Capgras+Syndrome

= What is Capgras Syndrome? = **Capgras Syndrome** is characterized by an individual’s primary **delusion** that close acquaintances – such as parents, siblings, children, or a spouse – have been replaced by an imposter. The individual afflicted with this disorder will usually claim that the person in question looks like or is even identical to the family member or friend that has ‘been replaced.’ Along with people, this disorder may also extend to animals, objects, or places. [2] = The Visual System  = The visual system serves to pick up and process information coming from the eyes. Processing begins as visual information projected onto the retina is absorbed by rod and cones cells. These rod and cone cells then project their information to M type ganglion cells that deal with motion and spatial perception, and P type ganglion cells that deal with form and color. These ganglion cells have axons that leave the retina and form the left and right optic nerves. The **optic nerve** of each eye projects to the **optic chiasm** where lateral information (right and left nasal) travels ipsilaterally, and medial information (right and left temporal) crosses the chiasm and travels contralaterally. Left nasal and right temporal information travels from the optic chiasm through the left **optic tract** to the left **lateral geniculate nucleus (LGN)** of the thalamus, left hypothalamus, left pretectum, left superior colliculus. Right nasal and left temporal information travels from the optic chiasm through the right optic tract to the right lateral geniculate nucleus of the thalamus, right hypothalamus, right pretectum, right superior colliculus. Visual information that traveled to the LGN of the thalamus is then projected through the **optic radiation** to its respective side of the brain’s **primary visual cortex**, also known as area V1 or Brodmann’s Area 17. [3]

Information from the primary visual cortex then travels to the visual association cortex, also called Brodmann’s Area 18 or area V2. From there, the visual information moves to higher order visual association cortices. The specific visual information dealing with motion and spatial analysis travels in a dorsal pathway to the dorsolateral parietotemporal cortex. This higher order dorsal pathway handles “where” information that is processed in the parietal lobe, essentially everything about movement, location, and the collective effect of what is being seen and what is moving in a given direction. The visual information for form and color is projected through a ventral pathway to the inferior occipitotemporal cortex in the temporal lobe that handles “what” information, meaning anything about object characteristics, shape, form, and color. The visual input from the inferior occipitotemporal cortex than goes to the hippocampus, which deals with memory, and the amygdala, which mainly handles emotional response and some memory. [3]

