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.

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.

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.

The best treatment for light sensitivity is to address the underlying cause. Once the triggering factor is treated, photophobia disappears in many but not all cases.

People with photophobia will avert their eyes from direct light, such as sunlight and room lights. They may seek the shelter of a dark room. They may wear sunglasses designed to filter peripheral light and wide-brimmed sun hats.

Wearing sunglasses indoors can make symptoms worse over time as it will dark-adapt the retina which aggravates sensitivity to light. Indoor photophobia symptoms may be relieved with the use of precision tinted lenses which block the green-to-blue end of the light spectrum without blurring or impeding vision.

A paper by Stringham and Hammond, published in the "Journal of Food Science", reviews studies of effects of consuming Lutein and Zeaxanthin on visual performance, and notes a decrease in sensitivity to glare.

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.

Treatment depends on identifying behavior that triggers migraine such as stress, sleep deprivation, skipped meals, food sensitivities, or specific activities. Medicines used to treat retinal migraines include aspirin, other NSAIDS, and medicines that reduce high blood pressure.

Photophobia may also affect patients' socioeconomic status by limiting their career choices, since many workplaces require bright lights for safety or to accommodate the work being done. Sufferers may be shut out of a wide range of both skilled and unskilled jobs, such as in warehouses, offices, workshops, classrooms, supermarkets and storage spaces. Some photophobes are only able to work night shifts, which reduces their prospects for finding work.

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.

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.

The following may provide relief:

- Cold compresses

- Pad and bandage with antibiotics drops for 24 hours, heals most of the cases

- anaesthetic drops should not be used

- Oral analgesics if pain is intolerable

- Single dose of tranquilizers

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).

Individuals with quadrantanopia often modify their behavior to compensate for the disorder, such as tilting of the head to bring the affected visual field into view. Drivers with quadrantanopia, who were rated as safe to drive, drive slower, utilize more shoulder movements and, generally, corner and accelerate less drastically than typical individuals or individuals with quadrantanopia who were rated as unsafe to drive. The amount of compensatory movements and the frequency with which they are employed is believed to be dependent on the cognitive demands of the task; when the task is so difficult that the subject's spatial memory is no longer sufficient to keep track of everything, patients are more likely to employ compensatory behavior of biasing their gaze to the afflicted side. Teaching individuals with quadrantanopia compensatory behaviors could potentially be used to help train patients to re-learn to drive safely.

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

Current experimental evidence focuses on the involvement of the occipitotemporal pathway in both the perceptual equivalence of objects across translations of retinal position and also across size modifications. Recent evidence points to this pathway as a mediator for an individual's perception of size. Even further, numerous cases suggest that size perception may be dissociated from other aspects of visual perception such as color and movement. However, more research is called for to correctly relate the condition to defined physiological conditions.

Current research is being done on macular degeneration which could help prevent cases of micropsia. A variety of drugs that block vascular endothelial growth factors (VEGFs) are being evaluated as a treatment option. These treatments for the first time have produced actual improvements in vision, rather than simply delaying or arresting the continued loss of vision characteristic of macular degeneration. A number of surgical treatments are also being investigated for macular degeneration lesions that may not qualify for laser treatment, including macular translocation to a healthier area of the eye, displacement of submacular blood using gas, and removing membranes by surgery.

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.

Prisms or "field expanders" that bend light have been prescribed for decades in patients with hemianopsia. Higher power Fresnel ("stick-on") prisms are commonly employed because they are thin and light weight, and can be cut and placed in different positions on a spectacle lens.

Peripheral prism spectacles expand the visual field of patients with hemifield visual defects and have the potential to improve visual function and mobility. Prism spectacles incorporate higher power prisms, with variable shapes and designs. The Gottlieb button prism, and the Peli superior and inferior horizontal bands are some proprietary examples of prism glasses. These high power prisms "create" artificial peripheral vision into the non-blind field for obstacle avoidance and motion detection.

While surgeries do exist to correct for severe cases of floaters, there are currently no medications (including eye drops) that can correct for this vitreous deterioration. Floaters are often caused by the normal aging process and will usually disappear as the brain learns to ignore them. Looking up/down and left/right will cause the floaters to leave the direct field of vision as the vitreous humour swirls around due to the sudden movement. If floaters significantly increase in numbers and/or severely affect vision, then one of the below surgeries may be necessary.

Currently, insufficient evidence is available to compare the safety and efficacy of surgical vitrectomy with laser vitreolysis for the treatment of floaters. A 2017 Cochrane Review did not find any relevant studies that compared the two treatments.

