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

Most optometrists agree that Streff syndrome is a generalized reduction in visual performance that is not caused by structural damage. It is a disease involving vision distress primarily of the accommodation system. Hans Selye described stress, distress and eustress. It is most common in girls ages 8 to 14. Hand held reading material is often positioned excessively close. Reading aloud shows signs of elevated pitch and stumbling over common words. History of homework avoidance and falling class performance are often present. If the patient is directed to read aloud and +.50 lenses are then used, there is usually a dramatic improvement as observed by patient and parent. Abnormal results on color vision or visual field testing is not uncommon. Visual field often presents as constricted 'tubular' at multiple test distances. The poor visual performance is understood as distress, and treatments are usually to provide the patient with low powered reading glasses. The "relaxing" nature of reading glasses is believed to reduce the near vision stress and allow normal function. The emotional effects of chronic near vision stress are also reduced.

The "non-Malingering" name is a refutation that the patient is malingering.

There have not been sufficient studies conducted to make conclusive statements about prevalence nor who tends to suffer EHS. One study found that 13.5% of a sample of undergrads reported at least one episode over the course of their lives, with higher rates in those also suffering from sleep paralysis.

The optokinetic response is a combination of a slow-phase and fast-phase eye movements. It is seen when an individual follows a moving object with their eyes, which then moves out of the field of vision at which point their eye moves back to the position it was in when it first saw the object. The reflex develops at about 6 months of age.

Optokinetic nystagmus (OKN) is nystagmus that occurs in response to a rotation movement. It is present normally. The optokinetic response allows the eye to follow objects in motion when the head remains stationary (e.g., observing individual telephone poles on the side of the road as one travels by them in a car, or observing stationary objects while walking past them).

As of 2014, no clinical trials had been conducted to determine what treatments are safe and effective; a few case reports had been published describing treatment of small numbers of people (two to twelve per report) with clomipramine, flunarizine, nifedipine, topiramate, carbamazepine, methylphenidate. Studies suggest that education and reassurance can reduce the frequency of EHS episodes. There is some evidence that individuals with EHS rarely report episodes to medical professionals.

Perioperative PION patients have a higher prevalence of cardiovascular risk factors than in the general population. Documented cardiovascular risks in people affected by perioperative PION include high blood pressure, diabetes mellitus, high levels of cholesterol in the blood, tobacco use, abnormal heart rhythms, stroke, and obesity. Men are also noted to be at higher risk, which is in accordance with the trend, as men are at higher risk of cardiovascular disease. These cardiovascular risks all interfere with adequate blood flow, and also may suggest a contributory role of defective vascular autoregulation.

If an optokinetic drum is available, rotate the drum in front of the patient. Ask the patient to look at the drum as you rotate it slowly. If an optokinetic drum is not available, move a strip of paper with alternating 2-inch black and white strips across the patient's visual field. Pass it in front of the patient's eye at reading distance while instructing the patient to look at it as it rapidly moves by. With normal vision, a nystagmus develops in both adults and infants. The nystagmus consists of initial slow phases in the direction of the stimulus (smooth pursuits), followed by fast, corrective phases (saccade). Presence of nystagmus indicates an intact visual pathway.

Another effective method is to hold a mirror in front of the patient and slowly rotate the mirror to either side of the patient. The patient with an intact visual pathway will maintain eye contact with herself or himself. This compelling optokinetic stimulus forces reflex slow eye movements.

OKN can be used as a crude assessment of the visual system, particularly in infants. When factitious blindness or malingering is suspected, check for optokinetic nystagmus to determine whether there is an intact visual pathway.

The disorder is extraordinarily rare. While individuals of all backgrounds have been reported with the disorder, there is a higher inclination towards males (75% or more). The average age of those with Ganser syndrome is 32 and it stretches from ages 15 to 62 years old. It has been reported in children.

The disorder is apparently most common in men and prisoners, although prevalence data and familial patterns are not established.

