Cotard’s syndrome was originally described in 1880 by the French psychiatrist Jules Cotard; this relatively rare disorder is characterized by the presence of nihilistic delusion (délire des négations). Typically, patients believe they have lost their organs, blood or body parts, or even they are dead; the delusion is accompanied by guilt as well as the belief to be immortal. This highly impressive psychopathological condition exists in patients with depression, schizophrenia, and other psychotic disorders but it may also occur in neurological practice.
A propos of one case seen in our hospital, we present an overview of the historical aspects, classification, neurological characteristics (neurostructural, neurophysiological and neuropsychological), etiology and the more recent view of pathogenesis of Cotard’s syndrome.
We searched electronic databases and key journals using appropriate search terms: Jules Cotard; Cotard syndrome; Cotard’s delusion; nihilistic delusion; internalising attributional style and depression.
Various organic conditions such as multiple sclerosis, temporal lobe epilepsy, brain tumors, brain injuries, and migraine have been reported in association with Cotard’s syndrome. The most commonly reported neurological abnormalities in these patients include structural brain changes (bilateral cerebral atrophy, enlarged interhemispheric fissure), functional brain changes (hypoperfusion in the frontal and parietal cortices) and neuropsychological abnormalities (impaired face recognition, impaired executive functions and internalising attributional style) (Fig. 1). The pharmacological treatment must be congruent with the underlying disorder. There are several reports of successful pharmacologic treatment of Cotard’s syndrome, most often regarding monotherapy with antidepressant agents or with combinations strategies.
The presented case set the issue of the differential diagnosis between dementia and Cotard’s syndrome. Fast cognitive and psychopathological symptom progression combined with substantially negative clinical investigations (brain NMR, EEG, blood chemistry) and the response to administered drug treatment prompted us to diagnose Cotard’s syndrome in the context of a major depressive episode.