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Cotard’s syndrome is a rare psychiatric condition, first described in 1880 by Jules Cotard, whose central symptom is delusions of negation and which, in its entire form, the patient deny the existence of parts of their bodies or even their whole bodies, leading to denial of the world around them. Ramirez-Bermudez et al. reported that of 479 Mexican patients with a primary psychiatric disorder, including 150 patients with schizophrenia, three had Cotard’s syndrome (0.62%), all of them with psychotic depression. In 2013, Stompe and Schanda reviewed 346 cases of schizophrenia and found three patients with Cotard’s syndrome (0.87%).

Objectives:Describe the neuroimaging findings of Brain Single-Photon Emission Computed Tomography (SPECT) of a patient with catatoniaBackground:Catatonia was originally described as a psychomotor disease by Karl Ludwig Kahlbaum in 1874. Initially it was considered as the motor manifestation of schizophrenia. However, during the last decades it has been documented a greater prevalence of catatonic symptoms in affective disorders. In addition, we recently observed a renewed interest in this syndrome due to functional neuroimaging techniques, as these could be useful in the study of the pathophysiology of catatonia.Materials and Methods:We report the case of a 49-year-old male patient, who presented severe depressive and catatonic symptoms simultaneously.Results and Conclusions:The patient was treated with diazepam at 40 mg / day and venlafaxine 150 mg / day. Brain SPECT of the patient showed signs of global decreased perfusion and in the frontal and parietal lobes of frontal predominance (dorsolateral, prefrontal orbitofrontal). Discrete greater perfusion in temporal lobes of left predominance. These findings are similar to those reported in other cases, where it is documented in studies of functional neuroimaging of catatonic patients: right inferior lateral prefrontal cortex hypoperfusion, right posterior parietal hypoperfusion, also left temporal hypoperfusion and asymmetric uptake in basal ganglia with left hypoperfusion. These neuroimaging findings support the idea that catatonia would be associated with possible dysfunction of the frontal lobes. According to the literature, the premotor and motor cortex would be functionally altered due to abnormalities in the cortical GABAergic control, which would also produce affective and behavioral symptoms.