There are few treatments for many types of hallucinations. However, for those hallucinations caused by mental disease, a psychologist or psychiatrist should be alerted, and treatment will be based on the observations of those doctors. Antipsychotic and atypical antipsychotic medication may also be utilized to treat the illness if the symptoms are severe and cause significant distress. For other causes of hallucinations there is no factual evidence to support any one treatment is scientifically tested and proven. However, abstaining from hallucinogenic drugs, stimulant drugs, managing stress levels, living healthily, and getting plenty of sleep can help reduce the prevalence of hallucinations. In all cases of hallucinations, medical attention should be sought out and informed of one's specific symptoms.

The treatment for delirium with medications depends on its cause. Antipsychotics, particularly haloperidol, are the most commonly used drugs for delirium and the most studied. Evidence is weaker for the atypical antipsychotics, such as risperidone, olanzapine and quetiapine. British professional guidelines by the National Institute for Health and Clinical Excellence advise haloperidol or olanzapine. Antipsychotics however are not supported for the treatment or prevention of delirium among those who are in hospital.

Benzodiazepines themselves can cause delirium or worsen it, and there is no reliable evidence for use in non-alcohol-related delirium. If delirium is due to alcohol withdrawal or benzodiazepine withdrawal or if antipsychotics are contraindicated (e.g. in Parkinson's disease or neuroleptic malignant syndrome), then benzodiazepines are recommended. Similarly, people with dementia with Lewy bodies may have significant side-effects to antipsychotics, and should either be treated with a small dose or not at all.

The antidepressant trazodone is occasionally used in the treatment of delirium, but it carries a risk of oversedation, and its use has not been well studied.

The treatment of psychosis depends on the specific diagnosis (such as schizophrenia, bipolar disorder or substance intoxication). The first-line psychiatric treatment for many psychotic disorders is antipsychotic medication, which can reduce the positive symptoms of psychosis in about 7 to 14 days.

The choice of which antipsychotic to use is based on benefits, risks, and costs. It is debatable whether, as a class, typical or atypical antipsychotics are better. Tentative evidence supports that amisulpride, olanzapine, risperidone and clozapine may be more effective for positive symptoms but result in more side effects. Typical antipsychotics have equal drop-out and symptom relapse rates to atypicals when used at low to moderate dosages. There is a good response in 40–50%, a partial response in 30–40%, and treatment resistance (failure of symptoms to respond satisfactorily after six weeks to two or three different antipsychotics) in 20% of people. Clozapine is an effective treatment for those who respond poorly to other drugs ("treatment-resistant" or "refractory" schizophrenia), but it has the potentially serious side effect of agranulocytosis (lowered white blood cell count) in less than 4% of people.

Most people on antipsychotics get side effects. People on typical antipsychotics tend to have a higher rate of extrapyramidal side effects while some atypicals are associated with considerable weight gain, diabetes and risk of metabolic syndrome; this is most pronounced with olanzapine, while risperidone and quetiapine are also associated with weight gain. Risperidone has a similar rate of extrapyramidal symptoms to haloperidol.

Psychological treatments such as acceptance and commitment therapy (ACT) are possibly useful in the treatment of psychosis, helping people to focus more on what they can do in terms of valued life directions despite challenging symptomology.

Treatment of delirium involves two main strategies: first, treatment of the underlying presumed acute cause or causes; secondly, optimising conditions for the brain. This involves ensuring that the person with delirium has adequate oxygenation, hydration, nutrition, and normal levels of metabolites, that drug effects are minimised, constipation treated, pain treated, and so on. Detection and management of mental stress is also important. Therefore, the traditional concept that the treatment of delirium is 'treat the cause' is not adequate; people with delirium require a highly detailed and expert analysis of all the factors which might be disrupting brain function.

Non medication treatments are the first measure in delirium, unless there is severe agitation that places the person at risk of harming oneself or others. Avoiding unnecessary movement, involving family members, having recognizable faces at the bedside, having means of orientation available (such as a clock and a calendar) may be sufficient in stabilizing the situation. If this is insufficient, verbal and non-verbal de-escalation techniques may be required to offer reassurances and calm the person experiencing delirium. Only if this fails, or if de-escalation techniques are inappropriate, is pharmacological treatment indicated.

