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.

There is limited data on treating the visual disturbances associated with HPPD, persistent visual aura, or post-head trauma visual disturbances, and pharmaceutical treatment is empirically-based. It is not clear if the etiology or type of illusory symptom influences treatment efficacy. Since the symptoms are usually benign, treatment is based on the patient’s zeal and willingness to try many different drugs. There are cases which report successful treatment with clonidine, clonazepam, lamotrigine, nimodipine, topiramate, verapamil, divalproex sodium, gabapentin, furosemide, and acetazolamide, as these drugs have mechanisms that decrease neuronal excitability. However, other patients report treatment failure from the same drugs. Based on the available evidence and side-effect profile, clonidine might be an attractive treatment option. Many patients report improvement from sunglasses. FL-41 tinted lenses may provide additional relief, as they have shown some efficacy in providing relief to visually-sensitive migraineurs.

Given the unknown nature of MES, treatments have been largely dependent on an individual basis. Treatments can vary from being as little as self-reassurance to pharmaceutical medications.

Medications can be helpful, such as antipsychotics, benzodiazepines or antiepileptics, but there is very limited evidence for this. Some case studies have found that switching to a prednisolone steroid after a betamethasone steroid which caused MES helped alleviate hallucinations or the use of the acetylcholinesterase inhibitor, Donepezil, have also found that it successfully treated an individual's MES. However, because of the heterogeneous etiology, these methods cannot be applied as general treatment.

Other than treatment by medicinal means, individuals have also successfully alleviated musical hallucinations by cochlear implants, listening to different songs via an external source, or by attempting to block them through mental effort, depending on how severe their condition is.

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).

There is no established treatment for visual snow. It is difficult to resolve visual snow with treatment, but it is possible to reduce symptoms and improve quality of life through treatment.

Medications that may be used include lamotrigine, acetazolamide, or verapamil. But these do not always result in benefits.

Since this condition is usually coupled with other neurological disorders or deficits, there is no known cure for cerebral polyopia. However, measures can be taken to reduce the effects of associated disorders, which have proven to reduce the effects of polyopia. In a case of occipital lobe epilepsy, the patient experienced polyopia. Following administration of valproate sodium to reduce headaches, the patient’s polyopia was reduced to palinopsia. Further, after administering the anticonvulsant drug Gabapentin in addition to valproate sodium, the effects of palinopsia were decreased, as visual perseveration is suppressed by this anticonvulsant drug. Thus, in cases of epilepsy, anticonvulsant drugs may prove to reduce the effects of polyopia and palinopsia, a topic of which should be further studied.

In other cases of polyopia, it is necessary to determine all other present visual disturbances before attempting treatment. Neurological imaging can be performed to determine if there are present occipital or temporal lobe infarctions that may be causing the polyopia. CT scans are relatively insensitive to the presence of cerebral lesions, so other neurological imaging such as PET and MRI may be performed. The presence of seizures and epilepsy may also be assessed through EEG. In addition, motor visual function should be assessed through examination of pupillary reactions, ocular motility, optokinetic nystagmus, slit-lamp examination, visual field examination, visual acuity, stereo vision, bimicroscopic examination, and funduscopic examination. Once the performance of such functions have been assessed, a plan for treatment can follow accordingly. Further research should be conducted to determine if the treatment of associated neurological disturbances can reduce the effects of polyopia.

Inconspicuous akinetopsia can be triggered by high doses of certain antidepressants with vision returning to normal once the dosage is reduced.

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.

Inconspicuous akinetopsia can be selectively and temporarily induced using transcranial magnetic stimulation (TMS) of area V5 of the visual cortex in healthy subjects. It is performed on a 1 cm² surface of the head, corresponding in position to area V5. With an 800-microsecond TMS pulse and a 28 ms stimulus at 11 degrees per second, V5 is incapacitated for about 20–30 ms. It is effective between −20 ms and +10 ms before and after onset of a moving visual stimulus. Inactivating V1 with TMS could induce some degree of akinetopsia 60–70 ms after the onset of the visual stimulus. TMS of V1 is not nearly as effective in inducing akinetopsia as TMS of V5.

