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.

Though no topical treatment has been proven to be effective in the treatment of Central Serous Retinopathy. Some doctors have attempted to use nonsteroidal topical medications to reduce the subretinal fluid associated with CSR. The nonsteroidal topical medications that are sometimes used to treat CSR are, Ketorolac, Diclofenac, or Bromfenac.

Spironolactone is a mineralocorticoid receptor antagonist that has been proven to help reduce the fluid associated with Central Serous Retinopathy. In a study noted by Acta Ophthalmologica also noted that the Spironolactone improved the visual acuity over the course of 8 weeks.

Epleronone is a mineralocorticoid receptor antagonist that has been proven to reduce the subretinal fluid that is present in Central Serous Retinopathy. This is a similar treatment to Spironolactone. In a study noted in International Journal of Ophthalmology, results showed Epleronone decreased the SRF both horizontally and vertically over time. Though after stopping the medication the fluid also appeared to return and patients needed further treatment.

Low dosage ibuprofen has been shown to quicken recovery in some cases, whilst avoiding naturally occurring blood thinners such as garlic, turmeric, cinnamon, which can enhance leakage from capillaries behind the retina.

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.

CNV is conventionally treated with intravitreal injections of angiogenesis inhibitors (also known as "anti-VEGF" drugs) to control neovascularization and reduce the area of fluid below the retinal pigment epithelium. Angiogenesis inhibitors include pegaptanib, ranibizumab and bevacizumab (known by a variety of trade names, such as Macugen, Avastin or Lucentis). These inhibitors slow or stop the formation of new blood vessels (angiogenesis), typically by binding to or deactivating the transmission of vascular endothelial growth factor ('VEGF'), a signal protein produced by cells to stimulate formation of new blood vessels. The effectiveness of angiogenesis inhibitors has been shown to significantly improve visual prognosis with CNV, the recurrence rate for these neovascular areas remains high.

CNV may also be treated with photodynamic therapy coupled with a photosensitive drug such as verteporfin (Visudyne). The drug is given intravenously. It is then activated in the eye by a laser light. The drug destroys the new blood vessels, and prevents any new vessels forming by forming thrombi.

Optic pits themselves do not need to be treated. However, patients should follow up with their eye care professional annually or even sooner if the patient notices any visual loss whatsoever. Treatment of PVD or serous retinal detachment will be necessary if either develops in a patient with an optic pit.

It can be treated with laser coagulation, and more commonly with medication that stops and sometimes reverses the growth of blood vessels.

A randomized control trial found that bevacizumab and ranibizumab had similar efficacy, and reported no significant increase in adverse events with bevacizumab. A 2014 Cochrane review found that the systemic safety of bevacizumab and ranibizumab are similar when used to treat neovascular AMD, except for gastrointestinal disorders. Bevacizumab however is not FDA approved for treatment of macular degeneration. A controversy in the UK involved the off-label use of cheaper bevacizumab over the approved, but expensive, ranibizumab. Ranibizumab is a smaller fragment, Fab fragment, of the parent bevacizumab molecule specifically designed for eye injections. Other approved antiangiogenic drugs for the treatment of neo-vascular AMD include pegaptanib and aflibercept.

The American Academy of Ophthalmology practice guidelines do not recommend laser coagulation therapy for macular degeneration, but state that it may be useful in people with new blood vessels in the choroid outside of the fovea who don't respond to drug treatment. There is strong evidence that laser coagulation will result in the disappearance of drusen but does not affect choroidal neovascularisation. A 2007 Cochrane review on found that laser photocoagulation of new blood vessels in the choroid outside of the fovea is effective and economical method, but that the benefits are limited for vessels next to or below the fovea.

Photodynamic therapy has also been used to treat wet AMD. The drug verteporfin is administered intravenously; light of a certain wavelength is then applied to the abnormal blood vessels. This activates the verteporfin destroying the vessels.

Cataract surgery could possibly improve visual outcomes for people with AMD, though there have been concerns of surgery increasing the progression of AMD. A randomized controlled trial found that people who underwent immediate cataract surgery (within 2 weeks) had improved visual acuity and better quality of life outcomes than those who underwent delayed cataract surgery (6 months).

No medical or surgical treatment is available for this condition.

Careful eye examination by an ophthalmologist or optometrist is critical for diagnosing symptomatic VMA. Imaging technologies such as optical coherence tomography (OCT) have significantly improved the accuracy of diagnosing symptomatic VMA.

A new FDA approved drug was released on the market late 2013. Jetrea (Brand name) or Ocriplasmin (Generic name) is the first drug of its kind used to treat vitreomacular adhension.

Mechanism of Action: Ocriplasmin is a truncated human plasmin with proteolytic activity against protein components of the vitreous body and vitreretinal interface. It dissolves the protein matrix responsible for the vitreomacular adhesion.

