Ever Wonder if You're Mom was Double? Part 2

Search for an Explanation

        What makes CS such an interesting subject for neuroscientists is the fact that CS patients believe that loved ones such as family members, long-time friends, and close co-workers have been replaced. But this delusional belief of doubles or impostors does not extend to those who they have no emotional connection with. In most CS cases the patients do not regard acquaintances, nurses, grocery store clerks or anyone else that they do not have a strong emotional tie with as a double or impostor (Ramachandran, 1998). Furthermore, in most CS case reports, patients believe that they are addressing their actual loved ones or family members when speaking to them on the phone (Yalin et al, 2008; Ramachandran, 1998). This point was further illustrated by a study done by Pick (1903), in which he studied a young man who believed that his mother had been replaced by an impostor when he looked at her. However, “her voice still elicited a strong feeling of familiarity.” This suggests that the cause of CS may be contained to an optical malfunction or lesion in the visual pathway; since patients do not experience any CS symptoms when listening to their loved ones.

        Ellis, Lewis, Moselhy & Young, (2000) and Schweinberger & Burton, (2003) wanted to see if there was any validity to the optical theory. They discovered that individuals with Capgras syndrome do not have any optical impairment. If patients did this finding would explain their inability to recognize family members, friends and co-workers faces. But the research showed that they do recognize faces; however, they lack the ability to match a face that they recognized with the any emotions. “Opposite to the pattern observed in prosopoagnosia, Capgras subjects recognize the structural features of familiar faces but may have impairments in the affective route to face recognition as documented by the SCR hyporesponsiveness”( Brighetti, Bonifacci, Borlimi & Ottaviani, 2007). Ellis et al. and Schweinberger et al. demonstrated that CS patients have no optical malfunctions and that they can recognize loved ones faces normally. CS patients possess the ability of emotional expression and of facial recognition; however, there seems to be a severing in the link between the primary emotional and recognition centers. In his book, “Phantoms in the Brain”, Ramachandran proposes his own theory for CS. He thought there was a neurological disconnection between temporal lobe areas involved with facial recognition, such as the Hippocampus, and the emotional center in the brain, the amygdala. Along with Ramachandran many other neuroscientists are arriving at similar conclusions, that CS has an organic basis in the brain.

        As stated before, investigations into the neurological causation of Capgras Syndrome are a recent phenomenon, taking place within the last forty years. One of the first studies that drew attention to the organic etiology of CS was done by Gluckman in 1968. The woman he studied believed that her husband was an impostor; she was subsequently diagnosed with paranoid Schizophrenia. Gluckman put her through a computerized axial tomography scan and found “severe cerebral atrophy” (Doran, 1990). This study and the growing suspicion of other researchers, that CS has an organic causation, opened the door to further neurological research. Three years later Weston & Whitlock (1971) presented their case of a twenty year old man who underwent severe head trauma and then exhibited symptoms of CS. Weston & Whitlock (1971) described the damage as “frontal lobe syndrome with evidence of bilateral temporoparietal damage, a severe memory defect, and mixed dysphasia along with generalized impairment” (Doran, 1990). They suggested that this damage to the temporal and parietal lobes lead to the patient’s inability to “integrate memory, perception, and affect.” And that these dysfunctions were primary factors in the formation of CS (Doran, 1990).

         Other studies have demonstrated a strong link between CS and physical disorders. In certain cases CS symptoms remitted at the same time that the physical illness remitted (Christodoulou, 1977b).  Further evidence of CS’s organic basis was found by MacCallum (1973). In three out of five cases MacCullum demonstrated the onset of CS as a result of “anoxia, basilar migraine, [and] alcoholic encephalopathy” (Doran, 1990). He also observed that when the physical symptoms were remedied so were the delusional perceptions and beliefs of the patients.  Based on these results, “MacCallum hypothesized that these organic conditions caused a change in the patients' affects and perceptions, which then led to the appearance of the Capgras syndrome. With a remission of the organic condition, affect and perception returned to normal” (Doran, 1990). These findings strongly support the suggestion that CS is caused by organic factors. Other studies have linked CS with “right-sided cerebral dysfunction” (Hayman & Abrams, 1977), which turns the focus of this discussion to current emerging theories of CS.

        Doran (1990) reviewed the current neurological theory on Capgras Syndrome. He pointed out that initial importance is given to the distinction between the reduplication of a person or place. In neurological literature the reduplication of a place is termed “reduplicative paramnesia”; however, within psychiatric literature the reduplication of a person is termed Capgras Syndrome. The common perception is that these reduplicative disorders are one in the same; the only difference between the two is the object of the duplication, a person or a place. Doran went on to say that, “The cerebral localization and mechanism of action could essentially be the same.” Alexander, Stuss & Benson (1979) and Staton, Brumback & Wilson (1982) both had cases in which duplication of a “person” and of a “place” were demonstrated in their patient. Lesions in the right hemisphere have been found to be the primary cause of duplicative symptoms.

        This finding leads to the central thrust of this theory, the right hemisphere. Research of the,

“Right hemisphere lesions may lead to disturbed visuospatial analysis (Paterson & Zangwill, 1944), impaired facial recognition and memory (Hacaen & Angelergues, 1962; Milner, 1968), abnormal sensations of general familiarity andjamais vu (Mullan & Penfield, 1959), and abnormally flat or euphoric disorders (Gainotti, 1972)”(Doran, 1990). Furthermore, the right hemisphere has connections between “facial recognition, visual memory, and feeling and familiarity” (Quinn, 1980; Schraberg & Weitzel, 1979; Synodinou, Christodoulou, & Tzavaros, 1977).

         According to these findings, Alexander (1979) and numerous other researchers concluded that the “right hemisphere is the seat of dysfunction producing the delusional symptom of Capgras” (emphasis in original).  The dysfunctions that occur if the right hemisphere is damaged fit the descriptions of Capgras Syndrome perfectly. Staton (1982) hypothesized that a disconnection occurs between old memory stores and new memory registration. He also suggests this area of damage happens specifically in the “right posterior hippocampus and right temporo-parieto-occipital junction.” Another recent study proposes that the dysfunction is subcortical (Anderson, 1980). Based on this evidence, it is hypothesized that Capgras Syndrome is the result of a disconnect between the “hippocampus and the hypothalamic/amygdala circuit” (Doran, 1990). In other words, a CS patient still recognizes a loved one in every sensory way, but does not recognize them emotionally; due to a disconnection between emotion and memory. This conclusion, again, supports the previous assertion that Capgras Syndrome is the result of an organic disconnection between emotion and memory made by Ramachandran, Ellis (2000), and Schweinberger (2003).