= The Amygdala  =



The **amygdala**, one located in both the left and right temporal lobes, is a small almond shaped structure that is known as the emotion center of the brain. This structure is involved in appraising the emotional valence of situations, meaning that it judges circumstances and allows the brain to determine if it is happy, sad, frightening, etc. The amygdala functions to prepare the body for its fight-or-flight reaction by helping the brain to recognize potential threats and therefore increasing heart rate and breathing rate. The amygdala is also partially responsible for the modulation of memory consolidation, particularly for memories related to emotion. [7] = = = What Causes Capgras Syndrome? = There are a handful of disorders that have similar symptoms to Capgras Syndrome, including Schizophrenia, Alzheimer’s Disease, Huntington’s Disease, Multiple Sclerosis, Traumatic Brain Injury, Substance-Induced Delusional Disorders from hallucinogens and alcohol, manic and depressive types of Mood Disorders with delusions, and Dementia. Capgras Syndrome appears to have somewhat of an organic etiology. Some believe that this disorder can be due to failure of normal brain recognition abilities resulting from a stroke, drug overdose, traumatic brain injury, or other causes that damage the brain. In the entire scientific realm, there are controversies about the exact trigger for improper brain function causing Capgras Syndrome, but it may be due to organic factors, psychodynamic factors, or a combination of the two. [2] Capgras Syndrome is often compared to the disorder of **prosopagnosia**, but these two disorders are somewhat like opposites of each other. Prosopagnosia, also known as face blindness, is the inability to recognize the faces of familiar people. These individuals do not consciously know the familiar people they come in contact with, yet their bodies demonstrate changes in their **galvanic skin response** when presented with familiar faces, indicating an unconscious emotional recognition. On the other hand, people with Capgras Syndrome can perceive faces and recognize that they look familiar, yet they are unable to connect the faces with the actual emotional aspect of familiarity. The galvanic skin response of individual’s with Capgras Syndrome remains unaffected, as it would if looking at a total stranger. This research conducted in this area of bodily response has revealed that Capgras Syndrome results from a disconnection somewhere in the brain. [6] According to V.S. Ramachandran, Capgras Syndrome results from a disconnection between the areas of the brain that process visual information and areas of the brain that control the limbic system’s emotional response and memory function, specifically, the amygdala. When a normal functioning individual sees someone familiar, a part of the brain’s visual system identifies the face. That facial identification information is then sent to the amygdala where emotions are activated that associate themselves with the familiar person being looked at. The brain is then able to consolidate all the information about the recognized individual and allow for proper emotional response. In those suffering from Capgras Syndrome, Ramachandran claims that the connection between the visual recognition and emotional recognition is damaged. Thus, the individual with Capgras is able to identify the distinguishable person as familiar, but the inability to associate emotions with such identification results in the patient being left with an unfamiliar emotional response about such person, triggering feelings and claims that the person is an imposter [7]. Principally, the cause of Capgras Syndrome is a failure in proper communication between the brain’s areas of ventral stream processing in the temporal lobe and the limbic system, mainly the amygdala. This inability to communicate effectively is what leads to the disruption of memory management dealing with identifying individuals. Patients with Capgras usually possess a fairly intact or even amplified ability to individuate different **episodic memories**, yet their ability to generate continuing memory classifications about individuals close to them is largely impaired. [4] Once Capgras Syndrome manifests the individual’s brain, it becomes more of a general memory management problem when meeting new people. In normal functioning human beings, meeting a new person triggers our brain to ‘open a new file’ in which all of the memories and interactions with this new person will go. In those with Capgras Syndrome, the brain functions in a way that does not allow for the retrieval of the ‘file’ filled with memories of a new person, therefore creating a new file each time that person is interacted with. This causes the person with Capgras Syndrome to claim that he or she is meeting a new person, one who looks very similar or identical to the new person they met before. Ramachandran suggests that this deficit occurs due to the missing aspect of emotional activation during memory creation in the amygdala. The absence of this factor signals to the brain to create a new memory file, not add to the previous memory file already created about this specific person. In addition to this explanation, there may be a more basic flaw in the brain of those with Capgras Syndrome that deals with the ability to extract and integrate successive episodic memories with a common denominator, which in this case, is the familiar individual. Individuals with Capgras Syndrome have not lost their previous memories of the identified person; the ‘other’ person is remembered, yet the syndrome stricken person behaves as if he or she has met two different but very similar people, and the brain creates separate memory files for them. [4] An extremely interesting aspect of Capgras Syndrome that supports Ramachandran’s theory is the fact that when a person with the syndrome speaks to the ‘imposter’ on the phone, that person is instantly recognized and is not considered an imposter. However, if that person walks into the room after the call and is seen by the individual with Capgras, the recognized individual is once again considered an imposter. Ramachandran asserts this is due to the brain’s visual system and auditory system possessing separate pathways to the amygdala. Because the auditory connection to the amygdala is not damaged, the brain is able to produce a normal emotional response needed for recognition of a familiar person over the phone. [1] media type="youtube" key="dqBGzkz1oDU" width="560" height="315" align="center" The video above documents VS Ramachandran and his patient, David, who suffers from Capgras Syndrome. = Treatment  = As the specific cause and manifestation of Capgras Syndrome is not known for certain, the treatment of such individuals is based mainly on each individual and what works best for them. Individual therapy allows for the establishment of proper cognitive-behavioral techniques, including reality testing and reframing, that provide discussion about evidence that may help the patient overcome the issue of believing the delusions. If a pharmacological approach is taken, a standard trial of a **selective serotonin reuptake inhibitor (SSRI)** or an **antipsychotic** may be prescribed. [2] = Glossary  = > **Delusion** - a belief that is held with strong conviction despite superior evidence to the contrary.
 * **Amygdala** - an almond-shaped mass in the temporal lobe that is considered the emotional center of the brain, dealing primarily with emotional valence and the modulcation of emotional memory consolidation.
 * **Antipsychotic** - a class of medicine used to treat psychosis and other mental and emotional conditions.
 * **Capgras Syndrome** - a disorder characterized by an individual’s primary delusion that close acquaintances have been replaced by an imposter.
 * **Episodic Memory** - the memory of autobiographical events (times, places, associated emotions, and other contextual who, what, when, where, and why knowledge) that can be explicitly stated.
 * **Galvanic Skin Response** - also known as skin conductance, this is a method of measuring the electrical conductance of the skin by examining the state of sweat glands on the skin, typically with the index and/or middle finger.
 * **Lateral Geniculate Nucleus (LGN)** - an area of the thalamus that functions as a relay center for the visual pathway by recieving visual input from the retina and projecting visual information through the optic radiation to the primary visual cortex.
 * **Optic Chiasm** - the X-shaped structure formed at the point below the brain where the left and right optic nerve cross over each other.
 * **Optic Nerve** - also known as Cranial Nerve 2, the optic nerve (one for each eye) is formed by axons from the ganglion cells of the retina and allows for the retina to pass its information to the optic chiasm.
 * **Optic Radiation** - axons from the neurons of the lateral geniculate nucleus of the thalamus that project to the primary visual cortex.
 * **Optic Tract** - a continuation of the optic nerves past the optic chiasm that relays information to the lateral geniculate nucleus of the thalamus.
 * **Primary Visual Cortex** - also called area V1 or Brodmann's Area 17, it is the region of the cerebral cortex located in the occipital lobe that receives visual information from the lateral geniculate nucleus of the thalamus.
 * **Prosopagnosia** - also known as face blindness, it is the cognitive disorder in which an individual is unable to recognize familiar faces.
 * **Selective Serotonin Reuptake** **Inhibitor** - a commonly prescribed drug for treating depression, working by blocking the reabsorption (reuptake) of the neurotransmitter serotonin in the brain.