Adverse drug reactions: Decreased vision, potential for lens sublaxation, dyschromatopsia (yellow vision), eye pain, floaters, blurred vision.

New Drug comparison Rating gave Jetea a 5 indicating an important advance.

Previously, no recommended treatment was available for the patient with mild symptomatic VMA. In symptomatic VMA patients with more significant vision loss, the standard of care is pars plana vitrectomy (PPV), which involves surgically removing the vitreous from the eye, thereby surgically releasing the symptomatic VMA. In other words, vitrectomy induces PVD to release the traction/adhesion on the retina. An estimated 850,000 vitrectomy procedures are performed globally on an annual basis with 250,000 in the United States alone.

A standard PPV procedure can lead to serious complications including small-gauge PPV. Complications can include retinal detachment, retinal tears, endophthalmitis, and postoperative cataract formation. Additionally, PPV may result in incomplete separation, and it may potentially leave a nidus for vasoactive and vasoproliferative substances, or it may induce development of fibrovascular membranes. As with any invasive surgical procedure, PPV introduces trauma to the vitreous and surrounding tissue.

There are data showing that nonsurgical induction of PVD using ocriplasmin (a recombinant protease with activity against fibronectin and laminin) can offer the benefits of successful PVD while eliminating the risks associated with a surgical procedure, i.e. vitrectomy. Pharmacologic vitreolysis is an improvement over invasive surgery as it induces complete separation, creates a more physiologic state of the vitreomacular interface, prevents the development of fibrovascular membranes, is less traumatic to the vitreous, and is potentially prophylactic. As of 2012, ThromboGenics is still developing the ocriplasmin biological agent. Ocriplasmin is approved recently under the name Jetrea for use in the United States by the FDA.view.

An experimental test of injections of perfluoropropane (CF) on 15 symptomatic eyes of 14 patients showed that vitreomacular traction resolved in 6 eyes within 1 month and resolved in 3 more eyes within 6 months.

To date, there is no known effective treatment for the non-proliferative form of macular telangiectasia type 2.

Treatment options are limited. No treatment has to date been shown to prevent progression. The variable course of progression of the disease makes it difficult to assess the efficacy of treatments. Retinal laser photocoagulation is not helpful. In fact, laser therapy may actually enhance vessel ectasia and promote intraretinal fibrosis in these individuals. It is hoped that a better understanding of the pathogenesis of the disease may lead to better treatments.

The use of vascular endothelial growth factor (VEGF) inhibitors, which have proven so successful in treating age-related macular degeneration, have not proven to be effective in non-proliferative MacTel type 2. Ranibizumab reduces the vascular leak seen on angiography, although microperimetry suggests that neural atrophy may still proceed in treated eyes.In proliferative stages (neovascularisation), treatment with Anti-VEGF can be helpful.

CNTF is believed to have neuroprotective properties and could thus be able to slow down the progression of MacTel type 2. It has been shown to be safe to use in MacTel patients in a phase 1 safety trial.

The most crucial aspect of managing patients with macular telangiectasia is recognition of the clinical signs. This condition is relatively uncommon: hence, many practitioners may not be familiar with or experienced in diagnosing the disorder. MacTel must be part of the differential in any case of idiopathic paramacular hemorrhage, vasculopathy, macular edema or focal pigment hypertrophy, especially in those patients without a history of retinopathy or contributory systemic disease.

Treatment options for macular telangiectasia type 1 include laser photocoagulation, intra-vitreal injections of steroids, or anti-vascular endothelial growth factor (anti-VEGF) agents. Photocoagulation was recommended by Gass and remains to date the mainstay of treatment. It seems to be successful in causing resolution of exudation and VA improvement or stabilization in selected patients. Photocoagulation should be used sparingly to reduce the chance of producing a symptomatic paracentral scotoma and metamorphopsia. Small burns (100–200 μm) of moderate intensity in a grid-pattern and on multiple occasions, if necessary, are recommended. It is unnecessary to destroy every dilated capillary, and, particularly during the initial session of photocoagulation, those on the edge of the capillary-free zone should be avoided.

Intravitreal injections of triamcinolone acetonide (IVTA) which have proved to be beneficial in the treatment of macular edema by their anti-inflammatory effect, their downregulation of VEGF production, and stabilization of the blood retinal barrier were reported anecdotally in the management of macular telangiectasia type 1. In two case reports, IVTA of 4 mg allowed a transitory reduction of retinal edema, with variable or no increase in VA. As expected with all IVTA injections, the edema recurred within 3–6 months, and no permanent improvement could be shown.14,15 In general, the effect of IVTA is short-lived and complications, mainly increased intraocular pressure and cataract, limit its use.