Hallucinatory palinopsia (Greek: "palin" for "again" and "opsia" for "seeing") is a subtype of palinopsia, a visual disturbance defined as the persistent or recurrence of a visual image after the stimulus has been removed. Palinopsia is a broad term describing a heterogeneous group of symptoms which is divided into hallucinatory palinopsia and illusory palinopsia. Hallucinatory palinopsia refers to the projection of an already-encoded visual memory and is similar to a complex visual hallucination: the creation of a formed visual image where none exists.

Hallucinatory palinopsia usually arises from posterior cortical lesions or seizures and can be the presenting symptom of a serious neurological disease. Hallucinatory palinopsia describes afterimages or scenes that are formed, long-lasting, high resolution, and isochromatic. The palinoptic images are not typically reliant on environmental parameters and often present with homonymous visual field deficits. Hallucinatory palinopsia occurs unpredictably and the persistent images can appear anywhere in the visual field, regardless of the location of the original stimulus. A patient will often have only a few episodes of hallucinatory palinopsia. Visual perseveration is synonymous with palinopsia.

Illusory palinopsia (Greek: "palin" for "again" and "opsia" for "seeing") is a subtype of palinopsia, a visual disturbance defined as the persistence or recurrence of a visual image after the stimulus has been removed. Palinopsia is a broad term describing a heterogeneous group of symptoms, which is divided into hallucinatory palinopsia and illusory palinopsia. Illusory palinopsia is likely due to sustained awareness of a stimulus and is similar to a visual illusion: the distorted perception of a real external stimulus.

Illusory palinopsia is caused by migraines, hallucinogen persisting perception disorder (HPPD), prescription drugs, and head trauma, but is also sometimes idiopathic. Illusory palinopsia consists of afterimages that are short-lived or unformed, occur at the same location in the visual field as the original stimulus, and are often exposed or exacerbated based on environmental parameters such as stimulus intensity, background contrast, fixation, and movement. Illusory palinopsia symptoms occur continuously or predictably, based on environmental conditions.

Palinopsia (Greek: "palin" for "again" and "opsia" for "seeing") is the persistent recurrence of a visual image after the stimulus has been removed. Palinopsia is not a diagnosis, it is a diverse group of pathological visual symptoms with a wide variety of causes. Visual perseveration is synonymous with palinopsia.

In 2014, Gersztenkorn and Lee comprehensively reviewed all cases of palinopsia in the literature and subdivided it into two clinically relevant groups: illusory palinopsia and hallucinatory palinopsia. Hallucinatory palinopsia, usually due to seizures or posterior cortical lesions, describes afterimages that are formed, long-lasting, and high resolution. Illusory palinopsia, usually due to migraines, head trauma, prescription drugs, or hallucinogen persisting perception disorder (HPPD), describes afterimages that are affected by ambient light and motion and are unformed, indistinct, or low resolution.

Oneirophrenic patients are resistant to insulin and when injected with glucose, these patients take 30 to 50% longer to return to normal glycemia. The meaning of this finding is not known, but it has been hypothesized that it may be due to an insulin antagonist present in the blood during psychosis. However, There is currently no known treatment for oneiophrenia.

In most of the reported cases, the treatment options were very similar. Plasmapheresis alone or in combination with steroids, sometimes also with thymectomy and azathioprine, have been the most frequently used therapeutic approach in treating Morvan’s Syndrome. However, this does not always work, as failed response to steroids and to subsequently added plasmapheresis have been reported. Intravenous immunoglobulin was effective in one case.

In one case, the dramatic response to high-dose oral prednisolone together with pulse methylprednisolone with almost complete disappearance of the symptoms within a short period should induce consideration of corticosteroids.

In another case, the subject was treated with haloperidol (6 mg/day) with some improvement in the psychomotor agitation and hallucinations, but even high doses of carbamazepine given to the subject failed to improve the spontaneous muscle activity. Plasma Exchange (PE) was initiated, and after the third such session, the itching, sweating, mental disturbances, and complex nocturnal behavior improved and these symptoms completely disappeared after the sixth session, with improvement in insomnia and reduced muscle twitching. However, one month after the sixth PE session, there was a progressive worsening of insomnia and diurnal drowsiness, which promptly disappeared after another two PE sessions.

In one case there high dose steroid treatment resulted in a transient improvement, but aggressive immuno-suppressive therapy with cyclophosphamide was necessary to control the disease and result in a dramatic clinical improvement.

