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Mania Presenting As Capgras Syndrome
Raj Kumar Lenin Singh* MD Phd, Ningombam Heramani Singh * MD, Mohammad
Munnawar Sameer Hussain*MBBS, Magong Pangkam*MBBS.
*Department of Psychiatry, Regional Institute of Medical Sciences (RIMS),
Imphal, Manipur, PIN-795004, India.
Corresponding Author:
Dr Mohammad Munnawar Sameer Hussain MBBS (MD)
Junior Resident
Department Of Psychiatry
Regional Institute of Medical Sciences
Imphal West
Manipur-795004
Telephone: 00913852411484
Fax : 0385-2414625
Email:Munnawar1986@gmail.com
Stastical summary of manuscript:
Total Number Of Words: 998
Total Number of Words in Abstract:129
Number of References:16
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Abstract:Objective: This case report highlights a case of mania with an initial presentation as capgrass
syndrome. Capgras syndrome is a part of delusional disorder’s called delusional
misidentification syndrome(DMS). The causes of DMS are some neurological disordes like
Alzheimer’s disease, and psychiatric conditions like schizophrenia and bipolar affective
disorders. Method: We report a case previously healthy 20 yr old female whose initial
presentation of mania was in the form of capgras syndrome. Result: The prominent delusion
in the form of capgras syndrome improved within 20 days. Delusion and mania responded to
an antipsychotic and a mood stabiliser. Conclusion: Mania rarely presents as capgras
syndrome as an intial manifestation hence mania should also be considered as a cause of
capgras syndrome as the response to treatment is favourable in mania.
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Introduction
Capgras syndrome was named after Joseph Capgras, who first reported a case, co-authored
with Reboul-Lachaux, in 1923 [1]. This disorder is characterised under the constellation of
Delusional Misidentity Syndrome(DMS) or Redeuplicative paramnesias. The main
neuropathology in capgras syndrome is disconnection of pathways between face recognition
areas in the inferior temporal lobe and the amygdala, which regulates the emotional response
to faces. Reports of an association between CS and medical and neurological conditions have
led to the belief that cerebral dysfunction underlies the delusion’s development [2]. The
syndrome has been linked to dopaminergic overactivity, and serotonin abnormality has been
implicated in some but not all studies [3-5]. Similarly, reduced platelet monoamine oxidase
activity has been noted by some [6] but not by others [7] .DMS are characterized by the
delusion that either another person or the self has undergone radical mental and/or bodily
changes [2]. Capgras syndrome can be present in schizophrenia, mood disorders, Alzheimer’s
disease and traumatic brain injury. CS may develop in women with oedipal issues as a
defence against hostility or incestuous desires [8-10]. Later attempts to account for CS
resulted in hypotheses of anxiety-induced regression of cognitive and emotional functioning
[11], pathological splitting of internalized object representations [12], inadequately repressed
conflicting or ambivalent feelings toward the implicated person [13], and the projection of
negative emotions arising from these conflicting feelings [12].
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Case Report:
We report a case of a 20 yr old female from North East Indian state of Manipur. The patient’s
immediate stressor identified for her current illness was death of her mother, six days after
the said event the patient suddenly became fear full of her husband and started talking
irrelevantly that he has been replaced by an imposter; his face has been replaced by that of a
stranger’s face. She denied any relationship with this person and was ready to sign any legal
document which declared that the person is not her husband .She also alleged that she has an
ex-boyfriend whom she intended to marry. She would be angry and aggressive on seeing her
husband’s face. She was indulging in self smiling; self singing and intermittent bouts of
crying spells with rapid mood fluctuations with auditory hallucinations and delusion of
persecution towards her mother in law and brother in law were also prominent with decreased
need for sleep and wandering tendency as an additional symptom. She was brought to
emergency department regional institute of medical sciences, imphal after 20 days of onset of
illness and later admitted in the psychiatry ward.
Her Mental status Examination revealed a moderately built and nourished female in an
inappropriate attire, with increased amount of speech with preservation, her affect was
irritable and labile, flight of ideas, loosening of association, tangentiality and preservation of
thought, delusion of doubles and delusion of persecution, auditory hallucination. Insight
grade I. Initially she was started on injectable haloperidol 10mg per day in two divided doses
and Olanzapine 15mg orally per day. Her mood was sustained in an irritable state with
labiality. Later on Quetiapine 400mg and Valproic acid 750mg per day in divided doses were
calibrated. Her investigations revealed Anemia with Hb of 8.8mg% and an ESR of 30mm/1st
hour. CT brain and MRI were not done due to financial constraints of the patient’s family.
During the course of her stay in hospital she showed considerable improvement in her mood
symptoms and started identifying her husband by 20th day of her hospitalisation. She
improved remarkably by 27th day and was continued on the same medication used during
acute phase of treatment and was discharged on request. Later on at review at 6 weeks there
were no features of capgras syndrome and her mania was well controlled with the
medication.
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Discussion:DMS can occur in the presence of idiopathic psychiatric illness, in diffuse brain illness such
as dementia, and in focal neurologic disease. In patients who have focal lesions, there is
evidence that right hemisphere damage is necessary for the production of DMS. Although
DMS is associated with a pattern of neuropsychologic impairments in the domains of
memory, perception, and executive function, these impairments alone do not account for the
selectivity and delusional nature of DMS. Hirstein and Ramachandran in a study of a patient
suffering from Capgras syndrome using skin conductance response, found that the patient's
Capgras delusion was “modality specific: they claimed that his parents were imposters when
he was looking at them but not when speaking to them on the telephone.” The authors stated
that in such patients, the connections from face-processing areas of temporal lobe to the
limbic system may be faulty and that far from being a “medical curiosity,” Capgras syndrome
may help explore the formation of new memories caught in flagrante delicto, a Latin term
that means “in the act of committing the error”[14] . Feinberg and associates in 1999 reported
the case of a 61-year-old man who suffered traumatic brain injury resulting in right frontal
and left temporoparietal contusions and subsequently developed florid Fregoli-type DMS.
This patient's “neuropsychological profile” closely resembled that of patients with Capgras
syndrome previously reported in the literature. The authors concluded that a combination of
executive and memory deficits may account for DMS associated with brain lesions [15].
Manic and patients with delusional misidentification syndrome are prone to be aggressive.
Hence the combination of mania and DMS is therefore a very potent cause of aggression.
Silva and colleagues found the association of mania and DMS in three of their patients with
aggression [16].
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Conclusion:
DMS symptoms in some patients remit with the resolution of the underlying or associated
illness, but in other cases, they remain unchanged even after the associated psychiatric illness
remits. A thorough evaluation by neuroimaging, neuropsychological and other
psychodynamic factors have to be taken into consideration to identify a treatable cause of
capgrass syndrome. The present knowledge regarding the DMS is still in a preliminary level
of understanding and it calls for a more focussed research mainly using the neuroimaging
techniques as the tolls of investigation.
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