Exploring the Etiology of Capgras Syndrome

The following is a paper on the Capgras Delusion written for my Neuropsychology class in the final year of my Psychology B.A.

Doctor, There’s an Impostor in My Bed! Perceptual Anomalies in the Capgras Delusion
November 2006

Imagine that you are eating lunch with your mother when you realize something about her is different. It is not a physical alteration, such as a new haircut or glasses, so much as the uneasy feeling you get while looking at her. As the weeks go by you continue to treat her with suspicion; you carefully inspect her behaviour and notice that she is responding strangely. The obvious truth finally sinks in—she is not your real mother! Though practically identical, this woman is clearly an impostor!

Welcome to the life of a Capgras syndrome patient, where anything from the people or pets to the places and objects you hold most dear may suddenly feel so unfamiliar that a delusion emerges: that of their substitution or duplication, perhaps by an actor, a robot, or simply, innocently, their identical twin figure.

The first well-documented case of this syndrome was an article by Capgras and Reboul-Lachaux (1923, as cited in Doran, 1990). Their patient was a 53-year-old woman who had the illusion that people in her life were being replaced by identical doubles; at one point, she came to believe that she herself had been duplicated. This “illusion of doubles” came to be coined ‘Capgras Syndrome’, and is now considered the prototype of various delusional anomalies categorized as misidentification syndromes.

Symptoms of Capgras tend to be monothematic and circumscribed. In other words, the impostor delusion tends to stand out against an otherwise normal belief system—“an island of irrationality within a sea of rationality” (Stone and Young, 1997). General trends within these patients, as summarized by Stone and Young, include difficulty in certain facial processing tasks, lack of interest concerning the fate of the “original” duplicated person, suspiciousness and occasional hostility (but mainly agreeableness) toward the double, and little recasting of beliefs to accommodate the delusional one. There is no evidence of overall reasoning deficits among these patients, especially considering that most feel it necessary to provide evidence for their claim.

Though Capgras typically accompanies a diagnosis of paranoid schizophrenia and is most often encountered in patients of middle or old age, over one third of cases occur in conjunction with traumatic brain lesion (Ramachandran and Blakeslee, 1998), especially injury to regions of the brain implicated in the processing of faces. As discussed in a detailed review by Stone and Young (1997), the delusions are often linked to lesions in the parieto-temporal regions of the right hemisphere.

Specifically, facial recognition is thought to be processed along two neural routes of the visual system, as proposed by Bauer (1984, as cited in Stone and Young, 1997): the ventral route for overt recognition or identification, and the dorsal route to the limbic system for affective significance. Cognitive dissonance resulting from a dysfunction in this second pathway is hypothesized to be at the root of Capgras syndrome. Brain imaging studies have provided evidence of dysfunctional connections among frontal cortex, multimodal association areas and paralimbic structures, resulting in cognitive-perceptual-affective dissonance (Papageorgiou et al., 2003); this suggestion of dissonance is consistent with the popular hypothesis that Capgras patients are able to recognize someone but not experience the appropriate affective responses. Since prosopagnosia, an inability to recognize faces, is thought to result from damage to the ventral route, these two syndromes are often considered mirror images of one another (Young and Ellis, 1990, as cited in Stone and Young, 1997). Finally, worsening of the condition is promoted by the vicious circle of confirmation bias: the patient looks for strange behaviours in others, and in response to this unusual behaviour, others act strangely toward the patient. This makes it difficult to break from a cycle of self-fulfilling prophecy.

Most reported cases of Capgras were diagnosed before modern diagnostic criteria and current neuroimaging methods; therefore, it should come as no surprise that the previously widely accepted explanation for the delusion was proposed by the psychodynamic field of psychology. It was believed that a patient created a double according to a defense mechanism due to guilt or conflicting emotions, most notably the Oedipus or Electra complex. Since a person would experience internal dissonance at discovering sexual feelings toward a parent or family member, it was proposed that they created a double in order to replace the object of their emotions and relieve this tension. However, current technology caused a shift from the psychodynamic foundation to viewing Capgras as a disorder of the central nervous system (Doran, 1990); advances in brain imaging clearly show some neurological damage in the majority of cases. Furthermore, the fact that Capgras delusions exist for pets, among other things, further weakens the psychodynamic approach.

