Because it is a rare and poorly understood condition, there is no definitive way to diagnose the Capgras delusion. Diagnosis is primarily made on psychological evaluation of the patient, who is most likely brought to a psychologist's attention by a family member or friend believed to be an imposter by the person under the delusion.

Individual therapy may be best suited to treat the individual's delusions. Persistence is needed in establishing a therapeutic empathy without validating the patient’s delusional system or overtly confronting the system. Cognitive techniques that include reality testing and reframing can be used. Antipsychotics and other therapeutic drugs have been used with relative success.

Reduplicative paramnesia is the delusional belief that a place or location has been duplicated, existing in two or more places simultaneously, or that it has been 'relocated' to another site. It is one of the delusional misidentification syndromes and, although rare, is most commonly associated with acquired brain injury, particularly simultaneous damage to the right cerebral hemisphere and to both frontal lobes.

The term "reduplicative paramnesia" was first used in 1903 by psychiatrist Arnold Pick to describe a condition in a patient with suspected Alzheimer's disease who insisted that she had been moved from Pick's city clinic to one she claimed looked identical but was in a familiar suburb. To explain the discrepancy she further claimed that Pick and the medical staff worked at both locations.

In retrospect, however, the phenomenon has been found to have been first reported by the Swiss naturalist Charles Bonnet in 1788, who described a woman who also had what would now be called Cotard delusion. Henry Head and Paterson and Zangwill later reported on soldiers who had the delusional belief that their hospital was located in their home town, although in these cases traumatic brain injury seemed to be the most likely cause.

It wasn't until 1976 that serious consideration was given to the disorder, when three cases were reported by Benson and colleagues. Benson not only described striking reduplication syndromes in his patients, but also attempted to explain the phenomena in terms of the neurocognitive deficits also present in the patients. This was one of the first attempts to give a neuropsychological explanation for the disorder.

A monothematic delusion is a delusional state that concerns only one particular topic. This is contrasted by what is sometimes called "multi-thematic" or "polythematic" delusions where the person has a range of delusions (typically the case of schizophrenia). These disorders can occur within the context of schizophrenia or dementia or they can occur without any other signs of mental illness. When these disorders are found outside the context of mental illness, they are often caused by organic dysfunction as a result of traumatic brain injury, stroke, or neurological illness.

People who experience these delusions as a result of organic dysfunction often do not have any obvious intellectual deficiency nor do they have any other symptoms. Additionally, a few of these people even have some awareness that their beliefs are bizarre, yet they cannot be persuaded that their beliefs are false.

The delusions that fall under this category are:

- Capgras delusion: the belief that (usually) a close relative or spouse has been replaced by an identical-looking impostor.

- Fregoli delusion: the belief that various people whom the believer meets are actually the same person in disguise.

- Intermetamorphosis: the belief that people in one's environment swap identities with each other while maintaining the same appearance.

- Subjective doubles: a person believes there is a doppelgänger or double of him- or herself carrying out independent actions.

- Cotard delusion: the belief that oneself is dead or does not exist; sometimes coupled with the belief that one is putrefying or missing internal organs.

- Mirrored-self misidentification: the belief that one's reflection in a mirror is some other person.

- Reduplicative paramnesia: the belief that a familiar person, place, object, or body part has been duplicated. For example, a person may believe that they are, in fact, not in the hospital to which they were admitted, but in an identical-looking hospital in a different part of the country.

- Somatoparaphrenia: the delusion where one denies ownership of a limb or an entire side of one's body (often connected with stroke).

Note that some of these delusions are sometimes grouped under the umbrella term of delusional misidentification syndrome.

Delusional misidentification syndrome is an umbrella term, introduced by Christodoulou (in his book "The Delusional Misidentification Syndromes", Karger, Basel, 1986) for a group of delusional disorders that occur in the context of mental and neurological illness. They all involve a belief that the identity of a person, object, or place has somehow changed or has been altered. As these delusions typically only concern one particular topic, they also fall under the category called monothematic delusions.

This psychopathological syndrome is usually considered to include four main variants:

- The Capgras delusion is the belief that (usually) a close relative or spouse has been replaced by an identical-looking impostor.