“The T-A-DA method (tolerate, anticipate, don't agitate)” can be an effective management technique for older people with delirium. All unnecessary attachments are removed (IVs, catheters, NG tubes) which allows for greater mobility. Patient behavior is tolerated even if it is not considered normal as long as it does not put the patient or other people in danger. This technique requires that patients are isolated in a specific area designated for patients of old age dealing with symptoms of delirium. Patient behavior is anticipated so care givers can plan required care. Patients are treated to reduce agitation. Reducing agitation may mean that patients are not reoriented if reorientation causes agitation.

Physical restraints are occasionally used as a last resort with patients in a severe delirium. Restraint use should be avoided as it can increase agitation and risk of injury. In order to avoid the use of restraints some patients may require constant supervision.

The primary means of treating auditory hallucinations is antipsychotic medications which affect dopamine metabolism. If the primary diagnosis is a mood disorder (with psychotic features), adjunctive medications are often used (e.g., antidepressants or mood stabilizers). These medical approaches may allow the person to function normally but are not a cure as they do not eradicate the underlying thought disorder.

Psychopharmacological treatments include anti-psychotic medications. Psychology research shows that first step in treatment is for the patient to realize that the voices they hear are creation of their own mind. This realization is argued to allow patients to reclaim a measure of control over their lives. Some additional psychological interventions might allow for the process of controlling these phenomena of auditory hallucinations but more research is needed.

Treatment of any kind of complex visual hallucination requires an understanding of the different pathologies in order to correctly diagnose and treat. If a person is taking a pro-hallucinogenic medication, the first step is to stop taking it. Sometimes improvement will occur spontaneously and pharmacotherapy is not necessary. While there is not a lot of evidence of effective pharmacological treatment, antipsychotics and anticonvulsants have been used in some cases to control hallucinations. Since peduncular hallucinosis occurs due to an excess of serotonin, modern antipsychotics are used to block both dopamine and serotonin receptors, preventing the overstimulation of the lateral geniculate nucleus. The drug generically called carbamazepine increases GABA, which prevents the LGN from firing, thereby increasing the inhibition of the LGN. Regular antipsychotics as well as antidepressants can also be helpful in reducing or eliminating peduncular hallucinosis.

More invasive treatments include corrective surgery such as cataract surgery, laser photocoagulation of the retina, and use of optical correcting devices. Tumor removal can also help to relieve compression in the brain, which can decrease or eliminate peduncular hallucinosis. Some hallucinations may be due to underlying cardiovascular disease, so in these cases the appropriate treatment includes control of hypertension and diabetes. As described, the type of treatment varies widely depending on the causation behind the complex visual hallucinations.

To date, there is no successful method of treatment that "cures" musical hallucinations. There have been successful therapies in single cases that have ameliorated the hallucinations. Some of these successes include drugs such as neuroleptics, antidepressants, and certain anticonvulsive drugs. A musical hallucination was alleviated, for example, by antidepressant medications given to patients with depression. Sanchez reported that some authors have suggested that the use of hearing aids may improve musical hallucination symptoms. They believed that the external environment influences the auditory hallucinations, showing worsening of symptoms in quieter environments than in noisier ones. Oliver Sacks' patient, Mrs. O'C, reported being in an "ocean of sound" despite being in a quiet room due to a small thrombosis or infarction in her right temporal lobe. After treatment, Mrs. O'C was relinquished of her musical experience but said that, "I do miss the old songs. Now, with lots of them, I can't even recall them. It was like being given back a forgotten bit of my childhood again." Sacks also reported another elderly woman, Mrs. O'M, who had a mild case of deafness and reported hearing musical pieces. When she was treated with anticonvulsive medications, her musical hallucinations ceased but when asked if she missed them, she said "Not on your life."

Because there is no prescribed treatment, the first starting place is to reassure the CBS sufferer of their sanity, and some charities provide specialist hallucination counselling "buddies" (people who have had CBS, or have CBS and are no longer fazed by it) to talk to on the telephone. Sometimes it is carers and/or physicians that need advice and guidance.

