A link between increased ICP and altered sodium and water retention was suggested by a report in which 77% of IIH patients had evidence of peripheral edema and 80% with orthostatic retention of sodium and water. Impaired saline and water load excretions were noted in the upright position in IIH patients with orthostatic edema compared to lean and obese controls without IIH. However, the precise mechanisms linking orthostatic changes to IIH were not defined, and many IH patients do not have these sodium and water abnormalities. Astronauts are well known to have orthostatic intolerance upon reentry to gravity after long-duration spaceflight, and the dietary sodium on orbit is also known to be in excess of 5 grams per day in some cases. The Majority of the NASA cases did have high dietary sodium during their increment. The ISS program is working to decrease in-flight dietary sodium intake to less than 3 grams per day. Prepackaged foods for the International Space Station were originally high in sodium at 5300 mg/d. This amount has now been substantially reduced to 3000 mg/g as a result of NASA reformulation of over ninety foods as a conscious effort to reduce astronaut sodium intake.

While exercise is used to maintain muscle, bone and cardiac health during spaceflight, its effects on ICP and IOP have yet to be determined. The effects of resistive exercise on the development of ICP remains controversial. An early investigation showed that the brief intrathoractic pressure increase during a Valsalva maneuver resulted in an associated rise in ICP. Two other investigations using transcranial Doppler ultrasound techniques showed that resistive exercise without a Valsalva maneuver resulted in no change in peak systolic pressure or ICP. The effects of resistive exercise in IOP are less controversial. Several different studies have shown a significant increase in IOP during or immediately after resistive exercise.

There is much more information available regarding aerobic exercise and ICP. The only known study to examine ICP during aerobic exercise by invasive means showed that ICP decreased in patients with intracranial hypertension and those with normal ICP. They suggested that because aerobic exercise is generally done without Valsalva maneuvers, it is unlikely that ICP will increase during exercise. Other studies show global brain blood flow increases 20-30% during the transition from rest to moderate exercise.

More recent work has shown that an increase in exercise intensity up to 60% VOmax results in an increase in CBF, after which CBF decreases towards (and sometimes below) baseline values with increasing exercise intensity.

Many cases resolve within 1–2 weeks of controlling blood pressure and eliminating the inciting factor. However some cases may persist with permanent neurologic impairment in the form of visual changes and seizures among others. Though uncommon, death may occur with progressive swelling of the brain (cerebral edema), compression of the brainstem, increased intracranial pressure, or a bleed in the brain (intracerebral hemorrhage). PRES may recur in about 5-10% of cases; this occurs more commonly in cases precipitated by hypertension as opposed to other factors (medications, etc.).

The predominant cause of nutritional optic neuropathy is thought to be deficiency of B-complex vitamins, particularly thiamine (vitamin B), cyanocobalamin (vitamin B) and recently copper Deficiency of pyridoxine (vitamin B), niacin (vitamin B), riboflavin (vitamin B), and/or folic acid also seems to play a role. Those individuals who abuse alcohol and tobacco are at greater risk because they tend to be malnourished. Those with pernicious anemia are also at risk due to an impaired ability to absorb vitamin B from the intestinal tract.

The number cases of PRES that occur each year is not known. It may be somewhat more common in females.

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.

Vitamin A supplementation plays an important role, specifically vitamin A deficiency is a top causes of preventable childhood blindness. Though in measles cases, the administration of the vitamin to offset visual impairment has not been proven effective, as of yet.

There are several causes of toxic optic neuropathy. Among these are: ingestion of methanol (wood alcohol), ethylene glycol (automotive antifreeze), disulfiram (used to treat chronic alcoholism), halogenated hydroquinolones (amebicidal medications), ethambutol and isoniazid (tuberculosis treatment), and antibiotics such as linezolid and chloramphenicol. Tobacco is also a major cause of toxic optic neuropathy.