- The Fregoli delusion is the belief that various people the believer meets are actually the same person in disguise.

- Intermetamorphosis is the belief that people in the environment swap identities with each other whilst maintaining the same appearance.

- Subjective doubles, described by Christodoulou in 1978 ("American Journal of Psychiatry" 135, 249, 1978), is the belief that there is a doppelgänger or double of him- or herself carrying out independent actions.

However, similar delusional beliefs, often singularly or more rarely reported, are sometimes also considered to be part of the delusional misidentification syndrome. For example:

- Mirrored-self misidentification is the belief that one's reflection in a mirror is some other person.

- Reduplicative paramnesia is the belief that a familiar person, place, object, or body part has been duplicated. For example, a person may believe that they are in fact not in the hospital to which they were admitted, but an identical-looking hospital in a different part of the country, despite this being obviously false.

- The Cotard delusion is a rare disorder in which people hold a delusional belief that they are dead (either figuratively or literally), do not exist, are putrefying, or have lost their blood or internal organs. In rare instances, it can include delusions of immortality.

- Syndrome of delusional companions is the belief that objects (such as soft toys) are sentient beings.

- Clonal pluralization of the self, where a person believes there are multiple copies of him- or herself, identical both physically and psychologically but physically separate and distinct.

There is considerable evidence that disorders such as the Capgras or Fregoli syndromes are associated with disorders of face perception and recognition. However, it has been suggested that all misidentification problems exist on a continuum of anomalies of familiarity, from déjà vu at one end to the formation of delusional beliefs at the other.

Experiences - are characterized by the presence of the following three factors:

- disembodiment, an apparent location of the self outside one's body;

- impression of seeing the world from an elevated and distanced visuo-spatial perspective or extracorporeal, but egocentric visuo-spatial perspective;

- impression of seeing one's own body from this perspective (autoscopy).

Laboratory of Cognitive Neuroscience, École Polytechnique Fédérale de Lausanne, Lausanne, and Department of Neurology, University Hospital, Geneva, Switzerland, have reviewed some of the classical precipitating factors of autoscopy. These are sleep, drug abuse, and general anesthesia as well as neurobiology. They have compared them with recent findings on neurological and neurocognitive mechanisms of the autoscopy. The reviewed data suggest that autoscopic experiences are due to functional disintegration of lower-level multisensory processing and abnormal higher-level self-processing at the temporoparietal junction.

Autoscopy is the experience in which an individual perceives the surrounding environment from a different perspective, from a position outside of his or her own body. Autoscopy comes from the ancient Greek ("self") and ("watcher").

Autoscopy has been of interest to humankind from time immemorial and is abundant in the folklore, mythology, and spiritual narratives of most ancient and modern societies. Cases of autoscopy are commonly encountered in modern psychiatric practice. According to neurological research, autoscopic experiences are hallucinations.

Breathing difficulties can occur, resulting from neuromyotonic activity of the laryngeal muscles. Laryngeal spasm possibly resulting from neuromyotonia has been described previously, and this highlights that, in patients with unexplained laryngospasm, neuromytonia should be added to the list of differential diagnoses.

Studies have shown subtly decreased metabolism on positron emission tomography (PET) and single photon emission computed tomography (SPECT) in the left inferior frontal and left temporal lobes. and or basal ganglia hypermetabolism. Ancillary laboratory tests including MRI and brain biopsy have confirmed temporal lobe involvement. Cranial MRI shows increased signal in the hippocampus.

Cerebral spinal fluid (CSF) shows normal protein, glucose, white blood cell, and IgG index but there are weak oligoclonal bands, absent in the blood. Marked changes in circadian serum levels of neurohormones and increased levels of peripheral neurotransmitters were also observed. The absence of morphological alterations of the brain pathology, the suggestion of diffusion of IgG into the thalamus and striatum, more marked than in the cortex (consistent with effects on the thalamolimbic system) the oligoclonal bands in the CSF and the amelioration after PE all strongly support an antibody-mediated basis for the condition. Raised CSF IgG concentrations and oligoclonal bands have been reported in patients with psychosis. Anti-acetylcholine receptors (anti-AChR) antibodies have also been detected in patients with thymoma, but without clinical manifestations of myasthenia gravis. There have also been reports of non-paraneoplastic limbic encephalitis associated with raised serum VGKC suggesting that these antibodies may give rise to a spectrum of neurological disease presenting with symptoms arising peripherally, centrally, or both. Yet, in two cases, oligoclonal bands were absent in the CSF and serum, and CSF immunoglobulin profiles were unremarkable.

