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.

One study from as early as 1895 reported that approximately 10% of the population experiences hallucinations. A 1996-1999 survey of over 13,000 people reported a much higher figure, with almost 39% of people reporting hallucinatory experiences, 27% of which daytime hallucinations, mostly outside the context of illness or drug use. From this survey, olfactory (smell) and gustatory (taste) hallucinations seem the most common in the general population.

There is substantial evidence that delirium results in long-term poor outcomes in older persons admitted to hospital. This systematic review only included studies that looked for an independent effect of delirium (i.e., after accounting for other associations with poor outcomes, for example co-morbidity or illness severity).

In older persons admitted to hospital, individuals experiencing delirium are twice as likely to die than those who do not (meta-analysis of 12 studies). In the only prospective study conducted in the general population, older persons reporting delirium also showed higher mortality (60% increase).

Institutionalisation was also twice as likely after an admission with delirium (meta-analysis of 7 studies). In a community-based population examining individuals after an episode of severe infection (though not specifically delirium), these persons acquired more functional limitations (i.e. required more assistance with their care needs) than those not experiencing infection. After an episode of delirium in the general population, functional dependence increased threefold.

The association between delirium and dementia is complex. The systematic review estimated a 13-fold increase in dementia after delirium (meta-analysis of 2 studies). However, it is difficult to be certain that this is accurate because the population admitted to hospital includes persons with undiagnosed dementia (i.e. the dementia was present before the delirium, rather than caused by it). In prospective studies, people hospitalised from any cause appear to be at greater risk of dementia and faster trajectories of cognitive decline, but these studies did not specifically look at delirium. In the only population-based prospective study of delirium, older persons had an eight-fold increase in dementia and faster cognitive decline. The same association is also evident in persons already diagnosed with Alzheimer’s dementia.

Multiple guidelines recommend that delirium should be diagnosed when it presents to healthcare services. Much evidence suggest, however, that delirium is greatly underdiagnosed. Higher rates of detection of delirium in general settings (for the ICU see below) can be assisted by the use of validated delirium screening tools. Many such tools have been published. They differ in duration, complexity, need for training, and so on. Examples of tools in use in clinical practice are: Delirium Observation Screening Scale, the Nursing Delirium Screening Scale (Nu-DESC), the Confusion Assessment Method, the Recognizing Acute Delirium As part of your Routine (RADAR) tool and the 4 "A"s Test or 4AT.

Palinopsia necessitates a full ophthalmologic and neurologic history and physical exam. Hallucinatory palinopsia warrants automated visual field testing and neuroimaging since the majority of hallucinatory palinopsia is caused by posterior cortical lesions and seizures. It is generally easy to diagnose the underlying cause of hallucinatory palinopsia. The medical history typically includes concerning symptoms, and neuroimaging usually reveals cortical lesions. In patients with hallucinatory palinopsia and unremarkable neuroimaging, blood tests or clinical history often hints at the cause. The practitioner should be considering visual seizures in these cases.

Tactile hallucination is the false perception of tactile sensory input that creates a hallucinatory sensation of physical contact with an imaginary object. It is caused by the faulty integration of the tactile sensory neural signals generated in the spinal cord and the thalamus and sent to the primary somatosensory cortex (SI) and secondary somatosensory cortex (SII). Tactile hallucinations are recurrent symptoms of neurological diseases such as schizophrenia, Parkinson's disease, Ekbom's syndrome and delerium tremens. Patients who experience phantom limb pains also experience a type of tactile hallucination. Tactile hallucinations are also caused by drugs such as cocaine and alcohol.

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.

Whatever the cause, the bodily related distortions can recur several times a day and may take some time to abate. Understandably, the person can become alarmed, frightened, and panic-stricken throughout the course of the hallucinations—maybe even hurt themselves or others around them. The symptoms of the syndrome themselves are not harmful and are likely to disappear with time.

Musical hallucinations fall under the category of auditory hallucinations and describe a disorder in which a sound is perceived as instrumental music, sounds, or songs. It is a very rare disorder, reporting only 0.16% in a cohort study of 3,678 individuals.

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.

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.

In 73 individual cases reviewed by Evers and Ellger, 57 patients heard tunes that were familiar, while 5 heard unfamiliar tunes. These tunes ranged from religious pieces to childhood favorites, and also included popular songs from the radio. Vocal and instrumental forms of classical music were also identified in some patients. Keshavan found that the consistent feature of musical hallucinations was that it represented a personal memory trace. Memory traces refer to anything that may seem familiar to the patient, which indicated why certain childhood or familiar songs were heard.

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.

Peduncular hallucinosis (PH), or Lhermitte's peduncular hallucinosis, is a rare neurological disorder that causes vivid visual hallucinations that typically occur in dark environments, and last for several minutes. Unlike some other kinds of hallucinations, the hallucinations that patients with PH experience are very realistic, and often involve people and environments that are familiar to the affected individuals. Because the content of the hallucinations is never exceptionally bizarre, patients can rarely distinguish between the hallucinations and reality.

