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Neuropsychology Copyright 1991 by the Educational Publishing Foundation

1991, Vol. 5, No. 3, 139-150 0894-4105/91/S3.00

A Neuropsychological Profile
of Capgras Syndrome

SCOTT W. SAUTTER
Division of Behavioral Medicine
Western State Hospital
Staunton, Virginia
Department of Behavioral Medicine and Psychiatry
University of Virginia School of Medicine

LEONARD BRISCOE
KAY FARKAS
Department of Behavioral Medicine and Psychiatry
University of Virginia School of Medicine

Abstract: The neuropsychological profile of a' woman with the delusion of


misidentification characteristic of Capgras syndrome is presented. Capgras syn-
drome can develop from both psychodynamic and neuropathological etiologies.
The available empirical data in the literature support a hypothesis ofbifrontal
and temporal cerebral dysfunction and a need for careful differential diagnosis
to rule out prosopagnosia and confusional states. The results of this specific case
suggest greater impairment in anterior right-hemisphere-mediated functions.
These findings are discussed in the context of clinical neuropsychological assess-
ment and treatment issues, and additional questions regarding use of the term
syndrome are raised.

Keywords: Capgras syndrome, neuropathology, psychodynamic therapy, neu-


ropsychology.

The delusion of misidentification has fascinated clinicians since its original descrip-
tion in the psychiatric literature almost seven decades ago (Capgras & Reboul-
Lachaux, 1923). Psychodynamic interpretations of this phenomenon were richly
described in colorful terms; however, recent advances in the clinical behavioral
neurosciences have helped to elucidate a possible neuropathological etiology. In
this article, we present a neuropsychological profile of Capgras syndrome. Both
psychodynamic and neuropathological interpretations are described in the litera-
ture review, and the results of this particular case support evidence of anterior
right-hemisphere-mediated dysfunction. Further questions are raised about com-
peting explanations and use of the term syndrome.
Most of the literature we reviewed provided case presentations with psycho-
dynamic interpretations involving "ego splitting and projection in defense of

Address correspondence to Scott W. Sautter, Behavioral and Neuropsychiatric Center,


1745 Camelot Drive, Suite 200, Virginia Beach, Virginia 23454.

139
140 Scott W. Sauter el al.

overwhelming erotic or aggressive impulses directed at a parental figure or intensive


ambivalent feelings directed toward a significant other, such as a spouse or sibling"
(Sullivan, Cavenor, Maltbie, & Silverstein, 1978, p. 275). The delusion arises in an
altered effective state toward others with intolerable ambivalent feelings that are
neutralized through imaginal existence of doubles (O'Reilly & Malhatra, 1987).
Berson (1983) reviewed 133 cases in the English-language literature and reported
that the syndrome is most commonly seen in paranoid schizophrenics; although
18 of these cases had neuropathological involvement, he suggested that brain
pathology could not account for the selectivity of the delusion. Berson (1983)
offered criteria for inclusion that required psychosis, paranoia, pathological splitting
of a significant other, and changes in the crucial interpersonal relationship. There
is a great deal of heterogeneity in the literature, implying a need to examine both
psychopathological and neuropathological evidence in a careful differential diag-
nosis (Bienenfield & Brott, 1989).
Others have described Capgras syndrome as a disorder that occurs in women
only (Vogel, 1974), that involves family systems dynamics (Moskowitz, 1975), or
that is associated with reduced platelet monoamine oxidase activity (Sullivan et
al., 1978), drug toxicity (Daniel, Swallows, & Wolff, 1987), hypothyroidism (Fish-
bain, 1989; Madakasira & Hall, 1981), or head trauma (Weston & Whitlock, 1971).
In a group comparison study, Joseph, O'Leary, and Wheeler (1990) examined 12
Capgras syndrome patients with matched controls and assessed computed tomo-
graphies (CTs) in a single blind paradigm; the results showed that Capgras syndrome
patients had significantly greater bilateral frontal and temporal atrophy. A brief
review of the literature that has been published since Berson's article is presented
in Table 1.
For the purpose of this article, Capgras syndrome is defined as occurring in a
psychotic state with paranoid features, manifested by a delusion of misidentification
of a significant other, and having greater anterior than posterior neuropsychological
dysfunction in the absence of gross visuoperceptual distortions, such as prosopag-
nosia or acute confusional states. The present case met the above criteria (as well
as Berson's 1983) but raised additional competing hypotheses that were not easily
ruled out.

