|
 
 |
| CASE REPORT |
|
| Year : 2018 | Volume
: 2
| Issue : 2 | Page : 150-151 |
|
Capgras syndrome, diarrhoea, and hyponatremia
Devesh Sharma1, Anchal Sharma2, Ramesh Kumar3, Sudhir Sharma4
1 Department of Psychiatry, Dr. YSPGMC, Nahan, Himachal Pradesh, India
2 Department of Radiodiagnosis, Dr. YSPGMC, Nahan, Himachal Pradesh, India
3 Department of Psychiatry, IGMC, Shimla, Himachal Pradesh, India
4 Department of Neurology, IGMC, Shimla, Himachal Pradesh, India
| Date of Web Publication | 30-Nov-2018 |
Correspondence Address:
Devesh Sharma
Department of Psychiatry, Dr. YSPGMC, Nahan, Himachal Pradesh
India
 Source of Support: None, Conflict of Interest: None  | 9 |
DOI: 10.4103/aip.aip_38_18
We present a case of a 56-year-old male who developed Capgras syndrome following hyponatremia consequent to dehydration. He was a previously healthy male who eventually developed secondary systematized delusions due to misidentification syndrome. This case highlights the need for evaluating the role of toxic/medical etiology in the causation of this syndrome that is more often encountered in schizophrenia.
Keywords: Capgras, delusional misidentification, diarrhoea, hyponatremia
How to cite this article:
Sharma D, Sharma A, Kumar R, Sharma S. Capgras syndrome, diarrhoea, and hyponatremia. Ann Indian Psychiatry 2018;2:150-1 |
| Introduction | |  |
Capgras syndrome or delusion is a type of condition where a person holds a belief that a close relative usually a husband/wife, parent has been replaced by a double. It is classified among a group of syndromes involving misidentification of people, places or objects (usually not in conjunction), called delusional misidentification syndrome. The overall prevalence of Capgras delusion is about 15% in patients of schizophrenia and about 0.12% in general population.[1] A similar type of case of a 63-year-old woman was reported in 2010 by Delaffon et al.[2] We are reporting a case of 56-year-old Indian male who developed Capgras delusion secondary to hyponatremia consequent to dehydration.
| Case Report | | |
A 56-year-old male adult presented with acute gastroenteritis for 2 days for which he was managed at a private clinic. Initially, he improved but after a week, developed lethargy and confusion. He was referred to our hospital and was admitted to Intensive Care Unit in an unconscious state. Blood investigations revealed a serum sodium level of 110 mEq/L and other blood parameters were within normal limits. Other investigations including cerebrospinal fluid examination, erythrocyte sedimentation rate, complete hemogram, C-reactive protein, liver function tests, and electroencephalography done at the time of admission were unremarkable. Magnetic resonance imaging brain revealed hyperintensity around the basal ganglia and along cortical gray matter. Dyselectrolytemia was corrected. He improved over the next week (total 2 weeks since the onset of complaints). The patient showed significant improvement and though was fully alert had a reduced verbal output. The patient was discharged and followed up after 2 weeks by the neurologist when patient presented with excess irritability and abusive behaviour. He complained that people accompanying him were unnecessarily trying to pose as his relatives. He said that the woman with him was not his wife but a look-alike and so was the person referring to himself as his brother. The patient was referred to psychiatry outpatient department and Mental State Examination revealed an irritable affect, persecutory delusions, and delusional misidentification. Neuropsychological evaluation was not carried out as patient had no dysfunction on Mini–Mental State Examination and basic cognitive tests done in mental status examination. The patient was diagnosed as Capgras syndrome with posthyponatremic brain injury. He was started on Haloperidol up to 2.5 mg that was increased to 5 mg over 2 weeks. The patient was followed up at a month's interval. Family members reported improvement in agitation. Patient was less distressed, happier, and enjoyed leisure activities however appeared indifferent to family members and did not interact with them. On follow-up visits, he appeared cheerful and greeted the doctor. He expressed gratitude to the woman accompanying him for taking care of him through his illness but still did not consider her to be his wife. He expressed that these people were probably paid to look after him and were not his real relatives. Even the place, he lived in was similar to but not his own, so was his belief about the state of Himachal Pradesh and the country India. He insisted that the India, he belonged to was a different one and so were the state and his city. He knew their names and their other details and agreed to all but their relation to him.
The patients did not have any contributory family or psychiatric history nor had any substance use habits and had been well-adjusted previously.
| Discussion | | |
This case report highlights the role of toxic/medical factors responsible for Capgras syndrome besides phenomenological explanations.[3] It is agreed that etiology of Capgras syndrome is a conjoint involvement of clinical, neuropsychiatric, and neuropsychological data with different theoretical models.[4]
Neurobiological hypothesis
Capgras delusion is not an exclusive dysfunction in facial recognition rather a dysfunction of integration of successive memories about a person along episodic experiences. It arises due to failure in reconciliation of identification of a person and its associated emotions due to disconnection of the frontal lobe and right temporolimbic hippocampal region.[5]
Psychosocial hypothesis
Delusions can be explained on the basis of 2-factor theory which involves the failure of autonomic arousal to familiar faces leading to delusional idea and defective belief evaluation system that sustains the idea against contrary evidence, arising primarily with right hemisphere involvement leading to impairment of several functions such as self-monitoring, reality monitoring, memory, and feelings of familiarity.[6]
In our patient, possible explanation is some subtle involvement of a crucial brain area due to hyponatremia that led to the disorder. Severe or rapidly progressing hyponatremia can result in swelling of the brain (cerebral edema), and the symptoms of hyponatremia are mainly neurological. A possibility arises that cerebral edema was followed by involvement of vital neurological circuits like the dorsal route from the visual cortex to the limbic system through the inferior parietal lobule which is responsible for covert recognition or recognition at an unconscious level. Whereas the ventral route from the visual cortex to the temporal lobes through the inferior longitudinal fasciculus responsible for overt or conscious recognition must have been spared.[7] This case provides a valuable insight into varied mechanisms operating in the causation of Capgras syndrome and possible etiologies ranging from a simple dehydration to a fully systematized schizophrenia thereby further strengthening the multifactorial etiology of Capgras syndrome.
Declaration of patient consent
The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
| References | | |
| 1. | Dohn HH, Crews EL. Capgras syndrome: A literature review and case series. Hillside J Clin Psychiatry 1986;8:56-74.  |
| 2. | Delaffon V, Vahabzadeh A, Naik S, Kinnair D, Bruce J. Capgras syndrome in a patient with severe hyponatremia. Ger J Psychiatry 2010;13:175-7. |
| 3. | Young G. Restating the role of phenomenological experience in the formation of the Capgras syndrome. Phenomenol Cogn Sci 2008;7:177-89. |
| 4. | Madoz-Gúrpide A, Hillers-Rodríguez R. Capgras delusion: A review of aetiological theories. Rev Neurol 2010;50:420-30. |
| 5. | Ramachandran VS. Consciousness and body image: Lessons from phantom limbs, Capgras syndrome and pain asymbolia. Philos Trans R Soc Lond B Biol Sci 1998;353:1851-9. |
| 6. | Coltheart M, Langdon R, McKay R. Schizophrenia and monothematic delusions. Schizophr Bull 2007;33:642-7. |
| 7. | Bauer RM. Autonomic recognition of names and faces in prosopagnosia: A neuropsychological application of the guilty knowledge test. Neuropsychologia 1984;22:457-69. |
|
Search Pubmed for