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.

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

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.

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.

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.

Arts syndrome should be included in the differential diagnosis of infantile hypotonia and weakness aggravated by recurrent infection with a family history of X-linked inheritance. Sequence analysis of PRPS1, the only gene associated with Arts syndrome, has detected mutations in both kindreds reported to date. Arts syndrome patients were also found to have reduced levels of hypoxanthine levels in urine and uric acid levels in the serum. In vitro, PRS-1 activity was reduced in erythrocytes and fibroblasts.

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).

Historically, misdiagnosis rates have been high due to the complex nature of the disorder although some research now indicates that misdiagnosis may be reducing.

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 diagnosis of a functional neurological disorder is dependent on positive features from the history and examination.

Patients with functional movement disorders and limb weakness may experience symptom onset triggered by an episode of acute pain, a physical injury or physical trauma. They may also experience symptoms when faced with a psychological stressor, but this isn't the case for most patients. Patients with functional neurological disorders are more likely to have a history of another illness such as irritable bowel syndrome, chronic pelvic pain or fibromyalgia but this cannot be used to make a diagnosis.

FND does not show up on blood tests or structural brain imaging such as MRI or CT scanning. However, this is also the case for many other neurological conditions so negative investigations should not be used alone to make the diagnosis. FND can, however, occur alongside other neurological diseases and tests may show non-specific abnormalities which cause confusion for doctors and patients.

The disorder can be considered very likely in a totally blind person with periodic insomnia and daytime sleepiness, although other causes for these common symptoms need to be ruled out. In the research setting, the diagnosis can be confirmed, and the length of the free-running circadian cycle can be ascertained, by periodic assessment of circadian marker rhythms, such as the core body temperature rhythm, the timing of melatonin secretion, or by analyzing the pattern of the sleep–wake schedule using actigraphy. Most recent research has used serial measurements of melatonin metabolites in urine or melatonin concentrations in saliva. These assays are not currently available for routine clinical use.

Individuals with a history of high blood pressure, diabetes, and smoking are most susceptible to PION as they have a compromised system of blood vessel autoregulation. Hence, extra efforts may need to be taken for them in the form of careful or staged surgery or the controlling the anemia from blood loss (by administration of blood transfusions), and the careful maintenance of their blood pressure.

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.

Since 1979, the disorder has been recognized by the American Academy of Sleep Medicine:

- "Diagnostic Classification of Sleep and Arousal Disorders" (DCSAD), 1979: Non-24-Hour Sleep–Wake Syndrome; code C.2.d

- "The International Classification of Sleep Disorders", 1st & Revised eds. (ICSD), 1990, 1997: Non-24-Hour Sleep–Wake Syndrome (or Non-24-Hour Sleep–Wake Disorder); code 780.55-2

- "The International Classification of Sleep Disorders", 2nd ed. (ICSD-2), 2005: Non-24-Hour Sleep–Wake Syndrome (alternatively, Non-24-Hour Sleep–Wake Disorder); code 780.55-2

Since 2005, the disorder has been recognized by name in the U.S. National Center for Health Statistics and the U.S. Centers for Medicare and Medicaid Services in their adaptation and extension of the WHO's "International Statistical Classification of Diseases and Related Health Problems" (ICD):

- ICD-9-CM: Circadian rhythm sleep disorder, free-running type; code 327.34 became effective in October 2005. Prior to the introduction of this code, the nonspecific code 307.45, Circadian rhythm sleep disorder of nonorganic origin, was available, and as of 2014 remains the code recommended by the DSM-5.

- ICD-10-CM: Circadian rhythm sleep disorder, free running type; code G47.24 is due to take effect October 1, 2014.

Since 2013, the disorder has been recognized by the American Psychiatric Association:

- DSM-5, 2013: Circadian rhythm sleep–wake disorders, Non-24-hour sleep–wake type; ICD-9-CM code 307.45 is recommended (no acknowledgment of 327.34 is made), and ICD-10-CM code G47.24 is recommended when it goes into effect.