Case History
Ms. C. is a 45-year-old, right-handed, divorced White woman with 11 years of
education and an episodic work history of unskilled jobs. She had a number of
psychiatric hospitalizations dating back to 1979 for psychotic symptomatology,
including paranoid delusions, depression, and noncompliance with medication
regimens. She had been diagnosed with schizophrenia and treated with Xanax and
Mellaril. When admitted to our facility on an involuntary, mentally ill status, she
exhibited marked paranoid delusions and reported that she felt someone had taken
the place of her real father and that this person was out to kill her. Three weeks
prior to this hospitalization, Ms. C. had been discharged from a psychiatric facility
in New Orleans with the diagnosis of undifferentiated schizophrenia. After dis-
charge, she traveled to Florida to meet her father for a return trip to Virginia,
during which they decided to take a vacation at a state park. Upon returning from
an evening walk in the park, the patient reportedly found a man in her room
claiming to be her father. She stated that this man was not her real father, but an
Capgras Syndrome 141

imposter, and became very angry and agitated. The park rangers were called to
subdue her and take her to a local emergency room, where she complained of
tactile hallucinations and thought broadcasting. She also reported that she felt she
may have done something to her real father and that this imposter wanted to kill
her.
Although Ms. C. has no history of neuropathology in her medical records, her
long history of alcohol abuse and numerous motor vehicle accidents suggested
otherwise. In one accident, she lost consciousness and was hospitalized for 5 days.
The duration of unconsciousness and probable posttraumatic amnesia was not
reported. Although she had been charged with driving while under the influence
earlier in that year, Ms. C. denied using alcohol or other drugs since that charge.
At admission, Ms. C.'s speech was quiet with decreased intonation and rate.
Her thought processes showed looseness of associations and tangentiality. She
denied any suicidal or homicidal ideation. Her judgment was poor, and insight was
absent. She was well dressed, groomed, and appeared slightly younger than her
chronological age of 45 years. At admission, she scored 20/30 on the Mini-Mental
State Examination (MMSE; Folstein, Folstein, & McHugh, 1975), the next day,
she scored 27/30. She remained reserved and suspicious and was quite guarded
when talking about her "father." She complained of decreased sleep and increased
feelings of guilt but not of anhedonia, change in energy, or decreased appetite. Ms.
C. was given the diagnosis of paranoid schizophrenia, chronic, with acute exacer-
bation, and was placed on a regimen of 100 mg of Thorazine twice a day for
attenuation of psychotic symptoms. After a brief hospital stay of 3 weeks and a
course of neuroleptics, her psychotic symptoms dissipated, and she was discharged
to her local community.

Neuropsychological Profile
Ms. C. was referred for neuropsychological evaluation for the purpose of providing
a differential diagnosis and documenting suspected brain-behavior dysfunction
resulting from multiple motor vehicle accidents and alcohol abuse. During the
evaluation, Ms. C. was initially suspicious about being tested. However, after the
type of procedures that would be given were explained to her, she relaxed. As a
result, she was pleasant and cooperative but remained guarded. She denied auditory
hallucinations but frequently smiled and laughed out loud at inappropriate times.
Ms. C. did not report that her father was an imposter during the testing, although
she appeared perplexed when confronted about this. An electroencephalograph
was within normal limits, and no further neuroradiological studies were pursued.
Neuropsychological impressions were consistent with greater anterior right-
hemisphere-mediated dysfunction of mild to moderate cognitive impairment,
particularly for tasks of memory and abstract reasoning. Right- and left-hemisphere-
mediated functions with respect to normative data are presented as z scores in
Figure 1. A breakdown of various neuropsychological functions (also z scores) are
presented in Figure 2. Relatively greater impairment can be seen in right-hemi-
sphere-mediated functions (Figure 1), as well as more anterior functions (Figure
2). Standard scores were computed by subtracting the mean of each test from the
raw score and dividing the result by the test's standard deviation as found in the
normative literature (Benton & Hamsher, 1976; Bornstein, 1984; Delis, Kramer,
Kaplan, & Ober, 1987; Fromm-Auch & Yeudall, 1983; Golden, 1978; Halstead &
text continues on p. 148
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Figure 1. Ms. C's left-hemisphere- versus right-hemisphere-mediated cognitive functioning,


presented as z scores (WAIS-R = Wechsler Adult Intelligence Scale-Revised; VIQ = verbal
IQ; PIQ = performance IQ; WMS = Wechsler Memory Scale; Hooper = Hooper Visual
Organization Test).
146 Scott W. Sauter et al.

