Neural misfiring in the fusiform face area, in the fusiform gyrus (orange), might be a cause of<unk> 's syndrome. In the cerebrum, organic lesions in the parietal lobe might cause<unk> 's syndrome. The underlying neurophysiology and psychopathology of<unk> 's syndrome might be related to problems of delusional misidentification. Neurologically,<unk> 's 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<unk> 's syndrome).<unk> 's syndrome is usually encountered in people afflicted 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<unk> 's delusion is associated with lesions in the parietal lobe. As such, the<unk> 's delusion patient presents a greater incidence of brain atrophy—especially of the median frontal lobe—than do people in control groups.<unk> 's delusion also has resulted from a patient's adverse physiological response to a drug (e.g., acyclovir) and to its prodrug precursor (e.g., valaciclovir). The occurrence of<unk> 's 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 patient's delusions (of negating the self) within hours of treatment, which suggests that the occurrence of<unk> 's delusion symptoms might not always be cause for psychiatric hospitalization of the patient.
Cotard delusion
Fregoli delusion
Capgras delusion
Monothematic delusion
Homicidal ideation
Pectoriloquy
Persecutory delusion
Grandiose delusions