It is generally agreed that the<unk>  has a complex and organic basis caused by structural damage to organs and can be better understood by examining neuroanatomical damage associated with the syndrome. In one of the first papers to consider the cerebral basis of the<unk> , Alexander, Stuss and Benson pointed out in 1979 that the disorder might be related to a combination of frontal lobe damage causing problems with familiarity and right hemisphere damage causing problems with visual recognition. Further clues to the possible causes of the<unk>  were suggested by the study of brain-injured patients who had developed prosopagnosia. In this condition, patients are unable to recognize faces consciously, despite being able to recognize other types of visual objects. However, a 1984 study by Bauer showed that even though conscious face recognition was impaired, patients with the condition showed autonomic arousal (measured by a galvanic skin response measure) to familiar faces, suggesting that there are two pathways to face recognition—one conscious and one unconscious. In a 1990 paper published in the British Journal of Psychiatry, psychologists Hadyn Ellis and Andy Young hypothesized that patients with<unk>  may have a "mirror image" or double dissociation of prosopagnosia, in that their conscious ability to recognize faces was intact, but they might have damage to the system that produces the automatic emotional arousal to familiar faces. This might lead to the experience of recognizing someone while feeling something was not "quite right" about them. In 1997, Ellis and his colleagues published a study of five patients with<unk>  (all diagnosed with schizophrenia) and confirmed that although they could consciously recognize the faces, they did not show the normal automatic emotional arousal response. The same low level of autonomic response was shown in the presence of strangers. Young (2008) has theorized that this means that patients with the disease experience a "loss" of familiarity, not a "lack" of it. Further evidence for this explanation comes from other studies measuring galvanic skin responses (GSR) to faces. A patient with<unk>  showed reduced GSRs to faces in spite of normal face recognition. This theory for the causes of<unk>  was summarised in Trends in Cognitive Sciences in 2001. William Hirstein and Vilayanur S. Ramachandran reported similar findings in a paper published on a single case of a patient with<unk>  after brain injury. Ramachandran portrayed this case in his book Phantoms in the Brain and gave a talk about it at TED 2007. Since the patient was capable of feeling emotions and recognizing faces but could not feel emotions when recognizing familiar faces, Ramachandran hypothesizes that the origin of<unk>  syndrome is a disconnection between the temporal cortex, where faces are usually recognized (see temporal lobe), and the limbic system, involved in emotions. More specifically, he emphasizes the disconnection between the amygdala and the inferotemporal cortex. In 2010, Hirstein revised this theory to explain why a person with<unk>  syndrome would have the particular reaction of not recognizing a familiar person. Hirstein explained the theory as follows: Furthermore, Ramachandran suggests a relationship between the<unk>  syndrome and a more general difficulty in linking successive episodic memories because of the crucial role emotion plays in creating memories. Since the patient could not put together memories and feelings, he believed objects in a photograph were new on every viewing, even though they normally should have evoked feelings (e.g., a person close to him, a familiar object, or even himself). Others like Merrin and Silberfarb (1976) have also proposed links between the<unk>  syndrome and deficits in aspects of memory. They suggest that an important and familiar person (the usual subject of the delusion) has many layers of visual, auditory, tactile, and experiential memories associated with them, so the<unk>  can be understood as a failure of object constancy at a high perceptual level. Most likely, more than a mere impairment of the automatic emotional arousal response is necessary to form the<unk> , as the same pattern has been reported in patients showing no signs of delusions. Ellis suggested that a second factor explains why this unusual experience is transformed into a delusional belief; this second factor is thought to be an impairment in reasoning, although no specific impairment has been found to explain all cases. Many have argued for the inclusion of the role of patient phenomenology in explanatory models of the<unk>  syndrome in order to better understand the mechanisms that enable the creation and maintenance of delusional beliefs.<unk>  syndrome has also been linked to reduplicative paramnesia, another delusional misidentification syndrome in which a person believes a location has been duplicated or relocated. Since these two syndromes are highly associated, it has been proposed that they affect similar areas of the brain and therefore have similar neurological implications. Reduplicative paramnesia is understood to affect the frontal lobe, and thus it is believed that<unk>  syndrome is also associated with the frontal lobe. Even if the damage is not directly to the frontal lobe, an interruption of signals between other lobes and the frontal lobe could result in<unk>  syndrome. Some authors have highlighted cannabis consumption as a trigger for<unk>  syndrome
Capgras delusion
Cotard delusion
Fregoli delusion
Visual hallucinations in psychosis
Monothematic delusion
Grandiose delusions
Homicidal ideation
Persecutory delusion