In 1922, the French neurologist Jean Lhermitte documented the case of a patient who was experiencing visual hallucinations that were suggestive of localized damage to the midbrain and pons. After other similar case studies were published, this syndrome was labeled "peduncular hallucinosis."

The accumulation of additional cases by Lhermitte and by others influenced academic medical debate about hallucinations and about behavioral neurology.

Lhermitte provided a full account of his work in this area in his book "Les hallucinations: clinique et physiopathologie," which was published in Paris in 1951 by Doin publishing.

Contemporary researchers, with access to new technologies in medical brain imaging, have confirmed the brain localization of these unusual hallucinations.

Psychosis is first and foremost a diagnosis of exclusion. So a new-onset episode of psychosis "cannot" be considered a symptom of a psychiatric disorder until other relevant and known causes of psychosis are properly excluded, or ruled out. Many clinicians improperly perform, or entirely miss this step, introducing avoidable diagnostic error and misdiagnosis.

An initial assessment includes a comprehensive history and physical examination by a physician, psychiatrist, psychiatric nurse practitioner or psychiatric physician assistant. Biological tests should be performed to exclude psychosis associated with or caused by substance use, medication, toxins, surgical complications, or other medical illnesses.

Delirium should be ruled out, which can be distinguished by visual hallucinations, acute onset and fluctuating level of consciousness, indicating other underlying factors, including medical illnesses. Excluding medical illnesses associated with psychosis is performed by using blood tests to measure:

- Thyroid-stimulating hormone to exclude hypo- or hyperthyroidism,

- Basic electrolytes and serum calcium to rule out a metabolic disturbance,

- Full blood count including ESR to rule out a systemic infection or chronic disease, and

- Serology to exclude syphilis or HIV infection.

Other investigations include:

- EEG to exclude epilepsy, and an

- MRI or CT scan of the head to exclude brain lesions.

Because psychosis may be precipitated or exacerbated by common classes of medications, medication-induced psychosis should be ruled out, particularly for first-episode psychosis. Both substance- and medication-induced psychosis can be excluded to a high level of certainty, using a

- Urinalysis and a

- Full serum toxicology screening.

Because some dietary supplements may also induce psychosis or mania, but cannot be ruled out with laboratory tests, a psychotic individual's family, partner, or friends should be asked whether the patient is currently taking any dietary supplements.

Common mistakes made when diagnosing people who are psychotic include:

- Not properly excluding delirium,

- Not appreciating medical abnormalities (e.g., vital signs),

- Not obtaining a medical history and family history,

- Indiscriminate screening without an organizing framework,

- Missing a toxic psychosis by not screening for substances "and" medications

- Not asking family or others about dietary supplements,

- Premature diagnostic closure, and

- Not revisiting or questioning the initial diagnostic impression of primary psychiatric disorder.

Only after relevant and known causes of psychosis are excluded, a mental health clinician may make a psychiatric differential diagnosis using a person's family history, incorporating information from the person with psychosis, and information from family, friends, or significant others.

Types of psychosis in psychiatric disorders may be established by formal rating scales. The Brief Psychiatric Rating Scale (BPRS) assesses the level of 18 symptom constructs of psychosis such as hostility, suspicion, hallucination, and grandiosity. It is based on the clinician's interview with the patient and observations of the patient's behavior over the previous 2–3 days. The patient's family can also answer questions on the behavior report. During the initial assessment and the follow-up, both positive and negative symptoms of psychosis can be assessed using the 30 item Positive and Negative Symptom Scale (PANSS).

Research needs to be performed on the efficacy of the various pharmaceuticals for treating illusory palinopsia. It is unclear if the symptoms' natural history and treatment are influenced by the cause. It is also not clear if there is treatment efficacy overlap for illusory palinopsia and the other co-existing diffuse persistent illusory phenomenon such as visual snow, oscillopsia, dysmetropsia, and halos.

Future advancements in fMRI could potentially further our understanding of hallucinatory palinopsia and visual memory. Increased accuracy in fMRI might also allow for the observation of subtle metabolic or perfusional changes in illusory palinopsia, without the use of ionizing radiation present in CT scans and radioactive isotopes. Studying the psychophysics of light and motion perception could advance our understanding of illusory palinopsia, and vice versa. For example, incorporating patients with visual trailing into motion perception studies could advance our understanding of the mechanisms of visual stability and motion suppression during eye movements (e.g. saccadic suppression).

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.

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.

EEG testing can diagnose patients with medial temporal lobe epilepsy. Epileptiform abnormalities including spikes and sharp waves in the medial temporal lobe of the brain can diagnose this condition, which can in turn be the cause of an epileptic patient's micropsia.

The Amsler grid test can be used to diagnose macular degeneration. For this test, patients are asked to look at a grid, and distortions or blank spots in the patient's central field of vision can be detected. A positive diagnosis of macular degeneration may account for a patient's micropsia.

