A widely accepted treatment for the syndrome of subjective doubles has not been developed. Treatment methods for this disease sometimes include the prescription of antipsychotic drugs, however, the type of drug prescribed depends on the presence of other mental disorders. Antipsychotic drugs (also known as neuroleptics) such as risperidone, pimozide, or haloperidol may be prescribed to treat the underlying psychiatric illness.

In addition to drug therapy, interpersonal counseling has also been suggested as a method to ease relations between the patient and his/her suspected doubles. However, the relationship between the patient and his/her double is not always negative.

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.

Once it has been positively identified, pharmacotherapy follows. Antipsychotic drugs are the frontrunners in treatment for Fregoli and other DMSs. In addition to antipsychotics, anticonvulsants and antidepressants are also prescribed in some treatment courses. If a Fregoli patient has other psychological disorders, treatment often results in the use of trifluoperazine.

An open study of cognitive behavior therapy has aimed to help patients reinterpret their symptoms in a nonthreatening way, leading to an improvement on several standardized measures. A standardized treatment for DPD based on cognitive behavioral principles was published in The Netherlands in 2011.

Primary depersonalization disorder is mostly refractory to current treatments. The disorder lacks effective treatment in part because it has been neglected within the field of psychiatry, which, in turn, is partly because funding has mainly been allocated to the search for cures of other illnesses, like alcoholism. However, recognizing and diagnosing the condition may in itself have therapeutic benefits, considering many patients express their problems as baffling and unique to them, but are in fact: one, recognized and described by psychiatry; and two, those affected by it are not the only individuals to be affected from the condition. A variety of psychotherapeutic techniques have been used to treat depersonalization disorder, such as cognitive behavioral therapy. Clinical pharmacotherapy research continues to explore a number of possible options, including selective serotonin reuptake inhibitors, tricyclic antidepressants, anticonvulsants, and opioid antagonists.

Recovery from this syndrome is situational, as some drug therapies have been effective in some individuals but not others. Patients may live in a variety of settings, including psychiatric hospitals, depending on the success of treatment. With successful treatment, an individual may live at home. In many of the reported cases, remission of symptoms occurred during the follow-up period.

This disorder can be dangerous to the patient and others, as a patient may interrogate or attack a person they believe to be a double. Inappropriate behavior such as stalking and physical or psychological abuse has been documented in some case studies. Consequently, many individuals suffering from this disorder are arrested for the resulting misconduct (see the case of Mr. B in #Presentation).

Treatment is dependent on the underlying cause, whether it is organic or psychological in origin. If depersonalization is a symptom of neurological disease, then diagnosis and treatment of the specific disease is the first approach. Depersonalization can be a cognitive symptom of such diseases as amyotrophic lateral sclerosis, Alzheimer's, multiple sclerosis (MS), neuroborreliosis (Lyme disease), or any other neurological disease affecting the brain. For those suffering from depersonalization with migraine, tricyclic antidepressants are often prescribed.

If depersonalization is a symptom of psychological causes such as developmental trauma, treatment depends on the diagnosis. In case of dissociative identity disorder or DD-NOS as a developmental disorder, in which extreme developmental trauma interferes with formation of a single cohesive identity, treatment requires proper psychotherapy, and—in the case of additional (co-morbid) disorders such as eating disorders—a team of specialists treating such an individual. It can also be a symptom of borderline personality disorder, which can be treated in the long term with proper psychotherapy and psychopharmacology.

The treatment of chronic depersonalization is considered in depersonalization disorder.

A recently completed study at Columbia University in New York City has shown positive effects from transcranial magnetic stimulation (TMS) to treat depersonalization disorder. Currently, however, the FDA has not approved TMS to treat DP.

A 2001 Russian study showed that naloxone, a drug used to reverse the intoxicating effects of opioid drugs, can successfully treat depersonalization disorder. According to the study: "In three of 14 patients, depersonalization symptoms disappeared entirely and seven patients showed a marked improvement. The therapeutic effect of naloxone provides evidence for the role of the endogenous opioid system in the pathogenesis of depersonalization."

The most common treatment for reducing bipolar II disorder symptoms is medication, usually in the form of mood stabilizers. However, treatment with mood stabilizers may produce a flat affect in the patient, which is dose-dependent. Concurrent use of SSRI antidepressants may help some with bipolar II disorder, though these medications should be used with caution because it is believed that they may cause a hypomanic switch.

