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 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.

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.

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.

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.

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.