The physician will consider on a case-by-case basis whether to treat any depression or other problems that may be related to CBS. A recent case report suggests selective serotonin reuptake inhibitors may be helpful.

The first-line psychiatric treatment for schizophrenia is antipsychotic medication, which can reduce the positive symptoms of psychosis in about 7 to 14 days. Antipsychotics, however, fail to significantly improve the negative symptoms and cognitive dysfunction. In those on antipsychotics, continued use decreases the risk of relapse. There is little evidence regarding effects from their use beyond two or three years. However use of anti-psychotics can lead to dopamine hypersensitivity increasing the risk of symptoms if antipsychotics are stopped.

The choice of which antipsychotic to use is based on benefits, risks, and costs. It is debatable whether, as a class, typical or atypical antipsychotics are better. Amisulpride, olanzapine, risperidone, and clozapine may be more effective but are associated with greater side effects. Typical antipsychotics have equal drop-out and symptom relapse rates to atypicals when used at low to moderate dosages. There is a good response in 40–50%, a partial response in 30–40%, and treatment resistance (failure of symptoms to respond satisfactorily after six weeks to two or three different antipsychotics) in 20% of people. Clozapine is an effective treatment for those who respond poorly to other drugs ("treatment-resistant" or "refractory" schizophrenia), but it has the potentially serious side effect of agranulocytosis (lowered white blood cell count) in less than 4% of people.

Most people on antipsychotics have side effects. People on typical antipsychotics tend to have a higher rate of extrapyramidal side effects, while some atypicals are associated with considerable weight gain, diabetes and risk of metabolic syndrome; this is most pronounced with olanzapine, while risperidone and quetiapine are also associated with weight gain. Risperidone has a similar rate of extrapyramidal symptoms to haloperidol. It remains unclear whether the newer antipsychotics reduce the chances of developing neuroleptic malignant syndrome or tardive dyskinesia, a rare but serious neurological disorder.

For people who are unwilling or unable to take medication regularly, long-acting depot preparations of antipsychotics may be used to achieve control. They reduce the risk of relapse to a greater degree than oral medications. When used in combination with psychosocial interventions, they may improve long-term adherence to treatment. The American Psychiatric Association suggests considering stopping antipsychotics in some people if there are no symptoms for more than a year.

There is no treatment of proven effectiveness for CBS. Some people experience CBS for anywhere from a few days up to many years, and these hallucinations can last only a few seconds or continue for most of the day. For those experiencing CBS, knowing that they are suffering from this syndrome and not a mental illness seems to be the best treatment so far, as it improves their ability to cope with the hallucinations. Most people with CBS meet their hallucinations with indifference, but they can still be disturbing because they may interfere with daily life. Interrupting vision for a short time by closing the eyes or blinking is sometimes helpful.

A number of psychosocial interventions may be useful in the treatment of schizophrenia including: family therapy, assertive community treatment, supported employment, cognitive remediation, skills training, token economic interventions, and psychosocial interventions for substance use and weight management. Family therapy or education, which addresses the whole family system of an individual, may reduce relapses and hospitalizations. Evidence for the effectiveness of cognitive-behavioral therapy (CBT) in either reducing symptoms or preventing relapse is minimal. Evidence for metacognitive training is mixed with one 2016 review finding benefit and another not. Art or drama therapy have not been well-researched.

There are symptoms that are mechanism-based that are associated with hallucinations. These include superficial pressure and stabbing pain. Others include a burning-like sensation or electric shock feeling. Human studies of these symptoms remain mostly unclear unlike similar studies in animals.

Treatment initially may include ketamine or midazolam and haloperidol injected into a muscle to sedate the person. Rapid cooling may be required in those with high body temperature. Other supportive measures such as intravenous fluids and sodium bicarbonate may be useful.