Aggressive marketing campaigns are currently promoting the use of laser vitreolysis for the treatment of floaters. No strong evidence currently exists for the treatment of floaters with laser vitreolysis. Currently, the strongest available evidence comparing these two treatment modalities are retrospective case series.

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.

Medical treatment with anti-vertigo medications may be considered in acute, severe exacerbation of BPPV, but in most cases are not indicated. These primarily include drugs of the anti-histamine and anti-cholinergic class, such as meclizine and hyoscine butylbromide (scopolamine) respectively. The medical management of vestibular syndromes has become increasingly popular over the last decade, and numerous novel drug therapies (including existing drugs with new indications) have emerged for the treatment of vertigo/dizziness syndromes. These drugs vary considerably in their mechanisms of action, with many of them being receptor- or ion channel-specific. Among them are betahistine or dexamethasone/gentamicin for the treatment of Ménière's disease, carbamazepine/oxcarbazepine for the treatment of paroxysmal dysarthria and ataxia in multiple sclerosis, metoprolol/topiramate or valproic acid/tricyclic antidepressant for the treatment of vestibular migraine, and 4-aminopyridine for the treatment of episodic ataxia type 2 and both downbeat and upbeat nystagmus. These drug therapies offer symptomatic treatment, and do not affect the disease process or resolution rate. Medications may be used to suppress symptoms during the positioning maneuvers if the patient's symptoms are severe and intolerable. More dose-specific studies are required, however, in order to determine the most effective drug(s) for both acute symptom relief and long-term remission of the condition.

The pain may be temporarily alleviated with anaesthetic eye drops for the examination; however, they are not used for continued treatment, as anaesthesia of the eye interferes with corneal healing, and may lead to corneal ulceration and even loss of the eye. Cool, wet compresses over the eyes and artificial tears may help local symptoms when the feeling returns. Nonsteroidal anti-inflammatory drug (NSAID) eyedrops are widely used to lessen inflammation and eye pain, but have not been proven in rigorous trials. Systemic (oral) pain medication is given if discomfort is severe. Healing is usually rapid (24–72 hours) if the injury source is removed. Further injury should be avoided by isolation in a dark room, removing contact lenses, not rubbing the eyes, and wearing sunglasses until the symptoms improve.

Enzymatic vitreolysis has been trialled to treat vitreomacular traction (VMT) and anomalous posterior vitreous detachment. Whilst the mechanism of action may have an effect on clinically significant floaters, as of March 2015 there are no clinical trials being undertaken to determine whether this may be a therapeutic alternative to either i) conservative management, or ii) vitrectomy.

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.

Surgical treatments, such as a semi-circular canal occlusion, do exist for BPPV, but carry the same risk as any neurosurgical procedure. Surgery is reserved as a last resort option for severe and persistent cases which fail vestibular rehabilitation (including particle repositioning and habituation therapy).

If only small amounts of torsion are present, cyclotropia may be without symptoms entirely and may not need correction, as the visual system can compensate small degrees of torsion and still achieve binocular vision ("see also:" cyclodisparity, cyclovergence). The compensation can be a motor response (visually evoked cyclovergence) or can take place during signal processing in the brain. In patients with cyclotropia of vascular origin, the condition often improves spontaneously.

Cyclotropia cannot be corrected with prism spectacles in the way other eye position disorders are corrected. (Nonetheless two Dove prisms can be employed to rotate the visual field in experimental settings.)

For cyclodeviations above 5 degrees, surgery has normally been recommended. Depending on the symptoms, the surgical correction of cyclotropia may involve a correction of an associated vertical deviation (hyper- or hypotropia), or a Harada–Ito procedure or another procedure to rotate the eye inwards, or yet another procedure to rotate it outwards. A cyclodeviation may thus be corrected at the same time with a correction of a vertical deviation (hyper- or hypotropia); cyclodeviations without any vertical deviation can be difficult to manage surgically, as the correction of the cyclodeviation may introduce a vertical deviation.

It must be emphasized that individuals without HPPD will sometimes notice visual abnormalities. These include floaters (material floating in the eye fluid that appears as black/dark objects floating in front of the eyes and are particularly visible when looking at the bright sky or on a white wall) and the white blood cells of the retinal blood vessels (seen as tiny, fast-moving and quickly disappearing white specks). Likewise, bright lights in an otherwise dark environment may generate trails and halos. Most people don't notice these effects, because they are so used to them. A person fearful of having acquired HPPD may be much more conscious about any visual disturbance, including those that are normal. In addition, visual problems can be caused by migraines, brain infections or lesions, epilepsy, and a number of mental disorders (e.g., delirium, dementia, schizophrenia, Parkinson's disease). For an individual to be diagnosed with HPPD, these other potential causes must be ruled out.