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.

The appropriate treatment for binocular diplopia will depend upon the cause of the condition producing the symptoms. Efforts must first be made to identify and treat the underlying cause of the problem. Treatment options include eye exercises, wearing an eye patch on alternative eyes, prism correction, and in more extreme situations, surgery or botulinum toxin.

If diplopia turns out to be intractable, it can be managed as last resort by obscuring part of the patient's field of view. This approach is outlined in the article on diplopia occurring in association with a condition called "horror fusionis".

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).

Dry eye is a major symptom that is targeted in the therapy of CVS. The use of over-the-counter artificial-tear solutions can reduce the effects of dry eye in CVS.

Asthenopic symptoms in the eye are responsible for much of the severity in CVS. Proper rest to the eye and its muscles is recommended to relieve the associated eye strain. Various catch-phrases have been used to spread awareness about giving rest to the eyes while working on computers. A routinely recommended approach is to consciously blink the eyes every now and then (this helps replenish the tear film) and to look out the window to a distant object or to the sky—doing so provides rest to the ciliary muscles. One of the catch phrases is the "20 20 20 rule": every 20 mins, focus the eyes on an object 20 feet (6 meters) away for 20 seconds. This basically gives a convenient distance and timeframe for a person to follow the advice from the optometrist and ophthalmologist. Otherwise, the patient is advised to close his/her eyes (which has a similar effect) for 20 seconds, at least every half-hour.

Decreased focusing capability is mitigated by wearing a small plus-powered (+1.00 to +1.50) over-the-counter pair of eyeglasses. Wearing these eyeglasses helps such patients regain their ability to focus on near objects. People who are engaged in other occupations—such as tailors engaged in embroidery—can experience similar symptoms and can be helped by these glasses.

A Pacific University research study of 36 participants found significant differences in irritation or burning of the eyes, tearing, or watery eyes, dry eyes, and tired eyes, that were each improved by filtering lenses versus placebo lenses, but in a follow-up study in 2008, the same team was not able to reproduce the results of the first study.

Competing research has shown blue light-filtering lenses decrease specific aspects of light emissions. Theoretical reductions in phototoxicity were 10.6% to 23.6%. Additionally, melatonin suppression was reduced by 5.8% to 15.0% and scotpic sensitivity by 2.4% to 9.6%. Over 70% of the participants in this testing were unable to detect these changes. The expansion of technology has led to more individuals utilizing computers and televisions which increase the overall exposure to blue light. This has opened up opportunities for companies such as Gunnar Optiks and Razer Inc. to create glasses focused on reducing the exposure to blue light.

Temporary binocular diplopia can be caused by alcohol intoxication or head injuries, such as concussion (if temporary double vision does not resolve quickly, one should see an optometrist or ophthalmologist immediately). It can also be a side effect of benzodiazepines or opioids, particularly if used in larger doses for recreation, the anti-epileptic drugs Phenytoin and Zonisamide, and the anti-convulsant drug Lamotrigine, as well as the hypnotic drug Zolpidem and the dissociative drugs Ketamine and Dextromethorphan. Temporary diplopia can also be caused by tired and/or strained eye muscles or voluntarily. If diplopia appears with other symptoms such as fatigue and acute or chronic pain, the patient should see an ophthalmologist immediately.

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.

Hemianopsia or hemianopia is a visual field loss on the left or right side of the vertical midline. It can affect one eye but usually affects both eyes. Homonymous hemianopsia, or homonymous hemianopia, is hemianopic visual field loss on the same side of both eyes. Homonymous hemianopsia occurs because the right half of the brain has visual pathways for the left hemifield of both eyes, and the left half of the brain has visual pathways for the right hemifield of both eyes. When one of these pathways is damaged, the corresponding visual field is lost.

Cerebral achromatopsia is a type of color-blindness caused by damage to the cerebral cortex of the brain, rather than abnormalities in the cells of the eye's retina. It is often confused with congenital achromatopsia but underlying physiological deficits of the disorders are completely distinct.

Several other corneal ectatic disorders also cause thinning of the cornea:

- Keratoglobus is a very rare condition that causes corneal thinning primarily at the margins, resulting in a spherical, slightly enlarged eye. It may be genetically related to keratoconus.

- Pellucid marginal degeneration causes thinning of a narrow (1–2 mm) band of the cornea, usually along the inferior corneal margin. It causes irregular astigmatism that, in the early stages of the disease can be corrected by spectacles. Differential diagnosis may be made by slit-lamp examination.

- Posterior keratoconus, a distinct disorder despite its similar name, is a rare abnormality, usually congenital, which causes a nonprogressive thinning of the inner surface of the cornea, while the curvature of the anterior surface remains normal. Usually only a single eye is affected.

- Post-LASIK ectasia is a complication of LASIK eye surgery.

In early stages of keratoconus, glasses or soft contact lenses can suffice to correct for the mild astigmatism. As the condition progresses, these may no longer provide the person with a satisfactory degree of visual acuity, and most practitioners will move to manage the condition with rigid contact lenses, known as rigid, gas-permeable, (RGP) lenses. RGP lenses provide a good level of visual correction, but do not arrest progression of the condition.

In people with keratoconus, rigid contact lenses improve vision by means of tear fluid filling the gap between the irregular corneal surface and the smooth regular inner surface of the lens, thereby creating the effect of a smoother cornea. Many specialized types of contact lenses have been developed for keratoconus, and affected people may seek out both doctors specialized in conditions of the cornea, and contact lens fitters who have experience managing people with keratoconus. The irregular cone presents a challenge and the fitter will endeavor to produce a lens with the optimal contact, stability and steepness. Some trial-and-error fitting may prove necessary.