There is no agreed treatment protocol. In most reported cases of ORS the attempted treatment was antidepressants, followed by antipsychotics and various psychotherapies. Little data are available regarding the efficacy of these treatments in ORS, but some suggest that psychotherapy yields the highest rate of response to treatment, and that antidepressants are more efficacious than antipsychotics (response rates 78%, 55% and 33% respectively). According to one review, 43% of cases which showed overall improvement required more than one treatment approach, and in only 31% did the first administered treatment lead to some improvement.

Pharmacotherapies that have been used for ORS include antidepressants, (e.g. selective serotonin reuptake inhibitors, tricyclic antidepressants, monoamine oxidase inhibitors), antipsychotics, (e.g. blonanserin, lithium, chlorpromazine), and benzodiazepines. The most common treatment used for ORS is SSRIs. Specific antidepressants that have been used include clomipramine.

Psychotherapies that have been used for ORS include cognitive behavioral therapy, eye movement desensitization and reprocessing.

Palinopsia from cerebrovascular accidents generally resolves spontaneously, and treatment should be focused on the vasculopathic risk factors. Palinopsia from neoplasms, AVMs, or abscesses require treatment of the underlying condition, which usually also resolves the palinopsia. Palinopsia due to seizures generally resolves after correcting the primary disturbance and/or treating the seizures. In persistent hallucinatory palinopsia, a trial of an anti-epileptic drug can be attempted. Anti-epileptics reduce cortical excitability and could potentially treat palinopsia caused by cortical deafferentation or cortical irritation. Patients with idiopathic hallucinatory palinopsia should have close follow-up.

This antidepressant medication is a serotonin norepinephrine reuptake inhibitor (SNRI). In the case study of a 52-year-old female suffering from phantosmia for 27 years, a dose of 75 mg a day relieved and eliminated her symptoms. The drug was prescribed initially in order to treat her depression.

Another treatment option is the topical solution of cocaine HCl which also provides relief for a short time period by acting as an anesthetic and desensitizing the nasal neurons. The topical solution is applied on the nostril. This topical solution can have several side effects as it has been found that some patients suffering from troposmia started to show symptoms of phantosmia after its use. Other patients have lost complete function of the nostril where the drug was applied.

Intoxication accounts for a small percentage of musical hallucination cases. Intoxication leads to either withdrawal or inflammatory encephalopathy, which are major contributors to musical hallucinations. Some of the drugs that have been found to relate to musical hallucinations include salicylates, benzodiazepines, pentoxifylline, propranolol, clomipramine, amphetamine, quinine, imipramine, a phenothiazine, carbamazepine, marijuana, paracetamol, phenytoin, procaine, and alcohol. General anesthesia has also been association with musical hallucinations.

In a case study by Gondim et al. 2010, a seventy–seven-year-old woman with Parkinson's disease (PD) was administered amantadine after a year of various other antiparkinsonian treatments. Two days into her treatment, she started to experience musical hallucinations, which consisted of four musical pieces. The music persisted until three days after cessation of the drug. Although the patient was taking other medications at the same time, the timing of onset and offset suggested that amantadine either had a synergistic effect with the other drugs or simply caused the hallucinations. Although the case wasn't specific to intoxication, it leads to the idea that persons with PD who are treated with certain drugs can experience musical hallucinations.

Chronic hallucinatory psychosis is a psychosis subtype, classified under "Other nonorganic psychosis" by the . Other abnormal mental symptoms in the early stages are, as a rule, absent. The patient is most usually quiet and orderly, with a good memory.

It has often been a matter of the greatest difficulty to decide under which heading of the recognized classifications individual members of this group should be placed. As the hallucinations give rise to slight depression, some might possibly be included under melancholia. In others, paranoia may develop. Others, again, might be swept into the widespread net of dementia praecox. This state of affairs cannot be regarded as satisfactory, for they are not truly cases of melancholia, paranoia, dementia praecox or any other described affection.

This disease, as its name suggests, is a hallucinatory case, for it is its main feature. These may be of all senses, but auditory hallucinations are the most prominent. At the beginning, the patient may realize that the hallucination is a morbid phenomenon and unaccountable. They may claim to hear a "voice" speaking, though there is no one in the flesh actually doing so. Such a state of affairs may last for years and possibly, though rarely, for life, and the subject would not be deemed insane in the ordinary sense of the word.

