The most prevalent research on prescription drugs with side effects of macropsia deals with zolpidem and citalopram. Zolpidem is a drug prescribed for insomnia, and although it has proven beneficial effects, there have been numerous reported cases of adverse perceptual reactions. One of these cases discusses an anorexic woman’s episode of macropsia, which occurred twenty minutes after taking 10 mg zolpidem. The same woman later had two more episodes of zolpidem-induced macropsia, after taking 5 mg and 2.5 mg zolpidem, respective to each episode. The intensity of the macropsia episodes decreased with the decreasing amount of zolpidem administered; it is implied in the article that the level of intensity was based on the patients accounts of her macropsia episodes, and that no external diagnosis was used. Hoyler points out notable similarities among the different reported cases of zolpidem-induced disorganization. The similarities were that all the cases were reported by women, the disorganization and agitation followed the first administration of zolpidem, and once zolpidem was discontinued, there were no lasting residual effects. It is believed that zolpidem-related macropsia is more prevalent in women because plasma zolpidem concentration is 40% higher in women, a concentration that further increases in anorexic women.

Citalopram-induced macropsia is similar to zolpidem-induced macropsia since both types have been observed in relatively few cases, and neither of the drugs’ side effects can be supported by experimental evidence. Citalopram is an antidepressant that inhibits serotonin reuptake. The first case of macropsia thought to be induced by citalopram involves a woman who experienced macropsia after her first administration of 10 mg citalopram. Just as with zolpidem, after the immediate discontinuation of citalopram, there were no further episodes of macropsia.

Future research may focus on ways to limit the occurrence of retinally-induced macropsia due to surgery. In terms of treatment, the most effective optical correction is still being researched with respect to visual field angles and direction to a target. The susceptibility of certain age demographics to macropsia is a subject that requires further validation. Overall, there have not been very many reports of macropsia induced by certain drugs, specifically zolpidem and citalopram. Once a larger effort is made to compile such reports, there will inevitably be more research on the subject of macropsia.

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.

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 (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.

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).

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".

While preventive measures, such as taking breaks from activities that cause eye strain are suggested, there are certain treatments which a person suffering from the condition can take to ease the pain or discomfort that the affliction causes. Perhaps the most effective of these is to remove all light sources from a room and allow the eyes to relax in darkness. Free of needing to focus, the eyes will naturally relax over time, and relieve the discomfort that comes with the strain. Cool compresses also help to some degree, though care should be taken to not use anything cold enough to damage the eyes themselves (such as ice). A number of companies have released "computer glasses" which, through the use of specially tinted lenses, help alleviate many of the factors which cause eye strain, though they do not completely prevent it. Rather, they just make it harder to strain the eye.

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 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.

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

"Looming" is a term used in the study of the perception, as it relates directly to psychology. Looming refers to the rapid expansion in the size of any given image. As the image becomes increasingly large on the perceiver's retina, i.e., when an object "looms", there is an automatic physiological response to perceive the object as an approaching object or surface, instead of one that is or receding. The type of mirage described as looming, in which distant objects appear much nearer than they actually are, is explained in the same way as the image of the ship, except that the image is not inverted; the density variations may also act as a magnifying glass.

"Visual looming", which is the expansion of the projection size of an object on the retina, is usually the indication of an approaching object. It is normally perceived as a threat for a possible collision and is sufficient to elicit avoidance and escape behaviors in animals. Also using the same basic principles in robotics have been successful.

There have been hypotheses about visual looming syndrome to be linked with several neural and gastroenterology diseases, such as celiac disease, epilepsy and migraines. Also physical differences between the eyes, such as astigmatism may be a factor. There have not been any empirical medical studies about the syndrome, though the consensus is all these may have affect on the muscular function of the eye, but most likely the visual looming syndrome is a separate symptom. There have been studies of a similar neurological situation. Gabbiani Peron has studied the "looming stimulus selectivity in a collision-detecting neuron". Beverley Regan has studied "Binocular and monocular stimuli for motion in depth". Moors P, Huygelier H, Wagemans J, de-Wit L, van Ee R; "Suppressed visual looming stimuli are not integrated with auditory looming signals"

Peer to peer studies have shown many common symptoms, such are "fear of pointy objects hitting the eye", "weird sensation behind the eyes", "difficulty in focusing on objects nearby, which are moving and are not operated by the observer, such as windscreen wipers or a pencil someone else is holding". In these studies visual looming syndrome is often referred as sharp edges eye syndrome (SEES).

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).

Suppression may treated with vision therapy, though there is a wide range of opinions on long-term effectiveness between eye care professionals, with little scientific evidence of long-term improvement of suppression, if the underlying cause is not addressed (strabismus, amblyopia, etc.).

There are five known levels of CEV perception which can be achieved either through chemical stimuli or through meditative relaxation techniques. Level 1 and 2 are very common and often happen every day. It is still normal to experience level 3, and even level 4, but only a small percentage of the population does this without psychedelic drugs, meditation or extensive visualization training.

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.

