Correspondence Address:
Daniel Saldanha
Flat No 1102, N Block, Grevillea, Magarpattacity, Pune - 411 013
India

Full Text

Sir,

The imposter syndrome described by Capgras and Lachuk [1] in 1923 aroused nosological controversy due to its separate diagnostic status by the French authors. Considered to be rare, Capgras' patient believes that a person usually a close relative has been replaced by an exact double or imposter and maintains this false belief despite evidence to the contrary, i.e., a delusion. The delusion can extend from patients close relations to animals or objects. The appearance of the delusion is acute, transient, or chronic medical condition (diabetes, rt cerebral infarcts, and dementia). [2],[3] Toxic states due to drugs (ketamine, lithium) [4],[5] and psychiatric disorders (paranoid schizophrenia [6] ) have been reported. Therefore, the presence of this delusion should be a cause for concern to rule out organicity. We report a case of Capgras delusional symptom in a young girl who was brought to us with an acute onset of schizophrenia.

An 18-year-old girl was admitted with undue fear, suspiciousness, muttering to self, poor self-care, and sleeplessness of one and a half months duration. Her medical, obstetric history was unremarkable. Her parents had both been HIV positive cases, mother succumbing to HIV 15 months ago. Father is an alcoholic, lived on pension. Mental state revealed delusions of reference, believed her aunt has been replaced by her exact double. She believed that cameras had been placed to monitor her movements. She could not go out of the house as she feared for her life and constant monitoring of her activities. She thus became a recluse. She was convinced that people around her talked ill of her and the belief that her aunt had been replaced by someone who looked similar, this despite being told that is not the case. She was admitted and investigated to rule out organic causes for the symptoms. These included blood test for hemoglobin, RBC, WBC, platelet, blood sugar fasting and postprandial, urine, HIV status by ELISA (since both parents were HIV positive) liver function tests, renal function tests, and MRI brain. All were normal. The diagnosis of paranoid schizophrenia was made as per ICD 10 criteria. The patient was given parenteral haloperidol of 5 mg twice a day for 2 days along with parenteral phenergan 50 mg. As her investigations ruled out organic cause for her symptoms, she was given six electroconvulsive therapy's (ECT's) along with antipsychotic drug therapy with the consent of her next of kin who was explained the nature of treatment. Once she was stabilized and her financial state could afford to buy the atypical antipsychotic drugs, she was shifted to tab olanzapine 10 mg twice daily initially for 4 weeks and on recovery was reduced to 10 mg once daily. She was also given trihexiphenidyl 2 mg twice a day. Her delusional symptoms gradually reduced. At the time of discharge, she had regained her insight. At 6 week follow-up, her delusional symptoms had completely disappeared. She no longer believed that her aunt had been replaced by someone else.

Originally it was described in 1923 by Capgras [1] as an illness in which the individual is delusional convinced that someone familiar in the environment has been replaced by an almost exact double. The Capgras delusion is commonly called a syndrome because it can occur as a part of various other conditions as a result some argue that it should be considered a symptom, rather than syndrome in its own right. Capgras delusion is classified as delusional misidentification syndrome that involves the misidentification of people, places, or objects. In 1997, Ellis and his colleagues [7] published a study of five patients with Capgras delusion (all schizophrenics) confirmed "that although they could consciously recognize the faces, they did not show normal autonomic emotional arousal response same as it is shown in the presence of strangers." [7] Young theorized that patients with disease experienced a loss of familiarity not a lack of it. [8] Interestingly, Hirstein and Ramachandran [9] "hypothesized that "the origin of Capgras syndrome is a disconnection between the temporal cortex (where faces are usually recognized) and the limbic system (involved in emotions). Because a patient could not put together the memories and feelings, they believed objects /people were new on every viewing even though they should have evoked the feelings. They also believed that there was a close relationship between Capgras syndrome and a more difficulty in linking successive episodic memories." [9] It is believed that emotions are critical in reviving or for creating memories. However, with significant proportion of cerebral pathologies in a high proportion of cases, it is evident that there is an organic basis for its occurrence. [10] It appears that the most difficult task that the brain performs is recognition of the face. The center for recognition may be located in the medial occipitotemporal cortex or brain structures nearby, as damage to medial occipitotemporal structures on the right or bilaterally leads to prosopagnosia, the failure to recognize facial identity. It may be correct to assume that deficits in face perception contribute to Capgras syndrome. [11] Although it is difficult to explain this delusional symptom in the present case, the theoretical views explained by Ramachandran that emotions are critical in reviving or creating memories that should be remembered. The above case illustrates that an early and active intervention resulted in remission of her psychotic state and disappearance of Capgras delusion.

To conclude, an effort should be made to rule out organic causes whenever one is confronted with a Capgras delusion which has been shown to occur in a number of organic conditions ever since it was described by Joseph Capgras in 1923 and psychiatric disorders like schizophrenia are no exception.

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