caused the loss of emotion? it is still possible that extreme emotion caused the loss of emotion (the brain shutting down to protect itself). maybe. in severe depression, the brain does sort of shut down to prevent suicide.
so you are interested in localized brain damage causing specific delusions. and the whole time i have been focusing on delusions found in schizophrenia, BPD, and the mood disorders, etc. i really don't think that delusions caused by localized brain injury are really that different than those caused by extreme emotional distress. i mean, i think that eventually psychodynamic and neurological theories will mesh.
so a certain part of the brain is injured. the result is delusions 2-6. each of these bring to mind the test scientists do with chimps/gorillas to see if they recognize themselves in the mirror (i spent a semester in philosophy working on whether chimps/gorillas had the same moral status as human beings.) they put a spot on their face and then put them in front of a mirror to see if the primate will try to wipe off the dot, meaning that they know that it is them in the mirror. the results were mixed. highly educated and well trained primates recognized themselves whereas primates who had been kept in small cages and had been neglected did not. well-reared primates recognized their handlers by signing their names.
but of course, all that has to do with development of the brain. but i think what can be developed can also be lost through tramatic experiences. what if that certain part of the brain that is damaged is somehow connected directly to those specific experiences (memories)accumulated during infancy that allow a person to recognize themselves and/or others? i know that there are stages in infancy in which a baby LEARNS to recognize him/herself and LEARNS to recognize others as well as a host of other things. By learned i mean the the brain has developed.
there is plenty of debate as to whether these things are learned unintentionally or whether they are wired--meaning that they are inevitable in the span of infancy. all i know is that there is a time in infancy when, if the baby could talk, their utterances would be considered delusions 2-6. so somehow, it seems, the damage to that certain part of the brain has "set back" the adults to the point where they were in infancy. this is all my b*llsh*tting of course, i really don't know.
SM
Posted by alexandra_k on December 22, 2004, at 16:46:42
In reply to Re: 1.4, posted by smokeymadison on December 21, 2004, at 20:20:03
I agree that it could be the case that an extreme emotion preceeded the shutting down. This could be empirically supported or falsified. Even if it was the case, however, the delusion does not occur until after the shutting down has occured and so I think that it would be fair to say that it is LACK of emotion / affective response that is causally relevant to the production of the Cotard delusion.
> so you are interested in localized brain damage causing specific delusions. and the whole time i have been focusing on delusions found in schizophrenia, BPD, and the mood disorders, etc.
Yes. But the delusions that occur within the context of schizophrenia, BPD, and the mood disorders etc are the hardest cases for the cognitive neuro-psychological model, so it is good not to lose sight of those. Thats why I didn't say anything until now. What that means, however, is that my attempted explations / thoughts with respect to those sorts of delusions are a whole heap less well thought out than my attempted explanations of the Capgras and Fregoli delusions as they occur in response to cerebral injury.
>I think that eventually psychodynamic and neurological theories will mesh.
It would be nice indeed to be able to explain all of those delusions from within a single framework. This may involve a framework of explanation that is slightly different from either the cognitive neuropsychological or the psychodynamic frameworks, as they currently stand, however. And of course explanation isn't a fixed or absolute thing, anyhow. A good explanation should raise any number of new interesting questions, and new empirical findings should spur on the evolution of theories (and hence explanations).
>they put a spot on their face and then put them in front of a mirror to see if the primate will try to wipe off the dot, meaning that they know that it is them in the mirror.This has a lot to do with 6)Mirrored Self Mis-Identification. It has been found that there are two groups of people with this delusion. The first seem to have lost their ability to interact fluently with mirrors. If an experimentor stands behind a subject who is facing a mirror and holds up a ball then when the subject is asked to take the ball they claw at the surface of the mirror. They no longer seem to see mirrors AS mirrors. They no longer seem to see mirror images as REFLECTIONS. The other group do ok on these kinds of tasks, but they still claim that the person in the mirror is another person who is following them around. It would seem that the deficit in the first group is different from the deficit in the second. Both would fail the spot on the face task, however.
It is interesting that if you (as a comparatively 'normal' subject) are standing in front of a mirror with an experimentor behind you, if they make to suddenly wack you on the back of the head by throwing a ball or something then you will cringe AWAY from the mirror (back towards the thing that is being thrown so it is better able to hit you!). It seems as though our initial response to mirrors is to see them as gateways into reality, it is just that we are able to inhibit this response (that very small children have) and see the mirror space AS reflection.
Perhaps the delusional subjects have lost this ability to inhibit their natural response. It is interesting that you are considering the development of these abilities from the perspective of development within the lifetime of the individual. I guess I attempt the same manouver, but appeal to the development of abilities (or special purpose cognitive mechanisms or mental modules / structures) from the perspective of the course of evolution. Still they are similar (if not the same) things, over different time courses, I suppose.
>this is all my b*llsh*tting of course, i really don't know.
Don't worry, b*llsh*tt*ng is all there is. Nobody does it any differently. It is just that there are more or less plausible varieties of b*llsh*t, but he who b*llsh*ts best wins!
Or, of course some b*llsh*t has such lovely practical consequences that we are kind of forced to take it seriously (rockets to the moon, computers, the atomic bomb etc). AI, AI is the test, IMO
This is the end of the thread.
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