The pharmaceutical management of bipolar II disorder is not generally supported by strong evidence, with limited randomised controlled trials (RCTs) published in the literature. Some medications used are:

- Lithium - There is strong evidence that lithium is effective in treating both the depressive and hypomanic symptoms in bipolar II. In addition, its action as a mood stabilizer can be used to decrease the risk of hypomanic switch in patients treated with antidepressants.

- Anticonvulsants - there is evidence that lamotrigine decreases the risk of relapse in rapid cycling bipolar II. It appears to be more effective in bipolar II than bipolar I, suggesting that lamotrigine is more effective for the treatment of depressive rather than manic episodes. Doses ranging from 100–200 mg have been reported to have the most efficacy, while experimental doses of 400 mg have rendered little response. A large, multicentre trial comparing carbamazepine and lithium over two and a half years found that carbamazepine was superior in terms of preventing future episodes of bipolar II, although lithium was superior in individuals with bipolar I. There is also some evidence for the use of valproate and topiramate, although the results for the use of gabapentin have been disappointing.

- Antidepressants - there is evidence to support the use of SSRI and SNRI antidepressants in bipolar II. Indeed, some sources consider them to be one of the first line treatments. However, antidepressants also pose significant risks, including a switch to mania, rapid cycling, and dysphoria and so many psychiatrists advise against their use for bipolar. When used, antidepressants are typically combined with a mood stabilizer.

- Antipsychotics - there is good evidence for the use of quetiapine, and it has been approved by the FDA for this indication. There is also some evidence for the use of risperidone, although the relevant trial was not placebo controlled and was complicated by the use of other medications in some of the patients.

- Dopamine agonists - there is evidence for the efficacy of pramipexole from one RCT.

Treatment typically includes three things: the treatment of acute hypomania, the treatment of acute depression, and the prevention of the relapse of either hypomania or depression. The main goal is to make sure that patients do not harm themselves.

To date, cognitive behavioral therapy (CBT) is the best established treatment for a variety of somatoform disorders including somatization disorder. CBT aims to help patients realize their ailments are not catastrophic and to enable them to gradually return to activities they previously engaged in, without fear of "worsening their symptoms". Consultation and collaboration with the primary care physician also demonstrated some effectiveness. The use of antidepressants is preliminary but does not yet show conclusive evidence. Electroconvulsive shock therapy (ECT) has been used in treating somatization disorder among the elderly; however, the results were still debatable with some concerns around the side effects of using ECT. Overall, psychologists recommend addressing a common difficulty in patients with somatization disorder in the reading of their own emotions. This may be a central feature of treatment; as well as developing a close collaboration between the GP, the patient and the mental health practitioner.

There are multiple treatments that can be effective in treating children diagnosed with depression. Psychotherapy and medications are commonly used treatment options. In some research, adolescents showed a preference for psychotherapy rather than antidepressant medication for treatment. For adolescents, cognitive behavioral therapy and interpersonal therapy have been empirically supported as effective treatment options. The use of antidepressant medication in children is often seen as a last resort; however, studies have shown that a combination of psychotherapy and medication is the most effective treatment. Pediatric massage therapy may have an immediate effect on a child's emotional state at the time of the massage, but sustained effects on depression have not been identified.

Treatment programs have been developed that help reduce the symptoms of depression. These treatments focus on immediate symptom reduction by concentrating on teaching children skills pertaining to primary and secondary control. While much research is still needed to confirm this treatment program’s efficacy, one study showed it to be effective in children with mild or moderate depressive symptoms.

The Depersonalisation Research Unit at the Institute of Psychiatry in London conducts research into depersonalization disorder. Researchers there use the acronym DPAFU (Depersonalisation and Feelings of Unreality) as a shortened label for the disorder.

There are three common types of talk therapy. These can assist people to live more fully and have a better life. Men are encouraged to open up more emotionally and communicate their personal distress, while women are encouraged to be assertive of their own strengths

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.

Capgras delusion is a psychiatric disorder in which a person holds a delusion that a friend, spouse, parent, or other close family member (or pet) has been replaced by an identical impostor. The Capgras delusion is classified as a delusional misidentification syndrome, a class of delusional beliefs that involves the misidentification of people, places, or objects. It can occur in acute, transient, or chronic forms. Cases in which patients hold the belief that time has been "warped" or "substituted" have also been reported.