Though psychological factors cannot be ruled out of the etiology, there seems to be an undeniable organic or physiological basis to misidentification syndromes. Stone and Young (1997) discuss two factors that partially explain the existence of Capgras delusions: a perceptual deficit and a reasoning bias. The Perceptual Deficit Account, similar to Fine, Craigie and Gold’s (2005) Explanation Account, claims that the delusion is the sufferer’s attempt to account for an anomalous perceptual experience. This account is incomplete on its own because the questions of why the impostor belief persists or that other sensory modalities do not override the faulty interpretation of the visual experience remain to be answered.

The Reasoning Bias Account claims that the original misperception is triggered by an organic process but that the delusion itself is determined by the psychology of the patient; in other words, the delusion is caused by a misinterpretation of an unusual experience. Delusional patients have abnormal reasoning processes: they tend to request less information before making a decision and jumping to conclusions (Huq et al., 1988, as cited in Stone and Young, 1997) and they have a tendency to attribute even hypothetical negative events to external causes (Candido and Romney, 1990, as cited in Stone and Young, 1997). Therefore, they are experiencing biases (rather than deficits) by using available information in a certain way through otherwise normal processes; for instance, by attributing their lack of affect to external consequences, they may be mistaking changes in the self for changes in others.

Both accounts are insufficient to determine why Capgras patients maintain these implausible beliefs despite available contradicting evidence. Stone and Young (1997) explore a philosophical model of belief formation to determine how patients might validate their decisions. Maher (1988, as cited in Stone and Young, 1997) claimed that delusional beliefs are formed the same way as normal and scientific ones: through a balance of observational adequacy and conservationism. It was proposed therefore that Capgras patients rely too heavily on observational adequacy (they have a bias toward first-hand experiences or the evidence of their senses), but maintain the integrity of their own personal beliefs by isolating this delusional belief, which is why the delusion tends to be circumscribed.

When patients feel that they must further validate their claims or beliefs, they have tended to refer to slight physical differences between the original and the impostor. Though this exploration is a step closer to resolving the dilemma of why the impostor belief is not rejected, it cannot explain the consistency of the impostor belief over other potential rationalizations. As put by Fine, Craigie, and Gold (2005):

The delusional belief is just one of several hypotheses that are observationally adequate… Many neurologic conditions result in direct perceptual abnormalities (e.g., acquired color blindness), yet we would not expect a corresponding delusion (e.g., that the world has been drained of color) as a default.

Furthermore, hypothesizing an abnormality in a patient’s belief acceptance system insinuates general patient susceptibility to any number of beliefs when an experience conflicts with prior knowledge. It is yet unknown whether Capgras patients experience subtler but similarly strange delusions.

The possibility that Capgras patients experience widespread emotional impairments, and not simply those pertaining to their loved ones, has been explored. This accompanies the suggestion that the misinterpretation of sensory evidence results from the fact that there is a larger discrepancy between, say, the affective response you should have to your mother as opposed to the delivery boy, so the missing affect toward the mother would be more noticeable. It has indeed been noted that patients often report persistent loss of affective response and generalized feelings of unfamiliarity, and they often seem to lack appropriate accompanying emotion (Christodoulou, 1977, as cited in Stone and Young, 1997). This could also explain why patients show little concern regarding the whereabouts or wellbeing of the original that was replaced.

Though this idea (that all emotions have been reduced due to some injury to the amygdale) seems intuitive, a case study by Hirstein and Ramachandran (1997, as cited in Ramachandran and Blakeslee, 1998) showed that this is not necessarily the case. Ramachandran hypothesized that his Capgras patient would not register a change in skin conductance when looking at pictures of his family intermixed with those of strangers. Control participants had a large response to their parents as expected, whereas the delusional patient showed no increased response; however, at times there would be a blip after a long delay, as if the brain were doing a double take. This showed that the patient was not responding emotionally to his parents. The experimenter kept track of the patient’s other emotions over a period of months to determine whether there was a global disturbance in emotion, but his responses were appropriate and diverse in all other situations. It was hypothesized that the large discrepancy between expected and actual emotion when the patient should have been experiencing a “warm fuzzy” feeling is the cause of the rationalization or delusion, and supports the Perceptual Deficit/Explanation Account. Ramachandran also considered that Cotard’s syndrome, where a person believes they are dead, is an exaggerated form of Capgras, where all affect is diminished or absent.

