As yet, there is no cure available for HPPD. A study presented by Dr. Henry Abraham, at the Annual Meeting of the Biological Psychiatry Society in 2012, showed that two drugs, tolcapone and levocarb that are primarily used in the treatment of Parkinson's disease improved the symptoms of HPPD in one third of the 20 test subjects who had participated in the trial. As tolcapone, and levocarb, are not approved for use in HPPD, the principal treatments that are available seek to reduce distress without treating the underlying cause. Primarily benzodiazepines including clonazepam,

diazepam and alprazolam are prescribed with a fair amount of success. The anticonvulsant drug levetiracetam has been reported to diminish some of the visual symptoms, as well as reduce depersonalization and derealization symptoms, that can occur along with HPPD. The efficacy of levetiracetam in treating HPPD has been documented in a prospective study. Another anticonvulsant, lamotrigine, has also been used to successfully treat HPPD.

Some medications have been contraindicated on the basis of their effects on HPPD or the concurrent mental issues. The atypical antipsychotic risperidone is reported to worsen symptoms of HPPD during the drug's duration in some people.

Those with HPPD are often advised to discontinue all drug use, many of which are thought to increase visuals in the short-term. There are also less concrete factors that may be generally detrimental to those with HPPD. For example, sleep deprivation and stress are thought to increase HPPD symptoms.

The probability of developing HPPD after consuming a hallucinogen is unknown. In their review article, John Halpern and Harrison Pope write that "the data does not permit us to estimate, even crudely, the prevalence of ‘strict’ HPPD." These authors noted that they had not encountered it in their evaluation of 500 Native American Church members who had taken the hallucinogenic cactus peyote on at least 100 occasions. In a presentation of preliminary results from ongoing research, Matthew Baggott and colleagues from University of California Berkeley found that HPPD-like symptoms occurred in 4.1% of participants (107 of 2,679) in a web-based survey of hallucinogen users. These people reported visual problems after drug use that were serious enough that they considered seeking professional help. This number may overestimate the prevalence of HPPD, since people with visual problems may have been more interested in completing the researchers' questionnaire. The authors reported that 16,192 people viewed the study information but did not complete the questionnaire. If all these people had used hallucinogens without developing visual problems, then the prevalence of serious visual problems in this larger group would be 0.66%. Since these people were not formally diagnosed in person (and may have had visual problems caused by other disorders), this number may provide a reasonable upper limit on the prevalence of HPPD, or they might be statistically meaningless.

It is possible the prevalence of HPPD has been underestimated by authorities because many people with visual problems relating to drug use either do not seek treatment or, when they do seek treatment, do not admit to having used illicit drugs. In the sample of Baggott, only 16 of the 107 people with possible HPPD had sought help and two of these people had been diagnosed with HPPD. Thus, it may be that HPPD occurs more often than is detected by the health care system.

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 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.

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.

Phantosmia is most likely to occur in women between the ages of 15 and 30 years. The time of the first hallucination(s) lasts from anywhere from five to twenty minutes. It has also been found that the second hallucination will occur approximately a month later in the same manner as the first. Over time, the length of the hallucination will begin to increase.

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).

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.

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.

Episodes of micropsia or macropsia occur in 9% of adolescents.

10-35% of migraine sufferers experience auras, with 88% of these patients experiencing both visual auras (which include micropsia) and neurological auras.

Micropsia seems to be slightly more common in boys than in girls among children who experience migraines.

Approximately 80% of temporal lobe seizures produce auras that may lead to micropsia or macropsia. They are a common feature of simple partial seizures and usually precede complex partial seizures of temporal lobe origin.

Central Serous Chorioretinopathy (CSCR) which can produce micropsia predominantly affects persons between the ages of 20 and 50. Women appear to be affected more than men by a factor of almost 3 to 1.

Derealization can accompany the neurological conditions of epilepsy (particularly temporal lobe epilepsy), migraine, and mild head injury. There is a similarity between visual hypo-emotionality, a reduced emotional response to viewed objects, and derealization. This suggests a disruption of the process by which perception becomes emotionally coloured. This qualitative change in the experiencing of perception may lead to reports of anything viewed being unreal or detached.

Derealization can also manifest as an indirect result of certain vestibular disorders such as labyrinthitis. This is thought to result from the experience of anxiety precipitated by the functional disparity that arises between the ability to reconcile external stimuli relative to motion and equilibrioception that are compromised by vestibular dysfunction with the internal perceptions and expectations regarding the physical environment.

An alternative explanation holds that a possible effect of vestibular dysfunction includes responses in the form of the modulation of noradrenergic and serotonergic activity due to a misattribution of vestibular symptoms to the presence of imminent physical danger resulting in the experience of anxiety or panic, which subsequently generate feelings of derealization.

Cannabis, psychedelics, dissociatives, antidepressants, caffeine, nitrous oxide, albuterol, and nicotine can all produce feelings resembling derealization, particularly when taken in excess. It can result from alcohol withdrawal or benzodiazepine withdrawal. Opiate withdrawal can also cause feelings of derealization.

Derealization can also be a symptom of severe sleep disorders and mental disorders like depersonalization disorder, borderline personality disorder, bipolar disorder, schizophrenia, dissociative identity disorder, and anxiety disorders.

Interoceptive exposure can be used as a means to induce derealization, as well as the related phenomenon depersonalization.