A controlled size comparison task can be employed to evaluate objectively whether a person is experiencing hemimicropsia. For each trial, a pair of horizontally aligned circles is presented on a computer screen, and the person being tested is asked to decide which circle is larger. After a set of trials, the overall pattern of responses should display a normal distance effect where the more similar the two circles, the higher the number of errors. This test is able to effectively diagnose micropsia and confirm which hemisphere is being distorted.

Due to the large range of causes that lead to micropsia, diagnosis varies among cases. Computed tomography (CT) and magnetic resonance imaging (MRI) may find lesions and hypodense areas in the temporal and occipital lobes. MRI and CT techniques are able to rule out lesions as the cause for micropsia, but are not sufficient to diagnose the most common causes.

During ancient Greek times, touch was considered to be an unrefined perceptual system because it differed from the other senses on the basis of the distance and timing of perception of the stimulus. Unlike vision and audition, one perceives touch simultaneously with the medium and the stimulus is always proximal and not distal. By 17th century, the British empiricist John Locke attributed the word “feeling” with two types of sensation. Weber distinctly identified these two types of sensation as the sense of touch and common bodily sensibility. This distinction further helped 19th century psychiatrists to distinguish between tactile hallucinations and cenesthopathy. During the 19th century, tactile hallucinations were classified as symptoms associated with insanity, organic and toxic syndromes and delusional parasitosis yet there was no identification on how such hallucinations were caused. Currently, neuroscientists such Dr. Oliver Sacks and Dr. V.S. Ramachandran have analyzed and attributed tactile hallucinations as a dysfunctional perception of the brain as opposed just a symptom related to insanity. They have contributed significantly to propose tactile hallucinations as the false perception of tactile sensory input creating a sensation of touch with an imaginary object.

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 challenging task for the examiner is to determine and obtain the correct symptoms and associate them with one of the olfactory disorders, as there are several of them and they are related to each other.

The first step the examiner usually takes is to investigate if the problem is olfactory or gustatory related. As it may be that the patient releases certain bodily odors that are causing them to have this perception.

If the examiner is able to confirm that the problem is olfactory related, the next step is to determine which olfactory disorder the patient suffers from. The following is a list of possible olfactory disorders:

- anosmia

- dysosmia

- hyperosmia

- hyposmia

- parosmia or troposmia

- phantosmia

The second step is very difficult for both the examiner and the patient as the patient has some difficulty describing their perception of the phantom odor. Furthermore, the patient is in a position of stress and anxiety thus it is crucial that the examiner be patient.

After determining the nature of the disorder, and confirming phantosmia, the examiner must then have the patient describe their perception of the phantom odor. In many cases, patients have described the odor to be that of something burning and rotten and have described it to be unpleasant and foul.

The third step for the examiner is to determine the health history of the patient to take note of head trauma, accidents, upper respiratory infections, allergic rhinitis or chronic rhinitis. Although these may be events that have resulted in the phantom odor, studies conducted by Zilstrof have found that the majority of phantosmia patients have no previous history of head trauma and upper respiratory infections.

Alice in Wonderland syndrome is a disturbance of perception rather than a specific physiological change to the body's systems. The diagnosis can be presumed when other causes have been ruled out and if the patient presents symptoms along with migraines and complains of onset during the day (although it can also occur at night).

Another symptom of Alice in Wonderland syndrome is sound distortion, such as every little movement making a clattering sound.

There have not been sufficient studies conducted to make conclusive statements about prevalence nor who tends to suffer EHS. One study found that 13.5% of a sample of undergrads reported at least one episode over the course of their lives, with higher rates in those also suffering from sleep paralysis.

The most important factor in diagnosing a patient with vertiginous epilepsy is the subject’s detailed description of the episode. However, due to the associated symptoms of the syndrome a subject may have difficulty remembering the specifics of the experience. This makes it difficult for a physician to confirm the diagnosis with absolute certainty. A questionnaire may be used to help patients, especially children, describe their symptoms. Clinicians may also consult family members for assistance in diagnosis, relying on their observations to help understand the episodes. In addition to the description of the event, neurological, physical and hematologic examinations are completed to assist in diagnosis. For proper diagnosis, an otological exam (examination of the ear) should also be completed to rule out disorders of the inner ear, which could also be responsible for manifestations of vertigo. This may include an audiological assessment and vestibular function test. During diagnosis, history-taking is essential in determining possible causes of vertiginous epilepsy as well as tracking the progress of the disorder over time.

Other means used in diagnosis of vertiginous epilepsy include:

- Electroencephalography (EEG)

- Magnetic resonance imaging (MRI)

- Positron emission tomography (PET)

- Neuropsychological testing

The EEG measures electrical activity in the brain, allowing a physician to identify any unusual patterns. While EEGs are good for identifying abnormal brain activity is it not helpful in localizing where the seizure originates because they spread so quickly across the brain. MRIs are used to look for masses or lesions in the temporal lobe of the brain, indicating possible tumors or cancer as the cause of the seizures. When using a PET scan, a physician is looking to detect abnormal blood flow and glucose metabolism in the brain, which is visible between seizures, to indicate the region of origin.