= Quiz Questions  = **Multiple Choice:** 1. Visual information from the ganglionic cells' axons of retina exit the retina to form the: 2. The lateral geniculate nucleus relays its information directly to the: 3. The ventral pathway is involved in processing: **True/False:** 4. The primary visual cortex is also known as Brodmann's Area 18. 5. When meeting new people, Capgras Syndrome become more of a general management problem, especially with episodic memories. 6. Those with Capgras Syndrome had a higher galvanic skin response when seeing familiar faces than when viewing faces of strangers. 7. The brain disruption of Capgras Syndrome deals with the dorsal pathway in the brain. **Short Answer/Essay:** 1. Describe the visual processing pathway from the retina to the higher order visual processing cortices. 2. What is the difference between prosopagnosia and Capgras Syndrome? Include information about galvanic skin response. 3. What is Ramachandran's claim about altered brain function in those with Capgras Syndrome and what supporting evidence does he present? **Answers:** 1. C 2. B 3. F 4. F 5. T 6. F 7. F = Suggested Reading  =
 * A. optic chiasm
 * B. optic radiation
 * C. optic nerve
 * D. lateral geniculate nucleus
 * A. superior colliculus
 * B. primary visual cortex
 * C. pretectum
 * D. hypothalamus
 * E. none of the above
 * A. form
 * B. movement
 * C. color
 * D. spatial analysis
 * E. a & b
 * F. a & c
 * G. b & d
 * This article by goes into further detail about the reduced autonomic responses to familiar faces in those with Capgras Syndrome. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1688551/pdf/9263474.pdf
 * While the fusiform face area was not directly mentioned in any of the Capgras literature, it has been considered to be a cortical brain region that specializes in the recognition and perception of faces. This article delves into the possibility of this area to function in such a way, and the possible questions, concerns, and arguments against this theory. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1857737/
 * This article elaborates on the idea that patients with Capgras Syndrome may harbor a side of dangerousness that should be addressed and monitored for to protect others, especially those who are seen as the 'imposters'. http://jaapl.org/content/jaapl/17/1/5.full.pdf
 * Capgras Syndrome has been suggested to be related to neurodegenerative diseases, and this retrospective study served to examine that relationship to determine how strong it is. http://jamanetwork.com/journals/jamaneurology/fullarticle/794900

= References  =

[1] Abumrad, J., & Krulwich, R. (2010, March 30). Seeing Imposters: When Loved Ones Suddenly Aren’t. National Public Radio. Retrieved from []

[2] Capgras (Delusion) Syndrome. (n.d.). PsychNet-UK. Retrieved from []

[3] Dragoi, V. (n.d.) Chapter 15: Visual Processing: Cortical Pathways. Neuroscience Online, Department of Neurobiology and Anatomy, The UT Medical School at Houston. Retrieved from [] [4] Hirstein, W. & Ramachandran, V.S. (1997, March 22). Capgras Syndrome: A Novel Probe for Understanding the Neural Representation of the Identity and Familiarity of Persons. Proceedings: Biological Sciences, Volume 264, Issue 1380, 437-444. Retrieved from []

[5] Kanwisher, N., & Yovel, G. (2006). The fusiform face area: a cortical region specialized for the perception of faces. Philosophical Transactions of the Royal Society B: Biological Sciences, 361(1476), 2109-2128. Retrieved from []

[6] Lambert, K. (2007, December 6). How Capgras Syndrome Works. HowStuffWorks.com. Retrived from []

[7] The Limbic System. (n.d.). Boundless.com. Retrieved from [] = = = Image and Video Sources  = Image 1: https://blackboard.gordon.edu/webapps/blackboard/content/listContent.jsp?course_id=_15820_1&content_id=_254154_1

Image 2: http://kellogg.umich.edu/theeyeshaveit/anatomy/visual-pathway.jpg

Image 3: https://blackboard.gordon.edu/bbcswebdav/pid-254156-dt-content-rid-1190853_1/courses/KIN4502016FA/KIN4502016FA_ImportedContent_20160818062206/KIN4502012FA_ImportedContent_20120828012916%287%29/KIN4502011FA_ImportedContent_20110826042521/KIN4502010FA_ImportedContent_20100819090538/Content%20Areas/Visual%20System/Visual%20System%20Images%20%28from%20class%20textbooks%29/Neuroanatomy%20through%20Clinical%20Cases/Blum11-11-1.jpg

Image 4: https://blackboard.gordon.edu/bbcswebdav/pid-254156-dt-content-rid-1190854_1/courses/KIN4502016FA/KIN4502016FA_ImportedContent_20160818062206/KIN4502012FA_ImportedContent_20120828012916%287%29/KIN4502011FA_ImportedContent_20110826042521/KIN4502010FA_ImportedContent_20100819090538/Content%20Areas/Visual%20System/Visual%20System%20Images%20%28from%20class%20textbooks%29/Neuroanatomy%20through%20Clinical%20Cases/Blum11-11-2.jpg

Image 5: https://ivanlerma.files.wordpress.com/2013/02/amc3adgdala.png

Video 1: []