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studied a young man who believed that his mother had been replaced by an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).
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