Capgras syndrome (CS) is characterized by the delusional belief that a person, usually very close to the patient, has been replaced by a double who is physically very similar to the original. CS is relatively rare, occurring predominantly in course of schizophrenia, particularly of the paranoid subtype, and less frequently in association with schizoaffective and affective disorder. Recent years have witnessed a sharp increase in the number of published CS cases with an organic etiology; however, CS was considered to have its origins in psychodynamic conflict. We present a patient with the CS and brain SPECT findings whom without psychiatric disorder. As an evaluation of brain SPECT there have been found a significantly decreased blood flow in bilateral parietal regions and slightly decreased blood flow in bilateral posterior frontal regions. Cerebral dysfunction is proposed to be a central role in CS development. Unilateral right hemisphere lesions occur more frequently than the left; however, the majority of CS cases show bilateral involvement. Pathology involves many parts of the brain, most notably frontal and parietal cortex. Our findings support that frontoparietal dysfunction could be important in the pathogenesis of CS. We reviewed the neurobiology of CS and discussed our findings in this article. CS studies will give a better understanding of the neurobiological basis of psychotic experiences and may contribute to develop a paradigm on researches about other psychotic disorders.