At its core, Capgras syndrome is the delusional belief that someone close to you has been replaced by an identical imposter. Capgras has historically been explained with Freudian psychodynamic theories concerning latent hostility and a sense of personal or professional inadequacy. There is now widespread consensus in the scientific community that Capgras syndrome can arise from brain lesions. Various hypotheses have been proposed to explain its mechanism. The mirror-image-of-prosopagnosia hypothesis posits a disruption of the dorsal visual pathway. Another hypothesis emphasizes the role of a single lesion affecting the functional connectivity of the retrosplenial cortex. Our analysis of 10 case studies reveals inconsistencies with these hypotheses, particularly in accounting for the diverse lesion locations observed in Capgras patients. Our findings suggest that Capgras syndrome likely stems from a multifactorial aetiology involving neurological and neuropsychiatric factors. Lesions may impact multiple areas associated with facial processing and belief evaluation, challenging the notion of a single lesion explanation.