This finding is undermined by the argument that patients with similar perceptually anomalous experiences do not necessarily form Capgras syndrome; Coltheart et al. (2000, as cited in Fine, Craigie, and Gold, 2005) reported that patients with bilateral ventromedial frontal damage (an area thought to be important for integrating somatic state information) also failed to show increased autonomic responsiveness to familiar faces, though these patients did not develop delusional beliefs. Therefore, a lack of autonomic responses is itself insufficient to produce the delusion; there must be other determining factors (Ellis and Lewis, 2001).

Fine et al. (2005) also explore the Expression Account, where delusional beliefs are expressions of the content of a particular disordered experience. In other words, the disordered experience is directly that of replacement by an impostor, so the account eliminates the problem of why the impostor belief is invariably constructed. Dalgarrondo, Fijuisawa, and Banzato (2002) performed a case study on a 26-year-old blind woman with Capgras syndrome based on the sensory modalities of touch, smell, and taste. Neurological examinations, MRI, and SPECT were all normal. This case reinforces the argument that facial recognition impairment is an insufficient explanation for Capgras delusions, suggesting that psychological factors such as ambivalence and fear of losing someone may play a role. The authors believe that an anomalous perceptual process is the result of a delusional transformation of the world, rather than the cause. This is consistent with the Expression Account presented above; however, such an account must then explain how such a perceptual belief arises.

A case study by Dietl et al. (2003) presents another anomaly to the current hypotheses of Capgras delusions. A 59-year-old woman with paranoid psychosis developed Capgras regarding her daughter and a close friend. A few days on antipsychotic treatment with haloperidol resolved it concerning her daughter but the delusion regarding her friend persisted. A year later, she began experiencing delusions of plans for self-substitution, but did not expect this person to be physically similar to herself. Her delusions about her daughter returned and she eventually reached the conclusion that this girl may not be her real daughter but was a pleasant person nonetheless, so did not confront her with suspicions any longer. Several inconsistencies with current hypotheses include the fact that the woman did not expect that her substitute would physically resemble her, and that a delusion regarding her daughter’s substitute occurred in that person’s absence. Therefore, this patient was not simply experiencing a face processing problem. Furthermore, the patient did not develop Capgras delusions for her husband, but rather reported that his facial features were altered; this suggests that additional cognitive processes were malfunctioning.

One insight that this case study presents is the idea that Capgras syndrome can be maintained without current visual input, which suggests that a reduced feeling of familiarity can become more general and independent; this is consistent with reports of blind patients with Capgras. It is therefore illustrated that additional factors must be integrated into the current model of Capgras etiology. Caution must be used when interpreting these results, however, due to the fact that the patient suffered from a paranoid disorder.

There are no conclusive treatments currently available for Capgras syndrome. Sometimes remission occurs naturally and sometimes the disorder persists; in many cases antipsychotic medication or neuroleptic therapy is provided. When remission does occur, it is frequently due to the removal or modification of a concomitant neurological condition; MacCallum (1973, as cited in Doran, 1990) hypothesized that organic conditions cause a change in a patient’s affects and perceptions, thus presenting Capgras syndrome.

In conclusion, no existing account or theory of Capgras syndrome is sufficiently explanatory of the phenomenon. The most credible and supported position to date is summarized neatly by Stone and Young (1997):

People voicing [the Capgras] delusion suffer an impairment that leads to faces being perceived as drained of their normal affective significance, and an additional reasoning bias that leads them to put greater weight on forming beliefs that are observationally adequate rather than beliefs that are a conservative extension of their existing stock.

Scientific evaluation of the processes in Capgras syndrome has many implications for our understanding of normal object- and face-recognition processes and the nature of beliefs, teaching us important principles about brain function. For instance, the fact that objects can be duplicated shows that items with which we are familiar or are particularly fond of may enjoy special cognitive status; also, we can deem our perceptions to be governed by comparisons between states of an object rather than absolute values (Ellis and Lewis, 2001).