In most of the reported cases, the treatment options were very similar. Plasmapheresis alone or in combination with steroids, sometimes also with thymectomy and azathioprine, have been the most frequently used therapeutic approach in treating Morvan’s Syndrome. However, this does not always work, as failed response to steroids and to subsequently added plasmapheresis have been reported. Intravenous immunoglobulin was effective in one case.

In one case, the dramatic response to high-dose oral prednisolone together with pulse methylprednisolone with almost complete disappearance of the symptoms within a short period should induce consideration of corticosteroids.

In another case, the subject was treated with haloperidol (6 mg/day) with some improvement in the psychomotor agitation and hallucinations, but even high doses of carbamazepine given to the subject failed to improve the spontaneous muscle activity. Plasma Exchange (PE) was initiated, and after the third such session, the itching, sweating, mental disturbances, and complex nocturnal behavior improved and these symptoms completely disappeared after the sixth session, with improvement in insomnia and reduced muscle twitching. However, one month after the sixth PE session, there was a progressive worsening of insomnia and diurnal drowsiness, which promptly disappeared after another two PE sessions.

In one case there high dose steroid treatment resulted in a transient improvement, but aggressive immuno-suppressive therapy with cyclophosphamide was necessary to control the disease and result in a dramatic clinical improvement.

In another case, the subject was treated with prednisolone (1 mg/kg body weight) with carbamazepine, propanolol, and amitriptyline. After two weeks, improvement with decreased stiffness and spontaneous muscle activity and improved sleep was observed. After another 7–10 days, the abnormal sleep behavior disappeared completely.

In another case, symptomatic improvement with plasmapheresis, thymectomy, and chronic immunosuppression provide further support for an autoimmune or paraneoplastic basis.

Although thymectomy is believed to be a key element in the proposed treatment, there is a reported case of Morvan’s Syndrome presenting itself post-thymectomy.

The symptoms of DLB overlap clinically with those of Alzheimer's disease and Parkinson's disease, but are associated more commonly with the latter. Because of this overlap, early DLB is often misdiagnosed. The overlap of neuropathological and presenting symptoms (cognitive, emotional, and motor) may make an accurate differential diagnosis difficult. In fact, DLB often is confused in its early stages with Alzheimer's disease and/or vascular dementia (multi-infarct dementia). However, while Alzheimer’s disease usually begins gradually, DLB frequently has a rapid or acute onset, with an especially rapid cognitive and physical decline in the first few months. Thus, DLB tends to progress more rapidly than Alzheimer’s disease. Despite the difficulty, a prompt diagnosis is important because of the risks of sensitivity to certain neuroleptic (antipsychotic) medications and because appropriate treatment of symptoms may improve life for both the person with DLB and the person's caregivers.

Dementia with Lewy bodies is distinguished from the dementia that sometimes occurs in Parkinson's disease by the time frame in which dementia symptoms appear relative to Parkinson symptoms. Parkinson's disease with dementia (PDD) would be the diagnosis when the onset of dementia is more than a year after the onset of Parkinsonian symptoms. DLB is diagnosed when cognitive symptoms begin at the same time or within a year of Parkinson symptoms.

Currently, an estimated 60 to 75% of diagnosed dementias are of the Alzheimer's and mixed (Alzheimer's and vascular dementia) type, 10 to 15% are Lewy body type, with the remaining types being of an entire spectrum of dementias, including frontotemporal lobar degeneration (Pick's disease), alcoholic dementia, pure vascular dementia, etc. Dementia with Lewy bodies tends to be under-recognized. Dementia with Lewy bodies is slightly more prevalent in men than women. DLB increases in prevalence with age; the mean age at presentation is 75 years.

Dementia with Lewy bodies affects about one million individuals in the United States.