Closed-eye hallucinations and closed-eye visualizations (CEV) are a distinct class of hallucination. These types of hallucinations generally only occur when one's eyes are closed or when one is in a darkened room. They can be a form of phosphene. Some people report closed-eye hallucinations under the influence of psychedelics. These are reportedly of a different nature than the "open-eye" hallucinations of the same compounds.

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.

Although the best outcome is achieved if treatment is started before age 8, children older than age 12 and some adults can show improvement in the affected eye. Children from 9 to 11 who wore an eye patch and performed near-point activities (vision therapy) were four times as likely to show a two-line improvement on a standard 11-line eye chart than children with amblyopia who did not receive treatment. Adolescents aged 13 to 17 showed improvement, as well, albeit to a lesser degree than younger children. Whether such improvements are only temporary, however, is uncertain, particularly if treatment is discontinued.

Tentative evidence shows that perceptual training may be beneficial in adults.

Virtual-reality computer games where each eye receives different signals of the virtual world that the player's brain must combine to successfully play the game have shown some promise in improving both monocularity in the affected eye, as well as binocularity.

A 2009 study, widely reported in the popular press, has suggested that repetitive transcranial magnetic stimulation may temporarily improve contrast sensitivity and spatial resolution in the affected eye of adults with amblyopia. This approach is still under development, and the results await verification by other researchers. It has also been suggested that comparable results can be achieved using different types of brain stimulation such as anodal transcranial direct current stimulation and theta burst rTMS.

A 2013 study concluded that converging evidence indicates decorrelated binocular experience plays a pivotal role in the genesis of amblyopia and the associated residual deficits. Another study of 2013 suggests that playing a version of the popular game Tetris that is modified such that each eye sees separate components of the game may also help to treat this condition in adults. Furthermore, it has been proposed that the effects of this kind of therapy may be further enhanced by noninvasive brain stimulation as shown by a recent study using anodal tDCS.

A 2014 Cochrane review sought to determine the effectiveness of occlusion treatment on patients with sensory deprivation amblyopia, but no trials were found eligible to be included in the review. However, good outcomes from occlusion treatment for sensory deprivation amblyopia likely rely on compliance with the treatment.

Congenital nystagmus has traditionally been viewed as non-treatable, but medications have been discovered in recent years that show promise in some patients. In 1980, researchers discovered that a drug called baclofen could effectively stop periodic alternating nystagmus. Subsequently, gabapentin, an anticonvulsant, was found to cause improvement in about half the patients who received it to relieve symptoms of nystagmus. Other drugs found to be effective against nystagmus in some patients include memantine, levetiracetam, 3,4-diaminopyridine (available in the US to eligible patients with downbeat nystagmus at no cost under an expanded access program), 4-aminopyridine, and acetazolamide. Several therapeutic approaches, such as contact lenses, drugs, surgery, and low vision rehabilitation have also been proposed. For example, it has been proposed that mini-telescopic eyeglasses suppress nystagmus.

Surgical treatment of Congenital Nystagmus is aimed at improving the abnormal head posture, simulating artificial divergence or weakening the horizontal recti muscles. Clinical trials of a surgery to treat nystagmus (known as tenotomy) concluded in 2001. Tenotomy is now being performed regularly at numerous centres around the world. The surgery developed by Louis F. Dell'Osso Ph.D. aims to reduce the eye shaking (oscillations), which in turn tends to improve visual acuity.

Acupuncture has conflicting evidence as to having beneficial effects on the symptoms of nystagmus. Benefits have been seen in treatments where acupuncture points of the neck were used, specifically points on the sternocleidomastoid muscle. Benefits of acupuncture for treatment of nystagmus include a reduction in frequency and decreased slow phase velocities which led to an increase in foveation duration periods both during and after treatment. By the standards of evidence-based medicine, the quality of these studies can be considered poor (for example, Ishikawa has a study sample size of just six, is unblinded and without proper control), and given high quality studies showing that acupuncture has no effect beyond placebo, the results of these studies have to be considered clinically irrelevant until higher quality studies are produced.

Physical therapy or Occupational therapy is also used to treat nystagmus. Treatment consist of learning compensatory strategies to take over for the impaired system.

Riddoch syndrome (also known as the "Riddoch phenomenon") is an ocular affectation often caused by lesions in the occipital lobe which limit the sufferer's ability to distinguish objects. Only moving objects in a blind field are visible, static ones being invisible to the patient. The moving objects are not perceived to have color or detail. The subject may only have awareness of the movement without visual perception of it (gnosanopsia), or the general shape of a moving object may be perceivable as a shadow like outline.

At least one patient was able to use a rocking chair—putting non-moving surroundings in relative motion to her head—to improve her motion perception. She eventually was able to do the same with just voluntary movement of her head.

Young children with strabismus normally suppress the visual field of one eye (or part of it), whereas adults who develop strabismus normally do not suppress and therefore suffer from double vision (diplopia). This also means that adults (and older children) have a higher risk of post-operative diplopia after undergoing strabismus surgery than young children. Patients who have undergone strabismus surgery at a young age often have monofixation syndrome (with peripheral binocular fusion and a central suppression scotoma).

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.