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.

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).

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.

Exploding head syndrome is classified as a parasomnia and a sleep-related dissociative disorder by the 2005 International Classification of Sleep Disorders and is an unusual type of auditory hallucination in that it occurs in people who are not fully awake.

Exploding head syndrome (EHS), alternately termed episodic cranial sensory shock, is a benign condition in which a person hears loud "imagined" noises (such as a bomb exploding, a gunshot, or a cymbal crash) or experiences an explosive feeling when falling asleep or waking up. These noises have a sudden onset, are typically brief in duration, and are often jarring for the person. Neither the cause nor the mechanism is known. Though harmless in and of themselves, episodes have been known to create distress or impairment in the lives of individuals.

Symptoms reported by patients forced into a 24-hour schedule are similar to those of sleep deprivation and can include:

- Apraxia including ideational apraxia, ideomotor apraxia, kinetic apraxia, limb apraxia, verbal apraxia

- Cognitive dysfunction

- Difficulties concentrating

- Confusion

- Depressed mood

- Diarrhea

- Extreme nausea

- Extreme fatigue

- Hair loss

- Headaches

- Impaired balance

- Photosensitivity

- Joint pain

- Loss of muscle coordination (ataxia)

- Menstrual irregularities

- Muscle pain

- Suicidal thoughts

- Weight gain

- Hallucinations

Facial features found in this syndrome include

- dolichocephaly

- hypertelorism

- ptosis

- microretrognathia

- high arched palate

- long flat philtrum

- low set ears

Non facial features of this syndrome include

- hyperextensibility

- hypotonia

- lateral meningoceles

The lateral meningocoles are a common finding in this syndrome. They may be associated with neurological abnormalities and result in bladder dysfunction and neuropathy.

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.

The original description by Sigbert Josef Maria Ganser in 1898 pointed out their hysterical twilight state. They may also describe hallucinations which are usually more than those in schizophrenia. They may also have disorders of sensation similar to those in conversion disorder. They may be inattentive or drowsy.

Some workers believe there is a genuine psychosis underlying this, others believe it is a dissociative disorder, while still others believe it is the result of malingering. Over the years, opinions have seemed to move from the last view more towards the first.

Ganser syndrome is currently classified under dissociative disorders, to which it moved in the DSM IV from the factitious disorders.

There are a great number of symptoms experienced by those with a functional neurological disorder. It is important to note that the symptoms experienced by those with an FND are very real , and should not be confused with malingering, factitious disorders, or Munchausen syndrome. At the same time, the origin of symptoms is complex since it can be associated with physical injury, severe psychological trauma (conversion disorder), and idiopathic neurological dysfunction. The core symptoms are those of motor or sensory function or episodes of altered awareness

- Limb weakness or paralysis

- Blackouts (also called dissociative or non-epileptic seizures/attacks) – these may look like epileptic seizures or faints

- Movement disorders including tremors, dystonia (spasms), myoclonus (jerky movements)

- Visual symptoms including loss of vision or double vision

- Speech symptoms including dysphonia (whispering speech), slurred or stuttering speech

- Sensory disturbance including hemisensory syndrome (altered sensation down one side of the body)

It has been estimated that non-24 occurs in more than half of all people who are totally blind. The disorder can occur at any age, from birth onwards. It generally follows shortly after loss or removal of a person’s eyes, as the photosensitive ganglion cells in the retina are also removed.

Without light to the retina, the suprachiasmatic nucleus (SCN), located in the hypothalamus, is not cued each day to synchronize the circadian rhythm to the 24-hour social day, resulting in non-24 for many totally blind individuals. Non-24 is rare among visually impaired patients who retain at least some light perception. Researchers have found that even minimal light exposure at night can affect the body clock.

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.

Functional neurological disorders are a common problem, and are the second most common reason for a neurological outpatient visit after headache/migraine. Dissociative (non-epileptic) seizures account for about 1 in 7 referrals to neurologists after an initial seizure, and functional weakness has a similar prevalence to multiple sclerosis.

Males with 48, XXXY can have average or tall stature, which becomes more prominent in adulthood. Facial dysmorphism is common in males with 48, XXXY and can include increased distance between the eyes (hypertelorism), skin folds of the upper eyelid (epicanthal folds), up-slanting opening between the eyelids (palpebral fissures) and hooded eyelids. Other physical features include the fifth finger or "pinky" to be bent inwards towards the fourth finger (clinodactyly), short nail beds, flat feet, double jointedness (hyperextensibility) and prominent elbows with cubitus varus where the arm rests closer to the body. Musculoskeletal features may include congentical elbow dislocation and the limited ability of the feet to roll inwards while walking and upon landing. Micropenis is another common symptom of this syndrome.

