He thought he had "borrowed [his] mothers spirit to show [him] around Hell" and that she was asleep in Scotland. The article Recurrent Postictal Depression with Cotard Delusion (2005) describes the case of a 14-year-old epileptic boy who experienced Cotards syndrome after seizures. His mental health history showed themes of death, chronic sadness, decreased physical activity in leisure time, social withdrawal, and disturbed biological functions. About twice a year, the boy had episodes that lasted between three weeks and three months. In the course of each episode, he said that everyone and everything was dead (including trees), described himself as a dead body, and warned that the world would be destroyed within hours. Throughout the episode, the boy showed no response to pleasurable stimuli, and had no interest in social activities. Pathophysiology
The underlying neurophysiology and psychopathology of Cotards syndrome might be related to problems of delusional misidentification. Neurologically, Cotards delusion (negation of the self) is thought to be related to Capgras delusion (people replaced by impostors); each type of delusion is thought to result from neural misfiring in the fusiform face area of the brain, which recognizes faces, and in the amygdalae, which associate emotions to a recognized face.The neural disconnection creates in the patient a sense that the face they are observing is not the face of the person to whom it belongs; therefore, that face lacks the familiarity (recognition) normally associated with it. This results in derealization or a disconnection from the environment.
If the observed face is that of a person known to the patient, they experience that face as the face of an impostor (Capgras delusion). If the patient sees their own face, they might perceive no association between the face and their own sense of self—which results in the patient believing that they do not exist (Cotards syndrome). Cotards syndrome is usually encountered in people with psychosis, as in schizophrenia. It is also found in clinical depression, derealization, brain tumor, and migraine headaches. The medical literature indicate that the occurrence of Cotards delusion is associated with lesions in the parietal lobe. As such, the Cotards delusion patient presents a greater incidence of brain atrophy—especially of the median frontal lobe—than do people in control groups.Cotards delusion also has resulted from a patients adverse physiological response to a drug (e.g., acyclovir) and to its prodrug precursor (e.g., valaciclovir). The occurrence of Cotards delusion symptoms was associated with a high serum-concentration of 9-carboxymethoxymethylguanine (CMMG), the principal metabolite of acyclovir.As such, the patient with weak kidneys (impaired renal function) continued risking the occurrence of delusional symptoms despite the reduction of the dose of acyclovir. Hemodialysis resolved the patients delusions (of negating the self) within hours of treatment, which suggests that the occurrence of Cotards delusion symptoms might not always be cause for psychiatric hospitalization of the patient. Treatment
Pharmacological treatments, both mono-therapeutic and multi-therapeutic, using antidepressants, antipsychotics, and mood stabilizers have been successful.