In another case, the subject was treated with prednisolone (1 mg/kg body weight) with carbamazepine, propanolol, and amitriptyline. After two weeks, improvement with decreased stiffness and spontaneous muscle activity and improved sleep was observed. After another 7–10 days, the abnormal sleep behavior disappeared completely.

In another case, symptomatic improvement with plasmapheresis, thymectomy, and chronic immunosuppression provide further support for an autoimmune or paraneoplastic basis.

Although thymectomy is believed to be a key element in the proposed treatment, there is a reported case of Morvan’s Syndrome presenting itself post-thymectomy.

Musical ear syndrome (MES) describes a condition seen in people who have hearing loss and subsequently develop auditory hallucinations. "MES" has also been associated with musical hallucinations, which is a complex form of auditory hallucinations where an individual may experience music or sounds that are heard without an external source. It is comparable to Charles Bonnet syndrome (visual hallucinations in visually impaired people) and some have suggested this phenomenon could be included under this diagnosis.

Cerebral diplopia or polyopia describes seeing two or more images arranged in ordered rows, columns, or diagonals after fixation on a stimulus. The polyopic images occur monocular bilaterally (one eye open on both sides) and binocularly (both eyes open), differentiating it from ocular diplopia or polyopia. The number of duplicated images can range from one to hundreds. Some patients report difficulty in distinguishing the replicated images from the real images, while others report that the false images differ in size, intensity, or color. Cerebral polyopia is sometimes confused with palinopsia (visual trailing), in which multiple images appear while watching an object. However, in cerebral polyopia, the duplicated images are of a stationary object which are perceived even after the object is removed from the visual field. Movement of the original object causes all of the duplicated images to move, or the polyopic images disappear during motion. In palinoptic polyopia, movement causes each polyopic image to leave an image in its wake, creating hundreds of persistent images (entomopia).

Infarctions, tumors, multiple sclerosis, trauma, encephalitis, migraines, and seizures have been reported to cause cerebral polyopia. Cerebral polyopia has been reported in extrastriate visual cortex lesions, which is important for detecting motion, orientation, and direction. Cerebral polyopia often occurs in homonymous field deficits, suggesting deafferentation hyperexcitability could be a possible mechanism, similar to visual release hallucinations (Charles Bonnet syndrome).

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.

Current methods in treating early-onset schizophrenia follow a similar approach to the treatment of adult schizophrenia. Although modes of treatment in this population is largely understudied, the use of antipsychotic medication is commonly the first line of treatment in addressing symptoms. Recent literature has failed to determine if typical or atypical antipsychotics are most effective in reducing symptoms and improving outcomes. When weighing treatment options, it is necessary to consider the adverse effects of various medications used to treat schizophrenia and the potential implications of these effects on development. A 2013 systematic review compared the efficacy of atypical antipsychotics versus typical antipsychotics for adolescents:

Madaan et al. wrote that studies report efficacy of typical neuroleptics such as thioridazine, thiothixene, loxapine and haloperidol, high incidence of side effects such as extrapyramidal symptoms, akathisia, dystonias, sedation, elevated prolactin, tardive dyskinesia.

Visual snow, also known as visual static, is a proposed condition in which people see white or black dots in parts or the whole of their visual fields. The problem is typically always present and can last years. The severity of the "snow" differs; and it has been suggested that in some the condition may affect daily life, making it difficult to read, drive, or see in detail. The use of computer screens can exacerbate symptoms.

The cause is unclear. Typically it occurs in people with migraines. The underlying mechanism is believed to involve excessive excitability of neurons within the cortex of the brain. It is commonly confused with floaters, leading to misdiagnosis as well as underdiagnosis.

Medications that may be used include lamotrigine, acetazolamide, or verapamil. But these do not always result in benefits.

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.

Focal seizures (also called partial seizures and localized seizures) are seizures which affect initially only one hemisphere of the brain. The brain is divided into two hemispheres, each consisting of four lobes – the frontal, temporal, parietal and occipital lobes. A focal seizure is generated in and affects just one part of the brain – a whole hemisphere or part of a lobe. Symptoms will vary according to where the seizure occurs. In the frontal lobe symptoms may include a wave-like sensation in the head; in the temporal lobe, a feeling of déjà vu; in the parietal lobe, a numbness or tingling; and in the occipital lobe, visual disturbance or hallucination.

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.

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.

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.