The fact that Capgras patients do not recognize a loved one due to their impairments suggests that affective responses could be a key part of the ability to recognize a face; perhaps “affect and cognition are under the control of separate and partially independent systems” (Zajonc, 1980, as cited in Stone and Young, 1997). The fact that scientific studies have supported the dissociation hypothesis makes it no longer possible to interpret face recognition as proceeding in a strictly sequential fashion, but rather as a feeding process into an integrative device. Future studies should look into this possible attribution process, as this knowledge is critical for further understanding of Capgras syndrome.

References

Dalgalarrondo, P., Fujisawa, G., & Banzato, C.E.M. (2002). Capgras syndrome and blindness: Against the prosopagnosia hypothesis. Canadian Journal of Psychiatry, 47(4), 387-388.

Dietl, T., Herr, A., Brunner, H., & Friess, E. (2003). Capgras syndrome – out of sight, out of mind? Acta Psychiatry Scandinavica, 108, 460-463.

Doran, J.M. (1990). The Capgras syndrome: Neurological/neuropsychological perspectives. Neuropsychology, 4, 29-42.

Ellis, H.D., & Lewis, M.B. (2001). Capgras delusion: A window on face recognition. TRENDS in Cognitive Sciences, 5(4), 149-156.

Fine, C., Craigie, J., & Gold, I. (2005). Damned if you do; Damned if you don’t: The impasse in cognitive accounts of the Capgras delusion. PPP, 12(2), 143-151.

Papageorgiou, C., Ventouras, E., Lykouras, L., Uzunoglu, N., & Christodoulou, G.N. (2003). Psychophysiological evidence for altered information processing in delusional misidentification syndromes. Progress in Neuro-Psychopharmacology & Biological Psychiatry, 27, 365-372.

Ramachandan, V.S., & BlakeBlakeslee, S. (1998). Phantoms in the Brain. New York: HarperCollins.

Stone, T., & Young, A.W. (1997). Delusions and brain injury: The philosophy and psychology of belief. Mind & Language, 12(3/4), 327-364.

Phantoms in the Brain

When I was reading one of my favourite books to date, “Phantoms in the Brain” by V.S. Ramachandran, I kept note of some facts that I found useful or particularly interesting. 

Fun Facts:

• In multiple personality disorders, eye structures and blood chemistry can change with different personas
• You can identify certain diseases by a person’s smell, for instance: diabetic ketosis – sweetish nail polish breath, typhoid fever – freshly baked bread odor, scrofula – stale-beer stench, rubella – newly plucked chicken feathers, lung abscess – foul smell, liver failure – ammonia-like windex odor, pseudomonas infection – grape juice, isovaleric acidemia – sweaty feet smell (yum yum)
• Poetry is processed in the right temporal lobe
• A distressed person who experiences a stroke in the corpus collosum might experience her left hand trying to strangle her – this is because the suicidal tendencies of the right hemisphere are no longer inhibited by the rational left hemisphere
• A stroke in the left brain might result in a patient who is anxious, depressed, and worried about prospect for recovery; a stroke in the right brain, however, might result in a patient who is blissfully indifferent
• There are two different smile circuits: (1) spontaneous smile – basal ganglia (no thought), (2) conscious smile (brain giving direction) – auditory to motor cortex. Therefore, a stroke in the right motor cortex means the instruction to smile results in right-side only, while a spontaneous smile is normal. A stroke in the basal ganglia results in a patient being incapable of a normal spontaneous smile, but an actual attempt at smiling works out alright
• A paralyzed person may still lift their arms when yawning, because a different brain pathway is used than a conscious attempt to lift the arms (unconscious lifting linked to respiratory centers in the brain stem)
• The Penfield homunculus is the name for the “little man in the brain,” whereby the body is mapped on the cerebral cortex. Brain circuitry can be remapped because the brain is flexible to change even in adulthood, which is why phantom limbs appear. These phantoms limbs can often experience sensation when the area mapped closest on the brain is stimulated on the body (see map below):