Individuals affected with XXXY are also prone to developing Taurodontism, which often presents early in life, and can be an early indicator of XXY syndrome. Those with this syndrome are also prone to hip dysplasia, and other joint abnormalities. An individual’s symptoms vary due to differing androgen deficiencies, and also with alter with age. Prepubescent boys with XXXY syndrome may not differ in physical appearance from a child without the syndrome. This is likely because androgen levels do not differ among pre-pubescent boys, but a difference does arise as puberty progresses. Those with XXXY syndrome may also experience feminine distribution of adipose tissue, and gynecomastia may also be present. Tall stature is more likely to appear in adolescence, when androgen levels begin to differ between those with XXXY syndrome and those that do not have it.

Patients with stiff person syndrome (SPS) suffer progressive stiffness in their truncal muscles, which become rigid and stiff because the lumbar and abdominal muscles engage in constant contractions. Initially, stiffness occurs in the thoracolumbar paraspinal and

abdominal muscles. It later affects the proximal leg and abdominal wall muscles. The stiffness leads to a change in posture, and patients develop a rigid gait. Persistent lumbar hyperlordosis often occurs as it progresses. The muscle stiffness initially fluctuates, sometimes for days or weeks, but eventually begins to consistently impair mobility. As the disease progresses, patients sometimes become unable to walk or bend. Chronic pain is common and worsens over time but sometimes acute pain occurs as well. Stress, cold weather, and infections lead to an increase in symptoms, and sleep decreases them.

SPS patients suffer superimposed spasms and extreme sensitivity to touch and sound. These spasms primarily occur in the proximal limb and axial muscles. There are co-contractions of agonist and antagonist muscles. Spasms usually last for minutes and can recur over hours. Attacks of spasms are unpredictable and are often caused by fast movements, emotional distress, or sudden sounds or touches. In rare cases, facial muscles, hands, feet, and the chest can be affected and unusual eye movements and vertigo occur. There are brisk stretch reflexes and clonus occurs in patients. Late in the disease's progression, hypnagogic myoclonus can occur. Tachycardia and hypertension are sometimes also present.

Because of the spasms, patients may become increasingly fearful, require assistance, and lose the ability to work, leading to depression, anxiety, and phobias, including agoraphobia and dromophobia. Most patients are psychologically normal and respond reasonably to their situations.

Paraneoplastic SPS tends to affect the neck and arms more than other variations. It progresses very quickly, is more painful, and is more likely to include distal pain than classic SPS. Patients with paraneoplastic SPS generally lack other autoimmune issues but may have other paraneoplastic conditions.

Stiff-limb syndrome is a variant of SPS. This syndrome develops into full SPS about 25 percent of the time. Stiffness and spasms are usually limited to the legs and hyperlordoisis generally does not occur. The stiffness begins in one limb and remains most prominent there. Sphincter and brainstem issues often occur with stiff-limb syndrome. Progressive encephalomyelitis with rigidity, another variant of the condition, includes symptoms of SPS with brainstem issues and autonomic disturbances. It involves polio-encephalomyelitis in the spine and brainstem. There is cerebellar and brainstem involvement. In some cases, the limbic system is affected, as well. Most patients have upper motoneuron issues and autonomic disturbances. Jerking man syndrome or jerking SPS is another subtype of the condition. It begins like classical SPS and progresses for several years, up to 14 in some cases. It is then distinguished by the development of myoclonus as well as seizures and ataxia in some cases.

A-PION most commonly affects Caucasian women, with an average age of 73. At onset vision loss is unilateral, but without treatment it rapidly progresses to involve both eyes. Vision loss is usually severe, ranging from counting fingers to no light perception. Associated symptoms are jaw pain exacerbated by chewing, scalp tenderness, shoulder and hip pain, headache and fatigue.

Vision loss is usually apparent upon waking from general anesthesia. Signs observable to a bystander include long surgery duration and facial swelling. Vision loss is usually bilateral and severe, ranging from counting fingers to no light perception.

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

Neurological effects are believed to be more severe as the number of extra X chromosomes increases; a male with 48, XXXY is likely to have more severe symptoms than a male with Klinefelter syndrome. Developmental delays are common in infancy and childhood. Expected symptoms include speech delays, motor delays, and hypotonia (lack of muscle tone), also known as floppy baby syndrome.Individuals with XXXY syndrome exhibit cognitive and behavioral problems.