There are an estimated 140,000 people with N24 – both sighted and blind – in the European Union, a total prevalence of approximately 3 per 10,000, or 0.03%. It is unknown how many individuals with this disorder do not seek medical attention, so incidence may be higher. The European portal for rare diseases, Orphanet, lists Non-24 as a rare disease by their definition: fewer than 1 affected person for every 2000 population. The US National Organization for Rare Disorders (NORD) lists Non-24 as a rare disease by its definition.

As the syndrome is due to a chromosomal non-disjunction event, the recurrence risk is not high compared to the general population. There has been no evidence found that indicates non-disjunction occurs more often in a particular family.

As illustrated by the risk factors above, perioperative hypoxia is a multifactorial problem. Amidst these risk factors it may be difficult to pinpoint the optic nerve’s threshold for cell death, and the exact contribution of each factor.

Low blood pressure and anemia are cited as perioperative complications in nearly all reports of PION, which suggests a causal relationship. However, while low blood pressure and anemia are relatively common in the perioperative setting, PION is exceedingly rare. Spine and cardiac bypass surgeries have the highest estimated incidences of PION, 0.028% and 0.018% respectively, and this is still extremely low. This evidence suggests that optic nerve injury in PION patients is caused by more than just anemia and low blood pressure.

Evidence suggests that the multifactorial origin of perioperative PION involves the risks discussed above and perhaps other unknown factors. Current review articles of PION propose that vascular autoregulatory dysfunction and anatomic variation are under-investigated subjects that may contribute to patient-specific susceptibility.

This syndrome is predominantly found in young women, but also occurs in children, teenagers and octogenarians.

In mild cases, individuals with XXXY syndrome may lead a relatively good life. These individuals may face difficulties in communicating with others due to their language-based deficits. These deficits may make forming bonds with others difficult, but fulfilling relationships with others are still achievable. Those with higher scores in adaptive functioning are likely to have higher quality of life because they can be independent.

Functional neurological symptom disorder can mimic many other conditions. Some alternative diagnoses for FND include:

- Hemiplegic migraine

- Multiple sclerosis

- Motor neurone disease

- Parkinson's

- Autoimmune disorders

- Ehlers–Danlos syndrome

- Stroke

- Vitamin B12 deficiency or pernicious anaemia

- Myasthenia gravis

PEHO syndrome is a progressive encephalopathy with edema, hypsarrhythmia and optic atrophy. It is a very rare disease, one of the Finnish heritage diseases, although approximately half of the cases reported so far are not-Finnish and have been described worldwide .

It has been suggested that it may also be present in Australian and American populations.

A mutation in the ZNHIT3 gene - a nuclear zinc finger protein involved in transcriptional regulation and in small nucleolar ribonucleoprotein particle assembly has been shown to be the cause of the Finnish-type of PEHO syndrome. However, the syndrome appear to be genetically heterogeneous and it might reflect an underlying genetic tubulinopathy, with biallelic mutations in the gene PRUNE1 also identified in non-Finnish patients with PEHO syndrome.

Sighted people with non-24 appear to be more rare than blind people with the disorder and the etiology of their circadian disorder is less well understood. At least one case of a sighted person developing non-24 was preceded by head injury; another patient diagnosed with the disorder was later found to have a "large pituitary adenoma that involved the optic chiasma". Thus the problem appears to be neurological. Specifically, it is thought to involve abnormal functioning of the suprachiasmatic nucleus (SCN) in the hypothalamus. Several other cases have been preceded by chronotherapy, a prescribed treatment for delayed sleep phase disorder. "Studies in animals suggest that a hypernyctohemeral syndrome could occur as a physiologic aftereffect of lengthening the sleep–wake cycle with chronotherapy".

According to the American Academy of Sleep Medicine (AASM): "Patients with free-running (FRD) rhythms are thought to reflect a failure of entrainment".