Over time, it is common for the vitreous within the human eye to liquify and collapse in processes known as syneresis and synchisis respectively. This creates fluid-filled areas that can combine to form pockets of vitreous gel that are mostly liquid with very small concentrations of collagen. If these liquid pockets are close enough to the interface between the vitreous gel and the retina, they can cause complete separation of the vitreous from the retina in a normally occurring process in older humans called posterior vitreous detachment (PVD). PVD in of itself is not dangerous and a natural process.

If the separation of the vitreous from the retina is not complete, areas of focal attachment or adhesions can occur, i.e. a VMA. The pulling forces or traction from this adhesion on the retinal surface can sometimes cause edema within the retina, damage to retinal blood vessels causing bleeding, or damage to the optic nerve causing disruption in the nerve signals sent to the brain for visual processing. It is important to note that while the VMA itself is not dangerous, the resultant pulling on the retina called vitreomacular traction (VMT) causes the above damage. The size and strength of the VMA determine the variety of resulting pathologies or symptoms.

VMA can also lead to the development of VMT/traction-related complications such as macular puckers and macular holes leading to distorted vision or metamorphopsia; epiretinal membrane; tractional macular oedema; myopic macular retinoschisis; visual impairment; blindness. The incidence of VMA is reported as high as 84% for patients with macular hole, 100% for patients with vitreomacular traction syndrome, and 56% in idiopathic epimacular membrane.

Of these, cataract is responsible for >65%, or more than 22 million cases of blindness, and glaucoma is responsible for 6 million cases.

Cataracts: is the congenital and pediatric pathology that describes the greying or opacity of the crystalline lens, which is most commonly caused by intrauterine infections, metabolic disorders, and genetically transmitted syndromes. Cataracts are the leading cause of child and adult blindness that doubles in prevalence with every ten years after the age of 40. Consequently, today cataracts are more common among adults than in children. That is, people face higher chances of developing cataracts as they age. Nonetheless, cataracts tend to have a greater financial and emotional toll upon children as they must undergo expensive diagnosis, long term rehabilitation, and visual assistance. Also, according to the Saudi Journal for Health Sciences, sometimes patients experience irreversible amblyopia after pediatric cataract surgery because the cataracts prevented the normal maturation of vision prior to operation. Despite the great progress in treatment, cataracts remain a global problem in both economically developed and developing countries. At present, with the variant outcomes as well as the unequal access to cataract surgery, the best way to reduce the risk of developing cataracts is to avoid smoking and extensive exposure to sun light (i.e. UV-B rays).

Blindness can occur in combination with such conditions as intellectual disability, autism spectrum disorders, cerebral palsy, hearing impairments, and epilepsy. Blindness in combination with hearing loss is known as deafblindness.

It has been estimated that over half of completely blind people have non-24-hour sleep–wake disorder, a condition in which a person's circadian rhythm, normally slightly longer than 24 hours, is not entrained (synchronized) to the light/dark cycle.

The number of children who suffer from blindness worldwide is approximately 1.4 million. 75% of the world’s blind children live in Africa and Asia. A 2014 review indicated that an estimated of 238,500 children with bilateral blindness (rate 1.2/1,000) in the Eastern Mediterranean region.

Although it is frequently claimed that the retina is burned by looking at the sun, retinal damage appears to occur primarily due to photochemical injury rather than thermal injury. The temperature rise from looking at the sun with a 3-mm pupil only causes a 4 °C increase in temperature, insufficient to photocoagulate. The energy is still phototoxic: since light promotes oxidation, chemical reactions occur in the exposed tissues with unbonded oxygen molecules. It also appears that central serous retinopathy can be a result of a depression in a treated solar damaged eye.

The duration of exposure necessary to cause injury varies with the intensity of light, and also affects the possibility and length of recovery

In general, approximately one-third of congenital cataracts are a component of a more extensive syndrome or disease (e.g., cataract resulting from congenital rubella syndrome), one-third occur as an isolated inherited trait, and one-third result from undetermined causes. Metabolic diseases tend to be more commonly associated with bilateral cataracts.

Generally speaking, people diagnosed with photic retinopathy recover visual acuity completely within two months, though more severe cases may take longer, or not see complete recovery at all.