Indocyanine green angiography-guided laser photocoagulation directed at the leaky microaneurysms and vessels combined with sub-Tenon’s capsule injection of triamcinolone acetonide has also been reported in a limited number of patients with macular telangiectasia type 1 with improvement or stabilization of vision after a mean follow-up of 10 months.16 Further studies are needed to assess the efficacy of this treatment modality.

Recently, intravitreal injections of anti-VEGF agents, namely bevacizumab, a humanized monoclonal antibody targeted against pro-angiogenic, circulatory VEGF, and ranibizumab, a FDA-approved monoclonal antibody fragment that targets all VEGF-A isoforms, have shown improved visual outcome and reduced leakage in macular edema form diabetes and retinal venous occlusions. In one reported patient with macular telangiectasia type 1, a single intravitreal bevacizumab injection resulted in a marked increase in VA from 20/50 to 20/20, with significant and sustained decrease in both leakage on FA and cystoid macular edema on OCT up to 12 months. It is likely that patients with macular telangiectasia type 1 with pronounced macular edema from leaky telangiectasis may benefit functionally and morphologically from intravitreal anti-VEGF injections, but this warrants further studies.

Today, laser photocoagulation remains mostly effective, but the optimal treatment of macular telangiectasia type 1 is questioned, and larger series comparing different treatment modalities seem warranted. The rarity of the disease however, makes it difficult to assess in a controlled randomized manner.

However, these treatment modalities should be considered only in cases of marked and rapid vision loss secondary to macular edema or CNV. Otherwise, a conservative approach is recommended, since many of these patients will stabilize without intervention.

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.

Optic pits should be diagnosed by an eye care professional who can perform a thorough exam of the back of the eye using an ophthalmoscope.

More recently, the development of a special technology called optical coherence tomography (OCT) has allowed better visualization of the retinal layers. It has been used to demonstrate a marked reduction in the thickness of the retinal nerve fiber layer in the quadrant corresponding to the optic pit. This is not yet in standard use for diagnosis of an optic pit, but may be helpful in supporting a diagnosis.

Metamorphopsia is a type of distorted vision in which a grid of straight lines appears wavy and parts of the grid may appear blank. People with this condition often first notice this when looking at mini-blinds in their home.

It is mainly associated with macular degeneration, particularly age-related macular degeneration with choroidal neovascularization. Other conditions that can present with complaints of metamorphopsia include pathological myopia, presumed ocular histoplasmosis syndrome, choroidal rupture and multifocal choroiditis.

The term dysmorphopsia comes from the Greek words dus (bad), morphè (form), and opsis (seeing).

Dry (nonexudative, > 80%)—deposition of yellowish extracellular material in and between bruch membrane and retinal pigment epithelium (“drusen”) with gradual loss in vision.

Wet (exudative, 10–15%)—rapid loss of vision due to bleeding secondary to choroidal neovascularization.

Dysmorphopsia, in a broad sense, is a condition which causes the person affected to be unable to correctly perceive objects. It is a visual distortion, used to denote a variant of metamorphopsia in which lines appear wavy. These illusions may be restricted to certain visuals areas, or may affect the entire visual field.

It has been associated with meningioma tumors and bilateral lateral occipital corital damage, e.g. after carbon monoxide poisoning or drug abuse.

Vitreomacular adhesion (VMA) is a human medical condition where the vitreous gel (or simply vitreous) of the human eye adheres to the retina in an abnormally strong manner. As the eye ages, it is common for the vitreous to separate from the retina. But if this separation is not complete, i.e. there is still an adhesion, this can create pulling forces on the retina that may result in subsequent loss or distortion of vision. The adhesion in of itself is not dangerous, but the resulting pathological vitreomacular traction (VMT) can cause severe ocular damage.

The current standard of care for treating these adhesions is pars plana vitrectomy (PPV), which involves surgically removing the vitreous from the eye. A biological agent for non-invasive treatment of adhesions called ocriplasmin has been approved by the FDA on Oct 17 2012.

Choroidal neovascularization (CNV) is the creation of new blood vessels in the choroid layer of the eye. Choroidal neovascularization is a common cause of neovascular degenerative maculopathy (i.e. 'wet' macular degeneration) commonly exacerbated by extreme myopia, malignant myopic degeneration, or age-related developments.

Retinal vasculitis presents as painless, decrease of visual acuity (blurry vision), visual floaters, scotomas (dark spot in vision), decreased ability to distinguish colors, and metamorphopsia (distortion of images such as linear images).

Ophthalmic examination may reveal neovascularization (creation of new vessels in the retina), retinal vessel narrowing, retinal vessel cuffing, retinal hemorrhage, or possible vitritis (inflammation of the vitreous body) or choroiditis (inflammation of the choroid).