Once visual loss has occurred, it becomes more problematic, but there are reports of recovered vision if blood transfusions and agents that raise blood pressure are administered within hours.

Neuroimaging like MRI is important. However, there was considerable intrafamilial variability regarding neuroimaging, with some individuals showing normal MRI findings. Early individual prognosis of such autosomal recessive cerebellar ataxias is not possible from early developmental milestones, neurological signs, or neuroimaging.

According to the DSM-IV-TR, which classifies Ganser syndrome as a dissociative disorder, it is "the giving of approximate answers to questions (e.g. '2 plus 2 equals 5' when not associated with dissociative amnesia or dissociative fugue)."

Diagnosing Ganser syndrome is very challenging, because some measure of dishonesty is involved and because it is very rare.

Usually when giving wrong answers, they are only slightly off, showing that the individual understood the question. For instance, when asked how many legs a horse has they might say, "five." Although subjects appear confused in their answers, in other respects they appear to understand their surroundings.

Diagnosis of 48, XXXY is usually done by a standard karyotype. A karyotype is a chromosomal analysis in which a full set of chromosomes can be seen for an individual. The presence of the additional 2 X chromosomes on the karyotype are indicative of XXXY syndrome.

Another way to diagnosis 48, XXXY is by chromosomal microarray showing the presence of extra X chromosomes. Chromosomal microarray (CMA) is used to detect extra or missing chromosomal segments or whole chromosomes. CMA uses microchip-based testing to analyze many pieces of DNA. Males with 48, XXXY are diagnosed anywhere from before birth to adulthood as a result of the range in the severity of symptoms. The age range at diagnosis is likely due to the fact that XXXY is a rare syndrome, and does not cause as extreme phenotypes as other variants of Klinefelter syndrome (such as XXXXY).

Diagnostic testing could also be done via blood samples. Elevated levels of follicle stimulating hormone, luteinizing hormone, and low levels of testosterone can be indicative of this syndrome.

SPS is diagnosed by evaluating clinical findings and excluding other conditions. There is no specific laboratory test that confirms its presence. Underdiagnosis and misdiagnosis are common.

The presence of antibodies against GAD is the best indication of the condition that can be detected by blood and cerebrospinal fluid (CSF) testing. Anti-GAD65 is found in about 80 percent of SPS patients. Anti-thyroid, anti-intrinsic factor, anti-nuclear, anti-RNP, and anti-gliadin are also often present in blood tests. Electromyography (EMG) demonstrates involuntary motor unit firing in SPS patients. EMG can confirm the diagnosis by noting spasms in distant muscles as a result of subnoxious stimulation of cutaneous or mixed nerves. Responsiveness to diazepam helps confirm that the patient is suffering from SPS, as this decreases stiffness and motor unit potential firing.

The same general criteria are used to diagnose paraneoplastic SPS as the normal form of the condition. Once SPS is diagnosed, poor response to conventional therapies and the presence of cancer indicate that it may be paraneoplastic. CT scans are indicated for SPS patients who respond poorly to therapy to determine if this is the case.

A variety of conditions have similar symptoms to SPS, including myelopathies, dystonias, spinocerebellar degenerations, primary lateral sclerosis, neuromyotonia, and some psychogenic disorders. Tetanus, neuroleptic malignant syndrome, malignant hyperpyrexia, chronic spinal interneuronitis, serotonin syndrome, Multiple sclerosis, Parkinson's disease, and Isaacs syndrome should also be excluded.

Patients' fears and phobias often incorrectly lead doctors to think their symptoms are psychogenic, and they are sometimes suspected of malingering. It takes an average of six years after the onset of symptoms before the disease is diagnosed.