• There are two visual pathways: (1) old – goes to superior colliculus in brain stem, then to parietal lobes, used for orienting behaviour and nicknamed ‘the zombie in the brain’, (2) new – travels to lateral geniculate nucleus (a relay station for primary visual cortex), used for identifying objects. Damage to the new pathway is what we know as blindness in the conventional sense. Damage to the old pathway is known as “blindsight,” whereby patients can be somewhat oriented toward an object or target without consciously knowing how or what it is. 
• Charles Bonnet syndrome affects people whose vision has become compromised by glaucoma, cataracts, macular degeneration, or diabetic retinopathy. Many people develop hallucinations though they are either completely or partially blind (as if to replace reality) – it goes unreported for fear of being labeled senile or insane
• Everyone has a natural blind spot, called ‘scotoma’, but the region is automatically filled in by other visual areas of other brain

His distortions are due to the fact that the homunculus is proportioned according to the amount of cortex devoted to each body part (more devotion = more sensation)

Let Me Blow Your Mind

I’m not going to straight-up call this an IQ test the way the original image location did, but it is no doubt a test of hemispheric flexibility (right brain-left brain switching), which is related to many brain and behavioural capabilities apart from intelligence. Look at this gif image of a woman turning, apparently from a study devised at Yale; which way is she going, clockwise or counter-clockwise? Instructions (via ReadnRock):

If you see this lady turning clockwise you are using your right brain.
If you see her turning anti-clockwise, you are using your left brain.
Some people can see her turning both ways, but most people see her only one way.

See if you can make her go one way and then the other by shifting the brain’s current.

HINT: I was able to switch between the two much faster when I focused on the foot turning on the ground. And no, this is not a trick; the lady is not changing directions on her own (in the image coding). It is like those perspective illusions – remember those? – when the picture can be, say, an old lady or a young one based on your focus.

A Cure For What Ails Ya

Since I’m always looking for ways to improve quality of life without swallowing gigantic horse pills or experiencing side effects, I’m interested in what I Dose has to offer. The website employs specific auditory stimuli as a method of achieving desired effects; among their musical ‘doses’ one can find a ‘cure’ for PMS, lack of focus, depression, pain, fatigue, and so on. How they claim to achieve this:

Binaural beats affect our brainwaves directly and can alter moods, behavior, even consciousness. Sound crazy? We thought so too. But guess what? We tried it and it works!

Other than streamed tracks and testimonials, there is not a lot to this site – yet. The fact is, there’s no harm in trying it, there’s scientific truth in the claim that music helps set the tone for your mood, and, last but not least, it’s free! I’m going to give it a shot, and if you choose to take it for a spin, comment on your experience below :)

I Thought I Wanted This

Any friend who has seen me through heartbreak has heard me wish I could have the painful memories erased (though I wasn’t a fan of Eternal Sunshine of the Spotless Mind). So why is it just a little scary that this possibility may be on the horizon?

Scientists from the Medical College of Georgia in Augusta and the East ChinaNormal University in Shanghai selectively removed a shocking memory from a mouse’s brain, the team reports in the Oct. 23 Neuron.

Insight from such experiments may one day lead to therapies that can erase traumatic memories for people suffering from post-traumatic stress disorder, or wipe clean drug-associated cues that lead addicts to relapse. (via Science News.)

Yes, I understand the positive applications of such knowledge…but there are SO many worse consequences and vulnerabilities than we can begin to imagine. I guess it’s worthwhile to ponder an option you don’t have just for the fun of it; the reality of brain tampering, however, is making me consider perhaps the more Darwinian approach of letting my less pleasant experiences teach me a thing or two.

UPDATE: I like this article on similar findings a lot better, and not only because of this quote:

Tsien, however, cautions against applying his team’s results to expunging thoughts of broken hearts or limbs. “All memories, even very painful emotional memories, have their purposes. We learn from those experiences to avoid making the same kind of mistake.”

Keep that Brain Fit ‘n Sexy!

Got a case of brain rot, but don’t want to tune out of your favourite mind-numbing television series? Young or old, I think we can all appreciate the need to keep our minds sharp for the sake of general health. Below find [slightly edited descriptions of] four games that this article claims will “super charge your brain” – and if not, they’ll at least kill the commercial break.

1. Sudoku: …allows you to analyze a problem from all angles and reduces your trial and error practices. Neuro-scientists have proven that playing this game as a part of your everyday schedule can dramatically increase your brain cell functions, thus making you a better thinker. Research has also confirmed that playing these games can reduce the risk of Alzheimer’s disease and memory [loss]. 
    