The most common finding is oculomotor nerve dysfunction leading to ophthalmoplegia. This is often accompanied by ophthalmic nerve dysfunction, leading to hypoesthesia of the upper face. The optic nerve may eventually be involved, with resulting visual impairment.

Orbital apex syndrome, also known as Jacod syndrome, is a collection of cranial nerve deficits associated with a mass lesion near the apex of the orbit of the eye. This syndrome is a separate entity from Rochon–Duvigneaud syndrome, which occurs due to a lesion immediately anterior to the orbital apex. Most commonly optic nerve is involved.

Bonnet–Dechaume–Blanc syndrome results mainly from arteriovenous malformations. These malformations are addressed previously in the article, under “Signs and Symptoms.” Due to lack of research, it is difficult to provide a specific mechanism for this disorder. However, a number of examinations, mentioned under “Diagnosis,” can be performed on subjects to investigate the disorder and severity of the AVMs.

Streff syndrome is a vision condition primarily exhibited by children under periods of visual or emotional stress.

Frequently patients will have reduced stereopsis, large accommodative lag on dynamic retinoscopy, and a reduced visual field (tubular or spiral field). Streff Syndrome was first described in 1962 by an optometrist, Dr. John Streff as Non-malingering syndrome. In 1962, Dr. Streff and Dr. Richard Apell expanded the concept to add early adaptive syndrome as a precursor to Streff syndrome. Dr. Streff believed the visual changes were induced by stress from reading. There is dispute on the taxonomy of functional vision defects. Some research indicates that Streff syndrome may be caused by a dysfunction in the magnocellular pathway of the retinal ganglion cells. These cells are only 10% of the retinal nerve cells and register motion detection.

Early Adaptive Syndrome

The syndrome is a congenital disorder that begins to develop around the seventh week of gestation when the maturation of retinal mesenchymal cells do not properly grow. The abnormal development of vascular tissue leads to arteriovenous malformations. These malformations affect both the visual and cerebral structures and lead to the development of the syndrome.

Congenital cataracts occur in a variety of morphologic configurations, including lamellar, polar, sutural, coronary, cerulean, nuclear, capsular, complete, membranous.

Nystagmus is a relatively common clinical condition, affecting one in several thousand people. A survey conducted in Oxfordshire, United Kingdom found that by the age of two, one in every 670 children had manifested nystagmus. Authors of another study in the United Kingdom estimated an incidence of 24 in 10,000 (~0.240 %), noting an apparently higher rate amongst white Europeans than in individuals of Asian origin.

It may be acquired from:

- Diseases. Some of the diseases that present nystagmus as a pathological sign:

- Aniridia

- Toxic or metabolic reasons could be the result of the following:

- Central nervous system (CNS) disorders, such as with a cerebellar problem, the nystagmus can be in any direction "including" horizontal. Purely vertical nystagmus is usually central in origin, but it is also a frequent adverse effect of high phenytoin toxicity. Causes include:

Corneal-cerebellar syndrome (also known as Der Kaloustian-Jarudi-Khoury syndrome) is an autosomally resessive disease that was first described in 1985. Three cases are known: all are sisters in the same family.

The most common cause of cortical blindness is ischemia (oxygen deprivation) to the occipital lobes caused by blockage to one or both of the posterior cerebral arteries. However, other conditions have also been known to cause acquired and transient cortical blindness, including:

- Bilateral lesions of the primary visual cortex

- Side effect of some anti-epilepsy drugs (AEDs)

- Creutzfeldt–Jakob disease, in association with a rapid onset of dementia

- Infection

- Head trauma to the occipital lobe of the brain

- Congenital abnormalities of the occipital lobe

- Eclampsia and, rarely, pre-eclampsia

- Hyperammonemia

The most common causes of congenital cortical blindness are:

- Traumatic brain injury (TBI) to the occipital lobe of the brain

- Congenital abnormalities of the occipital lobe

- Perinatal ischemia

- Encephalitis

- Meningitis