The International Statistical Classification of Diseases and Related Health Problems (ICD), maintained by the World Health Organization, does not recognize multiple chemical sensitivity or environmental sensitivity as a valid diagnosis. The Australian Department of Health recognizes that sometimes debilitating symptoms are attributed to MCS but notes that diagnosis, treatment, and any underlying mechanism remain uncertain. The German Institute for Medical Documentation and Information recognizes MCS as a physical disease and is subsequentially recognized in Austria. The American Medical Association does not recognize MCS as an organic disease because of the lack of scientific evidence supporting a cause-and-effect relationship between very low level exposure and the symptoms of MCS. The American Academy of Allergy, Asthma, and Immunology, the California Medical Association, the American College of Physicians, and the International Society of Regulatory Toxicology and Pharmacology also do not recognize MCS. The US Occupational Safety and Health Administration (OSHA) indicates that MCS is highly controversial and that there is insufficient scientific evidence to explain the relationship between the suggested causes of MCS and its symptoms. OSHA recommends evaluation by a physician knowledgeable of the symptoms presented.

In most instances, stating categorically that an individual is malingering requires an explicit admission by that individual. Legally the term may be considered prejudicial and excluded on that basis. No current research exists regarding the frequency, behaviour or detection of successful malingerers. No neuropsychological inventories exist that can be used to conclusively determine if a patient is malingering, or to exclude a determination of malingering. Genuine neurological and psychiatric conditions may return false positives. Testing inventories cannot distinguish between exaggeration and fabrication. Psychological inventories rely on naivety. Criminally, an assessment may lead to punishment enhancement, and medically, to denial of future treatment. The DSM-V criteria faces scrutiny for providing poor guidelines. As such physicians ultimately rely on their intuition and gut feeling for any assessment, which is subject to prejudice and cognitive dissonance, and which has been shown to be unreliable in synthetic tests.

Malingering presumes an exhaustive diagnostic procedure has been performed. Exhaustive diagnostics are neither practical nor economically viable or judged to be in the best interests of the patient's health. Radiological and invasive exploratory procedures can be necessary for an accurate diagnosis yet pose a health risk to the patient. Radiographic diagnostics expose the patient to radiation and surgical diagnostic procedures can carry a high risk of complications and mortality, such as a lumbar puncture, the only reliable diagnostic procedure for diagnosing rare terminal forms of parasitization, which the CDC reports as only being diagnosed "post mortem" 75% of the time. A physician invariably faces limitations in the realms of resources, time and liability. Because an assessment, formal or informal, of malingering ceases the medical process, it may seem an attractive option for the physician and help them to cope with cognitive dissonance over their failure to effectively diagnose and treat a patient within constraints.

Patients with unresolved illness may be adversarial towards physicians, attempting to game the triage system in order to receive specialist care. Such cases fit the criteria for malingering, yet the patient is still in need of medical care.

For example, in a gatekeeper system, primary care physicians may restrict the availability of HIV testing to only patients who report high risk activity. A patient may then falsely report sexual and/or drug history and/or symptoms in order to elevate priority which can then go on to serve as diagnostically relevant history for an inaccurate path of further diagnosis.

Medical practitioners often believe that they can detect deception. In two studies, experienced medical practitioners including psychiatrists failed to perform better than chance when asked to detect lying and simulated patients. In 12 other studies, detection rates of simulated patients ranged between 0 and 25%. It's impossible to detect malingering from a clinical perspective.

In response to a WHO call for papers at the 5th Paris Appeal Congress of Environmental Idiopathic Intolerance conference that took place in Belgium on the 18th of May, a report that was generally supportive quoted a number of international practitioners. This was provisionally accepted by the Spanish health ministry, and later found proven by a judge in the case of a plumber in the Province of Castellón

MCS is a diagnosis of exclusion, and the first step in diagnosing a potential MCS sufferer is to identify and treat all other conditions which are present and which often explain the reported symptoms. For example, depression, allergy, thyroid disorders, orthostatic syndromes, lupus, hypercalcemia, and anxiety need to be carefully evaluated and, if present, properly treated. The "gold standard" procedure for identifying a person who has MCS is to test response to the random introduction of chemicals the patient has self-identified as relevant. This may be done in a carefully designed challenge booth to eliminate the possibility of contaminants in the room. Chemicals and controls, sometimes called prompts, are introduced in a random method, usually scent-masked. The test subject does not know when a prompt is being given. Objective and subjective responses are measured. Objective measures, such as the galvanic skin response indicate psychological arousal, such as fear, anxiety, or anger. Subjective responses include patient self-reports. A diagnosis of MCS can only be justified when the subject cannot consciously distinguish between chemicals and controls, and when responses are consistently present with exposure to chemicals and consistently absent when prompted by a control.