S3HOOS-Z

Figure 2. Ms. C's individual test results, presented as z scores, grouped by neuropsycholog-
ical function (DH = dominant hand; NDH = nondominant hand; REC = recognition;
Hooper = Hooper Visual Organization Test; WAIS-R = Wechsler Adult Intelligence Scale-
Revised; PIQ = performance IQ; VIQ = verbal IQ; CVLT = California Verbal Learning
Test; WMS = Wechsler Memory Scale; W = word; C = color, C-W = color and word;
WCST = Wisconsin Card Sort Test; RESP = response).
Capgras Syndrome 147

a s s

S3HODS-1

Figure 3. Ms. C's Minnesota Multiphasic Inventory (MMPI) profile (L = Lie scale; F =
Frequency scale; K = Correction scale; 1 = Hypochondriasis scale; 2 = Depression scale;
3 = Hysteria scale; 4 = Psychopathic Deviate scale; 5 = Masculinity-Femininity scale;
6 = Paranoia scale; 7 = Psychasthenia scale; 8 = Schizophrenia scale; 9 = Hypomania scale;
0 = Social Introversion scale).
148 Scott W. Sauter et al.

Wepman, 1978; Heaton, 1981; Hooper, 1985; Loring, Martin, Meador, & Lee,
1990; Wechsler, 1945, 1981; Yeudall, 1987).
Ms. C's language skills were seen as a relative strength, as were her attempts to
increase interpersonal contact. Interestingly, the personality assessment depicted a
profile uncharacteristic of paranoid schizophrenia; Ms. C.'s profile may best be
described as a resolving episodic psychotic depression (see Minnesota Multiphasic
Inventory profile in Figure 3). Ms. C.'s apparent need for nurturance and attempts
to increase interpersonal contact were viewed as a positive prognostic sign for
further gains in adaptive competency, as long as she complies with outpatient
follow-up (e.g., to the extent that she takes medication as prescribed, abstains from
alcohol, and receives supportive therapy). As her psychiatric symptomatology
clears, a return to work will become important for continued recovery.

Discussion
The results of this case presentation of Capgras syndrome support the literature in
describing the neuropathological aspects of this syndrome, as well as Berson's
(1983) criteria for Capgras syndrome. The use of the term syndrome may be
misleading because of the heterogeneity of possible etiologies. Symptoms of delu-
sional misidentification may be a more accurate description because it can occur
in varied presentations. Some clinicians have suggested that the use of multiple
and colorful descriptions of delusions of misidentification may not be as helpful as
a thorough and careful differential diagnosis based on neuropsychological and
personality testing, as well as neuroradiological evidence. Ms. C. was psychotic
with paranoid features, had a delusion of misidentification of a significant other,
and had neuropsychological impairment in the absence of prosopagnosia or an
acute confusional state.
Treatment typically follows a therapeutic regimen of antipsychotic medication
and supportive therapy in which areas of cognitive-behavioral strength are used to
overcome weaker areas of functioning. Ms. C.'s case was useful for documenting
the many competing explanations that clinicians are forced to rule out in a
hypothesis-testing model when making a differential diagnosis; her history included
alcohol abuse and withdrawal, along with neuropathological involvement, such as
head trauma, paranoid delusions, and psychodynamic issues. With regard to
assessment, differential diagnosis, and subsequent treatment, the context of the
referral and its specific question should dictate whether neuroradiological, neuro-
psychological, and psychodynamic perspectives ought to be considered. It may be
more appropriate to use the term symptoms of, rather than syndrome, when
describing delusions of misidentification because of the heterogeneity of etiologies
and varied clinical presentations.

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