Patients typically show altered adaptive behavior, which is the ability of an individual to demonstrate essential living skills, including: social skills, community living, safety, functional use of academic skills and self-care. People with XXXY syndrome were found to score significantly less in the domains of daily living skills and communication compared to XXYY, and XXY individuals. This means that they typically demonstrate little ability in the domains of self-care, social skills, safety, application of academic skills, and responsibility.

Individuals with this syndrome also experience emotional symptoms such as anxiety symptoms, obsessive-compulsive behaviors, behavioral dysregulational and emotional immaturity. People with this syndrome typically have an IQ in the range of 40-60, where the average IQ range is 95-110. They also experience language-based learning disabilities that can affect their communication with others. Those with XXXY syndrome tend to display less externalizing and internalizing behaviors compared to those with 48, XXYY syndrome, which may have a positive effect on their social functioning. These individuals may also have increased vulnerability for autistic features. Changes in testosterone as well as androgen deficits may contribute to these individuals’ social behaviors that put them at increased risk for autistic features.

Affected individuals typically experience limited relief from standard pain relieving medication, with the exception of some neuroleptic agents. Patients frequently experience 'pseudovisceral' phenomena or symptoms of altered autonomic nervous system function including nausea, bloating, abdominal swelling, loss of appetite with consecutively lowered body weight or an altered defecation process.

Pain is typically related to tensing the abdominal wall muscles, so any type of movement is prone to aggravate pain. Lying quietly can be the least painful position. Most patients report that they cannot sleep on the painful side.

Males show more serious symptoms than females affected by this disorder.

The symptoms for males are:

1. Profound sensorineural hearing loss i.e, a complete or almost complete loss of hearing caused by abnormalities in the inner ear.

2. Weak muscle tone - Hypotonia.

3. Impaired muscle coordination - Ataxia.

4. Developmental delay.

5. Intellecual disability.

6. Vision loss caused by optic nerve atrophy in early childhood.

7. Peripheral neuropathy.

8. Recurrent infections, especially in the respiratory system.

9. Muscle weakness caused by recurrent infections.

Symptoms for females:

Very rarely seen hearing loss that begins in adulthood (age > 20 years) combined with ataxia and neuropathy. Optic atrophy and retinitis pigmentosa observed in some cases too.

Stiff person syndrome (SPS), also known as stiff man syndrome (SMS), is a rare neurologic disorder of unclear cause characterized by progressive rigidity and stiffness. The stiffness primarily affects the truncal muscles and is superimposed by spasms, resulting in postural deformities. Chronic pain, impaired mobility, and lumbar hyperlordosis are common symptoms.

SPS occurs in about one in a million people and is most commonly found in middle-aged people. A small minority of patients have the paraneoplastic variety of the condition. Variants of the condition, such as stiff-limb syndrome which primarily affects a specific limb, are often seen.

SPS was first described in 1956. Diagnostic criteria were proposed in the 1960s and refined two decades later. In the 1990s and 2000s the roles of antibodies in the condition became more clear. SPS patients generally have GAD antibodies, which seldom occur in the general population. In addition to blood to tests for GAD, electromyography tests can help confirm the condition's presence.

Benzodiazepine-class drugs are the most common treatment; they are used for symptom relief from stiffness. Other common treatments include Baclofen, intravenous immunoglobin and rituximab. There has been limited but encouraging success with stem-cell treatment.

Jeavons syndrome is a type of epilepsy. It is one of the most distinctive reflex syndromes of idiopathic generalized epilepsy characterized by the triad of eyelid myoclonia with and without absences, eye-closure-induced seizures, EEG paroxysms, or both, and photosensitivity. Eyelid myoclonia with or without absences is a form of epileptic seizure manifesting with myoclonic jerks of the eyelids with or without a brief absence. These are mainly precipitated by closing of the eyes and lights. Eyelid myoclonia is the defining seizure type of Jeavons syndrome.

Anterior cutaneous nerve entrapment syndrome (ACNES) is a nerve entrapment condition that causes chronic pain of the abdominal wall. It occurs when nerve endings of the lower thoracic intercostal nerves (7–12) are 'entrapped' in abdominal muscles, causing a severe localized nerve (neuropathic) pain that is usually experienced at the front of the abdomen.

ACNES syndrome is frequently overlooked and unrecognized, although the incidence is estimated to be 1:2000 patients.

The relative unfamiliarity with this condition often leads to significant diagnostic delays and misdiagnoses, often resulting in unnecessary diagnostic interventions and futile procedures. Physicians often misdiagnose ACNES as irritable bowel syndrome or "functional disorders", as symptoms of the condition are not dispositive.