The delusion most commonly occurs in patients diagnosed with paranoid schizophrenia, but has also been seen in patients suffering from brain injury and dementia. It presents often in individuals with a neurodegenerative disease, particularly at an older age. It has also been reported as occurring in association with diabetes, hypothyroidism, and migraine attacks. In one isolated case, the Capgras delusion was temporarily induced in a healthy subject by the drug ketamine. It occurs more frequently in females, with a female:male ratio of approximately 3:2. It is worth noting that there is historical and quite probably modern use of the Political decoy as well as Celebrity lookalike, and impersonation is used by criminals, as well. Although 'delusion' is defined as when a patient holds a false belief "in spite of incontrovertible evidence", such evidence is difficult to produce (in the case of Capgras symptoms), whether lookalikes exist or not. This does not deter psychiatrists from prescribing pharmaceutical chemicals for persons describing these situations with little, if any, investigation into the claims, though it seems even one actual encounter with a genuine impersonator (whether sinister or not) has a notably unnerving effect on future interactions with that actual person, and possibly leading to paranoia of others being impersonated. Carefully targeted identity thefts in this sense can cause quite a few real problems, ranging from confusion to petty theft, business and domestic situations going awry, sexual relationship sabotage or confusion (possibility of unplanned pregnancy and risk of STD exposure), and financial fraud.

The condition usually resolves spontaneously within a timespan of weeks to months, with the severity of the symptoms reducing continuously over the period in question. A primary goal of treatment is to prevent patients from harming themselves or others during the episode.

Jungians emphasise the importance of recognising the patient's perspective throughout the episode, the danger being that

'if psychiatry itself considers the situation incomprehensible...many exclusion mechanisms will be set to work and [s]he will slide down the slope of a deeper and deeper regression'.

R. D. Laing pointed repeatedly to "the possibility that what we call psychosis may be sometimes a natural process of healing (a view for which I claim no priority)". Under the title "A Ten Day Voyage", he published an acquaintance's first-hand account of a reactive psychosis, triggered by a festering dog-bite. The protagonist reported

'"living in a - in another time dimension added to the time situation in which I am now...another sphere, another layer of existence lying above...the present"'.

At the close of the experience, the patient '"thought, well, somewhere or other I've got to sort of join up with my present - er - self, very strongly. So I...kept on saying my own name over and over again and all of a sudden, just like that - I suddenly realized that it was all over"'.

Psychologist Erik H. Erikson considered that whatever the causes, the psychotic break involved a primitive re-testing of the boundaries of self and other, words and meanings, in an effort to re-establish a new social mutuality.

Current cognitive neuropsychology research points toward a two-factor approach to the cause of monothematic delusions. The first factor being the anomalous experience—often a neurological defect—which leads to the delusion, and the second factor being an impairment of the belief formation cognitive process.

As an example of one of these first factors, several studies point toward Capgras delusion being the result of a disorder of the affect component of face perception. As a result, while the person can recognize their spouse (or other close relation) they do not feel the typical emotional reaction, and thus the spouse does not seem like the person they once knew.

As studies have shown, these neurological defects are not enough on their own to cause delusional thinking. An additional second factor—a bias or impairment of the belief formation cognitive process—is required to solidify and maintain the delusion. Since we do not currently have a solid cognitive model of the belief formation process, this second factor is still somewhat of an unknown.

Some research has shown that delusional people are more prone to jumping to conclusions, and thus they would be more likely to take their anomalous experience as veridical and make snap judgments based on these experiences. Additionally, studies have shown that they are more prone to making errors due to matching bias—indicative of a tendency to try and confirm the rule. These two judgment biases help explain how delusion-prone people could grasp onto extreme delusions and be very resistant to change.

Researchers claim this is enough to explain the delusional thinking. However, other researchers still argue that these biases are not enough to explain why they remain completely impervious to evidence over time. They believe that there must be some additional unknown neurological defect in the patient's belief system (probably in the right hemisphere).

The Fregoli delusion, or the delusion of doubles, is a rare disorder in which a person holds a delusional belief that different people are in fact a single person who changes appearance or is in disguise. The syndrome may be related to a brain lesion and is often of a paranoid nature, with the delusional person believing themselves persecuted by the person they believe is in disguise.

