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 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.

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.

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.

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.

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."

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.

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.

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.

Meditation-relaxation (MR) therapy is a published direct treatment for sleep paralysis. The treatment was partly derived from the neuroscientific hypothesis suggesting that attempting movement during sleep paralysis (e.g., due to panic-like reactions) can lead to neurological distortions of one's "body image", possibly triggering hallucinations of shadowy human-like figures. The therapy is based on four steps applied during sleep paralysis: (1) reappraisal of the meaning of the attack (cognitive reappraisal); which entails closing one's eyes, avoid panicking and re-appraising the meaning of the attack as benign. (2) psychological and emotional distancing (emotion regulation); the sleeper reminds him- or herself that catastrophizing the event (i.e., fear and worry) will worsen and possibly prolong it; (3) inward focused-attention meditation; focusing attention inward on an emotionally salient positive object; 4) muscle relaxation; relaxing one's muscles, avoid controlling breathing and avoid attempting to move.There are preliminary case reports supporting this treatment, although no randomized clinical trials yet to show its effectiveness.

Some of the earliest work in treating sleep paralysis was done using a culturally sensitive cognitive-behavior therapy called CA-CBT. The work focuses on psycho-education and modifying catastrophic cognitions about the sleep paralysis attack. This approach has previously been used to treat sleep paralysis in Egypt, although clinical trials are lacking.

The first published psychosocial treatment for recurrent isolated sleep paralysis was cognitive-behavior therapy for isolated sleep paralysis (CBT-ISP). CBT-ISP is manualized, has an adherence manual for research purposes, and is intended to both prevent and disrupt ISP episodes. It begins with self-monitoring of symptoms, cognitive restructuring of maladaptive thoughts relevant to ISP (e.g., "the paralysis will be permanent"), and psychoeducation about the nature of sleep paralysis. Prevention techniques include ISP-specific sleep hygiene and the preparatory use of various relaxation techniques (e.g. diaphragmatic breathing, mindfulness, progressive muscle relaxation, meditation). Episode disruption techniques are first practiced in session and then applied during actual attacks. No controlled trial of CBT-ISP has yet been conducted to prove its effectiveness.

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.

Orexin-A ( hypocretin-1) has been shown to be strongly wake-promoting in animal models, but unfortunately it does not cross the blood-brain barrier. Therefore, companies have developed orexin receptor antagonists, like suvorexant, for the treatment of insomnia. It is also likely that an orexin-A receptor agonist will be found and developed for the treatment of hypersomnia.

In a test tube model, clarithromycin (an antibiotic approved by the FDA for the treatment of infections) was found to return the function of the GABA system to normal in patients with primary hypersomnias. Investigators therefore treated a few patients with off-label clarithromycin, and most felt their symptoms improved with this treatment. In order to help further determine whether clarithromycin is truly beneficial for the treatment of narcolepsy and idiopathic hypersomnia, a small, double-blind, randomized, controlled clinical trial was completed in 2012. "In this pilot study, clarithromycin improved subjective sleepiness in GABA-related hypersomnia. Larger trials of longer duration are warranted." In 2013, a retrospective review evaluating longer-term clarithromycin use showed efficacy in a large percentage of patients with GABA-related hypersomnia. “It is important to note that the positive effect of clarithromycin is secondary to a benzodiazepine antagonist-like effect, not its antibiotic effects, and treatment must be maintained.”

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.

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.

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.

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.

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.

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.

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 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.

Future research may focus on ways to limit the occurrence of retinally-induced macropsia due to surgery. In terms of treatment, the most effective optical correction is still being researched with respect to visual field angles and direction to a target. The susceptibility of certain age demographics to macropsia is a subject that requires further validation. Overall, there have not been very many reports of macropsia induced by certain drugs, specifically zolpidem and citalopram. Once a larger effort is made to compile such reports, there will inevitably be more research on the subject of macropsia.

As of 2014, no clinical trials had been conducted to determine what treatments are safe and effective; a few case reports had been published describing treatment of small numbers of people (two to twelve per report) with clomipramine, flunarizine, nifedipine, topiramate, carbamazepine, methylphenidate. Studies suggest that education and reassurance can reduce the frequency of EHS episodes. There is some evidence that individuals with EHS rarely report episodes to medical professionals.