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 following two case reports are examples of the Capgras delusion in a psychiatric setting:

The following case is an instance of the Capgras delusion resulting from a neurodegenerative disease:

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.

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.

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.

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.

Pharmaceutical management, as with Parkinson's disease, involves striking a balance between treating the motor, emotive, and cognitive symptoms. Motor symptoms appear to respond somewhat to the medications used to treat Parkinson's disease (e.g. levodopa), while cognitive issues may improve with medications for Alzheimer's disease such as donepezil. Medications used in the treatment of ADHD (e.g. methylphenidate) might improve cognition or daytime sleepiness; however, medications for both Parkinson's disease and ADHD increase levels of the chemical dopamine in the brain, so increase the risk of hallucinations with those classes of pharmaceuticals.

Treatment of the movement and cognitive portions of the disease may worsen hallucinations and psychosis, while treatment of hallucinations and psychosis with antipsychotics may worsen parkinsonian or ADHD symptoms in DLB, such as tremor or rigidity and lack of concentration or impulse control. Physicians may find the use of cholinesterase inhibitors represents the treatment of choice for cognitive problems and donepezil (Aricept), rivastigmine (Exelon), and galantamine (Reminyl) may be recommended as a means to help with these problems and to slow or prevent the decline of cognitive function. DLB may be more responsive to donepezil than Alzheimer's disease. Memantine also may be useful. Levocarb may help with movement problems, but in some cases, as with dopamine agonists, may tend to aggravate psychosis in people with DLB. Clonazepam may help with rapid eye movement behavior disorder; table salt or antihypotensive medications may help with fainting and other problems associated with orthostatic hypotension. Botulinum toxin injections in the parotid glands may help with sialorrhea. Other medications, especially stimulants such as the ADHD drug methylphenidate (Ritalin) and modafinil, may improve daytime alertness, but as with the antiparkinsonian drug Levocarb, antihyperkinetics such as Ritalin increase the risk of psychosis. Experts advise extreme caution in the use of antipsychotic medication in people with DLB because of their sensitivity to these agents. When these medications must be used, atypical antipsychotics are preferred to typical antipsychotics; a very low dose should be tried initially and increased slowly, and patients should be carefully monitored for adverse reactions to the medications.

Due to hypersensitivity to neuroleptics, preventing DLB patients from taking these medications is important. People with DLB are at risk for neuroleptic malignant syndrome, a life-threatening illness, because of their sensitivity to these medications, especially the older typical antipsychotics, such as haloperidol. Other medications, including medications for urinary incontinence and the antihistamine medication diphenhydramine (Benadryl), also may worsen confusion.

Antibodies against voltage-gated potassium channels (VGKC), which are detectable in about 40% of patients with acquired neuromytonia, have been implicated in Morvan’s pathophysiology. Raised serum levels of antibodies to VGKCs have been reported in three patients with Morvan’s Syndrome. Binding of serum from a patient with Morvan’s Syndrome to the hippocampus in a similar pattern of antibodies to known VGKC suggest that these antibodies can also cause CNS dysfunction. Additional antibodies against neuromuscular junction channels and receptors have also been described. Experimental evidence exists that these anti-VGKC antibodies cause nerve hyperexcitability by suppression of voltage gated K+ outward currents, whereas other, yet undefined humoral factors have been implicated in anti-VGKC antibody negative neuromyotonia. It is believed that antibodies to the Shaker-type K+ channels (the Kv1 family) are the type of potassium channel most strongly associated with acquired neuromyotonia and Morvan’s Syndrome.

Whether VGKC antibodies play a pathogenic role in the encephalopathy as they do in the peripheral nervous system is as yet unclear. It has been suggested that the VGKC antibodies may cross the blood–brain barrier and act centrally, binding predominantly to thalamic and striatal neurons causing encephalopathic and autonomic features.

No cure for dementia with Lewy bodies is known. Treatment may offer symptomatic benefit, but remains palliative in nature. Current treatment modalities are divided into pharmaceutical and caregiving.