2. Lumosity: This game was designed collectively by a group of neuro-scientists and brain game developers as a part of a brain training program. The results show that the players of the game have improved memory in terms of numbers, names, directions etc. along with elevated mood and clearer thinking. It has even led creating better and more alert drivers!
    
3. Bloxorz: The creators of Miniclip.com have succeeded in making a unique and sharp game called Bloxorz. The objective is to get a block or brick to fall into a square hole. The game will help you become dexterous and improves your control on your reflexes. The perfect game for improving hand and eye coordination.
    
4. Chess: …the king of all strategy games. 

I haven’t tested out #2 or #3, so let me know what you think! I am already a big fan of lowering my average Sudoku game-time on my Blackberry…

An Electro Interstitial Scan showed my depression

UPDATE: Read this article only after the following warning post.

I took part in a very interesting diagnosis method yesterday as part of my treatment by the group I mentioned yesterday, ISM (Immune System Management), which is associated with the CCRG (Canadian Cancer Research Group, the target of much online controversy since, surprise, some of its cancer patients did not survive). Using a fairly new, noninvasive, and reliable technology, the Electro Interstitial Scanner, my entire body was scanned and analyzed for abnormalities within minutes. It was amazing to watch, actually, because all I had to do was place my bare hands and feet on titanium plates, with signals also being drawn from two pads on my forehead, and every organ was scanned and displayed on a computer monitor in front of me.

From this experience, I learned much more about a lot of issues I already knew were affecting my health (so nice to have this confirmed, despite quackwatch warnings – though I appreciate the nature of vigilant concern). Having my health problems expressed in terms of organic chemistry preserves my sanity and hope, for one thing. Please keep this in consideration if you are merely scanning the internet for issues to battle: what ISM is doing is well-grounded scientifically, though its position on the fringes of socially-accepted medicine place it under more than its share of scrutiny. 

Anyhow, it was fascinating to have my spinal problems displayed in a different method than the x-rays I’ve had taken so often, expressed in terms of swelling, irritation, and resource concentration rather than bone density and shape. Most interesting of all, however, I was able to visually observe my depression.

The estimation of interstitial cerebral neurotransmitters showed that I am low on serotonin, dopamine, and catecholamines. Before I describe the behavioural consequences of this, I will draw some explanations from Wikipedia on the roles of these specific neurotransmitters:

Dopamine has many functions in the brain, including important roles in behavior and cognition, motor activity, motivation and reward, inhibition of prolactin production (involved in lactation), sleep, mood, attention, and learning.

In the central nervous system, serotonin plays an important role as a neurotransmitter in the modulation of anger, aggression, body temperature, mood, sleep, sexuality, appetite, and metabolism, as well as stimulating vomiting.^[1]

Catecholamines are hormones that are released by the adrenal glands in situations of stress such as psychological stress or low blood sugar levels.^[2]

My low levels of dopamine and serotonin result in low or easily varying moods (depression), and many of the symptoms that accompany it (sleep problems, aggression, etc.). My abnormal level of catecholamines messes up my fear response; this would largely explain my lack of fear associated with self-harm, suicidal idea, the indifference that led to my car accident, and so on. A really poor combination, in other words. More now:

Shown in research to perform a primary role in the processing and memory of emotional reactions, the amygdalae are considered part of the limbic system.^[3]

Another thing this test showed in my brain was that my amygdalae were active beyond belief and were a risk to my health. What this means, basically, is that my fight-or-flight response is on overdrive, constantly activated. However, my frontal lobes, which interpret these signals, showed dampened activity, meaning that I don’t interpret the necessity for fear, judgment, … BAD THINGS. Bad things all around.

I had blood taken today, which will analyze my amino acid levels, and be used to create a customized protein powder that I will ingest once a day, designed to balance my levels for optimal health.

It’s nice to see there is an organic reason for my abnormal (but all too common) mental state…and if there is an organic cause, there is an organic solution. I will keep you up to date with my progress using ISM’s patented organic proteins!

Brain electrodes as depression treatment

This sounds interesting but, in the light of new and reliable amino acid technology that can identify and [organically] resolve specific underlying causes of “untreatable” depression (I will be highlighting details of this company‘s research in the near future), I wouldn’t give it too much credit yet.

The article on brain stimulating electrodes here.