Derealization (sometimes abbreviated as DR) is an alteration in the perception or experience of the external world so that it seems unreal. Other symptoms include feeling as though one's environment is lacking in spontaneity, emotional colouring, and depth. It is a dissociative symptom of many conditions.

Derealization is a subjective experience of unreality of the outside world, while depersonalization is sense of unreality in one's personal self, although most authors currently do not regard derealization (surroundings) and depersonalization (self) as separate constructs.

Chronic derealization may be caused by occipital–temporal dysfunction. These symptoms are common in the population, with a lifetime prevalence of up to 5% and 31–66% at the time of a traumatic event.

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.

Before delirium treatment, the cause must be established. Medication such as antipsychotics or benzodiazepines can help reduce the symptoms for some cases. For alcohol or malnourished cases, vitamin B supplements are recommended and for extreme cases, life-support can be used.

Neither antidepressants nor antipsychotics have been found to be useful, Additionally antipsychotics can worsen symptoms of depersonalisation. To date, no clinical trials have studied the effectiveness of benzodiazepines. Tentative evidence supports naloxone and naltrexone.

A combination of an SSRI and a benzodiazepine has been proposed to be useful for DPD patients with anxiety.

Modafinil used alone has been reported to be effective in a subgroup of individuals with depersonalization disorder (those who have attentional impairments, under-arousal and hypersomnia). However, clinical trials have not been conducted.

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.

The frequency of phantosmia is rare in comparison with the frequency of parosmia. Parosmia has been estimated to be in 10-60% of patients with olfactory dysfunction and from studies, it has been shown that it can last anywhere from 3 months to 22 years. Smell and taste problems result in over 200,000 visits to physicians annually in the US. Lately, it has been thought that phantosmia might co-occur with Parkinson's disease. However, its potential to be a premotor biomarker for Parkinson's is still up for debate as not all patients with Parkinson's disease have olfactory disorders

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.

Hyperreligiosity may be associated with epilepsy — in particular temporal lobe epilepsy involving complex partial seizures — mania, frontotemporal lobar degeneration, Anti-NMDA receptor encephalitis, hallucinogen related psychsis and psychotic disorder. In persons with epilepsy episodic hyperreligosity may occur ictally or postictally, but is usually a chronic personality feature that occurs interictally. Hyperrelgiosity was associated in one small study with decreased right hippocampal volume. The medial prefrontal cortex may play a role in controlling religiousness, and dysfunction may lead to hyperreligiosity. Increased activity in the left temporal regions of hyperreligiosity in psychotic disorders. Pharmacological evidence points towards dysfunction in the ventral dopaminergic pathway.

Hyperreligiosity is characterized by an increased tendency to report spiritual, religious or mystical experiences, religious delusions, rigid legalistic thoughts, and extravagant expression of religiosity. Hyperreligiosity may also include religious hallucinations.

Even though dysosmia often goes away on its own over time, there are both medical and surgical treatments for dysosmia for patients that want immediate relief. Medical treatments include the use of topical nasal drops and oxymetazoline HCL, which give an upper nasal block so that the air flow can't reach the olfactory cleft. Other medications suggested include sedatives, anti-depressants, and anti-epileptic drugs. The medications may or may not work and for some patients, the side effects may not be tolerable. Most patients benefit from medical treatment but for some surgical treatment is required. Options include a bifrontal craniotomy and an excision of the olfactory epithelium, which cuts all of the fila olfactoria. According to some studies, transnasal endoscopic excision of the olfactory epithelium has been described as a safe and effective phantosmia treatment. The bifrontal craniotomy results in permanent anosmia and both surgeries are accompanied with the risks associated with general surgery.

There is no cure for neurocognitive disorder or the diseases that cause it. Antidepressants, antipsychotics, and other medications that treat memory loss and behavioral symptoms are available and may help to treat the diseases. Ongoing psychotherapy and psychosocial support for patients and families are usually necessary for clear understanding and proper management of the disorder and to maintain a better quality of life for everyone involved. Speech therapy has been shown to help with language impairment.

Studies suggest that diets with high Omega 3 content, low in saturated fats and sugars, along with regular exercise can increase the level of brain plasticity. Other studies have shown that mental exercise such a newly developed “computerized brain training programs” can also help build and maintain targeted specific areas of the brain. These studies have been very successful for those diagnosed with schizophrenia and can improve fluid intelligence, the ability to adapt and deal with new problems or challenges the first time encountered, and in young people, it can still be effective in later life.

A person with amnesia may slowly be able to recall their memories or work with an occupational therapist to learn new information to replace what was lost, or to use intact memories as a basis for taking in new information. If it is caused by an underlying cause such as Alzheimer's disease or infections, the cause may be treated but the amnesia may not be.

Some neuro-ophthalmologists believe that visual snow is not a medical condition, but a poorly understood symptom. People report seeing "snow", much like the visual noise on a TV screen after transmission ends. These authors hypothesize that what the patients see as "snow" is their own intrinsic visual noise.

Many report more visual snow in low light conditions. This has a natural explanation. "The intrinsic dark noise of primate cones is equivalent to ~4000 absorbed photons per second at mean light levels below this the cone signals are dominated by intrinsic noise".

In addition to visual snow, many of those affected have other types of visual disturbances such as starbursts, increased afterimages, floaters, trails, and many others.

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