It's probable, however, that this condition forms the first stage of the illness, which eventually develops on definite lines. What usually happens is the patient seeks an explanation for the hallucinations. As none is forthcoming he/she tries to account for their presence and the result is a delusion, and, most frequently, a delusion of persecution. Also, it needs to be noted that the delusion is a comparatively late arrival and is the logical result of the hallucinations.

A religious delusion is any delusion involving religious themes or subject matter. Though a small minority of psychologists have characterized all or nearly all religion as delusion, others focus solely on a denial of any spiritual cause of symptoms exhibited by a patient and look for other answers relating to a chemical imbalance in the brain, although there is actually no evidence of pathology in any psychiatric illness which means a diagnosis is made purely on opinions of professionals based on symptoms the person exhibits.

Treatment varies for micropsia due to the large number of different causes for the condition.

Treatments involving the occlusion of one eye and the use of a prism fitted over an eyeglass lens have both been shown to provide relief from micropsia.

Micropsia that is induced by macular degeneration can be treated in several ways. A study called AREDS (age-related eye disease study) determined that taking dietary supplements containing high-dose antioxidants and zinc produced significant benefits with regard to disease progression. This study was the first ever to prove that dietary supplements can alter the natural progression and complications of a disease state. Laser treatments also look promising but are still in clinical stages.

A pseudohallucination is an involuntary sensory experience vivid enough to be regarded as a hallucination, but recognised by the patient not to be the result of external stimuli. Unlike normal hallucinations, which occurs when one sees, hears, smells, tastes or feels something that is not there, with a compelling feeling or thought that it is real, pseudohallucinations are recognised by the person as unreal.

In other words, it is a hallucination that is recognized as a hallucination, as opposed to a "normal" hallucination which would be perceived as real. An example used in psychiatry is the hearing of voices which are "inside the head" according to the patient; in contrast, a hallucination would be indistinguishable to the patient from a real external stimulus, e.g. "people were talking about me".

The term is not widely used in the psychiatric and medical fields, as it is considered ambiguous; the term "nonpsychotic hallucination" is preferred. Pseudohallucinations, then, are more likely to happen with a hallucinogenic drug. But "the current understanding of pseudohallucinations is mostly based on the work of Karl Jaspers".

A further distinction is sometimes made between pseudohallucinations and "parahallucinations", the latter being a result of damage to the peripheral nervous system.

They are considered a feature of conversion disorder, somatization disorder, and dissociative disorders. Also, pseudohallucinations can occur in people with visual/hearing loss, with the typical such type being Charles Bonnet syndrome.

The most prevalent research on prescription drugs with side effects of macropsia deals with zolpidem and citalopram. Zolpidem is a drug prescribed for insomnia, and although it has proven beneficial effects, there have been numerous reported cases of adverse perceptual reactions. One of these cases discusses an anorexic woman’s episode of macropsia, which occurred twenty minutes after taking 10 mg zolpidem. The same woman later had two more episodes of zolpidem-induced macropsia, after taking 5 mg and 2.5 mg zolpidem, respective to each episode. The intensity of the macropsia episodes decreased with the decreasing amount of zolpidem administered; it is implied in the article that the level of intensity was based on the patients accounts of her macropsia episodes, and that no external diagnosis was used. Hoyler points out notable similarities among the different reported cases of zolpidem-induced disorganization. The similarities were that all the cases were reported by women, the disorganization and agitation followed the first administration of zolpidem, and once zolpidem was discontinued, there were no lasting residual effects. It is believed that zolpidem-related macropsia is more prevalent in women because plasma zolpidem concentration is 40% higher in women, a concentration that further increases in anorexic women.

Citalopram-induced macropsia is similar to zolpidem-induced macropsia since both types have been observed in relatively few cases, and neither of the drugs’ side effects can be supported by experimental evidence. Citalopram is an antidepressant that inhibits serotonin reuptake. The first case of macropsia thought to be induced by citalopram involves a woman who experienced macropsia after her first administration of 10 mg citalopram. Just as with zolpidem, after the immediate discontinuation of citalopram, there were no further episodes of macropsia.