A person with the Fregoli delusion can also inaccurately recall places, objects, and events. This disorder can be explained by "associative nodes". The associative nodes serve as a biological link of information about other people with a particular familiar face (to the patient). This means that for any face that is similar to a recognizable face to the patient, the patient will recall that face as the person they know.

The Fregoli delusion is classed both as a monothematic delusion, since it only encompasses one delusional topic, and as a delusional misidentification syndrome (DMS), a class of delusional beliefs that involves misidentifying people, places, or objects. Like Capgras delusion, psychiatrists believe it is related to a breakdown in normal face perception.

Brief reactive psychosis generally follows a recognisably traumatic life event like divorce or homelessness, but may be triggered by any subjective experience which appears catastrophic to the person affected.

Among such stressors are the death of a loved one, professional loss such as unexpectedly losing one's job or otherwise becoming unemployed, or serious adverse changes in the patient's personal life, such as the breakdown of their family through divorce, etc.

It must be emphasised that this is by no means an exhaustive list of stressful life events, because the events which trigger brief reactive psychosis tend, due to the individualistic nature of human psychology, to be extremely personalized. BRP may be the first breakdown for someone with a chronic psychiatric disorder but only time will tell whether the disorder will be brief or lifelong, whether BRP or a chronic condition that is controlled well enough by medication that symptoms do not return.

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.

If the symptoms of alcohol dementia are caught early enough, the effects may be reversed. The person must stop drinking and start on a healthy diet, replacing the lost vitamins, including, but not limited to, thiamine. Recovery is more easily achievable for women than men, but in all cases it is necessary that they have the support of family and friends and abstain from alcohol.

Behavioral treatment can be effective in some cases. Sedative hypnotics may also help relieve the symptoms. Additionally, education about normal patterns of the sleep-wake cycle may alleviate anxiety in some patients. For patients with severe depression resulting from the fear of having insomnia, electroconvulsive therapy appears to be a safe and effective treatment.

Often in those who have experienced their first episode of hypomania – generally without psychotic features – there may be a long or recent history of depression or a mix of hypomania combined with depression (known as mixed-state) prior to the emergence of manic symptoms. This commonly surfaces in the mid to late teens. Because the teenage years are typically an emotionally charged time of life, it is not unusual for mood swings to be passed off as normal hormonal teen behavior and for a diagnosis of bipolar disorder to be missed until there is evidence of an obvious manic or hypomanic phase.

Hypomania may also occur as a side effect of pharmaceuticals prescribed for conditions or diseases other than psychological states or mood disorders. In those instances, as in cases of drug-induced hypomanic episodes in unipolar depressives, the hypomania can almost invariably be eliminated by lowering medication dosage, withdrawing the drug entirely, or changing to a different medication if discontinuation of treatment is not possible.

Hypomania may also be triggered by the occurrence of a highly exciting event in the patient's situation, such as a substantial financial gain or recognition.

Hypomania can be associated with narcissistic personality disorder.

Currently, there are no medications that have been approved specifically for prevention or treatment of vascular dementia. The use of medications for treatment of Alzheimer's dementia, such as cholinesterase inhibitors and memantine, has shown small improvement of cognition in vascular dementia. This is most likely due to the drugs' actions on co-existing AD-related pathology. Multiple studies found a small benefit in VaD treatment with: memantine, a non-competitive N-methyl-D-aspartate (NMDA) receptor antagonist; cholinesterase inhibitors galantamine, donepezil, rivastigmine; and ginkgo biloba extract.

The general management of dementia includes referral to community services, aid with judgment and decision-making regarding legal and ethical issues (e.g., driving, capacity, advance directives), and consideration of caregiver stress.

Behavioral and affective symptoms deserve special consideration in this patient group. These problems tend to be resistant to conventional psychopharmacological treatment and often lead to hospital admission and placement in permanent care.

The condition may worsen as a result of persistent attempts to treat the symptoms through conventional methods of dealing with insomnia. The prescription of hypnotics or stimulants may lead to drug dependency as a complication.

Nonetheless, chronic SSM may increase risk for depression, anxiety, and substance abuse. It has also been noted that patients with this condition may sometimes opt to take medications over other treatments "for the wrong reasons (e.g. because of euphoriant properties)."