A 1999 consensus statement recommends that MCS be diagnosed according to six standardized criteria:

1. Symptoms are reproducible with repeated (chemical) exposures

2. The condition has persisted for a significant period of time

3. Low levels of exposure (lower than previously or commonly tolerated) result in manifestations of the syndrome ("i.e." increased sensitivity)

4. The symptoms improve or resolve completely when the triggering chemicals are removed

5. Responses often occur to multiple chemically unrelated substances

6. Symptoms involve multiple-organ symptoms (runny nose, itchy eyes, headache, scratchy throat, ear ache, scalp pain, mental confusion or sleepiness, palpitations of the heart, upset stomach, nausea and/or diarrhea, abdominal cramping, aching joints).

Treatments exist for the various symptoms associated with XXXY syndrome. Testosterone therapy, which is giving affected individuals doses of testosterone on a regular basis, has been shown to reduce aggressive behavior in these patients. But, this therapy has also been associated with negative side effects: worsening of behavior, and osteoporosis. Not all individuals are applicable for testosterone therapy, as the best results are often achieved when dosage begins at the initiation of puberty, and these individuals are often diagnosed at a later age, or not at all. Testosterone therapy has been shown to have no positive effect on fertility.

Consideration of the psychological phenotype of individuals with XXXY should be taken into account when treating these patients, because these traits affect compliance with treatments. When caught early, Taurodontism can be treated with a root canal and is often successful. Appropriate planning to avoid Taurodontism is possible, but this syndrome must be diagnosed early, which is not common. Taurodontism can often be detected as a symptom of XXXY syndrome before other characteristics develop, and can be an early indicator for it. Surgical treatments to correct joint problems, such as hip dysplasia are common, and are often successful alongside physiotherapy.

Those with XXXY syndrome can also attend speech therapy. This form of therapy helps patients to understand and produce more complex language. Those with XXXY syndrome tend to experience more severe speech delays, so this form of treatment can be very beneficial to them, and can help them to communicate better with other people.

Since hypotonia is common in those with this syndrome, physical therapy can also be helpful. This form of therapy may help these individuals develop muscle tone, and increase balance and coordination.

Some features are more or less likely to suggest PNES but they are not conclusive and should be considered within the broader clinical picture. Features that are common in PNES but rarer in epilepsy include: biting the tip of the tongue, seizures lasting more than 2 minutes (easiest factor to distinguish), seizures having a gradual onset, a fluctuating course of disease severity, the eyes being closed during a seizure, and side to side head movements. Features that are uncommon in PNES include automatisms (automatic complex movements during the seizure), severe tongue biting, biting the inside of the mouth, and incontinence.

If a patient with suspected PNES has an episode during a clinical examination, there are a number of signs that can be elicited to help support or refute the diagnosis of PNES. Compared to patients with epilepsy, patients with PNES will tend to resist having their eyes forced open (if they are closed during the seizure), will stop their hands from hitting their own face if the hand is dropped over the head, and will fixate their eyes in a way suggesting an absence of neurological interference. Mellers et al. warn that such tests are neither conclusive nor impossible for a determined patient with factitious disorder to "pass" through faking convincingly.

Once ACNES is considered based on the patient's history, the diagnosis can be made via a thorough physical examination: looking for a painful spot, which worsens by tensing the abdominal muscles with lifting the head and straightened legs (Carnett's sign). Almost always, a small area of maximal pain is covered by a larger area of altered skin sensibility with somatosensory disturbances such as hypoesthesia as well as hyperesthesia or hyperalgesia and change of cool perception. Pinching the skin between thumb and index finger is extremely painful compared to the opposite non-involved side.

Confirmation of a diagnosis of ACNES is warranted using an abdominal wall infiltration with a local anesthetic agent near the painful spot.