There have been several experimental studies of sighted people with the disorder. McArthur et al. reported treating a sighted patient who "appeared to be subsensitive to bright light". In other words, the brain (or the retina) does not react normally to light (people with the disorder may or may not, however, be unusually "subjectively" sensitive to light; one study found that they were more sensitive than the control group.) In 2002 Uchiyama et al. examined five sighted non-24 patients who showed, during the study, a sleep–wake cycle averaging 25.12 hours. That is appreciably longer than the 24.02-hour average shown by the control subjects in that study, which was near the average innate cycle for healthy adults of all ages: the 24.18 hours found by Charles Czeisler. The literature usually refers to a "one to two hour" delay per 24-hour day (i.e. a 25- to 26-hour cycle).

Uchiyama et al. had earlier determined that sighted non-24 patients' minimum core body temperature occurs much earlier in the sleep episode than the normal two hours before awakening. They suggest that the long interval between the temperature trough and awakening makes illumination upon awakening virtually ineffective, as per the phase response curve (PRC) for light.

In their clinical review in 2007, Okawa and Uchiyama reported that people with Non-24 have a mean habitual sleep duration of nine to ten hours and that their circadian periods average 24.8 hours.

Hospitalization may be necessary during the acute phase of symptoms, and psychiatric care if the patient is a danger to self or others. A neurological consult is advised to rule out any organic cause.

A wide range of factors have been identified as being predictive of PCS, including low socioeconomic status, previous mTBI, a serious associated injury, headaches, an ongoing court case, and female gender. Being older than 40 and being female have also been identified as being predictive of a diagnosis of PCS, and women tend to report more severe symptoms. In addition, the development of PCS can be predicted by having a history of alcohol abuse, low cognitive abilities before the injury, a personality disorder, or a medical illness not related to the injury. PCS is also more prevalent in people with a history of psychiatric conditions such as clinical depression or anxiety before the injury.

Mild brain injury-related factors that increase the risk for persisting post-concussion symptoms include an injury associated with acute headache, dizziness, or nausea; an acute Glasgow Coma Score of 13 or 14; and suffering another head injury before recovering from the first. The risk for developing PCS also appears to be increased in people who have traumatic memories of the injury or expect to be disabled by the injury.

Functional neurological disorder is a common problem, with estimates suggesting that up to a third of neurology outpatients having functional symptoms. In Scotland, around 5000 new cases of FND are diagnosed annually. Furthermore, non-epileptic seizures account for 1 in 7 referrals to neurologists after an initial seizure, and functional weakness has a similar prevalence to multiple sclerosis.

Functional somatic syndromes may occur in 6 to 36% of the population.

This syndrome appears to be inherited in an autosomal dominant fashion.

Molecular analyses suggest that the causative mutations cause a truncation of the protein. These mutations result in the loss of PEST sequence in the protein. This loss is associated with a prolonged half life of the protein.

Mutations in Notch 3 were found to be associated with this syndrome.

Currently, purine replacement via S-adenosylmethionine (SAM) supplementation in people with Arts syndrome appears to improve their condition. This suggests that SAM supplementation can alleviate symptoms of PRPS1 deficient patients by replacing purine nucleotides and open new avenues of therapeutic intervention. Other non-clinical treatment options include educational programs tailored to their individual needs. Sensorineural hearing loss has been treated with cochlear implantation with good results. Ataxia and visual impairment from optic atrophy are treated in a routine manner. Routine immunizations against common childhood infections and annual influenza immunization can also help prevent any secondary infections from occurring.

Regular neuropsychological, audiologic, and ophthalmologic examinations are also recommended.

Carrier testing for at-risk relatives and prenatal testing for pregnancies at increased risk are possible if the disease-causing mutation in the family is known.

NPCA is a syndrome and can have diverse causes. It has a genetic basis and inheritance is considered to be autosomal recessive. However, autosomal dominant variety has also been reported. There may be familial balanced translocation t(8;20)(p22;q13) involved.

The lateral meningocele syndrome is a very rare skeletal disorder with facial anomalies, hypotonia and meningocele-related neurologic dysfunction.