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).

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.

Patients with cerebral achromatopsia deny having any experience of color when asked and fail standard clinical assessments like the Farnsworth-Munsell 100-hue test (a test of color ordering with no naming requirements). Patients may often not notice their loss of color vision and merely describe the world they see as being "drab". Most describe seeing the world in "shades of gray". This observation notes a key difference between cerebral and congenital achromatopsia, as those born with achromatopsia have never had an experience of color or gray.

According to the US National Institute for Occupational Safety and Health, computer vision syndrome affects about 90% of the people who spend three hours or more a day at a computer.

Another study in Malaysia was conducted on 795 university students aged between 18 and 25. The students experienced headaches along with eyestrain, with 89.9% of the students surveyed feeling any type of symptom of CVS. Americans spend an average of 8 hours a day in front of a screen, whether that be a television screen, phone/tablet, or a computer screen. This has increased the prevalence of individuals affected by computer vision syndrome.

Entomopia (from the Greek roots for "insect" and "eye"), is a form of polyopia in which a grid-like pattern of multiple copies of the same visual image is seen.

Entomopia may be due to disease of the occipital lobe, defects in visual integration and fixation or incomplete visual processing due to poor visuospatial localisation in the hemianopic field, although its causes are unknown. Reassurance may be the only treatment.

Penetrating karatoplasty and endothelial keratoplasty can be used as treatments for severe cases of ICE [2,8]. Because glaucoma and elevated intraocular pressure are often present in ICE patients, long term follow up may be needed to ensure adequate intraocular pressures are maintained [2,7]

The disease is chronic and often progresses slowly. Prognosis is generally poor when associated with glaucoma [1,2].

Unfortunately, cerebral atrophy is not usually preventable, however there are steps that can be taken to reduce the risks such as controlling your blood pressure, eating a healthy balanced diet including omega-3's and antioxidants, and staying active mentally, physically, and socially.

While most cerebral atrophy is said to be irreversible there are some recent studies that show this is not always the case. A child who was treated with ACTH originally showed atrophy, but four months after treatment the brain was seemingly normal again.

Chronic alcoholism is known to be associated with cerebral atrophy in addition to motor dysfunction and impairment in higher brain function. Because some of the behavioral deficits have shown improvement after abstinence from alcohol, a study looked to see if cerebral atrophy could be reversed too. Researchers took CT scans of the 8 study participants in order to measure cortical volume over time. Although decrease in atrophy does not equate clinical improvement, the CT scans of 50% of participants showed partial improvement, giving hope that cerebral atrophy could be a reversible process.

Polymicrogyria (PMG) is a condition that affects the development of the human brain by multiple small gyri (microgyri) creating excessive folding of the brain leading to an abnormally thick cortex. This abnormality can affect either one region of the brain or multiple regions.

The time of onset has yet to be identified; however, it has been found to occur before birth in either the earlier or later stages of brain development. Early stages include impaired proliferation and migration of neuroblasts, while later stages show disordered post-migration development.

The symptoms experienced differ depending on what part of the brain is affected. There is no specific treatment to get rid of this condition, but there are medications that can control the symptoms such as seizures, delayed development or weakened muscles as some of the noted effects.

The treatment for Bonnet–Dechaume–Blanc syndrome is controversial due to a lack of consensus on the different therapeutic procedures for treating arteriovenous malformations. The first successful treatment was performed by Morgan et al. They combined intracranial resection, ligation of ophthalmic artery, and selective arterial ligature of the external carotid artery, but the patient did not have retinal vascular malformations.

If lesions are present, they are watched closely for changes in size. Prognosis is best when lesions are less than 3 cm in length. Most complications occur when the lesions are greater than 6 cm in size. Surgical intervention for intracranial lesions has been done successfully. Nonsurgical treatments include embolization, radiation therapy, and continued observation. Arterial vascular malformations may be treated with the cyberknife treatment. Possible treatment for cerebral arterial vascular malformations include stereotactic radiosurgery, endovascular embolization, and microsurgical resection.

When pursuing treatment, it is important to consider the size of the malformations, their locations, and the neurological involvement. Because it is a congenital disorder, there are not preventative steps to take aside from regular follow ups with a doctor to keep an eye on the symptoms so that future complications are avoided.

Under the United States federal government, the National Institute of Neurological Disorders and Stroke and National Institute of Health are involved in conducting and supporting research related to normal and abnormal brain and nervous system development. Information gained from the research is used to develop understanding of the mechanism of porencephaly and used to offer new methods of treatment and prevention for developmental brain disorders such as porencephaly.

Limited information was known about cerebral disorders until the development of modern technologies. Brain imaging and genetic sequencing greatly increased the information known about polymicrogyria within the past decade. Understanding about development, classification and localization of the disorder have greatly improved. For instance, localization of specific cortex regions affected by the disease was determined. This allowed for clinical symptoms of patients to be linked with localized cortex areas affected. A gene that was identified to be a contributor to Bilateral frontoparietal polymicrogyria was GPR56. This is the only gene that has been directly linked to the disease.

Because pachygyria is a structural defect no treatments are currently available other than symptomatic treatments, especially for associated seizures. Another common treatment is a gastrostomy (insertion of a feeding tube) to reduce possible poor nutrition and repeated aspiration pneumonia.

The syndrome was first described in 1943 and believed to be associated with racemose hemangiomatosis of the retina and arteriovenous malformations of the brain. It is non-hereditary and belongs to phakomatoses that do not have a cutaneous (pertaining to the skin) involvement. This syndrome can affect the retina, brain, skin, bones, kidney, muscles, and the gastrointestinal tract.